Category Archive Cardiac & Respiratory Disease

Spirometry – Indications, Contraindications, Procedure

Spirometry is a simple test used to help diagnose and monitor certain lung conditions by measuring how much air you can breathe out in one forced breath. It’s carried out using a device called a spirometer, which is a small machine attached by a cable to a mouthpiece.

Spirometry is one of the most commonly used approaches to test pulmonary function. It measures the volume of exhaled air vs. time. This activity highlights its role in the evaluation of pulmonary disease by the interprofessional team.

Spirometry is one of the most readily available and useful tests for pulmonary function. It measures the volume of air exhaled at specific time points during complete exhalation by force, which is preceded by a maximal inhalation.

The most important variables reported include total exhaled volume, known as the forced vital capacity (FVC), the volume exhaled in the first second, known as the forced expiratory volume in one second (FEV1), and their ratio (FEV1/FVC). These results are represented on a graph as volumes and combinations of these volumes termed capacities and can be used as a diagnostic tool, as a means to monitor patients with pulmonary diseases and to improve the rate of smoking cessation according to some reports.

Anatomy and Physiology

Lungs provide life-sustaining gas exchange by way of introducing oxygen for metabolism and eliminating the by-product carbon dioxide. Air-inspired will pass through the oropharynx to the trachea, which is a membranous tube covered by cartilage bifurcating at the carina as two bronchi at the level of C6. After passing the trachea, the air enters the right and left bronchi, which divide to give several million terminal bronchioles that end in alveoli. The alveoli and surrounding vessels provide a surface where the gas exchange takes place.

Indications

Apart from being a key diagnostic test for asthma and chronic obstructive pulmonary disease, spirometry in indicated in several other places, as listed below:

Diagnostic Indications

  • Evaluation of the signs and symptoms of a patient or their abnormal investigations and lab tests
  • Evaluation of the effect a certain disease has on pulmonary function
  • Screening and early detection of individuals who are at risk of pulmonary disease
  • Assessing surgical patients for preoperative risk
  • Assessing the severity and the prognosis of pulmonary disease

Monitoring Indications

  • Assessment of the efficiency of a therapeutic intervention such as bronchodilator therapy
  • Describing the course and progression of a disease that is affecting pulmonary function such as interstitial lung disease or obstructive lung disease
  • Monitoring pulmonary function in individuals with high-risk jobs
  • Sampling data that can be used for epidemiologic surveys

Spirometry is indicated for the following reasons

  • to diagnose or manage asthma[rx][rx][rx]
  • to detect respiratory disease in patients presenting with symptoms of breathlessness, and to distinguish respiratory from cardiac disease as the cause[rx]
  • to measure bronchial responsiveness in patients suspected of having asthma[rx]
  • to diagnose and differentiate between obstructive lung disease and restrictive lung disease[rx]
  • to follow the natural history of disease in respiratory conditions[rx]
  • to assess impairment from occupational asthma[rx]
  • to identify those at risk from pulmonary barotrauma while scuba diving[rx]
  • to conduct a pre-operative risk assessment before anesthesia or cardiothoracic surgery[rx]
  • to measure response to treatment of conditions which spirometry detects[5]
  • to diagnose the vocal cord dysfunction.

Contraindications

Spirometry has proved itself as an accessible utility to assess lung function. However, it may not be for every patient, and care must be taken in some cases, where it may be absolutely or relatively contraindicated.

Absolute Contraindications

  • Hemodynamic instability
  • Recent myocardial infarction or acute coronary syndrome
  • Respiratory infection, a recent pneumothorax or a pulmonary embolism
  • A growing or large (>6 cm) aneurysm of the thoracic, abdominal aorta
  • Hemoptysis of acute onset
  • Intracranial hypertension
  • Retinal detachment
  • Hemoptysis of unknown origin
  • Pneumothorax
  • Unstable cardiovascular status (angina, recent myocardial infarction, etc.)
  • Thoracic, abdominal, or cerebral aneurysms
  • Cataracts or recent eye surgery
  • Recent thoracic or abdominal surgery
  • Nausea, vomiting, or acute illness
  • Recent or current viral infection
  • Undiagnosed hypertension

Relative Contraindications

  • Patients who cannot be instructed to use the device properly and are at risk of using the device inappropriately such as children and patients with dementia
  • Conditions that make it difficult to hold the mouthpiece such as facial pain
  • Recent abdominal, thoracic, brain, eye, ear, nose or throat surgeries
  • Hypertensive crisis

Equipment

The first requirement for spirometry is physical space in order for the patient to be positioned comfortably. The minimum space recommended is a 2.5* 3m room with 120 cm side doors.

Spirometers are classified into closed-circuit and open-circuit spirometers. Closed-circuit spirometers are further sub-classified into wet and dry spirometers, which consist of a piston or a bellow acting as an air collecting system and a supported recording system that moves at the desired rate.

Open-circuit spirometers, which are more commonly used at present, do not have an air collecting system and instead measure the airflow, integrate the results, and calculate the volume. The most commonly used open-circuit spirometer is the turbine flow meter, which records the rate at which turbines turn and derives the flow measurement based on proportionality. Pneumotachographs are another example, which measures the airflow by measuring the pressure difference generated as the laminar flow passes through a certain resistance. Hotwire spirometers, in which a hot metal wire is heated, and the air used to cool it is used to calculate the flow, are also an example of open-circuit spirometers. Ultrasound spirometers can be based on any of the aforementioned open-circuit spirometer principles.

The minimum specifications for a spirometer are the ability to measure a volume of 8L with an accuracy of ±3% or ±50ml with a flow measurement range of ±141 and a sensitivity of 200ml/s. It is recommended that the spirometer can record at 15 s of the expiration time for the forced maneuver.

Personnel

The personnel performing the procedure must be familiar with respiratory symptoms and signs. They have to undergo training to understand the technical and physiological background of the tests in order to be competent in performing the techniques of the operation of the device, be able to apply the universal precautions, instruct the patients properly to avoid complications, and act accordingly if any of the complications arise. The personnel should be able to identify responses to therapy, the need for initiating therapy or discontinuing an inefficient one. Continuity of training and periodic retraining is a must for staff in charge of spirometry.

Preparation

All patients must be informed that they must abstain from smoking, physical exercise in the hours before the procedure. Any bronchodilator therapy must also be stopped beforehand.

The procedure must be carefully explained to the patient focusing on the importance of the patient’s cooperation to provide the most accurate results. The patient’s weight and height must be recorded with the patient barefoot and wearing only light clothing. In the case of chest deformities such as kyphoscoliosis, the span should be measured from the tip of one middle finger to the tip of the other middle finger with the hands crossed, and the height can be estimated from the formula: height = span/1.06. The patient’s age must be recorded. The procedure should be performed with the patient sitting upright wearing light clothing and without crossing their legs. Children can perform the test sitting or standing, but the same procedure should be carried out for the same individual every time.

During the procedure, the back must be supported by a backrest and must not lead forward. Dentures have to be removed if they interfere with the procedure. Manual occlusion of the nares with the help of nose clips helps to prevent air leakage through the nasal passages, although it is not mandatory to occlude nasal passages. The calibration of the spirometer has to be confirmed on the day of the test.

Any contraindications or infectious diseases that require special measures will lead to a delay in the procedure.

Patient positioning

Correct measurement posture is as follows.

  • Sit upright: there should be no difference in the amount of air the patient can exhale from a sitting position compared to a standing position as long as they are sitting up straight and there are no restrictions.
  • Feet flat on the floor with legs uncrossed: no use of abdominal muscles for leg position.
  • Loosen tight-fitting clothing: if clothing is too tight, this can give restrictive pictures on spirometry (give lower volumes than are true).
  • Dentures normally left in: it is best to have some structure to the mouth area unless dentures are very loose.
  • Use a chair with arms: when exhaling maximally, patients can become light-headed and possibly sway or faint.

    Infection control

    Hands must be washed between patients. Bacterial–viral filters should be used for all patients and thrown away by the patient at the end of testing. If an infectious patient requires testing, this should be performed at the end of the session and the equipment should be stripped down and sterilized/parts replaced (depending on what is being used) before being used again.

    Technique

    The patient must place the mouthpiece in their mouth, and the technician must ensure that there are no leaks, and the patient is not obstructing the mouthpiece. The procedure is carried out as follows:

    • The patient must breathe in as much air as they can with a pause lasting for less than 1s at the total lung capacity.
    • The mouthpiece is placed just inside the mouth between the teeth, soon after the deep inhalation. The lips should be sealed tightly around the mouthpiece to prevent air leakage. Exhalation should last at least 6 seconds, or as long as advised by the instructor. If only the forced expiratory volume is to be measured, the patient must insert the mouthpiece after performing step 1 and must not breathe from the tube.
    • If any of the maneuvers are incorrectly performed, the technician must stop the patient in order to avoid fatigue and re-explain the procedure to the patient.
    • The procedure is repeated in intervals separated by 1 minute until two matching, and acceptable results are acquired.

    Complications

    The complications of spirometry are fairly limited and will render the procedure as inaccurate or ineffective once they occur. They include:

    • Respiratory alkalosis as a result of hyperventilation
    • Hypoxemia in a patient whose oxygen therapy has been interrupted
    • Chest pain
    • Fatigue
    • Paroxysmal coughing
    • Bronchospasm
    • Dizziness
    • Urinary incontinence
    • Increased intracranial pressure
    • Syncopal symptoms
    Flow-Volume loop showing successful FVC maneuver. Positive values represent expiration, negative values represent inspiration. At the start of the test both flow and volume are equal to zero (representing the volume in the spirometer rather than the lung). The trace moves clockwise for expiration followed by inspiration. After the starting point the curve rapidly mounts to a peak (the peak expiratory flow). (Note the FEV1 value is arbitrary in this graph and just shown for illustrative purposes; these values must be calculated as part of the procedure).
    MeSH D013147
    OPS-301 code 1-712
    Lungvolumes Updated.png
    TLC Total lung capacity: the volume in the lungs at maximal inflation, the sum of VC and RV.
    TV Tidal volume: that volume of air moved into or out of the lungs during quiet breathing (TV indicates a subdivision of the lung; when tidal volume is precisely measured, as in gas exchange calculation, the symbol TV or VT is used.)
    RV Residual volume: the volume of air remaining in the lungs after a maximal exhalation
    ERV Expiratory reserve volume: the maximal volume of air that can be exhaled from the end-expiratory position
    IRV Inspiratory reserve volume: the maximal volume that can be inhaled from the end-inspiratory level
    IC Inspiratory capacity: the sum of IRV and TV
    IVC Inspiratory vital capacity: the maximum volume of air inhaled from the point of maximum expiration
    VC Vital capacity: the volume of air breathed out after the deepest inhalation.
    VT Tidal volume: that volume of air moved into or out of the lungs during quiet breathing (VT indicates a subdivision of the lung; when tidal volume is precisely measured, as in gas exchange calculation, the symbol TV or VT is used.)
    FRC Functional residual capacity: the volume in the lungs at the end-expiratory position
    RV/TLC% Residual volume expressed as a percent of TLC
    VA Alveolar gas volume
    VL The actual volume of the lung including the volume of the conducting airway.
    FVC Forced vital capacity: the determination of the vital capacity from a maximally forced expiratory effort
    FEVt Forced expiratory volume (time): a generic term indicating the volume of air exhaled under forced conditions in the first t seconds
    FEV1 The volume that has been exhaled at the end of the first second of forced expiration
    FIFA Forced expiratory flow related to some portion of the FVC curve; modifiers refer to the amount of FVC already exhaled
    FEFmax The maximum instantaneous flow achieved during an FVC maneuver
    FIF Forced inspiratory flow: (Specific measurement of the forced inspiratory curve is denoted by nomenclature analogous to that for the forced expiratory curve. For example, maximum inspiratory flow is denoted FIFmax. Unless otherwise specified, volume qualifiers indicate the volume inspired from RV at the point of measurement.)
    PEF Peak expiratory flow: The highest forced expiratory flow measured with a peak flow meter
    MVV Maximal voluntary ventilation: volume of air expired in a specified period during repetitive maximal effort

    Pulmonary Function Tests – Indications, Contraindications

    Pulmonary function tests (PFTs) are noninvasive tests that show how well the lungs are working. The tests measure lung volume, capacity, rates of flow, and gas exchange. This information can help your healthcare provider diagnose and decide the treatment of certain lung disorders.

    Pulmonary function tests (PFTs) allow physicians to evaluate the respiratory function of their patients. They are reproducible and accurate. Ultimately, the results of the PFTs are affected by the effort of the patient. PFTs do not provide a specific diagnosis, but together with the history, physical exam, and laboratory data help clinicians reach a diagnosis. PFTs also allow physicians to quantify the severity of the pulmonary disease, follow it up over time, and assess its response to treatment.

    There are 2 types of disorders that cause problems with air moving in and out of the lungs:

    • Obstructive. This is when air has trouble flowing out of the lungs due to airway resistance. This causes a decreased flow of air.
    • Restrictive. This is when the lung tissue and/or chest muscles can’t expand enough. This creates problems with airflow, mostly due to lower lung volumes.

    PFT can be done with 2 methods. These 2 methods may be used together and perform different tests, depending on the information that your healthcare provider is looking for:

    • Spirometry. A spirometer is a device with a mouthpiece hooked up to a small electronic machine.
    • Plethysmography. You sit or stand inside an air-tight box that looks like a short, square telephone booth to do the tests.

    PFT measures

    • Tidal volume (VT). This is the amount of air inhaled or exhaled during normal breathing.
    • Minute volume (MV). This is the total amount of air exhaled per minute.
    • Vital capacity (VC). This is the total volume of air that can be exhaled after inhaling as much as you can.
    • Functional residual capacity (FRC). This is the amount of air left in the lungs after exhaling normally.
    • Residual volume. This is the amount of air left in the lungs after exhaling as much as you can.
    • Total lung capacity. This is the total volume of the lungs when filled with as much air as possible.
    • Forced vital capacity (FVC). This is the amount of air exhaled forcefully and quickly after inhaling as much as you can.
    • Forced expiratory volume (FEV). This is the amount of air that expired during the first, second, and third seconds of the FVC test.
    • Forced expiratory flow (FEF). This is the average rate of flow during the middle half of the FVC test.
    • Peak expiratory flow rate (PEFR). This is the fastest rate that you can force air out of your lungs.
    • Spirometry measures the rate of airflow and estimates lung size. For this test, you will breathe multiple times, with regular and maximal effort, through a tube that is connected to a computer. Some people feel lightheaded or tired from the required breathing effort.
    • Lung volume tests are the most accurate way to measure how much air your lungs can hold. The procedure is similar to spirometry, except that you will be in a small room with clear walls. Some people feel lightheaded or tired from the required breathing effort.
    • Lung diffusion capacity assesses how well oxygen gets into the blood from the air you breathe. For this test, you will breathe in and out through a tube for several minutes without having to breathe intensely. You also may need to have blood drawn to measure the level of hemoglobin in your blood.
    • Pulse oximetry estimates oxygen levels in your blood. For this test, a probe will be placed on your finger or another skin surface such as your ear. It causes no pain and has few or no risks.
    • Arterial blood gas tests directly measure the levels of gases, such as oxygen and carbon dioxide, in your blood. Arterial blood gas tests are usually performed in a hospital, but may be done in a doctor’s office. For this test, blood will be taken from an artery, usually in the wrist where your pulse is measured. You may feel brief pain when the needle is inserted or when a tube attached to the needle fills with blood. It is possible to have bleeding or infection where the needle was inserted.
    • Fractional exhaled nitric oxide tests measure how much nitric oxide is in the air that you exhale. For this test, you will breathe out into a tube that is connected to the portable device. It requires steady but not intense breathing. It has few or no risks.

    Normal values for PFTs vary from person to person. The amount of air inhaled and exhaled in your test results are compared to the average for someone of the same age, height, sex, and race. Results are also compared to any of your previous test results. If you have abnormal PFT measurements or if your results have changed, you may need other tests.

    Why might I need pulmonary function tests?

    There are many different reasons why pulmonary function tests (PFTs) may be done. They are sometimes done in healthy people as part of a routine physical. They are also routinely done in certain types of work environments to ensure employee health (such as graphite factories and coal mines). Or you may have PFTs if your healthcare provider needs help to diagnose you with a health problem such as:

    • Allergies
    • Respiratory infections
    • Trouble breathing from injury to the chest or a recent surgery
    • Chronic lung conditions, such as asthma, bronchiectasis, emphysema, or chronic bronchitis
    • Asbestosis, a lung disease caused by inhaling asbestos fibers
    • Restrictive airway problems from scoliosis, tumors, or inflammation or scarring of the lungs
    • Sarcoidosis, a disease that causes lumps of inflammatory cells around organs, such as the liver, lungs, and spleen
    • Scleroderma, a disease that causes thickening and hardening of connective tissue

    PFTs may be used to check lung function before surgery or other procedures in patients who have lung or heart problems, who are smokers, or who have other health conditions. Another use of PFTs is to assess treatment for asthma, emphysema, and other chronic lung problems. Your healthcare provider may also have other reasons to advise PFTs.

    Procedures

    Spirometry

    Spirometry is a physiological test that measures the ability to inhale and exhale air in relation to time. Spirometry is a screening test of general respiratory health. The main results of spirometry are forced vital capacity (FVC) and forced expiratory volume (FEV). The procedure of spirometry has 3 phases: 1) maximal inspiration; 2) a “blast” of exhalation; 3) continued complete exhalation to the end of the test. There are within-maneuver acceptability and between-maneuver reproducibility criteria for spirometry (Table 2).

    Vital capacity (VC) is the volume of gas expelled from full inspiration to residual volume. The FVC is similar, but the patient is exhaling at maximal speed and effort.

    The FEV is the forced expiratory volume in t seconds from a position of full inspiration. Forced expiratory volume in the first second (FEV)) is used to classify the severity of obstructive lung diseases. The reversibility testing is administered using a bronchodilator (short-acting beta 2-agonist or anticholinergic agent). An increase in either FEV or FVC of 3^12% and 3^200 mL is considered a positive bronchodilator response. A lack of a response does not predict lack of response to bronchodilators. The patient should hold their bronchodilators before the reversibility testing.

    The maximal flow-volume curves are a great asset to detect mild airflow obstruction. There is an inspiratory and expiratory loop.

    Lung Volume

    The key measurement of lung volumes is functional reserve capacity (FRC). Once FRC has been measured, all other volumes can be calculated. FRC is the volume of the amount of gas in the lungs at the end of expiration during tidal breathing. FRC is the sum of expiratory reserve volume (ERV) and residual volume (RV). ERV is the volume of gas maximally exhaled after end-inspiratory tidal breathing. RV is the volume of gas in the airways after a maximal exhalation.

    In addition to RV and ERV, there is tidal volume (TV) and inspiratory reserve volume (IRV). IRV is the volume of gas that can be maximally inhaled from the end-inspiratory tidal breathing. TV is the volume of gas inhaled or exhaled with each breath at rest.

    There are 2 methods to measure lung volumes: body plethysmography and gas dilution methods (nitrogen washout and inert gas dilution). Gas dilution method uses an inert gas (poorly soluble in alveolar blood and lung tissues), either nitrogen or helium. The subject breathes a gas mixture until equilibrium is achieved. The volume and mixture of gas exhaled after the equilibrium have been achieved permit the calculation of FRC. In body plethysmography, the subject sits inside a body box and breathes against a shutter valve. FRC is calculated using Boyle Law (at a given temperature, the product of gas volume and pressure is constant). FRC calculated by body plethysmography is usually larger in subjects with obstructive lung disease and air trapping than FRC calculated using gas dilution methods. Body plethysmography is considered the gold standard for lung volumes measurement.

    Capacities are the sum of 2 or more volumes (Figure 1). TLC is the gold standard for diagnosis of restrictive lung disease. TLC less than 5 percentile of predicted or less than 80% predicted are diagnostic of a restrictive ventilatory defect.

    Diffusion Capacity

    Diffusion studies the diffusion of gases across the alveolar-capillary membranes. Its measurement uses carbon monoxide (CO) to calculate the pulmonary diffusion capacity. The most common method is the standard single-breath D. It is measured in milliliters per minute per mm Hg.

    The factors affecting the D are volume and distribution of ventilation, mixing and diffusion, the composition of the gas, characteristics of the alveolar membrane and lung parenchyma, the volume of alveolar-capillary plasma, concentration, and binding properties of hemoglobin, and gas tensions in blood entering the alveolar capillaries. A detailed list of factors affecting DLCO is listed in Table 3.

    The diffusion capacity depends on multiple factors, and its value should be adjusted. Specific adjustments should be made for hemoglobin, carboxyhemoglobin, and FiO for a correct interpretation. Adjustment for lung volumes is controversial, and further studies are needed.

    The DLCO is interpreted in conjunction with spirometry and lung volumes. Table 3 shows the severity classification for DLCO. For example, high DLCO is associated with asthma, obesity, and intrapulmonary hemorrhage. Normal spirometry and lung volumes with low DLCO can be present in pulmonary vascular diseases, early ILD, or emphysema. An obstructive ventilatory defect with low DLCO suggests emphysema or lymphangiomyomatosis.

    Respiratory Muscle Pressures

    The respiratory muscle strength is assessed with the maximal inspiratory pressure (MIP); also called negative inspiratory force (NIF) and maximal expiratory pressure (MEP). The MIP reveals the strength of the diaphragm and other inspiratory muscles; whereas, the MEP indicates the strength of the abdominal and other expiratory muscles.

    MIP and MEP are measured three times, maximal value is reported. For adults 18 to 65 years old, MIP should be lower than -90 cmHO in men and -70 cmHO in women. In adults older than 65 years old, MIP should be less than -65 cmH2O in men and -45 cmH2O in women. MEP should be higher than 140 cmH2O in men and 90 cmH2O in women. MEP less than 60 cmH2O predicts a weak cough and difficulty clearing secretions.

    Central and Upper Airway Obstruction

    Central or upper airway obstruction (UAO) could occur in the extrathoracic (pharynx, larynx, and the extrathoracic part of the trachea) and intrathoracic airways (intrathoracic trachea and main bronchi). The FEV and/or FVC are not affected by this type of obstruction, but the peak expiratory flow (PEF) can be severely decreased. An FEV/PEF ratio of greater than 8 suggests central or UAO.

    Three maximal and repeatable forced inspiratory and expiratory flow-volume curves are necessary. It is key that efforts, both inspiratory and expiratory are maximal.

    The maximal inspiratory flow is largely decreased with an extrathoracic airway obstruction because there is a negative pressure inside the airways during inspiration. Inspiratory flows are not affected by intrathoracic lesions; the negative pleural pressure maintains the intrathoracic airways open. The maximal expiratory flow (peak flow) is decreased with intrathoracic and extrathoracic lesions.

    The obstructions can be intrathoracic or extrathoracic and variable or fixed. In summary, fixed obstructions will have decreased inspiratory and expiratory flows; variable obstruction will depend on the location (intrathoracic or extrathoracic). The flow curve is not a sensitive test; the absence of the classic pattern does not rule out a central or UAO.

    Indications

    There are multiple indications to obtain PFTs. Table 1 summarizes the most commons indications.

    • PFTs can be physically demanding for patients, and it is recommended to wait one month after an acute coronary syndrome or myocardial infarction.
    • Other relative contraindications are thoracic/abdominal surgery, brain/eye/ear/otolaryngological surgery, pneumothorax, ascending aortic aneurysm, hemoptysis, pulmonary embolism, severe hypertension (SBP greater than 200 mm Hg, DBP greater than 120 mm Hg).
    • asthma
    • allergies
    • chronic bronchitis
    • respiratory infections
    • lung fibrosis
    • bronchiectasis, a condition in which the airways in the lungs stretch and widen
    • COPD, which used to be called emphysema
    • asbestosis, a condition caused by exposure to asbestos
    • sarcoidosis, an inflammation of your lungs, liver, lymph nodes, eyes, skin, or other tissues
    • scleroderma, a disease that affects your connective tissue
    • pulmonary tumor
    • lung cancer
    • weaknesses of the chest wall muscles

    What are the risks of pulmonary function tests?

    Because pulmonary function testing is not an invasive procedure, it is safe and quick for most people. But the person must be able to follow clear, simple directions.

    All procedures have some risks. The risks of this procedure may include:

    • Dizziness during the tests
    • Feeling short of breath
    • Coughing
    • Asthma attack brought on by deep inhalation
    • Recent eye surgery, because of increased pressure inside the eyes during the procedure
    • Recent belly or chest surgery
    • Chest pain, recent heart attack, or an unstable heart condition
    • A bulging blood vessel (aneurysm) in the chest, belly, or brain
    • Active tuberculosis (TB) or respiratory infection, such as a cold or the flu

    Your risks may vary depending on your general health and other factors. Ask your healthcare provider which risks apply most to you. Talk with him or her about any concerns you have.

    Certain things can make PFTs less accurate. These include:

    • The degree of patient cooperation and effort
    • Use of medicines that open the airways (bronchodilators)
    • Use of pain medicines
    • Pregnancy
    • Stomach bloating that affects the ability to take deep breaths
    • Extreme tiredness or other conditions that affect a person’s ability to do the tests (such as a head cold)

    How do I get ready for pulmonary function tests?

    Your healthcare provider will explain the procedure to you. Ask him or her any questions you have. You may be asked to sign a consent form that gives permission to do the procedure. Read the form carefully. Ask questions if anything is not clear.

    Tell your healthcare provider if you take any medicines. This includes prescriptions, over-the-counter medicines, vitamins, and herbal supplements.

    Make sure to:

    • Stop taking certain medicines before the procedure, if instructed by your healthcare provider
    • Stop smoking before the test, if instructed by your healthcare provider. Ask your provider how many hours before the test you should stop smoking.
    • Not eat a heavy meal before the test, if instructed by your healthcare provider
    • Follow any other instructions your healthcare provider gives you

    Your height and weight will be recorded before the test. This is done so that your results can be accurately calculated.

    What happens during pulmonary function tests?

    You may have your procedure as an outpatient. This means you go home the same day. Or it may be done as part of a longer stay in the hospital. The way the procedure is done may vary. It depends on your condition and your healthcare provider’s methods. In most cases, the procedure will follow this process:

    • You’ll be asked to loosen tight clothing, jewelry, or other things that may cause a problem with the procedure.
    • If you wear dentures, you will need to wear them during the procedure.
    • You’ll need to empty your bladder before the procedure.
    • You’ll sit in a chair. A soft clip will be put on your nose. This is so all of your breathing is done through your mouth, not your nose.
    • You’ll be given a sterile mouthpiece that is attached to a spirometer.
    • You’ll form a tight seal over the mouthpiece with your mouth. You’ll be instructed to inhale and exhale in different ways.
    • You will be watched carefully during the procedure for dizziness, trouble breathing, or other problems.
    • You may be given a bronchodilator after certain tests. The tests will then be repeated several minutes later after the bronchodilator has taken effect.

    Below are the steps for the most common types of lung function tests.

    For a spirometry test

    • You’ll sit in a chair and a soft clip will be put on your nose. This is done so you’ll breathe through your mouth, rather than your nose.
    • You’ll be given a mouthpiece that is attached to a machine called a spirometer.
    • You’ll place your lips tightly around the mouthpiece, and breathe in and out as instructed by your provider.
    • The spirometer will measure the amount and rate of airflow over a period of time.

    For a lung volume (body plethysmography) test

    • You’ll sit in a clear, airtight room that looks like a telephone booth.
    • As with a spirometry test, you’ll wear a nose clip and place your lips around a mouthpiece connected to a machine.
    • You’ll breathe in and breathe out as instructed by your provider.
    • The pressure changes inside the room help measure lung volume.

    For a gas diffusion test

    • You’ll wear a mouthpiece connected to a machine.
    • You will be asked to inhale (breathe in) a very small, non-dangerous amount of carbon monoxide or other types of gas.
    • Measurements will either be taken as you breathe in or as you breathe out.
    • The test can show how effective your lungs are in moving gases to your bloodstream.

    For an exercise test, you will

    • Ride a stationary bike or walk on a treadmill.
    • You’ll be attached to monitors and machines that will measure blood oxygen, blood pressure, and heartbeat.
    • This helps show how well your lungs perform during exercise.

    Normal Results

    Normal values are based on your age, height, ethnicity, and sex. Normal results are expressed as a percentage. A value is usually considered abnormal if it is approximately less than 80% of your predicted value.

    Normal value ranges may vary slightly among different laboratories, based on slightly different ways to determine normal values. Talk to your provider about the meaning of your specific test results.

    Different measurements that may be found on your report after pulmonary function tests include:

    • Diffusion capacity to carbon monoxide (DLCO)
    • Expiratory reserve volume (ERV)
    • Forced vital capacity (FVC)
    • Forced expiratory volume in 1 second (FEV1)
    • Forced expiratory flow 25% to 75% (FEF25-75)
    • Functional residual capacity (FRC)
    • Maximum voluntary ventilation (MVV)
    • Residual volume (RV)
    • Peak expiratory flow (PEF)
    • Slow vital capacity (SVC)
    • Total lung capacity (TLC)

    What Abnormal Results Mean

    Abnormal results usually mean that you may have chest or lung disease.

    Some lung diseases (such as emphysema, asthma, chronic bronchitis, and infections) can make the lungs contain too much air and take longer to empty. These lung diseases are called obstructive lung disorders.

    Other lung diseases make the lungs scarred and smaller so that they contain too little air and are poor at transferring oxygen into the blood. Examples of these types of illnesses include:

    • Extreme overweight
    • Pulmonary fibrosis (scarring or thickening of the lung tissue)
    • Sarcoidosis and scleroderma

    Muscular weakness can also cause abnormal test results, even if the lungs are normal, that is, similar to the diseases that cause smaller lungs.

    Normal and Critical Findings

    Normal findings of spirometry are FEV/FVC ratio of greater than 0.70 and both FEV and FVC above 80% of the predicted value. If lung volumes are performed, TLC above 80% of the predictive value is normal. Diffusion capacity above 75% of the predicted value is considered normal as well.

    Complications

    PFTs are safe in general, and there are no complications. There is some potential harm from 4 key factors:

    • Maximal pressures generated in the thorax and their impact on abdominal and thoracic organs/tissues
    • Large swings in blood pressure causing stresses on tissues in the body
    • Expansion of the chest wall and lungs
    • Spread of infections (e.g., tuberculosis, hepatitis B, HIV)

    Contraindications of PFTs are related to those 4 factors to prevent potential complications like acute coronary syndrome, rupture of aneurysms, and dehiscence of the surgical wound.

    Non-Respiratory Functions of Lungs

    Non-respiratory functions of lungs/These nonrespiratory functions of the lung include its own defense against inspired particulate matter, the storage and filtration of blood for the systemic circulation, the handling of vasoactive substances in the blood, and the formation and release of substances used in the alveoli or circulation.

    Non-respiratory functions of lungs

    •  In addition to their functions in gas exchange, the lungs have a no. Of metabolic functions: 1.Defence mechanism 2.Maintenance of water balance 3.Regulation of body temperature 4.Regulation of acid-base balance 5.Metabolism of biologically active substances
    • Like the skin, the lung is exposed to the external environment, the membranes are delicate and need to be kept moist. Every day the lungs are exposed to >7000lit. Of air and its fine tissues req. Protection from the daily bombardment of particles incl. Dust, pollen, pollutants, viruses, bacteria The respiratory tract is protected by different mechanisms at its various levels. Physical mechs. Incl. COUGH is imp. In the upper airways.
    • The lower airways are served by the mucociliary clearance mechanism The gas exchange units are protected by surfactant& cellular defenders including the patrolling alveolar macrophages
    • The nose is the 1st imp. contributor to the physical defences of the upper airway It comprises a stack of fine aerodynamic filters of respiratory epithelium covering the turbinate bones that remove most large particles from the inspired air. The filtering effect is greatly enhanced by fine hairs in the entire. nares &by mucociliary action which apart from a small area anterior to the info. turbinates is directed mostly such that trapped particles are swallowed or expectorated.
    • During cough & expectoration, the larynx acts as a sphincter, which is an essential protective mechanism for the lower airways during swallowing & vomiting. Larger particles that penetrate the nose and are deposited by impaction or sedimentation in the main airways are trapped by the lining fluids of the trachea & bronchi and cleared by the mucociliary clearance mechanism. (mucociliary escalator)Those smaller particles, down to a few nm in size, deposited in the acinar part of the lung are dealt with by the alveolar macrophages
    • Cough is generated in 4distinctphases 1.Inspiration 2.Compression of intrathoracic gas against a closed glottis 3.Explosive expulsion as the glottis opens 4.relaxation of the airways
    • Its entirely responsible for tracheobronchial cleanliness The mucus forms a raft on the top of the cilia, which sweep in a cephalic direction Each epithelium lining the bronchi possess about 200cilia on its surface The cilia beat 12-14 times/sec
    • Saccharin is placed in the entire. Nares The time taken to observe sweet taste is calculated Normally its <30sec Its a simple & practical clinical test to assess ciliary function
    • 1.direct cine bronchographic measurement of the movement of the Teflon discs 2.assessment of the rate of clearance of radio aerosols by external imaging techniques
    • The main functions of mucus are to trap & clear particles, Dilute noxious influences Lubricate the airways Humidy the inspired air
    • Complex surface-active material lining the alveolar surface that reduces the surface tension And prevents the lung from collapsing at resting transpulmonary pressures Surfactant also provides a simple but elegant mechanism for alveolar clearance, since at end-expiration surface tension decreases and the surface film moves from the alveolus towards the bronchioles thus carrying small particles towards the mucociliary transport system
    • Surfactant is synthesised by alveolar type2 pneumocytes Comprises at least 4 different specific proteins Sp –A, B, C, D These proteins have important roles in host defence Many studies show that surfactant exerts a variety of influences on alveolar macrophages,incl., chemotaxis & enhancement of phagocytosis & killing of microbes
    • Normal surfactant also enhances local pulmonary non-specific immune defence mechanism by suppressing the development of specific T lymphocyte-mediated immune responses to inhaled antigens and T cell proliferation Its also likely that surfactant exerts influences on neutrophil functions incl., neutrophil adherence
    • ANTI bacterial ANTI Proteinases Surfactant proteins Alpha1 proteinase inhibitor Igs display IgA Alpha1 antichymotrypsin defensins alpha2macroglobulin Lactoferrins, lysozyme Secretory mucoproteinase inhibitor Complement display c3 ELAFFIN, Tissue inhibitors of metalloproteinases
    • These are derived from blood-borne monocytes that originate in the bone marrow Possess marked phagocytic ability, being able to ingest and destroy pathogenic bacteria & particles Able to generate mediators in the initiation of inflammation and to present Ags in the initiation of immune responses
    • Primary host defence phagocytosis & killing of microorganisms by oxygen radicals and Nitric oxide-dependent mechanisms and enzymes Inflammatory response. Initiation generation of neutrophil chemokines eg.IL8 generation of monocyte chemokines eg. MIP-1 alpha Generation of agents that activate endothelial cells eg.IL1, TNFalpha Generation of acute-phase response.IL1,TNFalpha,IL6
    • Local intracellular generation of NO is an imp., a defence mechanism against microorganisms Activated macrophages also form nitrate & nitrite which contribute to antifungal & antiparasitic, activities of macrophages
    • Unlike RBCs, up to 12 of neutrophils remain in the vascular compartment at any given time are not circulating but form the marginated pool which is in dynamic equilibrium with the circulating pool of vascular neutrophils The marginated pool can be released into the circulating pool by exercise or epinephrine The vascular bed of the lung &spleen make the most important contributions to the marginated pool and therefore serve as a source of rapidly releasable neutrophils in time of stress or injury
    • The presence of a large no. Of neutrophils loitering in the pulmonary microvascular bed may be of local advantage in host defence Their mobilisation and effectiveness is likely to be augmented in local lung responses to inhaled microbes or toxins and in the generation of the local inflammatory response to lung invasion by streptococci there may be a downside to the presence of this marginated pool of neutrophils in pulmonary microvessels they may put the lung particularly at risk of developing injury in multiorgan failure
    • The respiratory tract plays a role in the water loss mechanism. During expiration, water evaporates through the expired air and some amount of body water is lost by this process In COPD patients Expiration is prolonged…..so more water is lost l/t dehydration.
    • During expiration, along with water, heat is also lost from the body. Thus respiratory tract plays a role in the heat loss mechanism
    • Lungs play a role in the maintenance of the acid-base balance of the body by regulating the CO2 content in blood CO2 is produced during various metabolic reactions in tissues of the body When it enters the blood, CO2 combines with water to form carbonic acid Since carbonic acid is unstable, it splits into hydrogen and bicarbonate ions CO2 +H2OH2CO3H+ +HCO3-
    • The entire reaction is reversed in the lungs when CO2 is removed from the blood into the alveoli of lungs H+ +HCO3–H2CO3CO2 +H2O As CO2 is a volatile gas, it is practically blown out by ventilation.
    • When metabolic activities are accelerated, more amount of CO2 is produced in the tissues Concentration of H+ is also increased This leads to a reduction in pH. Increased H+ ion conc., causes increased pulmonary ventilation(hyperventilation) By acting through various mechanisms like chemoreceptors in aortic & carotid bodies and in the medulla of the brain Due to hyperventilation, excess CO2 is removed from body fluids and the pH. is brought back to normal
    •  Lungs contain a fibrinolytic system that lyses clots in the pulmonary vessels i.e why breathing exercises (alternate nose breathing) are advised to DVT (deep vein thrombosis), Thromboembolic cases
    • By renin-angiotensin metabolism angiotensin, II causes the release of aldosterone from the adrenal cortex, which in turn causes Na+ retention, + angiotensin II causes vasoconstriction= increased BP
    • Lungs release a variety of substances that enter the systemic arterial blood They remove other substances from the systemic venous blood that reach via the pulmonary artery Prostaglandins are removed from the circulation, but PGs are also synthesised in the lungs and released into the blood when lung tissue is stretched
    • Prostaglandins are powerful locally acting vasodilators and inhibit the aggregation of blood platelets. Through their role in vasodilation, prostaglandins are also involved in inflammation
    • Substances are synthesised and used in the lungs surfactant Substances which are synthesised or stored and released into the blood PGs, histamine, kallikrein Substances which are partially removed from the lungs PGs ,bradykinin, adenine nucleotides, serotonin, norepinephrine, acetylcholine Substances which are activated in the lungs Angiotensin 1 angiotensin2
    • Large amounts of the angiotensin-converting enzyme responsible for this activation are located on the surface of the endothelial cells of the pulmonary capillaries. The converting enzyme also inactivates bradykinin Circulation time through the pulmonary capillaries is <1sec Yet 70% of the angiotensin1 reaching the lungs is converted to angiotensin2 in a single trip through the capillaries
    • Four other peptidases have been identified on the surface of the pulmonary endothelial cells, but their physiological role is unsettled. Removal of serotonin and norepinephrine reduces the amounts of these vasoactive substances reaching the systemic circulation so that the effect of these stress hormones is decreased
    • Many other vasoactive substances pass through the lung without being metabolised Epinephrine Dopamine Oxytocin Vasopressin Angiotensin2

    Lung Capacity and Volume

    Lung volumes and capacities refer to phases of the respiratory cycle; lung volumes are directly measured while capacities are inferred.

    Key Points

    Lung capacity is a measure of lung volume inferred from the exhaled during the various cycles of breathing.

    There is residual air leftover in the lungs during normal breathing.

    Vital capacity is used to diagnose restrictive diseases, while the FEV1/FVC ratio is used to diagnose obstructive diseases.

    FEV1/FVC ratio declines as someone ages, but declines faster in those who smoke due to damage caused by smoking.

    Key Terms

    • FEV1/FVC ratio: The ratio between forced expiratory volume and forced vital capacity, which is used to measure the level of obstruction in the lungs.
    • vital capacity: The maximum volume of air that can be discharged from the lungs following maximum inspiration.

    EXAMPLES

    • Pulmonary function tests (PFTs) may be used to help diagnose different pulmonary diseases. The two most often used measurements are FVC (forced vital capacity) and FEV1 (forced expiratory volume in one second).
    • An FEV1/FVC ratio of >80% indicates a restrictive lung disease like pulmonary fibrosis or infant respiratory distress syndrome.
    • An FEV1/FVC ratio of <70% indicates an obstructive lung disease like asthma or COPD.

    Lung Capacity

    Lung capacity generally refers to the total amount of air inside the lungs at certain phases of the respiratory cycle. It is usually measured as the amount of air that is exhaled after inhalation; this is measured with a device called a spirometer.

    There are many different types and terms for the different components of lung capacity that all have different characteristics. In general, measuring lung capacity is important because it serves as the best indicator of lung health by quantifying the functional ability of the lungs to cycle air.

    Vital Capacity

    Vital capacity (VC) is the maximum amount of air that a person can exhale after inhaling as much air as possible. It is also the sum of tidal volume and the inspiratory and expiratory reserve volumes, which capture the differences between normal breathing and maximal breathing.

    The inspiratory reserve volume is the extra space for air after a normal inspiration, and the expiratory reserve volume is the extra air that can be exhalaed after a normal expiration. VC tends to be decreased in those with restrictive lung diseases, such as pulmonary fibrosis, making VC a good diagnostic indicator of restrictive lung diseases.

    Other important lung volumes related to lung capacity are residual volume (RV) and total lung capacity (TLC).

    • RV: The amount of air left in the lungs after a maximal expiration.
    • TLC: The volume of the lungs at maximal inflation, which is the sum of VC and RV.

    FEV1/FVC Ratio

    The most widely used diagnostic application for lung capacities is the ratio between forced expiratory volume (FEV1) and forced vital capacity (FVC).

    • FEV1: The volume of air exhaled in one second of forced expiration.
    • FVC: The total volume of exhaled air during forced expiration.

    The FEV1/FVC ratio is an important indicator of lung health and is the standard approach for diagnosing COPD (chronic pulmonary obstructive disease), which includes emphysema and bronchitis, which are both caused by smoking. An FEV1/FVC ratio that is greater than .8 indicates a normal lung with generally healthy function, however, a ratio below .8 indicates a significant degree of airway obstruction and suggests COPD.

    This is a graph of lung capacity at the various stages of the respiratory cycle, which is one inhalation followed by an exhalation. The events during this cycle are labeled, from left to right: resting tidal volume, inspiratory reserve volume, residual volume, expiratory reserve volume, total lung capacity, and vital capacity.

    Lung Capacity: Lung capacity at the various stages of the respiratory cycle, which is one inhalation followed by an exhalation.

    The obstruction becomes worse the lower the ratio becomes, which increases the likelihood of respiratory failure and death. The FEV1/FVC ratio naturally falls as humans age, however, smoking (the cause of COPD) will cause much larger decreases in FEV1/FVC ratio than what is normal.

    Smoking causes this damage by initiating an inflammatory response in the lungs. Those who quit smoking will not experience a regain the FEV1/FVC ratio lost from smoking, however, their rate of FEV1/FVC ratio decline will slow to normal, and their life expectancy will be less impacted.

    Those with asthma, an acute form obstructive lung disease, will show a low FEV1/FVC ratio during an asthma attack, which returns to normal after the attack is over. Therefore, to diagnose asthma, many clinicians expose patients to methacholine or histamine to trigger mild asthma attacks to measure FEV1/FVC ratios.

    Nonrespiratory Air Movements

    The lungs have a number of metabolic functions in addition to their functions in gas exchange.

    Key Points

    The lungs have a number of metabolic functions, such as the secretion of ACE (angiotensin-converting enzyme), which converts angiotensin I to angiotensin II to stimulate changes in the renal system.

    Higher levels of ACE lead to higher blood pressure. ACE inhibitors are used to treat hypertension by reducing ACE to reduce blood pressure.

    Airway epithelial cells can secrete a variety of molecules—immunoglobulins (IgA), proteases, reactive oxygen species, and antimicrobial peptides—that all help protect the lungs and body from pathogens.

    Non-respiratory air movements are mechanical functions that aren’t involved in gas exchange, such as voice production and coughing.

    Key Terms

    • ACE: Angiotensin-converting enzyme, which is secreted in the lungs and helps to increase blood pressure in the body through renal system feedback loops.
    • Airway epithelial cells: Airway epithelial cells can secrete a variety of molecules that aid in the immune system defense of the lungs.

    EXAMPLE

    Non-respiratory air movements do not involve gas exchange. Examples are: sneezing, coughing, burping, laughing, singing, and talking.

    While the primary function of the lungs is gas exchange, they have several other functions, which are both metabolic and mechanical. These include the secretion of many enzymes and proteins involved in other body systems and nonrespiratory air movements.

    Metabolic Functions

    The lungs secrete many enzymes and proteins that serve non-respiratory metabolic functions.

    ACE (angiotensin-converting enzyme) is an enzyme secreted by the endothelial cells of the capillaries in the lungs. ACE converts angiotensin I into angiotensin II, which are two important hormones in the renin-angiotensin feedback loop of the renal system.

    This is a schematic diagram of the renin-angiotensin-aldosterone system. It shows how the renin-angiotensin system is dependent on ACE from the lungs to regulate blood pressure. ACE converts angiotensin I into angiotensin II, which are two important hormones in the renin-angiotensin feedback loop of the renal system. ACE activity results in increased blood pressure.

    The renin-angiotensin-aldosterone system: The renin-angiotensin-aldosterone system is dependent on ACE from the lungs to regulate blood pressure. ACE activity results in increased blood pressure.

    This system works to regulate blood pressure and blood volume by changing the amount of water retained by the kidneys. In general, more ACE leads to more angiotensin II, which leads to more aldosterone, which leads to more retained water through sodium reabsorption in the kidney, which leads to increased blood volume and blood pressure.

    ACE inhibitors are a common treatment for those with hypertension, as it will reduce the amount of ACE, which will cause the kidney to excrete more water, which lowers blood volume and blood pressure.

    The epithelial cells and macrophages of the lungs secrete many molecules that have immune system functions. In general these molecules have anti-microbial functions.

    • Immunoglobin A (IgA): An antibody that can attack pathogens and mark them for phagocytosis from macrophages and neutrophils.
    • Protease: Secreted from lung macrophages and neutrophils during inflammatory response to damage pathogens. A fibrinolytic that can break up thrombosis (blood clots) in the lungs.
    • Reactive oxygen species (ROS): Free radicals, which are any substance with an unpaired electron in the valence shell, can cause oxidative stress (damage) in cells. They are used to kill pathogens after being engulfed (phagocytized) by immune cells.
    • Anti-microbial peptides: Various chemokines and proteins that are secreted by the mucus membranes of the airways. They can damage and inhibit pathogens and are considered a barrier component of the immune system.

    Mechanical Functions

    There are several types of non-respiratory air movements that have important functions that are not primarily related to gas exchange. One example is voice production for speaking and singing, which involves fine control over the direction and flow of the air as it passes into the upper respiratory tract.

    Other mechanical functions include sneezing and coughing, which protect the lungs and airways from irritants that could potentially cause damage. Coughing is a result of constriction from nervous stimulation in the trachea and larynx and also serves to dislodge mucus trapped inside the lungs.

    Postural and ventilatory changes

    A change in posture from supine to erect in normal individuals results in ∼400 ml of pulmonary blood volume being redistributed to the systemic circulation. During forced expiration against a closed glottis (e.g. valsalva manoeuvre), the pulmonary blood volume decreases by 50%. On the other hand, the pulmonary blood volume doubles with forced inspiration. Changes in pulmonary vascular volume are also influenced by the activity of the sympathetic nervous system.1

    Filter for blood borne substances

    The lung is ideally positioned to filter out particulate matter such as clots, fibrin clumps, and other endogenous and exogenous materials from entering the systemic circulation. This plays an important role in preventing ischaemia or even infarction to vital organs.

    Physical filtration

    The lung acts as a physical barrier to various blood-borne substances but is not completely efficient in protecting systemic circulation. Pulmonary capillaries have a diameter of 7 µm. But it has been shown in animal studies that glass beads of up to 500 µm can pass through a perfused lung.3 Post-mortem studies have shown that almost 25% (15–40%) of the population have a probe patent foramen ovale. Increased pressure in the right atrium secondary to events such as coughing or Valsalva manoeuvre produces demonstrable blood flow between the right and left atria. Therefore, emboli, particularly fat and gas emboli, can still pass through the pulmonary capillary filter, or bypass the lung entirely via the foramen ovale. The pulmonary microcirculation is designed to maintain alveolar perfusion in the face of substantial embolization. However, emboli blocking major vessels or extensive micro-embolization can result in a life-threatening ventilation-perfusion mismatch. Pulmonary micro-embolism also initiates neutrophil activation leading to increased permeability and alveolar oedema in the affected area and has been implicated in the aetiology of acute lung injury.

    Chemical filtration

    Pulmonary capillaries also produce substances that break down blood clots. Pulmonary endothelium is a rich source of fibrinolysin activator, which converts plasminogen present in plasma to fibrinolysin, which subsequently breaks down fibrin-to-fibrin degradation products. The lung thus has an efficient fibrinolytic system, which lyses clots in the pulmonary circulation.2 In addition, the lung is the richest source of heparin (which inhibits coagulation) and thromboplastin (which by converting prothrombin to thrombin, promotes coagulation).1 Hence the lung may play a role in the overall coagulability of blood to promote or delay coagulation and fibrinolysis.

    Defence against inhaled substances

    Every day, about 10 000 litres of air comes into contact with 50–100 m2 of the alveolar epithelium. There are various mechanisms along the respiratory tract that are involved in providing protection against inhaled physical and chemical substances.

    Defence against inhaled particles

    A pseudo-stratified ciliated columnar epithelium lines the upper airway from the posterior two-thirds of the nose to the respiratory bronchioles. This is covered with a ‘mucous blanket’ that is composed of a highly viscous mucopolysaccharide gel secreted by goblet cells in the epithelium and mucous cells of the submucosal glands, floating on a low-viscosity serous fluid layer secreted by the bronchial glands. This ‘mucous blanket’ forms the first line of defence against inhaled physical substances.

    Mucociliary escalator

    The cilia beat within the serous layer of the airway lining fluid in a coordinated fashion at a frequency of 10–15 Hz. In healthy individuals, this action moves the overlying mucus towards the pharynx at a rate of about 1 mm min−1 in the small peripheral airways but can be as quick as 20 mm min−1 in the trachea. This is known as the ‘mucociliary escalator’. Inspired particles >5 µm are deposited by impaction on the mucus covering the nose and larger airways. Particles between 2 and 5 µm in diameter are deposited by sedimentation in smaller airways, where the airflow rates are extremely low. The cilia propel this outer ‘blanket’ of mucus with the entrapped particles and microorganisms over the serous layer. They act together to move the mucus from peripheral airways to central airways, from which the mucus is expectorated or swallowed. Smaller particles (<2 µm) reach the alveoli as aerosols and about 80% is exhaled.4 The rest may be deposited in the alveoli as a result of Brownian motion. The random movement of microscopic particles suspended in a liquid or gas is caused by collisions with molecules of the surrounding medium is termed Brownian motion after its identifier, Scottish botanist Robert Brown (1773–1858).

    Factors affecting the mucociliary function

    The impaired mucociliary function may be because of abnormal mucus production or defective ciliary motility. The secretions of goblet cells are stimulated by inhaled irritant gases and inflammatory mediators. Neural control of bronchial gland secretions is mediated by the parasympathetic nervous system via the vagus nerve, increasing secretions with vagal stimulation, and vice versa. Secretions are also reduced by the administration of opioids. Ciliary motility is impaired by dehydration, smoking, anaesthesia, dry inspired gases, extremes of temperature, and ciliary dysmotility syndromes,  for example, Kartagener syndrome. Drugs that depress ciliary motility include inhaled anaesthetic agents, local anaesthetics, opioids, atropine, and alcohol. In Vitro studies have shown that midazolam, propofol, thiopental, and dexmedetomidine do not directly impair ciliary motility, whereas high doses of ketamine and fentanyl stimulate ciliary motility.

    Effects of impaired mucociliary function

    A defective mucociliary escalator can lead to chronic sinusitis, recurrent chest infections, and bronchiectasis. When mucociliary clearance is decreased, the cough becomes increasingly important for the removal of secretions from the airways. In intensive care, the disruption of this function by critical illness, intubation, ventilation, and prolonged high-inspired oxygen concentrations predisposes the patient to atelectasis, hypoxia, and infection.

    Immune function

    Optimal lung defences require the coordinated action of multiple cell types. Immune function within the lung is mediated by pulmonary alveolar macrophages (PAMs) and a variety of immune mediators.

    Pulmonary alveolar macrophages

    Amoeboid PAMs engulf the particles that reach the alveoli and deposit them on the mucociliary escalator or remove them via blood or lymph. The macrophages are particularly effective against bacteria and ensure that the alveolar region of the lung is effectively sterile. Pam also have a role in antigen presentation, T-cell activation, and immunomodulation. When PAMs ingest large amounts of inhaled particles, especially cigarette smoke, silica, and asbestos, they release lysosomal products into the extracellular space causing inflammation and eventually fibrosis. Neutrophil activation within the lung also leads to the release of proteases such as trypsin and elastase. These chemicals, while very effective at destroying pathogens, can also damage normal lung tissue. This is prevented by the proteases being swept away by the mucus coating the respiratory tree, and by conjugation with alpha1-antitrypsin, which renders them inactive.4 Hence, in alpha1-antitrypsin deficiency, surplus trypsin and elastase lead to tissue destruction that in turn leads to pulmonary emphysema.

    Immune mediators in the lung

    The airway epithelial cells secrete a variety of substances such as mucins, defensins, lysozyme, lactoferrin, and nitric oxide, which non-specifically shield the lung from microbial attack.7 They also produce a number of mediators of inflammation such as reactive oxygen species, cytokines [tumour necrosis factor (TNFα), interleukins (IL-1β), granulocyte/macrophage colony-stimulating factor (GM-CSF)], and platelet-activating factor to recruit inflammatory cells to the site of inflammation. Immunoglobulins, mainly IgA, present in the bronchial secretions resist infections and help maintain the integrity of the respiratory mucosa.8

    Immunomodulation therapies in lung disease

    New therapies using immunomodulating agents to prevent or minimize non-specific inflammation within the lungs are being developed. Broncho-Vaxom® (OM-85 BV; OM Laboratories, Geneva, Switzerland), a lyophilized bacterial extract from eight species of bacteria (Haemophilus influenzaeNeisseria catarrhalisKlebsiella pneumoniaeStreptococcus pyogenesStreptococcus viridansStaphylococcus aureusKlebsiella ozaenaeDiplococcus pneumoniae), has been found to enhance antibody synthesis together with better resistance to bacterial infection resulting in a well-balanced, non-inflammatory immune response against invading pathogens. This results in a reduction in the number and duration of chest infections in chronic obstructive pulmonary disease (COPD) patients.9 Recombinant interferon-γ1b administered as an adjuvant along with anti-tuberculosis therapy has been shown to reduce the inflammatory response in the lung, improve clearance of pathogenic tuberculosis bacteria, and improve constitutional symptoms in patients suffering from pulmonary tuberculosis.10

    Defence against inhaled chemicals

    The large surface area of the alveoli is perfectly suited for gas exchange, but can also serve as a portal of entry for inhaled toxic agents. The fate of these inhaled chemical substances depends on their size, water-solubility, inspired concentration, and their metabolism within the lung.4 Akin to hepatic metabolism, both phase I and II metabolism takes place within the lungs. The metabolism of inhaled chemicals is detailed in a separate section of this article.

    Endocrine and metabolic functions

    Isolated pulmonary neuroendocrine cells (PNECs) and innervated cell clusters called neuroepithelial bodies (NEBs) are widely distributed in the airway mucosa and are together referred to as the ‘pulmonary neuroendocrine system’. The role played by these cells in health and disease is becoming clearer.11 They secrete a wide variety of amines (e.g. serotonin) and peptides (e.g. bombesin). PNEC play a significant role in cell growth, differentiation, and branching morphogenesis in the developing lung. NEBs are located at airway bifurcations and degranulate in the presence of hypoxia. It is postulated that they act as hypoxia-sensitive chemoreceptors linked to the central nervous system by their vagal afferent sensory fibres.

    While some of the endocrine and metabolic functions of the lung are ill-defined and poorly understood, others are well established and summarized in Table 1.

    Summary of metabolic changes to hormones on passing through the pulmonary circulation. 5-HT, 5-hydroxytryptamine; ANP, atrial natriuretic peptide; PG, prostaglandin; ATP, adenosine triphosphate; ADP, adenosine diphosphate; AMP, adenosine monophosphate. Reproduced with permission from Lumb.

    Group Effect of passing through the pulmonary circulation


    Activated No change Inactivated
    Amines Dopamine 5-HT
    Epinephrine Norepinephrine
    Histamine
    Peptides Angiotensin I Angiotensin II Bradykinin
    Oxytocin ANP
    Vasopressin Endothelins
    Arachidonic acid derivatives Arachidonic acid PGI2 PGD2
    PGA2 PGE2
    PGF2 alfa
    Leukotrienes
    Purine derivatives Adenosine
    ATP
    ADP
    AMP

    Amines

    The pulmonary endothelium selectively takes up norepinephrine and serotonin (5HT) from the blood while sparing histamine, dopamine, and epinephrine. This results in the removal of 30% of norepinephrine and 98% of 5HT in a single pass through the lungs.4 Norepinephrine is metabolized by intracellular monoamine oxidase (MAO) and catechol-O-methyl transferase, while MAO breaks down 5HT. There are no effects on histamine, dopamine, or epinephrine because these compounds cannot be transported into the pulmonary endothelial cells due to the lack of an active transport mechanism.

    Peptides

    Angiotensin-converting enzyme (ACE) is found in plasma and systemic vascular endothelium, but is present in much larger quantities on the endothelium of pulmonary vessels. On passage through the lung, the inert decapeptide angiotensin I is converted into the vasoactive octapeptide angiotensin II by ACE. Although the circulation time within the pulmonary capillaries is <1 s, 70% of the angiotensin I reaching the lung is converted to angiotensin II.2 The latter is 50 times more active than its precursor and is unaffected on passing through the lung. Similarly, the vasoactive nonapeptide bradykinin is also broken down by ACE in the lung. Atrial natriuretic peptides and endothelins are also removed by the lung.

    Arachidonic acid derivatives

    Arachidonic acid metabolites PGE, PGE2, PGF, and leukotrienes are metabolized extensively in the lung by specific enzymes, while PGA2 and PGI2 pass through unchanged. As with catecholamines, the selectivity for specific prostaglandins is attributed to selectivity in uptake pathways and not to intracellular enzymes.

    Purine derivatives

    The purines adenosine monophosphate (AMP), adenosine diphosphate, and adenosine triphosphate are metabolized to adenosine by specific enzymes on the surface of the pulmonary endothelial cells. Adenosine is taken up rapidly into the endothelial cells where it is phosphorylated to AMP or deaminated to inosine and ultimately to uric acid.

    This selectivity of the lung seems to imply that it acts as a metabolic filter removing certain locally important vasoactive substances, while substances important to systemic regulation pass unaffected. It also implies that vasoactive substances normally removed by the lung may have profound systemic effects if they were to bypass the lung.

    Pulmonary drug metabolism

    The lung is an important extra-hepatic site for mixed-function oxidation by the cytochrome P450 system but unlike hepatocytes, their activity cannot be induced. Their metabolic capacity is small and easily saturated. An important role of lungs may therefore be to act as a buffer by binding i.v. drugs, preventing an acute increase in systemic concentrations. The same metabolic systems also play a role in the biotransformation and detoxification of inhaled substances.

    Pulmonary extraction

    Pulmonary extraction refers to the transfer of a drug from the blood into the lung. The drug may then be metabolized or released unchanged back into the blood. Several drugs, including some used during anaesthesia, are taken up, metabolized, or released slowly from the lungs.12 Pulmonary endothelial cells are the primary site for binding or metabolism of i.v. drugs. They have high metabolic activity and an important role in breaking down endogenous substrates, but their metabolic capacity is low and easily saturated.

    Effects of pulmonary drug extraction

    In most patients, i.v. drugs are retained in the lungs by binding to specific sites on the pulmonary endothelium. Pulmonary extraction buffers the rate of rising in drug concentration within the systemic circulation. Pulmonary extraction may also help maintain a steady-state concentration by releasing ‘excess’ bound drug as the plasma concentration decreases. In the presence of moderate-to-severe right-to-left shunts, loss of buffering from lungs could result in a dangerous rise in the plasma concentration for certain drugs, for example, lidocaine. Co-administration of drugs such as antidepressants and beta-blockers, which compete for similar binding sites, or the presence of significant lung disease has also been shown to decrease pulmonary uptake of drugs resulting in potentially toxic systemic concentrations. Conversely, some drugs tend to accumulate within the lung causing dangerous local toxicity, for example, paraquat, nitrofurantoin, bleomycin, and amiodarone.

    Pulmonary extraction of anaesthetic drugs

    While most drugs used in anaesthesia are taken up by the lung to some extent, only prilocaine is metabolized within the lung.12 Drugs with a significant pulmonary uptake are basic amines with a pKa of >8. Other factors known to influence the pulmonary uptake are molecular weight, lipophilicity, protein binding, ventilation, perfusion, oxygenation, co-administration of other drugs, cardio-pulmonary bypass, ageing, lung pathology, and anaesthesia.10 None of the drugs with high pulmonary extraction undergo significant metabolism within the lung. As the systemic levels decrease, drug is released from the lung. The extent of pulmonary extraction for anaesthetic agents is shown in Table 2.

    Pulmonary extraction, metabolism or both of drugs used in anaesthesia

    Drugs Extraction
    Local anaesthetics
     Lidocaine 41–51%
     Prilocaine 40%
     Mepivacaine 20%
     Bupivacaine 12%
    I.V. anaesthetic agents
     Diazepam 30%
     Propofol 28%
     Thiopental 14%
    Opioids
     Fentanyl 75%
     Meperidine 65%
     Alfentanil 10%
     Morphine 4–7%
    Neuromuscular blocking agents
     Vecuronium No significant pulmonary uptake
     Atracurium No significant pulmonary uptake
    D-Tubocurarine No significant pulmonary uptake
     Rocuronium No significant pulmonary uptake
    Catecholamines
     Norepinephrine 16%
     Dopamine 20%

    Pulmonary metabolism of inhaled drugs

    There are three major benefits that may be attained by delivering medication to the lungs via the inhaled route: rapid onset of action, high local concentration by delivery directly to the airways (and hence high therapeutic ratio and increased selectivity), and needle-free systemic delivery of drugs with poor oral bioavailability.13 As a consequence of rapid absorption and low metabolic activity, many inhaled drugs have near-complete bioavailability via the lung. However, some isoforms of the cytochrome P450 enzymes are present in higher quantities in the lung in comparison with the liver. This may explain why some inhaled drugs such as theophylline, salmeterol, isoprenaline, budesonide, and ciclesonide undergo significant metabolism in the lung, while others do not. Metabolism of inhaled chemicals is not always beneficial. For example, some innocuous chemicals in cigarette smoke are metabolized into potential carcinogens by the lung. In an attempt to improve airway selectivity and minimize systemic side-effects; several drugs particularly inhaled steroids, have been designed to take advantage of biotransformation within the lungs as prodrugs or soft drugs.

    Prodrugs

    An inactive drug that is metabolized to its active form before or at its biological target within the lung is called a ‘prodrug’. The prodrug beclomethasone dipropionate is metabolized to the more potent 17-beclomethasone monopropionate by esterases in the lungs. This reduces the risks of side effects within the oropharyngeal tract from this steroid.13 Another steroid, ciclesonide, is metabolized into its active form by esterases in the lungs and further reversibly conjugated to fatty acids. Similarly, reversible conjugation of budesonide with fatty acids within the lung helps to retain it within the larger airways. Budesonide conjugates are gradually hydrolyzed and free budesonide is regenerated. This results in prolonged lung retention, increased duration of action, and a lower elimination time.

    Soft drugs

    An active drug molecule that is readily inactivated by hydrolysis at its target site within the lung or blood is called a ‘soft drug’. Several soft drug steroids (itrocinonide, γ-butyrolactone steroids, fluocortin butyl-ester, and butixocort propionate) have been in clinical development as inhaled drugs with the purpose of maintaining a high local intrinsic activity, but are readily inactivated in the lung or blood avoiding systemic spillover and side-effects.

    Conclusion

    • Trap for airborne particles:  generally, nothing larger than 2.5μm gets to the alveoli

    • Reservoir of blood: the lungs contain about 10% of the circulating blood volume

    • Route of drug administration (eg. nebulised steroids and bronchodilators)

    • Route of drug elimination  (eg. volatile anaesthetics)

    • Metabolism (eg. conversion of of angiotensin-I, and degradation of neutrophil elastase by α1-antitrypsin)

    • Modulator of acid-base balance by virtue of CO2 elimination

    • Modulator of the clotting cascade: the lungs contain thromboplastin, heparin and tissue plasminogen activator

    • Filter for the bloodstream: particles larger than an RBC are trapped (~8  μm size barrier), which includes clots, tumour cells and other emboli

    • Antimicrobial and immune functions: Alveolar macrophages and sequestered neutrophils, mast cells in the lung and bronchi, immunoglobulin in the respiratory mucus (IgA)

    • Modulation of body temperature: heat loss can occur by respiration

    • Organ of speech: the lungs form a part of the system which permits communication by sound and language

     

    Positive End-expiratory Pressure

    Positive end-expiratory pressure (PEEP) is a value that can be set up in patients receiving invasive or non-invasive mechanical ventilation. This activity reviews the indications, contraindications, complications, and other key elements of the use of PEEP in the clinical setting as relates to the essential points needed by members of an interprofessional team managing the care of patients requiring assisted ventilation.

    Positive end-expiratory pressure (PEEP) is the positive pressure that will remain in the airways at the end of the respiratory cycle (end of exhalation) that is greater than the atmospheric pressure in mechanically ventilated patients.

    An analogous term used for non-invasive ventilation is end positive airway pressure (EPAP) for patients receiving bi-level positive airway pressure (BPAP).

    Continuous positive airway pressure therapy (CPAP), although not an interchangeable term, works by delivering a constant pressure, which at the time of exhalation works in the same way as PEEP.

    PEEP can be a therapeutic parameter set in the ventilator (extrinsic PEEP), or a complication of mechanical ventilation with air trapping (auto-PEEP).

    Function

    Extrinsic PEEP can be used to increase oxygenation. By Henry’s law, the solubility of a gas in a liquid is directly proportional to the pressure of that gas above the surface of the solution. This applies to mechanical or noninvasive ventilation in that increasing PEEP will increase the pressure in the system. This, in turn, increases the solubility of oxygen and its ability to cross the alveolocapillary membrane and increase the oxygen content in the blood.

    Extrinsic PEEP also can be used to improve ventilation-perfusion (VQ) mismatches. The application of positive pressure inside the airways can open or “splint” airways that may otherwise be collapsed, decreasing atelectasis, improving alveolar ventilation, and, in turn, decreasing VQ mismatch.

    The application of extrinsic PEEP will, therefore, have a direct impact on oxygenation and an indirect impact on ventilation. By opening up airways, the alveolar surface increases, creating more areas for gas exchange and somewhat improving ventilation. Nevertheless, extrinsic PEEP should never be used for the sole purpose of increasing ventilation. If a patient needs to clear CO2 by improving ventilation, he should receive some level of pressure support for his ventilation, either via BPAP or invasive ventilation.

    Extrinsic PEEP also significantly decreases the work of breathing. This is especially important for stiff lungs with low compliance. In intubated patients with low compliance, work of breathing can represent an important part of their total energy expenditure (up to 30%). This increases CO2 and lactate production, both of which may be problems of their own. By decreasing work of breathing, CO2 and lactate production decreases, decreasing the need for high minute ventilation (to correct the hypercapnia and acidosis) and thereby decreasing respiratory drive and further decreasing the work of breathing needed by the patient in a positive-effect loop.

    Issues of Concern

    The use of Extrinsic PEEP also can cause some complications. Normal respiratory physiology works as a negative pressure system. When the diaphragm pushes down during inspiration, negative pressure in the pleural cavity is generated, creating negative pressure in the airways that suck air into the lungs. This same negative intrathoracic pressure decreases the right atrial (RA) pressure and generates a sucking effect on the IVC increasing venous return. The application of extrinsic PEEP changes this physiology. The positive pressure generated by the ventilator or BPAP transmits to the upper airways and finally to the alveoli which are transmitted to the alveolar space and thoracic cavity, creating positive pressure (or at least less negative pressure). This increases RA pressure and decreases venous return, generating a decrease in preload. This has a double effect in decreasing cardiac output: less blood in RV means less blood reaching LV and less blood that can be pumped out decreasing cardiac output, at the same time, the decreased preload means that the heart works at a less efficient point in the frank-startling curve, generating less effective work and further decreasing cardiac output and resulting in a drop in mean arterial pressure (MAP) if there is not a compensatory response by increasing systemic vascular resistance (SVR). This is a very important point to have in mind, especially with patients who may not be able to increase their SVR, such as those with distributive shock (e.g., septic, neurogenic, or anaphylactic).

    This effect on RA pressure and venous return (VR) may be beneficial when used in patients with cardiogenic pulmonary edema. In patients with volume overload, decreasing VR will have a dual beneficial effect: the LV may be over distended, also be working at a less-than-optimal point of the frank starling curve. Decreasing VR will again decrease preload, but in this particular case, it has been proposed that the decrease in preload will place the LV at a more efficient workload, possibly increasing cardiac output and improving pulmonary edema, although it has never been shown that higher PEEP directly improves LV function. At the same time, decreased VR means less blood pumped by RV and less pulmonary edema being generated.

    Another special circumstance in which extrinsic PEEP’s effect on CO and MAP is important to consider is in patients in whom a cerebral perfusion pressure (CCP) has to be maintained after a stroke or subarachnoid hemorrhage. In this case, although PEEP does not directly affect CCP, and cerebral autoregulation will normally compensate for changes in MAP, special attention has to be given in cases of disturbed cerebrovascular autoregulation, as the decrease in MAP can directly affect CCP causing adverse effects.

    Other adverse effects of extrinsic PEEP include its capacity for generating barotrauma, especially in non-compliant lungs by increasing plateau pressures, and its interference with hemodynamic measurements in patients with right-heart catheters.

    Clinical Significance

    Using extrinsic PEEP clinically requires an understanding of all the principles discussed and will depend on many factors including the type of ventilation the patient is receiving (nasal intermittent positive pressure ventilation versus invasive mechanical ventilation) and the mode of ventilation (assist control, synchronized intermittent mandatory ventilation, airway pressure release ventilation). All of these different setups have a way to set extrinsic PEEP or an equivalent measure of positive pressure, and their specific set up in each case escapes the scope of this review. Nonetheless, there are some basic principles that apply to all modes of ventilation for PEEP:

    • Start low and increase as tolerated and dial to patient comfort and desired oxygenation.
    • Constantly check your plateau pressures to prevent barotrauma. As a general rule of thumb, you should aim the keep a plateau pressure below 30 cm H2O.
    • Follow the MAP as you are dialing up or down the PEEP.
    • When extubating a patient with cardiogenic pulmonary edema who are receiving extrinsic PEEP, consider its effects on VR as removing PEEP may precipitate new pulmonary edema and re-intubation.
    • When managing patients with acute respiratory distress syndrome, the ARDSnet protocol provides clear guidance on how to titrate extrinsic PEEP and FiO2%.

    Other Issues

    Auto-PEEP or intrinsic PEEP

    Intrinsic or auto-PEEP is a complication of mechanically ventilated patients. Usually, passive exhalation will permit complete emptying of the air in the lungs until lung pressure equalized with atmospheric pressure, but in some cases the lungs may not completely deflate, leaving air trapped inside the lung at the end of exhalation which generates a positive pressure that remains in the lungs. This pressure is called auto or intrinsic PEEP. When this process repeatedly happens with each respiratory cycle, the amount of air trapping increases with each breath and consequently the intrathoracic pressure increases pathologically, compressing the RA and decreasing VR causing hypotension, as well as increasing plateau pressure (intra-alveolar pressure) and causing barotrauma. The increased air trapping also will make it harder for the patient to bring new air in, increasing the work of breathing, which increases oxygen consumption and CO2 production, thereby increasing the need for ventilation, increasing respiratory rate, and worsening auto-PEEP in a vicious cycle.

    Factors leading to auto-PEEP 

    • Airway inflammation and mucus plugs generate dynamic airflow obstruction as a forced expiratory effort will increase the pressure around the airway leading to closure around the plugs or inflamed area and trapping air in the alveoli that are dependent on that airway.
    • High lung compliance as in chronic obstructive pulmonary disease (COPD) works similarly, as the airways lack scaffolding to stay open during forced exhalation, leading to dynamic airway collapse and air trapping.
    • High tidal volume ventilation, where the tidal volume may be too high to be exhaled in a set amount of time, so air is retained by the time the next breath is delivered.
    • The high respiratory rate is generating a short exhalation time.
    • Slow inspiratory flow generating a higher inspiratory to expiratory time ratio (too much time taken during inhalation does not leave enough time for a full exhalation).

    Two types of auto-PEEP

    • Dynamic hyperinflation with intrinsic expiratory flow obstruction is the most common cause of auto-PEEP in COPD patients in whom alveolar collapse during expiration leads to air trapping. It has been stipulated that low-level extrinsic PEEP can help decrease auto-PEEP in these patients by splinting airways open, leading to the easier release of air from the alveoli. Airway inflammation and mucus plugs also cause dynamic hyperinflation in a similar fashion, although the use of extrinsic PEEP in these patients has not been shown to be beneficial as in COPD.
    • Dynamic hyperinflation without airflow obstruction occurs when not enough time is given for the patient to exhale, for example in high respiratory rate, low inspiratory flow, or high tidal volume in which there may not be enough time for the air to leave the lungs before the next respiratory cycle leading to air trapping. In cases like this application of extrinsic PEEP would be detrimental as it would generate backpressure preventing air to flow freely out of the lungs.

    When to suspect auto-PEEP

    • Exhalation is still ongoing when the next respiratory cycle starts. This can be easily checked by looking at the volume curve in the ventilator display. If this curve fails to go back to zero, then it is a sign that air is being trapped.
    • Increasing plateau pressures on the ventilator.
    • Active exhalation by the patient as seen by the use of accessory muscles of respiration during exhalation.
    • Drop-in blood pressure.
    • Long expiratory times.
    • Respiratory distress.

    Although there is a big differential for an intubated patient, who develops respiratory distress, the presence of a volume curve that does not go back to zero before the next breath is delivered is very highly suggestive of auto-PEEP.

    Treating auto-PEEP

    It is important to minimize or prevent the development of auto-PEEP in the ventilated population as its consequences may be dire.

    In the most extreme case in which patients are in respiratory distress and shock, disconnecting the patient from the ventilator and allowing enough time for exhalation before manually bagging the patient is a quick life-saving measure.

    For less dramatic cases, several measures can be taken to reduce the amount and prevent the development of auto-PEEP.

    Assuring enough time for exhalation so that all the air in the lungs can get out is the most important principle governing the prevention of auto-PEEP. This may be achieved by multiple methods:

    • Decreasing respiratory rate will increase the time between breaths and decrease the inspiratory to expiratory (I:E) ratio to 1:3 to 1:5.
    • Increasing the inspiratory rate to 60 to 100 L/min will assure fast delivery of air during inspiration, lending more time for exhalation.
    • Utilize a square waveform for ventilation delivery. This is uncomfortable for the patient but speeds the inspiration process.
    • Decrease tidal volume. When there is less air being pushed into the lungs, there is less air needed to be pushed out and less time is required to finish a full exhalation.
    • Decrease respiratory demand by decreasing CO2 and lactate production (minimize work of breathing, control fever and pain, ensure adequate sedation, control anxiety, treat sepsis)

    If there is also flow obstruction, minimize it by treating bronchoconstriction with bronchodilators and suctioning mucus plugs. Treat airway inflammation with steroids when indicated.

    The use of extrinsic PEEP is tricky, and although it may be beneficial, it has to be guided by good clinical sense. In cases of dynamic flow obstruction, especially in COPD where there is alveolar collapse, (Note: This does not include asthma where there is inflammation of the airway but not necessarily airway collapse.) the application of extrinsic PEEP will splint the airways open, permitting this way for air to be flushed from alveolar pouches and decreasing auto-PEEP. Extrinsic PEEP will also decrease the work of breathing in the appropriate setting. Nevertheless, when applied in the wrong setting, like in patients without dynamic airflow obstruction, the application of extrinsic PEEP will generate back pressure that will prevent air from getting out of the lungs, worsening air trapping. It is also important to understand that the extrinsic PEEP initially will add to the auto-PEEP, increasing the intrathoracic pressure. When used, it is recommended to maintain extrinsic PEEP below 75% to 85% of the auto-PEEP. Again, the use of extrinsic PEEP to treat auto-PEEP has to be driven by strong clinical sense as not all patients will benefit from it and others will be harmed. A practical way to assess the effects of extrinsic PEEP in auto-PEEP is to apply small increments of extrinsic PEEP and check the static pressures in the lungs. If the static pressures do not increase, then applying extrinsic PEEP may benefit the patient, but if the pressures increase, then it is time to back down on this strategy.

     

    Hypoxia – Causes, Symptoms, Diagnosis, Treatment

    Hypoxia is a state in which oxygen is not available in sufficient amounts at the tissue level to maintain adequate homeostasis; this can result from inadequate oxygen delivery to the tissues either due to low blood supply or low oxygen content in the blood (hypoxemia). Hypoxia can vary in intensity from mild to severe and can present in acute, chronic, or acute and chronic forms. This activity reviews the etiology, pathophysiology, and presentation of hypoxia and highlights the role of the interprofessional team in the management of affected patients.

    Hypoxia is a state in which oxygen is not available in sufficient amounts at the tissue level to maintain adequate homeostasis; this can result from inadequate oxygen delivery to the tissues either due to low blood supply or low oxygen content in the blood (hypoxemia).

    Hypoxia can vary in intensity from mild to severe and can present in acute, chronic, or acute and chronic forms. The response to hypoxia is variable; while some tissues can tolerate some forms of hypoxia/ischemia for a longer duration, other tissues are severely damaged by low oxygen levels.

    Hypoxia is a condition in which tissues of the body do not receive sufficient oxygen (O2) supply. The imbalance between tissue O2 supply and consumption results in an insufficient O2 supply to maintain cellular function. Hypoxia is defined as an O2 saturation (SpO2) < 90%. Hypoxemia is a decrease in oxygen tension in the arterial blood (PaO2) and is defined as a PaO2 < 60 mmHg. A SpO2 < 90% or a PaO2 < 60 mmHg places a patient on the “steep” area of the oxygen–hemoglobin dissociation curve, where small changes in PaO2 cause large changes in SpO2 and rapid clinical deterioration

    Types of Hypoxia

    • Asphyxia – condition of severely deficient supply of oxygen to the body caused by abnormal breathing
    • Cerebral hypoxia – Oxygen shortage of the brain or cerebral anoxia, a reduced supply of oxygen to the brain
    • Erotic asphyxiation – Intentional restriction of oxygen to the brain for sexual arousal or autoerotic hypoxia, intentional restriction of oxygen to the brain for sexual arousal
    • Fink effect – Changes of oxygen partial pressure in the pulmonary alveoli caused by a soluble anesthetic gas, or diffusion hypoxia, a factor that influences the partial pressure of oxygen within the pulmonary alveolus
    • G-LOC cerebral hypoxia induced by excessive g-forces
    • histotoxic hypoxia, the inability of cells to take up or utilize oxygen from the bloodstream
    • Hyperoxia – exposure of tissues to abnormally high concentrations of oxygen.
    • Hypoventilation training – Physical training method in which reduced breathing frequency are interspersed with periods with normal breathing
    • Hypoxemia – Abnormally low level of oxygen in the blood or hypoxemic hypoxia, a deficiency of oxygen in arterial blood
    • Hypoxia in fish – Response of fish to environmental hypoxia, responses of fish to hypoxia
    • Hypoxia-inducible factors
    • Hypoxic hypoxia, a result of insufficient oxygen available to the lungs
    • Hypoxic ventilatory response
    • Hypoxicator a device intended for hypoxia acclimatisation in a controlled manner
    • Intermittent hypoxic training
    • Intrauterine hypoxia, when a fetus is deprived of an adequate supply of oxygen
    • Latent hypoxia – Tissue oxygen concentration which is sufficient to support consciousness at depth, but not at surface pressure or deep water blackout, loss of consciousness on ascending from a deep freedive
    • Pseudohypoxia, increased cytosolic ratio of free NADH to NAD+ in cells
    • Rhinomanometry
    • Sleep apnea – Disorder involving pauses in breathing during sleep
    • Time of useful consciousness
    • Tumor hypoxia, the situation where tumor cells have been deprived of oxygen

    Causes of Hypoxia

    There are two major causes of hypoxia at the tissue level, low blood flow to the tissue, or low oxygen content in the blood (hypoxemia).

    In order to understand the mechanism of hypoxia, we have to know that in order to have the oxygen carried by hemoglobin, direct interaction between red blood cells in pulmonary capillaries and the air in the alveoli is needed. This process can be compromised at any one of the following three points: blood flow to the lung (perfusion), airflow to the alveoli (ventilation), and the gas exchange through the interstitial tissue (diffusion).

    The brain depends on the blood to provide it with a constant supply of oxygen. Thus disruptions to any part of the body that plays a role in blood or oxygen supply can lead to hypoxia. The four primary causes of hypoxia are:

    • No blood supply to the brain – This occurs when the blood vessels that supply the brain with blood are completely obstructed. This is extremely rare and usually fatal.
    • Low blood supply to the brain – Low blood supply can occur when even a single blood vessel is blocked or partially obstructed, as often happens with a stroke. This form of hypoxia frequently affects a specific region of the brain, interfering with functions governed by that region.
    • No blood oxygen – When the body can’t take in oxygen, or the heart or lungs can’t properly provide the blood with oxygen, the brain — and all other organs — suffer from hypoxia. This is quickly fatal.
    • Low blood oxygen – When the body can’t properly oxygenate the blood, often due to illnesses such as emphysema or a crisis such as a heart attack, the brain gets less oxygen than it needs to properly function.

    Reduced Oxygen Tension

    As in cases of high altitude.

    Hypoventilation

    • Airway obstruction can be proximal as in laryngeal edema or foreign body inhalation, or distal as in bronchial asthma or chronic obstructive pulmonary disease (COPD).
    • Impaired respiratory drive as in cases of deep sedation or coma.
    • Restricted movement of the chest wall as in obesity hypoventilation syndrome, circumferential burns, massive ascites, or ankylosing spondylitis.
    • Neuromuscular diseases, such as myasthenia gravis, muscular dystrophy, amyotrophic lateral sclerosis, or phrenic nerve injuries.

    Ventilation-Perfusion Mismatch (V/Q Mismatch)

    • Decreased V/Q Ratio (impaired ventilation or high perfusion) such as chronic bronchitis, obstructive airway disease, mucus plugs, pulmonary edema impair the ventilation and therefore decrease the ratio of ventilation to perfusion.
    • Increased V/Q Ratio (impaired perfusion): such as in cases of pulmonary embolism or increased ventilation as in emphysema (large bullae in the lungs) the surface area available for gas exchange is decreased, which causes higher ventilation in comparison to perfusion leading to a high V/Q ratio.

    Others

    • Hypoxemic Hypoxia – Low oxygen tension in the arterial blood (PaO2) is due to the inability of the lungs to properly oxygenate the blood. Causes include hypoventilation, impaired alveolar diffusion, and pulmonary shunting.
    • Circulatory Hypoxia – It is due to pump failure (heart is unable to pump enough blood, and therefore oxygen delivery is impaired).
    • Anemic Hypoxia – It is because of a decrease in oxygen-carrying capacity due to low hemoglobin leading to inadequate oxygen delivery.
    • Histotoxic Hypoxia (Dysoxia) – Cells are unable to utilize oxygen effectively, the best example of this is Cyanide poisoning which inhibits the enzyme cytochrome C oxidase in the mitochondria, blocking the use of oxygen to make ATP.
    • Traveling to high altitudes, especially for people in poor health and for those who quickly rise to high altitudes.
    • Carbon monoxide poisoning.
    • Strangulation or smothering. For example, the choke holds that some law enforcement officers use can cause hypoxia if held too long.
    • Very low blood pressure, which is usually caused by something else, such as a hemorrhage.
    • Smoke inhalation.
    • Choking.
    • Heart attack or stroke.
    • Medical conditions such as a heart attack or stroke.
    • Allergic reactions that lead to anaphylactic shock.
    • Severe cases of asthma.
    • Allergies
    • In infants, improper sleep positions or unsafe sleep environments. For example, young babies can be smothered in crib bumpers, or get inadequate oxygen while sleeping on their stomachs.
    • Hyperventilation.

    Right to Left Shunt

    The blood crosses from the right to the left side of the heart without being oxygenated. Causes include:

    • Anatomic Shunts: Blood bypasses the alveoli, e.g., intracardiac shunts (ASD, VSD, PDA), pulmonary arteriovenous malformations, fistulas, and hepato-pulmonary syndrome.
    • Physiologic Shunting: Blood passes through non-ventilated alveoli, for example, pneumonia, atelectasis, and ARDS.

    Impaired Diffusion of Oxygen

    Oxygen diffusion is impaired between the alveolus and the pulmonary capillaries. Causes are usually interstitial edema, interstitial inflammation, or fibrosis. Clinical examples include pulmonary edema and interstitial lung disease.

    Hypoventilation

    This includes the factors that decrease the percentage of oxygen in the alveoli, either due to obstruction of the airways or an increase in partial pressure of alveolar gases other than oxygen. Carbon dioxide is one example. Hypoventilation can also occur due to impaired respiratory drive as in cases of deep sedation or because of restricted movement of the chest wall as in obesity hypoventilation syndrome or ankylosing spondylitis. In this setting, the A-a gradient will be normal as the oxygen is deficient in both alveoli and the bloodstream.

    In alveoli, an increase in partial pressure of one gas will be on the cost of the other gases composing the air, e.g., an increase in carbon dioxide partial pressure results in a decrease of partial pressure of oxygen, both at alveolar as well as the arterial level. This type of hypoxemia is easily corrected with supplemental oxygen.

    Ventilation-Perfusion Mismatch (V/Q Mismatch)

    This occurs when there is an imbalance between lung ventilation and blood flow. Even in the normal lung, there is a V/Q mismatch. In an upright individual, the V/Q ratio is higher in the apices than at the lung base. This difference is responsible for the normal A-a gradient. V/Q mismatch increases in pulmonary vascular disease, thromboembolic disease, or atelectasis to name a few. Such a process ultimately results in hypoxemia which is more difficult to correct with supplemental oxygen.

    Right to Left Shunt

    Occurs when blood passes from the right to the left side of the heart without being oxygenated. Anatomic abnormalities, such as atrial or ventricular septal defects as well as pulmonary arteriovenous malformations can cause hypoxemia that is notoriously difficult to correct with supplemental oxygen. Similar physiology is observed in hepato-pulmonary syndrome. Physiologic right-to-left shunt exists when the blood passes through non-ventilated alveoli in cases of atelectasis, pneumonia, and acute respiratory distress syndrome (ARDS).

    Impaired Diffusion of Oxygen Across the Alveoli into Blood

    The usual causes are interstitial edema, lung tissue inflammation, or fibrosis. Depending on the disease’s extent, a moderate to a large amount of supplemental oxygen may be required to correct this type of hypoxemia. Exercise can worsen hypoxemia resulting from impaired diffusion. An increase in cardiac output with exercise results in accelerated blood flow through alveoli, reducing the time available for gas exchange. In the case of the abnormal pulmonary interstitium, gas exchange time becomes insufficient, and hypoxemia ensues.

    Symptoms of Hypoxia

    Oxygen plays an important part in your body’s cells and tissues. The only way for your body to get oxygen is through your lungs.

    COPD results in inflammation and swelling of your airways. It also causes the destruction of the lung tissue called alveoli. COPD causes a restricted flow of oxygen in your body as well.

    Symptoms of hypoxia often include:

    • shortness of breath while resting
    • severe shortness of breath after physical activity
    • decreased tolerance to physical activity
    • waking up out of breath
    • feelings of choking
    • wheezing
    • frequent cough
    • bluish discoloration of the skin
    • Changes in the color of your skin, ranging from blue to cherry red
    • Confusion
    • Cough
    • Fast heart rate
    • Rapid breathing
    • Shortness of breath
    • Slow heart rate
    • Sweating
    • Wheezing

    Symptoms of oxygen deprivation include

    • Something obstructing the face, mouth, or nose; increased carbon monoxide exposure can be a problem in enclosed areas, so a person in a very small space or whose face is covered may suffer from oxygen deprivation even if they can breathe.
    • Changes in mood or personality; the victim may seem confused.
    • Loss of consciousness, including fainting or seizures.
    • Blue or white lips, tongue, or face.
    • Tingling in the extremities.
    • Pupils that don’t respond normally to light.
    • Not breathing, or not expelling air when exhaling.
    • Hyperventilating or gasping for air.
    • Unable to speak; a person who is truly choking may not cough.

    COPD is a chronic condition, so you may experience any of these symptoms on an ongoing basis. If you experience any of these symptoms, it’s considered a medical emergency.

    You should call your local emergency services, or go to an emergency room, if you experience a change from your baseline or if your symptoms worsen. This is especially important if the symptoms are associated with chest pain, fever, fatigue, or confusion.

    Diagnosis of Hypoxia

    The presentation of hypoxia can be acute or chronic; acutely the hypoxia may present with dyspnea and tachypnea. Symptom severity usually depends on the severity of hypoxia. Sufficiently severe hypoxia can result in tachycardia to provide sufficient oxygen to the tissues. Some of the signs are very evident on physical exam; stridor can be heard once the patient arrives in cases of upper airway obstruction. Skin can be cyanotic, which might indicate severe hypoxia.

    When oxygen delivery is severely compromised, organ function will start to deteriorate. Neurologic manifestations include restlessness, headache, and confusion with moderate hypoxia. In severe cases, altered mentation and coma can occur, and if not corrected quickly may lead to death.

    The chronic presentation is usually less dramatic, with dyspnea on exertion as the most common complaint. Symptoms of the underlying condition that induced the hypoxia can help in narrowing the differential diagnosis. For instance, productive cough and fever will be seen in cases of lung infection, leg edema, and orthopnea in cases of heart failure, and chest pain and unilateral leg swelling may point to pulmonary embolism as a cause of hypoxia.

    The physical exam may show tachycardia, tachypnea, and low oxygen saturation. Fever may point to infection as the cause of hypoxia.

    Lung auscultation can yield a lot of useful information. Bilateral basilar crackles may indicate pulmonary edema or volume overload, other signs of that includes jugular venous distention and lower limb edema. Wheezing and rhonchi can be found in obstructive lung disease. Absent unilateral air entry can be caused by either massive pleural effusion or pneumothorax. Chest percussion can help differentiate the two and will reveal dullness in cases of pleural effusion and hyper-resonance in cases of pneumothorax. Clear lung fields in a setting of hypoxia should raise suspicion of pulmonary embolism, especially if the patient is tachycardic and has evidence of deep vein thrombosis (DVT).

    Lab Test And Imaging

    Evaluation of Acute Hypoxia

    Pulse Oximetry to Evaluate Arterial Oxygen Saturation (SaO2)

    The arterial oxygen saturation (SaO2) refers to the amount of oxygen bound to hemoglobin in arterial blood. The measurement is given as a percentage. Resting SaO2 less than or equal to 95% or exercise desaturation greater than or equal to 5% is considered abnormal. However, clinical correlation is always necessary as the exact cutoff below which tissue hypoxia ensues has not been defined.

    Arterial Blood Gas

    It is a useful tool to evaluate hypoxemia. Aside from the diagnosis of hypoxemia, additional information obtained, such as PCO2, can shed light on the etiology of the process.

    • Arterial oxygen tension (PaO2): Partial pressure of oxygen is the amount of oxygen dissolved in the plasma. A PaO2 less than 80 mmHg is considered abnormal. However, this should be in line with the clinical situation.
    • The partial pressure of CO2: It is an indirect measure of exchange of CO2 with the air via the alveoli, its level is related to minute ventilation. PCO2 is elevated in hypoventilation like in obesity hypoventilation, deep sedation, or maybe in the setting of acute hypoxia secondary to tachypnea and washout of CO2.

    PaO2:FiO2 ratio (Normal ratio is 300 to 500), if this ratio drops this may indicate a deterioration in gas exchange, this is particularly important in defining ARDS.

    Imaging

    Imaging studies of the chest, such as chest x-rays or CT help in identifying the cause of the hypoxia, e.g., pneumonia, pulmonary edema, hyperinflated lungs in COPD, and other conditions. CT chest can give more detailed images that outline the exact pathology, CT angiogram of the chest is of particular importance in detecting the pulmonary embolism. Another modality is the VQ scan which can detect the ventilation-perfusion mismatch, which is helpful in diagnostics of acute or chronic pulmonary embolism. VQ scan can be particularly useful when renal failure or allergy to iodinated contrast increases the risks of CT angiography.

    The first step in evaluating the hypoxia is to calculate the A-a gradient of oxygen. This is the difference in the amount of oxygen between the Alveoli “A” and the amount of oxygen in the blood “a.” In other terms, the A-a oxygen gradient = PAO2 – PaO2.

    PaO2 can be obtained from the arterial blood gas; however, PAO2 is calculated using the alveolar gas equation:

    • PAO2 = (FiO2 x [760-47]) – PaCO2/0.8)

    760 is the atmospheric pressure at the sea level in mmHg, 47 is the partial pressure of water at a temperature of 37 C, and 0.8 is the steady-state respiratory quotient.

    The A-a gradient changes with age, and thus it is corrected for age using this equation; A-a gradient = (age/4+4).

    If the A-a gradient is normal, then the cause of hypoxia is low oxygen content in the alveoli, either due to low O2 content in the air (low FiO2, as in the high altitude) or more commonly due to hypoventilation like the central nervous system (CNS) depression, OHS, or obstructed airways as in COPD exacerbation.

    If the gradient is height then the cause of hypoxia is either due to a diffusion defect or perfusion defect (VQ mismatch), an alternative explanation is shunting of blood flow around the alveolar circulation, administering 1.0 FiO2 may help differentiate the two, as the oxygenation will improve in VQ mismatch in contrast to cases where shunt physiology is present.

    PaO2:FiO2 Ratio

    This ratio is another way to measure the degree of hypoxia. A normal PaO2/FiO2 ratio is about 300 to 500 mmHg. The ratio of less than 300 indicates abnormal gas exchange, and values less than 200 mmHg indicate severe hypoxemia. The PaO2/FiO2 ratio is used mostly as a definition of acute respiratory distress syndrome severity.

    Evaluation of Chronic Hypoxia

    Pulmonary Function Test (PFT)

    PFT provides a direct measure of the lung volumes, bronchodilator response, and diffusion capacity, which can help in establishing the diagnosis and guiding the treatment of lung disorders. Aiding the history and physical exam, PFTs can be used to differentiate between the obstructive (bronchial asthma, COPD, upper airway obstruction) versus restrictive lung diseases (interstitial lung diseases, chest wall abnormalities). PFTs play a role in the assessment of airway obstruction severity as well as a response to therapy. One has to keep in mind that PFTs are effort-dependent and require the patient’s ability to cooperate and understand instructions.

    Nocturnal (overnight) Trend Oximetry

    It provides information about oxyhemoglobin saturation over a period (usually overnight). This test is primarily used to assess adequacy or need for oxygen supplementation at night. Use of overnight trend oximetry as a surrogate for a diagnostic sleep study is possible, however, is discouraged. A formal sleep study should be used whenever possible.

    Six-Minute Walk Test

    This test provides information on oxyhemoglobin saturation response to exercise as well as the total distance a patient can walk in 6 minutes on a ground level. This information can be used to titrate oxygen supplementation as well as evaluate the response to therapy. The 6-minutes walk test is frequently used in the preoperative pulmonary evaluation, pulmonary hypertension treatment and assessment of supplemental oxygen need with exercise.

    Hemoglobin

    Secondary polycythemia can be an indicator of chronic hypoxia.

    Treatment of Hypoxia

    Management of hypoxia falls under 3 categories: maintaining patent airways, increasing the oxygen content of the inspired air, and improving the diffusion capacity.

    Maintaining Patent Airways

    Ensure patency of the upper airways with good suctioning, maneuvers that prevent occlusion of the throat (head tilt and jaw thrust if necessary), sometimes the placement of an endotracheal tube or tracheostomy is necessary.

    In chronic conditions like obesity hyperventilation syndrome, maintaining patent airways can be achieved with positive pressure ventilation like CPAP or BiPAP.

    Bronchodilators and aggressive pulmonary hygiene, such as chest physiotherapy, the flutter valve, and incentive spirometry can be used to maintain the patency of the lower airways.

    Increase Fraction of the Inspired O2 (FiO2)

    This is indicated for low PaO2 less than 60 or SaO2 less than 90, and this can be achieved by increasing the percentage of oxygen in the inspired air that reaches the alveoli.

    Low-Flow Devices

    Nasal Cannula
    • Use: mild hypoxia (with FiO2 approximately 92%)
    • Flow rate: up to 6 L per minute
    • FiO2 delivered: up to 45% (0.45)
    • Advantage: Easy to use and more convenient to the patient (can be used during eating, drinking, talking)
    • Disadvantage: Dry nasal mucosa (humidify if the flow is greater than or equal to 4 L per minute), FiO2 being delivered varies greatly. Mouth breathers derive less benefit from using a nasal cannula.
    • The following formula can be used to approximate the percentage of FiO2; FiO2 = 20% + (4 times oxygen flow liters) For example, oxygen flow 2L/min would deliver approximately FiO2 of 0.3, 6 L per minute would deliver approximately FiO2 of 0.45 (more commonly known as 45%).
    Simple Face Mask
    • Use: Moderate to severe hypoxia, initial treatment
    • Flow rate: up to 10 L per minute
    • FiO2 delivered: 35% to 50%
    • Advantage: provides higher FiO2, no pressures involved, well tolerated by patients
    • Disadvantage: Dry oral mucosa (needs humidification), the flow must be at least 5 L per minute to flush CO2, not high flow. Also, the mask itself can interfere with activities of daily living.
    Reservoir Cannulas (Oxymizer)
    • The device uses a reservoir space, which stores O2 during expiration, making it available as a bolus during the next inspiration. This way the patient gets a higher oxygen delivery without increasing flow.
    • Flow rate: up to 16 L per minute.
    • FiO2 = up to 90% (0.9)
    • Reservoir cannulas are available as mustache configuration (Oxymizer), where the  reservoir is located directly beneath the nose, pendant configuration (Oxymizer Pendant) which is connected to a plastic reservoir on the anterior chest
    Partial-rebreather Mask
    • Has a 300 to 500 mL reservoir bag and 2 one-way valves to prevent exhaling into the reservoir
    • Use: Moderate to severe hypoxia, initial treatment
    • Flow rate: 6 to 10 L per minute (flow must be sufficient to keep reservoir bag from collapse during inspiration)
    • FiO2 delivered: 50% to 70%
    • Advantage: Higher FiO2 can be delivered
    • Disadvantage: Interferes with activities of daily living
    Non-rebreather Mask
    • Has a 300 to 500 mL reservoir bag and 2 one-way valves
    • Use: Moderate to severe acute hypoxia, initial treatment
    • Flow rate: 10 to 15 (at least 10 L per minute to avoid bag collapse during inspiration)
    • FiO2 delivered: 85% to 90%
    • Advantage: even higher FiO2 can be achieved
    • Disadvantage: Interferes with activities of daily living

    High-Flow Devices 

    Usually, this requires an oxygen blender, humidifier, and heated tubing.

    Venturi Mask
    • Mask attached an air entrainment valve
    • Use: Moderate to severe hypoxia, initial treatment
    • The flow rate and FiO2: (depends on the color). (Blue = 2 to 4 L per minute = 24% O2, White = 4 to 6 L per minute = 28% O2, Yellow = 8 to 10 L per minute = 35% O2, Red = 10 to 12 L per minute = 40% O2, Green = 12 to 15 L per minute = 60% O2)
    • Advantage: provides the most accurate O2 delivery, high flow
    • Disadvantage: need to be removed for eating. Less accurate at high flow rates
    • Does not guarantee the total flow with O2 percentages above 35% in patients with high inspiratory flow demands; the problem with air entrainment systems is that as this is increased, the air to oxygen ratio decreases
    High-flow Nasal Cannula
    • High-flow oxygen (HFO) consists of a heated, humidified O2
    • Flow rate: 10 to 60 L per minute
    • FiO2 delivered: Up to 100%
    • Advantages: More convenient, Can deliver up to 100% heated and humidified oxygen at a maximum flow of 60 L
    • Disadvantages: Fairly large cannula, can be a source of (although usually rather minimal) discomfort
    Air/oxygen Blender
    • Provides accurate oxygen delivery independent of the patient’s inspiratory flow demands
    • Positive end-expiratory pressure may be generated
    • For approximately every 10 liters of flow delivered, about 1 cm/HO of positive pressure is obtained

    Positive Pressure Ventilation

    It allows for accurate delivery of any necessary FiO2 and includes the following:

    Non-Invasive Ventilation

    It is usually used as the last resort to avoid the intubation

    Continuous Positive Airways Pressure Mask (CPAP)
    • Mainly used in patients with obstructive sleep apnea or in acute pulmonary edema.
    • Delivers oxygen (or air) under pre-determined high pressure via a tightly fitting face mask.
    • Positive pressure is continuous, to ensure that the airways are open (split them)
    Bilevel Positive Airways Pressure (BiPAP)
    • Mainly used in patients with acute Hypercarbia as in patients with COPD exacerbation and ARDS patients.
    • High positive pressure on inspiration and lower positive pressure on expiration.
    • Pressure delivery is variable throughout the respiratory cycle, with high positive pressure on inspiration and lower positive pressure on expiration.

    Invasive Ventilation

    • Positive pressure ventilator attached to (usually) endotracheal tube.
    • Allows for accurate delivery of predetermined minute ventilation as well as accurate FiO2 and positive end-expiratory pressure.
    • Can be used electively during surgery.

    Improve the Diffusion of Oxygen through the Alveolar Interstitial Tissue

    The overall idea s to treat the underlying cause of respiratory failure:

    • Diuretics can be used in cases of pulmonary edema.
    • Steroids in certain cases of interstitial lung disease.
    • Extracorporeal membrane oxygenation (ECMO) can be used as an ultimate method of increasing oxygenation.

    Other Issues

    The characteristics of each category of hypoxemia are as follows:
    • Hypoventilation presents with an elevated PaCO2 with a normal A-a gradient.
    • Low-inspired oxygen presents with a normal PaC02 plus normal A-a gradient.
    • Shunting presents with a normal PaC02 and elevated A-a gradient that does not correct with the administration of 100% oxygen.
    • V/Q mismatch presents with a normal PaC02 and elevated A-a gradient that does correctly with 100% oxygen.
    • Oxygen supplementation varies between FiO2 of 0.21 and 1.00. A variety of low and high flow devices exist to facilitate this process, each with unique advantages and disadvantages.
    • The delivery of oxygen depends on two variables:
      • FiO2
      • Flow rate
    • There are several devices designed to deliver oxygen at different rates and concentrations as described above.
    • Oxygen toxicity may result if oxygen is delivered at a higher concentration for a long duration of time.
    • Decreased body temperature decreases metabolic rate, which lowers oxygen consumption and minimizes the adverse effects of tissue hypoxia (especially brain) Therapeutic hypothermia is based on this principle.
    • Long-term oxygen therapy can reduce mortality, and it is indicated in these patient populations:
      • Group 1 (Absolute): PaO2 55 mm Hg or SaO2  88%
      • Group 2 (In the presence of cor pulmonale): PaO2 55 to 59 mm Hg or SaO2 89%, ECG evidence of right atrial enlargement, hematocrit greater than  55%, congestive heart failure

     

    Ventilator-Induced Lung Injury – Causes, Symptoms, Treatment

    Ventilator-induced lung injury is the acute lung injury inflicted or aggravated by mechanical ventilation during treatment and has the potential to cause significant morbidity and mortality. The potential morbidity and the mortality impact of ventilator-induced lung injury are increasingly recognized across the world. However, accurate data on the incidence and prevalence of this condition is still scanty. This activity covers the etiology, clinical evaluation, and measures to attenuate or prevent this dreaded condition highlighting the importance of an interprofessional team in the diagnosis and management.

    Ventilator-induced lung injury (VILI) is the acute lung injury inflicted or aggravated by mechanical ventilation during treatment. Ventilator-induced lung injury could occur during invasive as well as non-invasive ventilation and might contribute significantly to the morbidity and mortality of critically ill patients. Though mechanical ventilation potentially injures both normal and diseased lungs, the injury will be much more severe in the latter due to higher microscale stresses. Ventilator-induced lung injury (VILI) has been used synonymously with ventilator-associated lung injury (VALI). However, the latter terminology is more appropriate when the lung injury is strongly presumed to be due to ventilation but lacking any strong evidence to confirm the same.

    The concept of injury by mechanical ventilation dates back to 1744 when John Fothergill, after successful resuscitation of a patient by mouth to mouth respiration, expressed the view that mouth to mouth ventilation might be a better option than machine bellows in resuscitation since the latter could potentially harm the lungs with the uncontrolled push of air. Investigators during the 1952 polio epidemic had documented structural lung damages caused by mechanical ventilation.

    In 1967, the term “respirator lung” was coined to describe the post mortem lung pathology of patients who had undergone mechanical ventilation and whose lungs showed extensive alveolar infiltrates and hyaline membrane formation. Further confirmatory evidence for ventilator-induced lung injury comes from the landmark ARDS Nett trial, where low tidal volume ventilation was proved to be superior to high tidal volume ventilation in ARDS patients.

    Causes of Ventilator-Induced Lung Injury

    The predominant mechanisms by which the ventilator-induced lung injury occurs include alveolar overdistention (volutrauma), barotrauma, atelectotrauma, and inflammation (biotrauma). Other mechanisms that are attributed include adverse heart-lung interactions, deflation-related, and effort-induced injuries. Related factors being studied in this context also include heterogeneous local lung mechanics, alveolar stress frequency, and stress failure of pulmonary capillaries. Variation in the expression of genetically determined inflammatory mediators has been known to affect VILI susceptibility.

    In a study on  332 mechanically ventilated patients who were not having ARDS at the initiation of ventilation, the risk factors found for ventilator-induced lung injury were larger tidal volume, blood product transfusion, acidemia, and history of restrictive lung disease. Though factors such as respiratory acidosis, respiratory rate, pulmonary vascular pressures, and body temperature are found to be associated with ventilator-induced lung injury, many experts consider them only as second-order effects at this stage.

    The excessive stretch from high tidal volumes results in volutrauma. Faridy et al., in their study on dogs, found that increasing the tidal volume and decreasing the PEEP resulted in lower lung volumes for similar transpulmonary pressures. They concluded that high tidal volume and lower PEEP resulted in high surface-activ forces, which could cause collapse and inflammation of the lungs. Dreyfuss et al., in a 1988 paper, described the development of pulmonary edema in animals undergoing ventilation at high tidal volumes. It was also noticed that such edema did not develop in animals with similar airway pressures when the lower tidal volume is ensured with straps around the chest and abdomen. A randomized controlled trial by Amato et al., and subsequently, the landmark ARDS Nett study, have indisputably proved that low tidal volume ventilation improves the morality in ARDS patients. Even a higher tidal volume due to high patient efforts on non-invasive ventilation could result in self-inflicted lung injury.

    Barotrauma is a pressure-related lung injury. Limiting the inflation pressure to prevent overdistension has conventionally been used as a part of the lung-protective strategy(i.e., plateau pressure < 28 to 30 cms H2O) for ARDS patients. Air leaks, pneumothoraces, and pneumomediastinum could result from overdistention. One also needs to understand that regional lung overdistention is a key factor for such ventilator-induced lung injuries. However, the evaluation of local lung mechanics is experimental at this stage. Transpulmonary pressure, which is the difference between alveolar pressure and pleural pressure, is the pressure that keeps the lung inflated when the airflow is zero at end inspiration. Hence there is a strong relation between transpulmonary pressure and tidal volume. Plateau pressure has been used as a surrogate of transpulmonary pressure at the bedside despite certain inherent limitations.

    Animal experiments have shown that cyclical opening and closing of the atelectatic alveoli during the respiratory cycle could damage the adjacent non- atelectatic alveoli and airways by shear stress forces. This mechanism is called atelectotrauma. The application of optimal PEEP is important in the prevention of atelectrauma. Higher PEEP can cause alveolar overdistension, and lower PEEP may be inadequate to stabilize the alveoli and keep them open. The first in vivo study on VILI was published in 1974 by Webb and Tierney who found that rats ventilated at high airway pressures without PEEP died shortly with florid hemorrhagic pulmonary edema, and this could be mitigated by the application of PEEP  while maintaining the same airway pressure.

    Biotrauma is the release of inflammatory mediators from the cells in the injured lungs in response to volutrauma and atelectotrauma. In ventilator-induced lung injury, the neutrophils, macrophages, and probably alveolar epithelial cells secrete various inflammatory mediators, including TNF-alpha, interleukins 6 & 8, transcription factor nuclear factor(NF)-kB, and matrix metalloproteinase-9. These cytokines could trigger detrimental effects locally and systemically, resulting in multiorgan failure.

    Adverse heart-lung interaction could result in ventilator-associated lung injury, especially in the setting of high tidal volume and low PEEP, as observed in animal studies. During inspiration, the pulmonary blood flow is significantly decreased due to compression of the right ventricular cavity by the expanding lung, and the blood flow is exaggerated during expiration. This results in a  cyclic occurrence of high flow- no flow-high flow state, which damages pulmonary capillaries’ endothelium, termed capillary stress failure. An endothelial injury could result in increased permeability of capillaries, promoting leakage of protein and water, resulting in pulmonary edema. Within a period of about 20 minutes, left ventricular failure with pulmonary edema ensues as a result of right ventricular failure and RV dilatation, pushing the interventricular septum towards the left ventricle, thereby increasing the left ventricular end-diastolic pressure.

    In a 2018 publication, Katira et al. showed that abrupt deflation after sustained inflation could cause ventilator-induced lung injury in rat models. Extrapolating these findings into human scenarios, any abrupt disconnection from the mechanical ventilator could potentially cause lung injury by loss of PEEP with resultant alveolar collapse. The authors have termed this phenomenon as lung deflation injury. The authors attribute this phenomenon to decreased cardiac output during sustained inflation, which is usually compensated by increased systemic vascular resistance to maintain blood pressure. When there is sudden deflation, the cardiac output becomes normalized but faces significant afterload due to the increased systemic vascular resistance, which results in back pressure causing increased left ventricular end-diastolic pressure and pulmonary edema. Another contributory factor is the high pulmonary forward blood flow after sudden deflation causing sudden high pressure in capillaries, causing capillary injury. The authors suggest avoiding open suctioning and slow lowering of PEEP in ventilated ARDS patients. Abrupt disconnection from NIV could also cause potential harm, as per the authors.

    The following points need to be noted to understand the concept of effort-induced lung injury(self-inflicted lung injury). Early paralysis has been known to improve lung function and mortality.. A post hoc analysis of the LUNG SAFE study showed that patients with severe ARDS fared worse on NIV than mechanical ventilators. Airway pressure release ventilation(APRV) in a single centered randomized trial showed high mortality in the interventional group, promoting spontaneous breathing.

    Patients with already injured lung are much more susceptible to effort-induced lung injury. The proposed mechanisms of lung injury during spontaneous efforts at breathing include increased pleural negative pressure during spontaneous efforts causing increased transpulmonary pressure resulting in higher tidal volumes causing volutrauma, pendelluft phenomenon resulting in tidal recruitment of injured alveoli, increased transvascular pressure predisposing to pulmonary edema in volume cycled mode, and patient-ventilator asynchrony.

    Driving pressure is the difference between the plateau pressure and PEEP, and is also derived by dividing Vt by static compliance of the respiratory system (Crs). In 2002, Estenssoro et al. first described the consistent ability of driving pressure values in the first week to identify survivors versus non-survivors in ARDS patients (along with other variables, including P/F ratio and SOFA). Amato et al., in a 2015 meta-analysis on more than 3500 patients, showed that driving pressure is the physical variable that has correlated best with mortality. A driving pressure-based ventilatory strategy to prevent lung injury in ARDS patients on a ventilator has been proposed and debated actively.

    Ventilator-induced lung injury mostly occurs in patients with underlying physiological insults such as sepsis, trauma, and major surgery, where the immune system is already primed for a cascading response to mechanical lung injury. Volutrauma, atelectrauma, and biotrauma are the key mechanisms of ventilator-induced lung injury, although each component’s relative contribution is unclear at this stage. Alveolar distention and injury cause increased alveolar permeability, alveolar and interstitial edema, alveolar hemorrhage, and formation of hyaline membranes, resulting in diminished functional surfactant with resultant alveolar collapse.

    Diagnosis of Ventilator-Induced Lung Injury

    Clinical diagnosis of ventilator-induced lung injury is made at the bedside with a high degree of suspicion and ruling out of other causes that could closely mimic the picture. The patient on a mechanical ventilator typically develops worsening hypoxemia with low PaO2 and a fall in saturation. X-ray chest will show bilateral diffuse alveolar/interstitial infiltrates without cardiac enlargement. A CT scan thorax may show heterogeneous consolidation and atelectasis with focal areas of hyperlucencies suggestive of alveolar overdistension.

    New-onset pulmonary infections and pulmonary edema are the commonest differential diagnosis to be ruled out initially. A thorough bedside clinical evaluation needs to be performed to exclude new-onset bronchospasm or crackles. Evidence for pneumothorax, pleural effusion, limb edema, ascites, and intra-abdominal hypertension has to be evaluated. The history of drug allergy or blood product transfusion needs to be clarified. Ventilatory settings need to be cross-checked to look for any contributing factors for acute lung injury.

    Lab Test and Imaging

    Evaluation should be targeted at ruling out other associated etiologies causing hypoxemia in ventilated patients. Aspiration, infective pneumonia, auto PEEPing, acute coronary syndromes, venous, fat, air or amniotic fluid embolism, pneumothoraces, pleural effusion, and intra-abdominal distension are to be ruled out. A thorough clinical evaluation bedside chest X-ray, ultrasound of the chest and abdomen along with a 12 lead ECG with a bedside ECHO can throw light to rule out most of the above etiologies. Auto PEEPing could be detected by analyzing the flow-time curve.

    Chest X-ray in ventilator-induced lung injury could be almost similar to ARDS patients. It will show bilateral diffuse alveolar interstitial shadows without cardiomegaly. A CT scan thorax can show bilateral heterogeneous consolidation and atelectasis with focal areas of hyperlucency consistent with alveolar distension.

    Laboratory investigations include lipase levels, cardiac enzymes & blood culture, and other body secretions. A lower limb Doppler and CT pulmonary angiogram may be necessary in certain cases. Fiber-optic bronchoscopy and biopsy are rarely indicated.

    Gattinoni et al., in a 2016 paper, hypothesized that ventilator-related etiology of lung injury could be converted into a single variable called mechanical power. Mechanical power can be computed from tidal volume/driving pressure, flow, PEEP, and respiratory rate. They have proposed a simple ventilator software where the mechanical power equation (hence identifying the contribution of each component causing ventilator-induced lung injury) could be easily computed and analyzed at the bedside.

    A 2019 review mentions that quantitative bedside measurement of dynamic elastance (E) and the interpretation of the way it varies as a function of time and PEEP could be utilized to evaluate not only the degree and nature of lung injury but also the degree of contributions each from volutrauma, and atelectrauma.

    Treatment of Ventilator-Induced Lung Injury

    The most important measure to prevent ventilator-induced lung injury is to select appropriate ventilatory settings that prevent overdistension of alveoli, causing volutrauma and biotrauma and atelectrauma.

    The concept of “baby lung’ in ARDS represents the relatively small areas of aerated normal lung (which is just the size of a baby’s lung), which needs to be protected from injury during mechanical ventilation. Since most of the remaining alveoli are non-aerated and collapsed, delivery of a large tidal volume could overinflate the baby lung areas inciting lung injury. The baby lung is not a fixed anatomic structure since redistribution of dependent atelectasis occurs in prone positioning. The ideal tidal volume might have been the tidal volume required to ventilate the baby’s lung, which has been evaluated only in physiologic studies at this stage.

    In ARDS patients, a low tidal volume strategy of 6 ml /Kg of predicted body weight(PBW) has been shown to prevent overdistension of the alveoli and improved mortality when compared with a higher tidal volume (i.e., 12 ml/Kg of predicted body weight) as shown in the ARDS Nett trial. In non-ARDS patients, a meta-analysis of 15 small randomized control trials and 5 large observational studies concluded that a tidal volume of 6-8 ml/Kg of predicted body weight is associated with improved survival. Patients with mild to moderate ARDS who are on a trial of non-invasive ventilation could generate high efforts with large tidal volumes, which have the potential to harm the lung. It is better to abort NIV in such settings and consider early intubation.

    PEEP is an important aspect of the ARDS ventilatory strategy, offering protection from atelectrauma apart from improving alveolar recruitment & oxygenation. PEEP needs to be carefully titrated since an inappropriately high PEEP can cause overdistension injury, and a lower PEEP could be insufficient to stabilize and keep the alveoli open. The PEEP is most commonly selected at the bedside for a given FiO2 based on the PEEP selection criteria adopted at the landmark ARDS Nett trial. Optimal PEEP titration based on pressure-volume curve analysis, transpulmonary pressure measurements, CT, and ultrasound pictures have been tried in various studies though proved clinical benefits with such strategies are lacking. Closed suction catheters should be preferred in mechanically ventilated ARDS patients to avoid abrupt disconnection and PEEP derecruitment, which could cause hypoxemia as well as lung deflation injury.

    Recruitment maneuvers should reduce ventilator-associated injury in theory. However, due to concerns regarding complications (e.g., hemodynamic compromise, pneumothorax) and uncertainty regarding clinical benefits, they are not applied widely. High-frequency oscillatory ventilation(HFOV) is theoretically promising in providing a low tidal volume(even lower than dead space and high frequency). However, the landmark OSCILLATE and OSCAR trials failed to provide any clinical superiority in ARDS patients.

    The use of neuromuscular agents has been known to reduce cytokine levels in previous studies. The ACURASYS study on 340 patients published in 2010 showed approximately 10% morality benefit at 28 days and 90 days in ARDS patients who received a neuromuscular agent for 48 hours. The morality benefit attributed in the cisatracurium arm is likely due to decreased multiorgan dysfunction due to decreased biotrauma resulting from decreased effort-induced lung injury.

    Prone position ventilation has been known to increase the homogeneity of ventilation in animal studies, thus protecting from lung injury. A 2010 metanalysis of seven trials involving 1724 patients showed a reduction in absolute mortality by 10 % in severely hypoxemic patients with ARDS with a PaO2: FiO2 ratio < 100. The landmark PROSEVA trial on 466 patients with severe ARDS with a PaO2: FiO2 ratio < 150 also showed a significant 28-day mortality difference of 16.8 % compared to patients who were not prone.

    Partial or total extracorporeal support (ECMO/ECCO2-R) have been conceptually promising in the prevention of ventilator-related lung injury. However, data supporting clinical benefits prompting the routine initiation of extracorporeal support are scanty at this stage.

    Anti-inflammatory strategies and the use of mesenchymal stem cells have been employed in animal studies to prevent the consequences of ventilator-induced lung injury. However, their clinical utility in humans is yet to be proven. A 2017 Chinese study found that both ketamine and propofol could increase the pulmonary function index in patients with a ventilatory-induced injury. Ketamine was found to be superior to propofol as an anti-inflammatory agent in reducing IL-1β, Caspase-1, and NF-κB.

    Prevention

    • Preventing alveolar overdistension – Alveolar overdistension is mitigated by using small tidal volumes, maintaining a low plateau pressure, and most effectively by using volume-limited ventilation. A 2018 systematic review by The Cochrane Collaboration provided evidence that low tidal volume ventilation reduced postoperative pneumonia and reduced the requirement for both invasive and noninvasive ventilation after surgery[rx]
    • Preventing cyclic atelectasis (atelectotrauma) – Applied positive end-expiratory pressure (PEEP) is the principal method used to keep the alveoli open and lessen cyclic atelectasis.
    • Open lung ventilation – Open lung ventilation is a ventilatory strategy that combines small tidal volumes (to lessen alveolar overdistension) and an applied PEEP above the low inflection point on the pressure-volume curve (to lessen cyclic atelectasis).
    • High-frequency ventilation is thought to reduce ventilator-associated lung injury, especially in the context of ARDS and acute lung injury.[rx]
    • Permissive hypercapnia and hypoxemia allow the patient to be ventilated at less aggressive settings and can, therefore, mitigate all forms of ventilator-associated lung injury

    Diving Disorders – Causes, Symptoms, Diagnosis, Treatment

    Diving disorders are medical conditions specifically arising from underwater diving. The signs and symptoms of these may present during a dive, on the surfacing, or up to several hours after a dive. Divers have to breathe a gas that is at the same pressure as their surroundings (ambient pressure), which can be much greater than on the surface. The ambient pressure underwater increases by 1 standard atmosphere (100 kPa) for every 10 meters (33 ft) of depth.[1]

    The principal conditions are decompression illness (which covers decompression sickness and arterial gas embolism), nitrogen narcosis, high-pressure nervous syndrome, oxygen toxicity, and pulmonary barotrauma (burst lung). Although some of these may occur in other settings, they are of particular concern during diving activities.[rx]

    The disorders are caused by breathing gas at the high pressures encountered at depth, and divers will often breathe a gas mixture different from air to mitigate these effects. Nitrox, which contains more oxygen and less nitrogen, is commonly used as a breathing gas to reduce the risk of decompression sickness at recreational depths (up to about 40 meters (130 ft)). Helium may be added to reduce the amount of nitrogen and oxygen in the gas mixture when diving deeper, to reduce the effects of narcosis, and to avoid the risk of oxygen toxicity. This is complicated at depths beyond about 150 metres (500 ft), because a helium-oxygen mixture (heliox) then causes the high-pressure nervous syndrome.[rx] More exotic mixtures such as hydration, hydrogen–helium-oxygen mixture, are used at extreme depths to counteract this.[rx]

    The recompression chamber at the Neutral Buoyancy Laboratory used for treating DCS and training

    Decompression sickness (DCS) occurs when gas, which has been breathed under high pressure and dissolved into the body tissues, forms bubbles as the pressure is reduced on ascent from a dive. The results may range from pain in the joints where the bubbles form to blockage of an artery leading to damage to the nervous system, paralysis or death. While bubbles can form anywhere in the body, DCS is most frequently observed in the shoulders, elbows, knees, and ankles. Joint pain occurs in about 90% of DCS cases reported to the U.S. Navy, with neurological symptoms and skin manifestations each present in 10% to 15% of cases. Pulmonary DCS is very rare in divers.[rx] The table below classifies the effects by affected organ and bubble location.[rx]

    Signs and symptoms of decompression sickness
    DCS type Bubble location Clinical manifestations
    Musculoskeletal Mostly large joints
    • Localized deep pain, ranging from mild to excruciating; sometimes a dull ache, but rarely a sharp pain
    • Pain aggravated by active and passive motion of the joint
    • Pain may be reduced by bending the joint to find a more comfortable position
    • Pain occurring immediately on surfacing or up to many hours later
    Cutaneous Skin
    • Itching, usually around the ears, face, neck, arms, and upper torso
    • The sensation of tiny insects crawling over the skin (formication)
    • Mottled or marbled skin or subcutaneous crepitation, usually around the shoulders, upper chest, and abdomen, with itching
    • Swelling of the skin, accompanied by tiny scar-like skin depressions (pitting edema)
    Neurologic Brain
    • Altered sensation, paresthesia (tingling or numbness), hyperesthesia (increased sensitivity)
    • Confusion or memory loss (amnesia)
    • Visual abnormalities
    • Unexplained mood or behavior changes
    • Seizures, unconsciousness
    Neurologic Spinal cord
    • Ascending weakness or paralysis in the legs
    • Girdling abdominal or chest pain
    • Urinary incontinence and fecal incontinence
    Constitutional Whole-body
    • Headache
    • Unexplained fatigue
    • Generalized malaise, poorly localized aches
    Audiovestibular Inner ear
    • Loss of balance
    • Dizziness, vertigo, nausea, vomiting
    • Hearing loss
    Pulmonary Lungs
    • Dry persistent cough
    • Burning chest pain under the sternum, aggravated by breathing
    • Shortness of breath

    Arterial gas embolism and pulmonary barotrauma

    Diagram showing the four chambers of the heart and the pulmonary arteries and veins connecting it to both lungs

    The pulmonary circulation

    If the compressed air in a diver’s lungs cannot freely escape during an ascent, particularly a rapid one, then the lung tissues may rupture, causing pulmonary barotrauma (PBT). The air may then enter the arterial circulation producing arterial gas embolism (AGE), with effects similar to severe decompression sickness. Although AGE may occur as a result of other causes, it is most often secondary to PBT. AGE is the second most common cause of death while diving (drowning being the most common stated cause of death). Gas bubbles within the arterial circulation can block the supply of blood to any part of the body, including the brain, and can therefore manifest a vast variety of symptoms. The following table presents those signs and symptoms which have been observed in more than ten percent of cases diagnosed as AGE, with approximate estimates of frequency.[rx]

    Other conditions that can be caused by pulmonary barotrauma include pneumothorax, mediastinal emphysema and interstitial emphysema.

    Signs and symptoms of arterial gas embolism
    Symptom Percentage
    Loss of consciousness 81
    Pulmonary rales or wheezes 38
    Blood in the ear (Hemotympanum) 34
    Decreased reflexes 34
    Extremity weakness or paralysis 32
    Chest pain 29
    Irregular breathing or apnea 29
    Vomiting 29
    Coma without convulsions 26
    Coughing blood (Hemoptysis) 23
    Sensory loss 21
    Stupor and confusion 18
    Vision changes 20
    Cardiac arrest 16
    Headache 16
    Unilateral motor changes 16
    Change in gait or ataxia 14
    Conjunctivitis 14
    Sluggishly reactive pupils 14
    Vertigo 12
    Coma with convulsions 11

    Nitrogen narcosis

    Nitrogen narcosis is caused by the pressure of dissolved gas in the body and produces impairment to the nervous system. This results in an alteration to thought processes and a decrease in the diver’s ability to make judgments or calculations. It can also decrease motor skills, and worsen performance in tasks requiring manual dexterity. As depth increases, so do the pressure and hence the severity of the narcosis. The effects may vary widely from individual to individual, and from day to day for the same diver. Because of the perception-altering effects of narcosis, a diver may not be aware of the symptoms, but studies have shown that impairment occurs nevertheless.[rx] Since the choice of breathing gas also affects the depth at which narcosis occurs, the table below represents typical manifestations when breathing air.[rx]

    Signs and symptoms of narcosis
    Pressure (bar) Depth (m) Depth (ft) Manifestations
    1–2 0–10 0–33
    • Unnoticeable small symptoms, or no symptoms at all
    2–4 10–30 33–100
    • Mild impairment of performance of unpracticed tasks
    • Mildly impaired reasoning
    • Mild euphoria possible
    4–6 30–50 100–165
    • Delayed response to visual and auditory stimuli
    • Reasoning and immediate memory affected more than motor coordination
    • Calculation errors and wrong choices
    • Idea fixation
    • Overconfidence and sense of well-being
    • Laughter and loquacity which may be overcome by self-control
    • Anxiety (common in cold murky water)
    6–8 50–70 165–230
    • Sleepiness, impaired judgment, confusion
    • Hallucinations
    • Severe delay in response to signals, instructions and other stimuli
    • Occasional dizziness
    • Uncontrolled laughter, hysteria
    • Terror in some
    8–10 70–90 230–300
    • Poor concentration and mental confusion
    • Stupefaction with some decrease in dexterity and judgment
    • Loss of memory, increased excitability
    10+ 90+ 300+
    • Hallucinations
    • Increased intensity of vision and hearing (Hyperesthesia)
    • Sense of impending blackout, euphoria, dizziness
    • Manic or depressive states
    • A sense of levitation and disorganisation of the sense of time
    • Changes in facial appearance
    • Unconsciousness, death

    High-pressure nervous syndrome

    Helium is the least narcotic of all gases, and divers may use breathing mixtures containing a proportion of helium for dives exceeding about 40 meters (130 ft) deep. In the 1960s it was expected that helium narcosis would begin to become apparent at depths of 300 metres (1,000 ft). However, it was found that different symptoms, such as tremors, occurred at shallower depths around 150 meters (500 ft). This became known as a high-pressure nervous syndrome, and its effects are found to result from both the absolute depth and the speed of descent. Although the effects vary from person to person, they are stable and reproducible for each individual; the list below summarises the symptoms observed underwater and in studies using simulated dives in the dry, using recompression chambers and electroencephalography (EEG) monitors.[rx]

    Signs and symptoms of HPNS
    Symptom Notes
    Impairment Both intellectual and motor performance is impaired. A 20% decrease in the ability to perform calculations and in manual dexterity is observed at 180 meters (600 ft), rising to 40% at depths of 240 meters (800 ft)
    Dizziness Vertigo, nausea, and vomiting may occur in divers at depths of 180 meters (600 ft). Animal studies under more extreme conditions have produced convulsions.
    Tremors Tremors of the hands, arms, and torso are observed from 130 meters (400 ft) onward. The tremors occur with a frequency in the range of 5–8 hertz (Hz), and their severity is related to the speed of compression; the tremors reduce and may disappear when the pressure has stabilized.
    EEG changes At depths exceeding 300 meters (1,000 ft), changes in the electroencephalogram (EEG) are observed; the appearance of theta waves (4–6 Hz) and depression of alpha waves (8–13 Hz).
    Somnolence At depths beyond the onset of EEG changes, test subjects intermittently fall asleep, with sleep stages 1 and 2 observed in the EEG. Even when decompressed to shallower depths, the effect continues for 10–12 hours.

    Oxygen toxicity

    During World War II Professor Kenneth Donald carried out extensive testing for oxygen toxicity in divers. The chamber is pressurised with air to 3.7 bars (370 kPa; 54 psi). The subject in the center is breathing 100% oxygen from a mask.

    Although oxygen is essential to life, in concentrations greater than normal it becomes toxic, overcoming the body’s natural defenses (antioxidants), and causing cell death in any part of the body. The lungs and brain are particularly affected by high partial pressures of oxygen, such as are encountered in diving. The body can tolerate partial pressures of oxygen around 0.5 bars (50 kPa; 7.3 psi) indefinitely, and up to 1.4 bars (140 kPa; 20 psi) for many hours, but higher partial pressures rapidly increase the chance of the most dangerous effect of oxygen toxicity, a convulsion resembling an epileptic seizure.[10] Susceptibility to oxygen toxicity varies dramatically from person to person, and to a much smaller extent from day to day for the same diver.[11] Prior to convulsion, several symptoms may be present – most distinctly that of an aura.

    During 1942 and 1943, Professor Kenneth W Donald, working at the Admiralty Experimental Diving Unit, carried out over 2,000 experiments on divers to examine the effects of oxygen toxicity. To date, no comparable series of studies has been performed. In one seminal experiment, Donald exposed 36 healthy divers to 3.7 bars (370 kPa; 54 psi) of oxygen in a chamber, equivalent to breathing pure oxygen at a depth of 27 metres (90 ft), and recorded the time of onset of various signs and symptoms. Five of the subjects convulsed, and the others recovered when returned to normal pressure following the appearance of acute symptoms. The table below summarises the results for the relative frequency of the symptoms, and the earliest and latest time of onset, as observed by Donald. The wide variety of symptoms and large variability of onset between individuals typical of oxygen toxicity are clearly illustrated.[12]

    Signs and symptoms of oxygen toxicity observed in 36 subjects
    Signs and symptoms Frequency Earliest onset (minutes) Latest onset (minutes)
    Lip-twitching 25 6 67
    Vertigo 5 9 62
    Convulsion 5 20 33
    Nausea 4 6 62
    Spasmodic respiration 3 16 17
    Dazed 2 9 51
    Syncope 2 15 16
    Epigastric aura 2 18 23
    Arm twitch 2 21 62
    Dazzle 2 51 96
    Diaphragmatic spasm 1 7 7
    Tingling 1 9 9
    Confusion 1 15 15
    Inspiratory predominance[note 1] 1 16 16
    Amnesia 1 21 21
    Drowsiness 1 26 26
    Fell asleep 1 51 51
    Euphoria 1 62 62
    Vomiting 1 96 96

     

    Barotrauma – Causes, Symptoms, Diagnosis, Treatment

    Barotrauma is a potentially life-threatening complication in patients on mechanical ventilation. It is important to recognize and quickly act to prevent barotrauma for prolonged periods as this may lead to significant morbidity and mortality in patients intubated in the intensive care unit. This activity will highlight how to recognize, diagnose, prevent, and manage barotrauma in patients on mechanical ventilation.

    Pulmonary barotrauma is a damage to the lung from rapid or excessive pressure changes, as may occur when a patient is on a ventilator and is subjected to high airway pressure. Pulmonary barotrauma can also occur in scuba and other forms of diving.

    Barotrauma is damage to body tissue secondary to pressure difference in enclosed cavities within the body. Barotrauma is commonly observed in scuba divers, free-divers, or even in airplane passengers during ascent and descent. The most common organs affected by barotrauma are the middle ear (otic barotrauma), sinuses (sinus barotrauma), and the lungs (pulmonary barotrauma). This article will focus on pulmonary barotrauma.

    Barotrauma is tissue injury caused by a pressure-related change in body compartment gas volume. Factors increasing risk of pulmonary barotrauma include certain behaviors (eg, rapid ascent, breath-holding, breathing compressed air) and lung disorders (eg, COPD [chronic obstructive pulmonary disease]). Pneumothorax and pneumomediastinum are common manifestations. Patients require neurologic examination and chest imaging. Pneumothorax is treated. Prevention involves decreasing risky behaviors and counseling high-risk divers.

    Causes of Pulmonary Barotrauma

    Pulmonary barotrauma results from positive pressure mechanical ventilation. Positive pressure ventilation may lead to elevation of the trans-alveolar pressure or the difference in pressure between the alveolar pressure and the pressure in the interstitial space. Elevation in the trans-alveolar pressure may lead to alveolar rupture, which results in leakage of air into the extra-alveolar tissue.

    Every patient on positive pressure ventilation is at risk of developing pulmonary barotrauma. However, certain ventilator settings, as well as specific disease processes, may increase the risk of barotrauma significantly. When managing a ventilator, physicians and other health care professionals must be aware of these risks to avoid barotrauma.

    Specific disease processes, including chronic obstructive pulmonary disease (COPD), asthma, interstitial lung disease (ILD), pneumocystis jiroveci pneumonia, and acute respiratory distress syndrome (ARDS), may predispose individuals to pulmonary barotrauma. These diseases are associated with either dynamic hyperinflation or poor lung compliance, both of which predispose patients to increased alveolar pressure and ultimately barotrauma.

    Patients with obstructive lung disease, COPD, and asthma are at risk of dynamic hyperinflation. These patients have a prolonged expiratory phase, and therefore have difficulty exhaling the full volume before the ventilator delivers the next breath. As a result, there is an increase in the intrinsic positive end-expiratory pressure (PEEP), also known as auto-PEEP. The hyperinflation is progressive and worsens with each tidal volume delivered. It leads to overdistention of the alveoli and increases the risk for barotrauma. Dynamic hyperinflation can be managed by decreasing the respiratory rate, decreasing the tidal volume, prolonging the expiratory time, and in some cases by increasing the external PEEP on the ventilator. The static auto-peep is easily measurable on a ventilator by performing an expiratory pause; by using this method you would obtain the total PEEP, the external PEEP subtracted from the total PEEP will equal the intrinsic PEEP or auto-PEEP. In many cases, auto-PEEP results in ventilator asynchrony, which may result in an increased risk of barotrauma. For a patient to be able to trigger a breath on the ventilator and for the flow to begin, the inspiratory muscles must overcome the recoil pressure. When intrinsic PEEP is present, it imposes an additional force that the inspiratory muscles have to overcome to trigger a breath. In many instances, auto-PEEP may lead to ventilator asynchrony, increased alveoli distention, and ultimately barotrauma.

    Elevated plateau pressure is perhaps one of the most critical measurements of which to be aware. Plateau pressure is the pressure applied to the alveoli and other small airways during ventilation. Elevated plateau pressures, particularly pressures higher than 35 cmH2O, have been associated with an elevated risk for barotrauma. Plateau pressures are easily measurable on a ventilator by performing an inspiratory hold. Based on current data, as well as the increased mortality associated with barotrauma, the ARDSnet protocol suggests keeping plateau pressures below 30 cmH2O in patients on mechanical ventilation for ARDS management.

    Peak pressure is the plateau pressure in addition to the pressure needed to overcome flow resistance and the elastic recoil of the lungs and chest wall. The risk for barotrauma increases whenever the peak pressures and plateau pressures become elevated to the same degree.

    Elevated positive end-expiratory pressure (PEEP) may theoretically lead to overdistention of healthy alveoli in regions not affected by disease and ultimately barotrauma. However, clinical data has not associated increased PEEP with increased risk of barotrauma when used in conjunction with lung protective strategies, such as low tidal volume and target plateau pressure under 30 cmH2O. If higher PEEP is necessary for oxygenation, it should be titrated up slowly with close monitoring of the peak inspiratory and plateau pressures.

    The exact pathophysiology for lung injury and barotrauma due to mechanical ventilation remains unclear; however, evidence suggests that overdistention and increased pressures in the alveoli units lead to inflammatory changes and possibly rupture and leakage of air into the extra alveolar tissue.

    Researchers have described several mechanisms in the literature for the rupture of alveoli. Most of the mechanisms have their basis in overdistention and increased pressures in the alveoli. Historically, large tidal volumes were the approach in patients requiring mechanical ventilation to minimize atelectasis and improve oxygenation and ventilation. Such ventilatory settings usually lead to high inspiratory pressures and overdistention of the alveolar unit. Overdistention is more pronounced in patients with ARDS and other non-uniform lung diseases. In non-uniform lung disease, not every alveoli unit is affected equally; normal alveoli receive a greater percentage of the tidal volume, which leads to preferential ventilation and ultimately overdistention to accommodate the larger tidal volume.

    Some animal studies have looked at the association between alveolar overdistention and lung injury. Tsuno et al. looked at histopathologic changes in the lungs of baby pigs. The settings on the ventilator produced a peak inspiratory pressure (PIP) of 40 cmH2O for up to 32 hours as well as the tidal volume of 15 mL/kg. Pathological findings on the subject’s studies included interstitial lymphocyte proliferation, alveolar hemorrhage, and hyaline membrane formation; all of which are similar to the histopathology observed in patients with ARDS. Other studies in human subjects have also demonstrated an association between high volume ventilation and increased levels of TNF-alpha and MIP-2; both are inflammatory cytokines researchers believe are implicated in the multi-organ dysfunction associated with ARDS.

    Associate causes

    • Acute respiratory distress syndrome (ARDS)
    • Bacterial/viral pneumonia
    • Aspiration pneumonitis
    • Shock (distributive, cardiogenic, hemorrhagic)
    • Flail chest, chest trauma
    • Secondary pneumothorax
    • Pulmonary emboli
    • Asthma exacerbation
    • COPD exacerbation
    • Acute coronary syndrome

    Symptoms of Pulmonary Barotrauma

    Examples of organs or tissues easily damaged by barotrauma are:

    • Middle ear (barotitis or aerotitis)
    • Paranasal sinuses[rx][rx][rx] (causing aerosinusitis)
    • Lungs
    • Eyes (the under-pressure air space is inside the diving mask[rx])
    • Skin (when wearing a diving suit which creates an air space)
    • Brain and cranium (temporal lobe injury secondary to temporal bone rupture)[rx]
    • Teeth (causing barodontalgia, i.e., barometric pressure related dental pain, or dental fractures
    • Genital (squeeze and associated complications of P-valve use)[rx]

    or

    • Head and neck
      • Hypopharyngeal Petechiae
    • Lung findings
      • Dyspnea
      • Cough
      • Wheezing
      • Hemoptysis
      • Chest Pain
      • Hypoxia
      • Apnea
      • Decreased breath sounds
    • Cardiovascular findings
      • Bradycardia
      • Hypotension
      • Cyanosis
    • Skin findings
      • Subcutaneous Emphysema

    Diagnosis of Pulmonary Barotrauma

    The history and physical exam in patients with barotrauma secondary to mechanical ventilation are usually limited since those patients are sick and under sedation while on mechanical ventilation. In cases of clinically significant pneumothorax, patients will present with acute changes in vital signs, including tachypnea, hypoxia, and tachycardia. Patients may also present with obstructive shock if a tension pneumothorax occurs. Physical examination may be significant for absent breath sounds if a pneumothorax exists. Subcutaneous emphysema may also present in some cases. In some, less severe cases, no systemic or hemodynamic changes may be present.

    The patient’s past medical history is also essential when it comes to the diagnosis and management of pulmonary barotrauma. As mentioned previously, patients with a known history of chronic obstructive pulmonary disease (COPD), asthma, interstitial lung disease (ILD), pneumocystis jiroveci pneumonia, or ARDS, are at increased risk of developing pulmonary barotrauma. Underlying pulmonary pathology will also be important to be aware of when it comes to selecting the ventilator mode as well as the settings as we will discuss later.

    Lab Test and Imaging

    Ventilator data may be useful in the evaluation of pulmonary barotrauma. Ventilator asynchrony, acute elevation of the plateau and peak pressures above 30 cmH2O, or sudden decrease of delivered tidal volume may suggest respiratory distress secondary to pneumothorax or other complications from barotrauma. Ventilator data can give a clue to physicians regarding which patients are at higher risk for barotrauma.

    Once pulmonary barotrauma secondary to the mechanical ventilator is suspected, action must take place immediately. Pneumothorax is an acute complication from pulmonary barotrauma, which is an emergency. The physical exam will be remarkable for absent breath sounds, and in most cases, patients who can communicate will complain of shortness of breath and chest pain. Vital signs usually demonstrate hypoxia as well as hypotension secondary to obstructive shock in the case of a tension pneumothorax. In patients who develop a tension pneumothorax, action is necessary before obtaining a chest radiograph. Tension pneumothorax requires urgent needle decompression to evacuate the pneumothorax, followed by thoracotomy tube placement. In patients presenting with a less acute complication, such as a simple pneumothorax with stable vital signs, pneumomediastinum, or subcutaneous emphysema, the clinician should obtain a chest radiograph immediately. The chest radiograph is able to identify the presence of pneumothorax, pneumomediastinum, subcutaneous emphysema, and other less common manifestations of pulmonary barotrauma, such as pneumatoceles, sub-pleural air collections, and pulmonary interstitial emphysema (PIE). If a chest x-ray is obtained but inadequate for evaluation, a CT of the chest can be done. It is important to remember that barotrauma is a clinical diagnosis and should always be high in the differential diagnosis for patients on invasive and non-invasive mechanical ventilation presenting with acute decompensation.

    Treatment of Pulmonary Barotrauma

    First aid

    Pre-hospital care for lung barotrauma includes basic life support of maintaining adequate oxygenation and perfusion, assessment of airway, breathing and circulation, neurological assessment, and managing any immediate life-threatening conditions. High-flow oxygen up to 100% is considered appropriate for diving accidents. Large-bore venous access with isotonic fluid infusion is recommended to maintain blood pressure and pulse.[rx]

    Emergency treatment

    Pulmonary barotrauma:[rx]

    • Endotracheal intubation may be required if the airway is unstable or hypoxia persists when breathing 100% oxygen.
    • Needle decompression or tube thoracostomy may be necessary to drain a pneumothorax or haemothorax
    • Foley catheterization may be necessary for spinal cord AGE if the person is unable to urinate.
    • Intravenous hydration may be required to maintain adequate blood pressure.
    • Therapeutic recompression is indicated for severe AGE. The diving medical practitioner will need to know the vital signs and relevant symptoms, along with the recent pressure exposure and breathing gas history of the patient. Air transport should be below 1,000 feet (300 m) if possible, or in a pressurized aircraft which should be pressurized to as low an altitude as reasonably possible.

    Sinus squeeze and middle ear squeeze are generally treated with decongestants to reduce the pressure differential, with anti-inflammatory medications to treat the pain. For severe pain, narcotic analgesics may be appropriate.[49]

    Suit, helmet and mask squeeze are treated as trauma according to symptoms and severity.

    There is no single strategy to prevent pulmonary barotrauma on patients on mechanical ventilation. The most efficient mechanism that has been described to prevent the risk of developing barotrauma on mechanical ventilation involves maintaining the plateau and peak inspiratory pressures low. The goal plateau pressure should be below 35 cmH2O, and ideally below 30 cmH2O, on most patients on mechanical ventilation as recommended by the ARDS Network group. Various techniques may be employed to aid in maintaining the plateau pressure at goal. Various ventilator modes are available. The two modes most commonly used in intensive care units are volume assist control (volume AC), a volume cycled mode, and pressure assist control (pressure AC), a pressure cycled mode. Lung protective ventilator strategies should be used in every ARDS and most other patients, regardless of the mode of mechanical ventilation. Lung protective ventilator strategies derive for the most part from a study published in the year 2000 by the ARDS Network group. The study involved ARDS patients and compared outcomes in ARDS patients using higher tidal volume ventilation (about 12 mL/kg of IBW) and patients using lower tidal volume ventilation (about 6 mL/kg OF IBW). Although tidal volume was the variable in this study, the goal with the low volume ventilation group was to keep the plateau pressure below 30 cmH2O. The low tidal volume ventilatory strategy correlated with a lower mortality rate (31% vs. 40%). The incidence of barotrauma in this study was not lower when using lung-protective ventilator strategies; however, other studies have demonstrated a higher incidence of barotrauma when the plateau pressure rises above 35 cmH2O. Low tidal volume ventilation is especially important in patients at higher risk for barotrauma, such as patients with ARDS, COPD, asthma, Pneumocystis jiroveci pneumonia (PJP), and chronic interstitial lung disease (ILD).

    The driving pressure is another concept with which physicians managing patients at risk of barotrauma must be familiar. The driving pressure is measurable in patients not making an inspiratory effort; one can obtain the calculated pressure by subtracting the PEEP from the plateau pressure. Driving pressure became a hot topic of discussion after the ARDS trial proposed that high plateau pressures increase mortality in patients with ARDS but that high PEEP pressure is associated with improved outcomes. Amato et al., in 2015, proposed that the driving pressure was a better ventilation variable to stratify risk. In the trial, published in the NEJM in 2015, they concluded that an increment of 1 standard deviation in driving pressure was associated with increased mortality even in patients receiving protective plateau pressure and tidal volumes. Individual changes in tidal volume and PEEP were only associated with improved survival if these changes led to a reduction in driving pressure. Based on the data available, clinicians should maintain the optimal driving pressure between 13 and 15 cm H2O.

    As mentioned previously, patients with obstructive lung disease are at risk of dynamic hyperinflation due to a prolonged expiratory phase, and difficulty exhaling the full volume before the ventilator delivers the next breath. Physicians must be aware of intrinsic PEEP or auto-PEEP, particularly in patients at high risk, such as those with obstructive lung disease. An expiratory pause maneuver on the ventilator will provide static intrinsic pressure. If intrinsic PEEP is present, then the physician may increase the external PEEP to help with ventilator synchronization by allowing the patient to trigger the ventilator and initiate a breath more effectively. The goal is to increase the external PEEP by 75 to 85% of the intrinsic PEEP . Other methods that the physician may employ to decrease the intrinsic PEEP include decreasing the respiratory rate, decreasing the tidal volume, and prolonging the expiratory time.

    High positive end-expiratory pressure (PEEP) may theoretically lead to overdistention of healthy alveoli in regions not affected by disease and ultimately lead to barotrauma. Many conditions, such as moderate to severe ARDS, require the use of high PEEP pressures to improved oxygenation by recruiting as many alveoli units as possible. When used in conjunction with lung protective strategies, as described above, the risk of barotrauma due to high PEEP is minimal. Several methods exist to aid physicians in determining the adequate level of PEEP to treat individual patients based on lung compliance. A system pressure-volume curve may be used to determine the lower inflection point and the higher inflection point. The lower inflection point in the curve determines the minimal level of PEEP required to start alveolar recruitment. The upper inflection point in the curve determines the pressure level at which the risk of barotrauma and lung injury occurs.

    The stress index is another method that may be used by physicians to determine the adequate amount of PEEP for individual patients. For the stress index to be an accurate measurement, the patient must be well sedated, and the flow must be constant. The physician may look at the pressure waveform on the ventilator to determine the stress index. A pressure wave that is concave down indicates a stress index less than 1. A stress index of less than 1 indicates that the patient may benefit from increased PEEP to help with alveoli recruitment. A pressure wave that is concave up indicates a stress index higher than 1. A stress index higher than one should alert the physician that the patient’s alveoli unit is at risk of distention and barotrauma. A straight diagonal line in the pressure wave is ideal because it correlates with a stress index between 0.9 and 1.1, which is the ideal range for proper alveoli recruitment with a low risk of distention and rupture.

    Different ventilator modes also exist, which may be better tolerated by some patients and decrease the risk of barotrauma. There is no evidence to suggest that one ventilator mode is better than the other. However, in patients who are difficult to manage, physicians may try different modes to synchronize the patient with the ventilator better.

    Volume AC mode is a volume cycled mode. It will deliver a set volume on every ventilator-assisted breath, which will lead to significant variations in peak inspiratory pressures as well as plateau pressures depending on the compliance of the lung parenchyma. The peak inspiratory and plateau pressures may be kept at goal using this mode of ventilation by using low tidal volume ventilation (between 6 to 8 mL/kg based on the ideal body weight). The respiratory rate and inspiratory time may be adjusted as well to prevent intrinsic PEEP. In some cases, sedation, and even neuromuscular blocking agents may be to be used to improve ventilator synchrony and maintain inspiratory peak and plateau pressures at goal.

    Pressure AC mode is a pressure cycled mode. It allows medical personnel to set an inspiratory pressure level as well as the applied PEEP. The advantage of using a pressure cycled mode is that the peak inspiratory pressure will remain constant and will be equal to the inspiratory pressure in addition to the PEEP. The plateau pressure will also be lower or equal to the peak inspiratory pressure; therefore, this mode of ventilation correlates with a lower rate of barotrauma. The disadvantage, however, is that the tidal volume delivered will vary depending on lung compliance. Patients with poor lung compliance may not receive an adequate tidal volume using this ventilator mode.

    Effect Management

    The management of complications due to barotrauma depends on the specific complication. Pneumothorax, or tension pneumothorax, is a medical emergency. A tension pneumothorax must be treated immediately with needle decompression. The diagnosis of tension pneumothorax is made clinically and must be acted upon quickly without waiting for chest radiography. Signs and symptoms of tension pneumothorax include the absence of breath sounds, hemodynamic instability, as well as symptoms of chest pain and shortness of breath. The clinician must perform an urgent needle decompression followed by the placement of a thoracotomy tube.

    The management of most non-tension pneumothorax in patients on mechanical ventilation involves the placement of a thoracostomy tube to evacuate the air due to the high incidence of progression to tension pneumothorax while on mechanical ventilation. Once the thoracotomy tube is in place, additional changes in the ventilator may be made to help with the resolution of the pneumothorax. Tidal volume may be decreased to decrease the plateau and peak inspiratory pressures. FiO2 in the ventilator may be increased temporarily to help decrease the partial pressure of nitrogen and aid with the absorption of air from the pleural cavity and hasten lung re-expansion. PEEP should also be lowered to decrease overdistention of the alveoli units, and patients should be well sedated to prevent ventilator asynchrony and further trauma.

    Other complications, such as subcutaneous emphysema, pneumomediastinum, and pneumoperitoneum, are usually self-resolving and management is conservative. Conservative management involves reducing the plateau pressures below 30 cmH2O as well as continuous monitoring. Other strategies to minimize complications include reducing the PEEP on the ventilator, using sedation and neuromuscular blockade in patients who are difficult to synchronize with the ventilator, and decreasing the ventilatory pressures. Ultimately, the best way to prevent barotrauma and complications is liberating the patient from mechanical ventilation.

    Tension pneumomediastinum is an exception. Intension pneumomediastinum, the pressure in the mediastinum increases significantly and ultimately may lead to physiological effects similar to pericardial tamponade. It may cause compression of the great vessels and compromise the right heart filling leading to shock and eventually, cardiac arrest. Chest radiography will show a heart silhouette resembling a sphere. The initial management involves ventilator changes to decrease the airway pressures and increase the FiO2 in the ventilator to 100%. Ultimately surgical mediastinal decompression is required.

    Subcutaneous emphysema rarely may lead to compartment syndrome. Compartment syndrome should be suspected in patients with hemodynamic instability and elevated bladder pressures. Management involves decreasing the airway pressures, but ultimately, surgical evaluation is warranted. Surgical decompression must be performed in all patients with hemodynamic instability as this condition is associated with a high mortality rate.

    Patients presenting with pneumoperitoneum may also progress to compartment syndrome. An immediate surgical evaluation must take place due to the high mortality associated with this condition. Pneumoperitoneum due to barotrauma is rare, and other causes for pneumoperitoneum should be ruled out, such as ruptured viscus and abdominal trauma.

    Hypercapnia is among the most common side effects that present when managing a patient with lung-protective ventilatory strategies. The lower tidal volume may lead to decreased minute ventilation, and in some cases, hypercapnia. Guidelines for ARDS recommend allowing for permissive hypercapnia up to a pH of 7.2. If the pH drops below 7.2, the initiation of a bicarbonate infusion should be a therapeutic consideration to correct the pH to 7.2.

    Prevention

    In divers

    Barotrauma may be caused when diving, either from being crushed or squeezed, on descent or by stretching and bursting on the ascent; both can be avoided by equalizing the pressures. A negative, unbalanced pressure is known as a squeeze, crushing eardrums, dry suit, lungs, or mask inwards and can be equalized by putting air into the squeezed space. A positive unbalanced pressure expands internal spaces rupturing tissue and can be equalized by letting air out, for example by exhaling. Both may cause barotrauma. There are a variety of techniques depending on the affected area and whether the pressure inequality is a squeeze or an expansion:

    • Ears and sinuses: There is a risk of stretched or burst eardrums, usually crushed inwards during descent but sometimes stretched outwards on the ascent. The diver can use a variety of methods to let air into or out of the middle ears via the Eustachian tubes. Sometimes swallowing will open the Eustachian tubes and equalize the ears.
    • Lungs: There is a risk of pneumothorax, arterial gas embolism, and mediastinal and subcutaneous emphysema during ascent, which are commonly called burst lung or lung overpressure injury by divers. To equalize the lungs, all that is necessary is not to hold the breath during ascent. This risk does not occur when breath-hold diving from the surface, unless the diver breathes from an ambient pressure gas source underwater; breath-hold divers do suffer squeezed lungs on the descent, crushing in the chest cavity, but, while uncomfortable, this rarely causes lung injury and returns to normal at the surface. Some people have the pathology of the lung which prevents the rapid flow of excess air through the passages, which can lead to lung barotrauma even if the breath is not held during rapid depressurization. These people should not dive as the risk is unacceptably high. Most commercial or military diving medical examinations will look specifically for signs of this pathology.
    • Diving mask squeeze enclosing the eyes and nose: The main risk is rupture of the capillaries of the eyes and facial skin because of the negative pressure difference between the gas space and blood pressure, or orbital emphysema from higher pressures. This can be avoided by breathing air into the mask through the nose. Goggles covering only the eyes are not suitable for deep diving as they cannot be equalized.
    • Drysuit squeeze. The main risk is skin getting pinched and bruised by folds of the drysuit when squeezed on the descent. Most drysuits can be equalized against squeeze via a manually operated valve fed from a low-pressure gas supply. Air must be manually injected during the descent to avoid squeeze and is manually or automatically vented on the ascent to maintain buoyancy control.
    • Diving helmet squeeze: Helmet squeeze will occur if the gas supply hose is severed above the diver and the non-return valve at the helmet gas inlet fails or is not fitted. The severity will depend on the hydrostatic pressure difference. A very rapid descent, usually by accident, may exceed the rate at which the breathing gas supply can equalize the pressure causing a temporary squeeze. The introduction of the non-return valve and high maximum gas supply flow rates have all but eliminated both these risks. In helmets fitted with a neck dam, the dam will admit water into the helmet if the internal pressure gets too low; this is less of a problem than helmet squeeze but the diver may drown if the gas supply is not reinstated quickly. This form of barotrauma is avoidable by controlled descent rate, which is standard practice for commercial divers, who will use hotlines, diving stages and wet bells to control descent and ascent rates.

    Pulmonary Barotrauma – Causes, Symptoms, Treatment

    Pulmonary barotrauma is a potentially life-threatening complication in patients on mechanical ventilation. It is important to recognize and quickly act to prevent barotrauma for prolonged periods as this may lead to significant morbidity and mortality in patients intubated in the intensive care unit. This activity will highlight how to recognize, diagnose, prevent, and manage barotrauma in patients on mechanical ventilation.

    Pulmonary barotrauma is a damage to the lung from rapid or excessive pressure changes, as may occur when a patient is on a ventilator and is subjected to high airway pressure. Pulmonary barotrauma can also occur in scuba and other forms of diving.

    Barotrauma is damage to body tissue secondary to pressure difference in enclosed cavities within the body. Barotrauma is commonly observed in scuba divers, free-divers, or even in airplane passengers during ascent and descent. The most common organs affected by barotrauma are the middle ear (otic barotrauma), sinuses (sinus barotrauma), and the lungs (pulmonary barotrauma). This article will focus on pulmonary barotrauma.

    Barotrauma is tissue injury caused by a pressure-related change in body compartment gas volume. Factors increasing risk of pulmonary barotrauma include certain behaviors (eg, rapid ascent, breath-holding, breathing compressed air) and lung disorders (eg, COPD [chronic obstructive pulmonary disease]). Pneumothorax and pneumomediastinum are common manifestations. Patients require neurologic examination and chest imaging. Pneumothorax is treated. Prevention involves decreasing risky behaviors and counseling high-risk divers.

    Causes of Pulmonary Barotrauma

    Pulmonary barotrauma results from positive pressure mechanical ventilation. Positive pressure ventilation may lead to elevation of the trans-alveolar pressure or the difference in pressure between the alveolar pressure and the pressure in the interstitial space. Elevation in the trans-alveolar pressure may lead to alveolar rupture, which results in leakage of air into the extra-alveolar tissue.

    Every patient on positive pressure ventilation is at risk of developing pulmonary barotrauma. However, certain ventilator settings, as well as specific disease processes, may increase the risk of barotrauma significantly. When managing a ventilator, physicians and other health care professionals must be aware of these risks to avoid barotrauma.

    Specific disease processes, including chronic obstructive pulmonary disease (COPD), asthma, interstitial lung disease (ILD), pneumocystis jiroveci pneumonia, and acute respiratory distress syndrome (ARDS), may predispose individuals to pulmonary barotrauma. These diseases are associated with either dynamic hyperinflation or poor lung compliance, both of which predispose patients to increased alveolar pressure and ultimately barotrauma.

    Patients with obstructive lung disease, COPD, and asthma are at risk of dynamic hyperinflation. These patients have a prolonged expiratory phase, and therefore have difficulty exhaling the full volume before the ventilator delivers the next breath. As a result, there is an increase in the intrinsic positive end-expiratory pressure (PEEP), also known as auto-PEEP. The hyperinflation is progressive and worsens with each tidal volume delivered. It leads to overdistention of the alveoli and increases the risk for barotrauma. Dynamic hyperinflation can be managed by decreasing the respiratory rate, decreasing the tidal volume, prolonging the expiratory time, and in some cases by increasing the external PEEP on the ventilator. The static auto-peep is easily measurable on a ventilator by performing an expiratory pause; by using this method you would obtain the total PEEP, the external PEEP subtracted from the total PEEP will equal the intrinsic PEEP or auto-PEEP. In many cases, auto-PEEP results in ventilator asynchrony, which may result in an increased risk of barotrauma. For a patient to be able to trigger a breath on the ventilator and for the flow to begin, the inspiratory muscles must overcome the recoil pressure. When intrinsic PEEP is present, it imposes an additional force that the inspiratory muscles have to overcome to trigger a breath. In many instances, auto-PEEP may lead to ventilator asynchrony, increased alveoli distention, and ultimately barotrauma.

    Elevated plateau pressure is perhaps one of the most critical measurements of which to be aware. Plateau pressure is the pressure applied to the alveoli and other small airways during ventilation. Elevated plateau pressures, particularly pressures higher than 35 cmH2O, have been associated with an elevated risk for barotrauma. Plateau pressures are easily measurable on a ventilator by performing an inspiratory hold. Based on current data, as well as the increased mortality associated with barotrauma, the ARDSnet protocol suggests keeping plateau pressures below 30 cmH2O in patients on mechanical ventilation for ARDS management.

    Peak pressure is the plateau pressure in addition to the pressure needed to overcome flow resistance and the elastic recoil of the lungs and chest wall. The risk for barotrauma increases whenever the peak pressures and plateau pressures become elevated to the same degree.

    Elevated positive end-expiratory pressure (PEEP) may theoretically lead to overdistention of healthy alveoli in regions not affected by disease and ultimately barotrauma. However, clinical data has not associated increased PEEP with increased risk of barotrauma when used in conjunction with lung protective strategies, such as low tidal volume and target plateau pressure under 30 cmH2O. If higher PEEP is necessary for oxygenation, it should be titrated up slowly with close monitoring of the peak inspiratory and plateau pressures.

    The exact pathophysiology for lung injury and barotrauma due to mechanical ventilation remains unclear; however, evidence suggests that overdistention and increased pressures in the alveoli units lead to inflammatory changes and possibly rupture and leakage of air into the extra alveolar tissue.

    Researchers have described several mechanisms in the literature for the rupture of alveoli. Most of the mechanisms have their basis in overdistention and increased pressures in the alveoli. Historically, large tidal volumes were the approach in patients requiring mechanical ventilation to minimize atelectasis and improve oxygenation and ventilation. Such ventilatory settings usually lead to high inspiratory pressures and overdistention of the alveolar unit. Overdistention is more pronounced in patients with ARDS and other non-uniform lung diseases. In non-uniform lung disease, not every alveoli unit is affected equally; normal alveoli receive a greater percentage of the tidal volume, which leads to preferential ventilation and ultimately overdistention to accommodate the larger tidal volume.

    Some animal studies have looked at the association between alveolar overdistention and lung injury. Tsuno et al. looked at histopathologic changes in the lungs of baby pigs. The settings on the ventilator produced a peak inspiratory pressure (PIP) of 40 cmH2O for up to 32 hours as well as the tidal volume of 15 mL/kg. Pathological findings on the subject’s studies included interstitial lymphocyte proliferation, alveolar hemorrhage, and hyaline membrane formation; all of which are similar to the histopathology observed in patients with ARDS. Other studies in human subjects have also demonstrated an association between high volume ventilation and increased levels of TNF-alpha and MIP-2; both are inflammatory cytokines researchers believe are implicated in the multi-organ dysfunction associated with ARDS.

    Associate causes

    • Acute respiratory distress syndrome (ARDS)
    • Bacterial/viral pneumonia
    • Aspiration pneumonitis
    • Shock (distributive, cardiogenic, hemorrhagic)
    • Flail chest, chest trauma
    • Secondary pneumothorax
    • Pulmonary emboli
    • Asthma exacerbation
    • COPD exacerbation
    • Acute coronary syndrome

    Symptoms of Pulmonary Barotrauma

    Examples of organs or tissues easily damaged by barotrauma are:

    • Middle ear (barotitis or aerotitis)
    • Paranasal sinuses[rx][rx][rx] (causing aerosinusitis)
    • Lungs
    • Eyes (the under-pressure air space is inside the diving mask[rx])
    • Skin (when wearing a diving suit which creates an air space)
    • Brain and cranium (temporal lobe injury secondary to temporal bone rupture)[rx]
    • Teeth (causing barodontalgia, i.e., barometric pressure related dental pain, or dental fractures
    • Genital (squeeze and associated complications of P-valve use)[rx]

    or

    • Head and neck
      • Hypopharyngeal Petechiae
    • Lung findings
      • Dyspnea
      • Cough
      • Wheezing
      • Hemoptysis
      • Chest Pain
      • Hypoxia
      • Apnea
      • Decreased breath sounds
    • Cardiovascular findings
      • Bradycardia
      • Hypotension
      • Cyanosis
    • Skin findings
      • Subcutaneous Emphysema

    Diagnosis of Pulmonary Barotrauma

    The history and physical exam in patients with barotrauma secondary to mechanical ventilation are usually limited since those patients are sick and under sedation while on mechanical ventilation. In cases of clinically significant pneumothorax, patients will present with acute changes in vital signs, including tachypnea, hypoxia, and tachycardia. Patients may also present with obstructive shock if a tension pneumothorax occurs. Physical examination may be significant for absent breath sounds if a pneumothorax exists. Subcutaneous emphysema may also present in some cases. In some, less severe cases, no systemic or hemodynamic changes may be present.

    The patient’s past medical history is also essential when it comes to the diagnosis and management of pulmonary barotrauma. As mentioned previously, patients with a known history of chronic obstructive pulmonary disease (COPD), asthma, interstitial lung disease (ILD), pneumocystis jiroveci pneumonia, or ARDS, are at increased risk of developing pulmonary barotrauma. Underlying pulmonary pathology will also be important to be aware of when it comes to selecting the ventilator mode as well as the settings as we will discuss later.

    Lab Test and Imaging

    Ventilator data may be useful in the evaluation of pulmonary barotrauma. Ventilator asynchrony, acute elevation of the plateau and peak pressures above 30 cmH2O, or sudden decrease of delivered tidal volume may suggest respiratory distress secondary to pneumothorax or other complications from barotrauma. Ventilator data can give a clue to physicians regarding which patients are at higher risk for barotrauma.

    Once pulmonary barotrauma secondary to the mechanical ventilator is suspected, action must take place immediately. Pneumothorax is an acute complication from pulmonary barotrauma, which is an emergency. The physical exam will be remarkable for absent breath sounds, and in most cases, patients who can communicate will complain of shortness of breath and chest pain. Vital signs usually demonstrate hypoxia as well as hypotension secondary to obstructive shock in the case of a tension pneumothorax. In patients who develop a tension pneumothorax, action is necessary before obtaining a chest radiograph. Tension pneumothorax requires urgent needle decompression to evacuate the pneumothorax, followed by thoracotomy tube placement. In patients presenting with a less acute complication, such as a simple pneumothorax with stable vital signs, pneumomediastinum, or subcutaneous emphysema, the clinician should obtain a chest radiograph immediately. The chest radiograph is able to identify the presence of pneumothorax, pneumomediastinum, subcutaneous emphysema, and other less common manifestations of pulmonary barotrauma, such as pneumatoceles, sub-pleural air collections, and pulmonary interstitial emphysema (PIE). If a chest x-ray is obtained but inadequate for evaluation, a CT of the chest can be done. It is important to remember that barotrauma is a clinical diagnosis and should always be high in the differential diagnosis for patients on invasive and non-invasive mechanical ventilation presenting with acute decompensation.

    Treatment of Pulmonary Barotrauma

    First aid

    Pre-hospital care for lung barotrauma includes basic life support of maintaining adequate oxygenation and perfusion, assessment of airway, breathing and circulation, neurological assessment, and managing any immediate life-threatening conditions. High-flow oxygen up to 100% is considered appropriate for diving accidents. Large-bore venous access with isotonic fluid infusion is recommended to maintain blood pressure and pulse.[rx]

    Emergency treatment

    Pulmonary barotrauma:[rx]

    • Endotracheal intubation may be required if the airway is unstable or hypoxia persists when breathing 100% oxygen.
    • Needle decompression or tube thoracostomy may be necessary to drain a pneumothorax or haemothorax
    • Foley catheterization may be necessary for spinal cord AGE if the person is unable to urinate.
    • Intravenous hydration may be required to maintain adequate blood pressure.
    • Therapeutic recompression is indicated for severe AGE. The diving medical practitioner will need to know the vital signs and relevant symptoms, along with the recent pressure exposure and breathing gas history of the patient. Air transport should be below 1,000 feet (300 m) if possible, or in a pressurized aircraft which should be pressurized to as low an altitude as reasonably possible.

    Sinus squeeze and middle ear squeeze are generally treated with decongestants to reduce the pressure differential, with anti-inflammatory medications to treat the pain. For severe pain, narcotic analgesics may be appropriate.[49]

    Suit, helmet and mask squeeze are treated as trauma according to symptoms and severity.

    There is no single strategy to prevent pulmonary barotrauma on patients on mechanical ventilation. The most efficient mechanism that has been described to prevent the risk of developing barotrauma on mechanical ventilation involves maintaining the plateau and peak inspiratory pressures low. The goal plateau pressure should be below 35 cmH2O, and ideally below 30 cmH2O, on most patients on mechanical ventilation as recommended by the ARDS Network group. Various techniques may be employed to aid in maintaining the plateau pressure at goal. Various ventilator modes are available. The two modes most commonly used in intensive care units are volume assist control (volume AC), a volume cycled mode, and pressure assist control (pressure AC), a pressure cycled mode. Lung protective ventilator strategies should be used in every ARDS and most other patients, regardless of the mode of mechanical ventilation. Lung protective ventilator strategies derive for the most part from a study published in the year 2000 by the ARDS Network group. The study involved ARDS patients and compared outcomes in ARDS patients using higher tidal volume ventilation (about 12 mL/kg of IBW) and patients using lower tidal volume ventilation (about 6 mL/kg OF IBW). Although tidal volume was the variable in this study, the goal with the low volume ventilation group was to keep the plateau pressure below 30 cmH2O. The low tidal volume ventilatory strategy correlated with a lower mortality rate (31% vs. 40%). The incidence of barotrauma in this study was not lower when using lung-protective ventilator strategies; however, other studies have demonstrated a higher incidence of barotrauma when the plateau pressure rises above 35 cmH2O. Low tidal volume ventilation is especially important in patients at higher risk for barotrauma, such as patients with ARDS, COPD, asthma, Pneumocystis jiroveci pneumonia (PJP), and chronic interstitial lung disease (ILD).

    The driving pressure is another concept with which physicians managing patients at risk of barotrauma must be familiar. The driving pressure is measurable in patients not making an inspiratory effort; one can obtain the calculated pressure by subtracting the PEEP from the plateau pressure. Driving pressure became a hot topic of discussion after the ARDS trial proposed that high plateau pressures increase mortality in patients with ARDS but that high PEEP pressure is associated with improved outcomes. Amato et al., in 2015, proposed that the driving pressure was a better ventilation variable to stratify risk. In the trial, published in the NEJM in 2015, they concluded that an increment of 1 standard deviation in driving pressure was associated with increased mortality even in patients receiving protective plateau pressure and tidal volumes. Individual changes in tidal volume and PEEP were only associated with improved survival if these changes led to a reduction in driving pressure. Based on the data available, clinicians should maintain the optimal driving pressure between 13 and 15 cm H2O.

    As mentioned previously, patients with obstructive lung disease are at risk of dynamic hyperinflation due to a prolonged expiratory phase, and difficulty exhaling the full volume before the ventilator delivers the next breath. Physicians must be aware of intrinsic PEEP or auto-PEEP, particularly in patients at high risk, such as those with obstructive lung disease. An expiratory pause maneuver on the ventilator will provide static intrinsic pressure. If intrinsic PEEP is present, then the physician may increase the external PEEP to help with ventilator synchronization by allowing the patient to trigger the ventilator and initiate a breath more effectively. The goal is to increase the external PEEP by 75 to 85% of the intrinsic PEEP . Other methods that the physician may employ to decrease the intrinsic PEEP include decreasing the respiratory rate, decreasing the tidal volume, and prolonging the expiratory time.

    High positive end-expiratory pressure (PEEP) may theoretically lead to overdistention of healthy alveoli in regions not affected by disease and ultimately lead to barotrauma. Many conditions, such as moderate to severe ARDS, require the use of high PEEP pressures to improved oxygenation by recruiting as many alveoli units as possible. When used in conjunction with lung protective strategies, as described above, the risk of barotrauma due to high PEEP is minimal. Several methods exist to aid physicians in determining the adequate level of PEEP to treat individual patients based on lung compliance. A system pressure-volume curve may be used to determine the lower inflection point and the higher inflection point. The lower inflection point in the curve determines the minimal level of PEEP required to start alveolar recruitment. The upper inflection point in the curve determines the pressure level at which the risk of barotrauma and lung injury occurs.

    The stress index is another method that may be used by physicians to determine the adequate amount of PEEP for individual patients. For the stress index to be an accurate measurement, the patient must be well sedated, and the flow must be constant. The physician may look at the pressure waveform on the ventilator to determine the stress index. A pressure wave that is concave down indicates a stress index less than 1. A stress index of less than 1 indicates that the patient may benefit from increased PEEP to help with alveoli recruitment. A pressure wave that is concave up indicates a stress index higher than 1. A stress index higher than one should alert the physician that the patient’s alveoli unit is at risk of distention and barotrauma. A straight diagonal line in the pressure wave is ideal because it correlates with a stress index between 0.9 and 1.1, which is the ideal range for proper alveoli recruitment with a low risk of distention and rupture.

    Different ventilator modes also exist, which may be better tolerated by some patients and decrease the risk of barotrauma. There is no evidence to suggest that one ventilator mode is better than the other. However, in patients who are difficult to manage, physicians may try different modes to synchronize the patient with the ventilator better.

    Volume AC mode is a volume cycled mode. It will deliver a set volume on every ventilator-assisted breath, which will lead to significant variations in peak inspiratory pressures as well as plateau pressures depending on the compliance of the lung parenchyma. The peak inspiratory and plateau pressures may be kept at goal using this mode of ventilation by using low tidal volume ventilation (between 6 to 8 mL/kg based on the ideal body weight). The respiratory rate and inspiratory time may be adjusted as well to prevent intrinsic PEEP. In some cases, sedation, and even neuromuscular blocking agents may be to be used to improve ventilator synchrony and maintain inspiratory peak and plateau pressures at goal.

    Pressure AC mode is a pressure cycled mode. It allows medical personnel to set an inspiratory pressure level as well as the applied PEEP. The advantage of using a pressure cycled mode is that the peak inspiratory pressure will remain constant and will be equal to the inspiratory pressure in addition to the PEEP. The plateau pressure will also be lower or equal to the peak inspiratory pressure; therefore, this mode of ventilation correlates with a lower rate of barotrauma. The disadvantage, however, is that the tidal volume delivered will vary depending on lung compliance. Patients with poor lung compliance may not receive an adequate tidal volume using this ventilator mode.

    Effect Management

    The management of complications due to barotrauma depends on the specific complication. Pneumothorax, or tension pneumothorax, is a medical emergency. A tension pneumothorax must be treated immediately with needle decompression. The diagnosis of tension pneumothorax is made clinically and must be acted upon quickly without waiting for chest radiography. Signs and symptoms of tension pneumothorax include the absence of breath sounds, hemodynamic instability, as well as symptoms of chest pain and shortness of breath. The clinician must perform an urgent needle decompression followed by the placement of a thoracotomy tube.

    The management of most non-tension pneumothorax in patients on mechanical ventilation involves the placement of a thoracostomy tube to evacuate the air due to the high incidence of progression to tension pneumothorax while on mechanical ventilation. Once the thoracotomy tube is in place, additional changes in the ventilator may be made to help with the resolution of the pneumothorax. Tidal volume may be decreased to decrease the plateau and peak inspiratory pressures. FiO2 in the ventilator may be increased temporarily to help decrease the partial pressure of nitrogen and aid with the absorption of air from the pleural cavity and hasten lung re-expansion. PEEP should also be lowered to decrease overdistention of the alveoli units, and patients should be well sedated to prevent ventilator asynchrony and further trauma.

    Other complications, such as subcutaneous emphysema, pneumomediastinum, and pneumoperitoneum, are usually self-resolving and management is conservative. Conservative management involves reducing the plateau pressures below 30 cmH2O as well as continuous monitoring. Other strategies to minimize complications include reducing the PEEP on the ventilator, using sedation and neuromuscular blockade in patients who are difficult to synchronize with the ventilator, and decreasing the ventilatory pressures. Ultimately, the best way to prevent barotrauma and complications is liberating the patient from mechanical ventilation.

    Tension pneumomediastinum is an exception. Intension pneumomediastinum, the pressure in the mediastinum increases significantly and ultimately may lead to physiological effects similar to pericardial tamponade. It may cause compression of the great vessels and compromise the right heart filling leading to shock and eventually, cardiac arrest. Chest radiography will show a heart silhouette resembling a sphere. The initial management involves ventilator changes to decrease the airway pressures and increase the FiO2 in the ventilator to 100%. Ultimately surgical mediastinal decompression is required.

    Subcutaneous emphysema rarely may lead to compartment syndrome. Compartment syndrome should be suspected in patients with hemodynamic instability and elevated bladder pressures. Management involves decreasing the airway pressures, but ultimately, surgical evaluation is warranted. Surgical decompression must be performed in all patients with hemodynamic instability as this condition is associated with a high mortality rate.

    Patients presenting with pneumoperitoneum may also progress to compartment syndrome. An immediate surgical evaluation must take place due to the high mortality associated with this condition. Pneumoperitoneum due to barotrauma is rare, and other causes for pneumoperitoneum should be ruled out, such as ruptured viscus and abdominal trauma.

    Hypercapnia is among the most common side effects that present when managing a patient with lung-protective ventilatory strategies. The lower tidal volume may lead to decreased minute ventilation, and in some cases, hypercapnia. Guidelines for ARDS recommend allowing for permissive hypercapnia up to a pH of 7.2. If the pH drops below 7.2, the initiation of a bicarbonate infusion should be a therapeutic consideration to correct the pH to 7.2.

    Prevention

    In divers

    Barotrauma may be caused when diving, either from being crushed or squeezed, on descent or by stretching and bursting on the ascent; both can be avoided by equalizing the pressures. A negative, unbalanced pressure is known as a squeeze, crushing eardrums, dry suit, lungs, or mask inwards and can be equalized by putting air into the squeezed space. A positive unbalanced pressure expands internal spaces rupturing tissue and can be equalized by letting air out, for example by exhaling. Both may cause barotrauma. There are a variety of techniques depending on the affected area and whether the pressure inequality is a squeeze or an expansion:

    • Ears and sinuses: There is a risk of stretched or burst eardrums, usually crushed inwards during descent but sometimes stretched outwards on the ascent. The diver can use a variety of methods to let air into or out of the middle ears via the Eustachian tubes. Sometimes swallowing will open the Eustachian tubes and equalize the ears.
    • Lungs: There is a risk of pneumothorax, arterial gas embolism, and mediastinal and subcutaneous emphysema during ascent, which are commonly called burst lung or lung overpressure injury by divers. To equalize the lungs, all that is necessary is not to hold the breath during ascent. This risk does not occur when breath-hold diving from the surface, unless the diver breathes from an ambient pressure gas source underwater; breath-hold divers do suffer squeezed lungs on the descent, crushing in the chest cavity, but, while uncomfortable, this rarely causes lung injury and returns to normal at the surface. Some people have the pathology of the lung which prevents the rapid flow of excess air through the passages, which can lead to lung barotrauma even if the breath is not held during rapid depressurization. These people should not dive as the risk is unacceptably high. Most commercial or military diving medical examinations will look specifically for signs of this pathology.
    • Diving mask squeeze enclosing the eyes and nose: The main risk is rupture of the capillaries of the eyes and facial skin because of the negative pressure difference between the gas space and blood pressure, or orbital emphysema from higher pressures. This can be avoided by breathing air into the mask through the nose. Goggles covering only the eyes are not suitable for deep diving as they cannot be equalized.
    • Drysuit squeeze. The main risk is skin getting pinched and bruised by folds of the drysuit when squeezed on the descent. Most drysuits can be equalized against squeeze via a manually operated valve fed from a low-pressure gas supply. Air must be manually injected during the descent to avoid squeeze and is manually or automatically vented on the ascent to maintain buoyancy control.
    • Diving helmet squeeze: Helmet squeeze will occur if the gas supply hose is severed above the diver and the non-return valve at the helmet gas inlet fails or is not fitted. The severity will depend on the hydrostatic pressure difference. A very rapid descent, usually by accident, may exceed the rate at which the breathing gas supply can equalize the pressure causing a temporary squeeze. The introduction of the non-return valve and high maximum gas supply flow rates have all but eliminated both these risks. In helmets fitted with a neck dam, the dam will admit water into the helmet if the internal pressure gets too low; this is less of a problem than helmet squeeze but the diver may drown if the gas supply is not reinstated quickly. This form of barotrauma is avoidable by controlled descent rate, which is standard practice for commercial divers, who will use hotlines, diving stages and wet bells to control descent and ascent rates.

    Breathing Exercise and Techniques for Stress Relief

    Breathing Exercise and Techniques for Stress Relief/Breathing is a necessity of life that usually occurs without much thought. When you breathe in air, blood cells receive oxygen and release carbon dioxide. Carbon dioxide is a waste product that’s carried back through your body and exhaled.

    breathing also goes by the names of diaphragmatic breathing, abdominal breathing, belly breathing, and paced respiration. When you breathe deeply, the air coming in through your nose fully fills your lungs, and the lower belly rises.

    For many of us, deep breathing seems unnatural. There are several reasons for this. For one, body image has a negative impact on respiration in our culture. A flat stomach is considered attractive, so women (and men) tend to hold in their stomach muscles. This interferes with deep breathing and gradually makes shallow “chest breathing” seem normal, which increases tension and anxiety.

    Shallow breathing limits the diaphragm’s range of motion. The lowest part of the lungs doesn’t get a full share of oxygenated air. That can make you feel short of breath and anxious.

    Deep abdominal breathing encourages full oxygen exchange — that is, the beneficial trade of incoming oxygen for outgoing carbon dioxide. Not surprisingly, it can slow the heartbeat and lower or stabilize blood pressure.

    Improper breathing can upset the oxygen and carbon dioxide exchange and contribute to anxiety, panic attacks, fatigue, and other physical and emotional disturbances.

    Breathing Exercise and Techniques for Stress Relief

    If you’re interested in trying breathing exercises to reduce stress or anxiety or improve your lung function, we’ve got 10 different ones to sample. You may find that certain exercises appeal to you right away. Start with those so that the practice is more enjoyable.

    How to add breathing exercises to your day

    Breathing exercises don’t have to take a lot of time out of your day. It’s really just about setting aside some time to pay attention to your breathing. Here are a few ideas to get started:

    • Begin with just 5 minutes a day, and increase your time as the exercise becomes easier and more comfortable.
    • If 5 minutes feels too long, start with just 2 minutes.
    • Practice multiple times a day. Schedule set times or practice conscious breathing as you feel the need.

    1. Pursed lip breathing

    • This simple breathing technique makes you slow down your pace of breathing by having you apply deliberate effort in each breath.
    • You can practice pursed-lip breathing at any time. It may be especially useful during activities such as bending, lifting, or stair climbing.
    • Practice using this breath 4 to 5 times a day when you begin in order to correctly learn the breathing pattern.

    To do it

    • Relax your neck and shoulders.
    • Keeping your mouth closed, inhale slowly through your nose for 2 counts.
    • Pucker or purse your lips as though you were going to whistle.
    • Exhale slowly by blowing air through your pursed lips for a count of 4.

    2. Diaphragmatic breathing

    • Belly breathing can help you use your diaphragm properly. Do belly breathing exercises when you’re feeling relaxed and rested.
    • Practice diaphragmatic breathing for 5 to 10 minutes 3 to 4 times per day.
    • When you begin you may feel tired, but over time the technique should become easier and should feel more natural.

    To do it

    • Lie on your back with your knees slightly bent and your head on a pillow.
    • You may place a pillow under your knees for support.
    • Place one hand on your upper chest and one hand below your rib cage, allowing you to feel the movement of your diaphragm.
    • Slowly inhale through your nose, feeling your stomach pressing into your hand.
    • Keep your other hand as still as possible.
    • Exhale using pursed lips as you tighten your stomach muscles, keeping your upper hand completely still.

    You can place a book on your abdomen to make the exercise more difficult. Once you learn how to do belly breathing lying down you can increase the difficulty by trying it while sitting in a chair. You can then practice the technique while performing your daily activities.

    3. Breath focus technique

    • This deep breathing technique uses imagery or focuses words and phrases.
    • You can choose a focus word that makes you smile, feel relaxed, or that is simply neutral to think about. Examples include peacelet go, or relaxation, but it can be any word that suits you to focus on and repeat through your practice.
    • As you build up your breath focus practice you can start with a 10-minute session. Gradually increase the duration until your sessions are at least 20 minutes.

    To do it

    • Sit or lie down in a comfortable place.
    • Bring your awareness to your breaths without trying to change how you’re breathing.
    • Alternate between normal and deep breaths a few times. Notice any differences between normal breathing and deep breathing. Notice how your abdomen expands with deep inhalations.
    • Note how shallow breathing feels compared to deep breathing.
    • Practice your deep breathing for a few minutes.
    • Place one hand below your belly button, keeping your belly relaxed, and notice how it rises with each inhales and falls with each exhale.
    • Let out a loud sigh with each exhale.
    • Begin the practice of breath focus by combining this deep breathing with imagery and a focused word or phrase that will support relaxation.
    • You can imagine that the air you inhale brings waves of peace and calm throughout your body. Mentally say, “Inhaling peace and calm.”
    • Imagine that the air you exhale washes away tension and anxiety. You can say to yourself, “Exhaling tension and anxiety.

    4. Lion’s breath

    • Lion’s breath is an energizing yoga breathing practice that is said to relieve tension in your chest and face.
    • It’s also known in yoga as Lion’s Pose or simhasana in Sanskrit.

    To do this

    • Come into a comfortable seated position. You can sit back on your heels or cross your legs.
    • Press your palms against your knees with your fingers spread wide.
    • Inhale deeply through your nose and open your eyes wide.
    • At the same time, open your mouth wide and stick out your tongue, bringing the tip down toward your chin.
    • Contract the muscles at the front of your throat as you exhale out through your mouth by making a long “ha” sound.
    • You can turn your gaze to look at the space between your eyebrows or the tip of your nose.
    • Do this breath 2 to 3 times.

    5. Alternate nostril breathing

    • Alternate nostril breathing, known as nadi shodhana pranayama in Sanskrit, is a breathing practice for relaxation.
    • Alternate nostril breathing has been shown to enhance cardiovascular function and lower heart rate.
    • Nadi shodhana is best practiced on an empty stomach. Avoid the practice if you’re feeling sick or congested. Keep your breath smooth and even throughout the practice.

    To do this

    • Choose a comfortable seated position.
    • Lift up your right hand toward your nose, pressing your first and middle fingers down toward your palm and leaving your other fingers extended.
    • After an exhale, use your right thumb to gently close your right nostril.
    • Inhale through your left nostril and then close your left nostril with your right pinky and ring fingers.
    • Release your thumb and exhale out through your right nostril.
    • Inhale through your right nostril and then close this nostril.
    • Release your fingers to open your left nostril and exhale through this side.
    • This is one cycle.
    • Continue this breathing pattern for up to 5 minutes.
    • Finish your session with an exhale on the left side.

    6. Equal breathing

    • Equal breathing is known as sama vritti in Sanskrit. This breathing technique focuses on making your inhales and exhales the same length. Making your breath smooth and steady can help bring about balance and equanimity.
    • You should find a breath length that is not too easy and not too difficult. You also want it to be too fast, so that you’re able to maintain it throughout the practice. Usually, this is between 3 and 5 counts.
    • Once you get used to equal breathing while seated you can do it during your yoga practice or other daily activities.

    To do it

    • Choose a comfortable seated position.
    • Breathe in and out through your nose.
    • Count during each inhale and exhale to make sure they are even in duration. Alternatively, choose a word or short phrase to repeat during each inhale and exhale.
    • You can add a slight pause or breath retention after each inhales and exhales if you feel comfortable. (Normal breathing involves a natural pause.)
    • Continue practicing this breath for at least 5 minutes.

    7. Resonant or coherent breathing

    • Resonant breathing, also known as coherent breathing, is when you breathe at a rate of 5 full breaths per minute. You can achieve this rate by inhaling and exhaling for a count of 5.
    • Breathing at this rate maximizes your heart rate variability (HRV), reduces stress, and, according to one 2017 study, can reduce symptoms of depression when combined with Iyengar yoga.

    To do this

    • Inhale for a count of 5.
    • Exhale for a count of 5.
    • Continue this breathing pattern for at least a few minutes.

    8. Sitali breath

    • This yoga breathing practice helps you lower your body temperature and relax your mind.
    • Slightly extend your breath in length but don’t force it. Since you inhale through your mouth during Sitali breath, you may want to choose a place to practice that’s free of any allergens that affect you and air pollution.

    To do this

    • Choose a comfortable seated position.
    • Stick out your tongue and curl your tongue to bring the outer edges together.
    • If your tongue doesn’t do this, you can pursue your lips.
    • Inhale through your mouth.
    • Exhale out through your nose.
    • Continue breathing like this for up to 5 minutes.

    9. Deep breathing

    • Deep breathing helps to relieve shortness of breath by preventing air from getting trapped in your lungs and helping you to breathe in the more fresh air. It may help you to feel more relaxed and centered.

    To do this

    • While standing or sitting, draw your elbows back slightly to allow your chest to expand.
    • Take a deep inhalation through your nose.
    • Retain your breath for a count of 5.
    • Slowly release your breath by exhaling through your nose.

    10. Humming bee breath (bhramari)

    • The unique sensation of this yoga breathing practice helps to create an instant calm and is especially soothing around your forehead.
    • Some people use humming bee breaths to relieve frustration, anxiety, and anger. Of course, you’ll want to practice it in a place where you are free to make a humming sound.

    To do this

    • Choose a comfortable seated position.
    • Close your eyes and relax your face.
    • Place your first fingers on the tragus cartilage that partially covers your ear canal.
    • Inhale, and as you exhale gently press your fingers into the cartilage.
    • Keeping your mouth closed, make a loud humming sound.
    • Continue for as long as is comfortable.

    You can try most of these breath exercises right away. Take the time to experiment with different types of breathing techniques. Dedicate a certain amount of time at least a few times per week. You can do these exercises throughout the day.

    Check-in with your doctor if you have any medical concerns or take any medications. If you want to learn more about breathing practices you can consult a respiratory therapist or a yoga teacher who specializes in breathing practices. Discontinue the practice if you experience any feelings of discomfort or agitation.

    The 9 Best Breathing Techniques for Sleep

    If you find it difficult to fall asleep, you’re not alone.

    According to the American Sleep Association (ASA), insomnia is the most common sleep disorder. About 30 percent of American adults report short-term problems, and 10 percent experience chronic trouble falling or staying asleep.

    Our busy and fast-paced society, filled with homework, long work days, financial strains, parenting burnout, or other emotionally exhausting situations, can make it difficult to unwind, calm down, and get restful sleep. When it’s hard to sleep, focusing on your breath may help.

    Let’s take a look at some breathing exercises to calm your mind and body to help you fall asleep.

    Things to remember before getting started

    Although there are a number of breathing exercises you can try to relax and fall asleep, a few basic principles apply to all of them.

    It’s always a good idea to close your eyes, which may help you shut out distractions. Focus on your breathing and think about the healing power of your breath.

    Each of these nine different exercises has slightly different benefits. Try them and see which one is the best match for you. Soon you’ll be sleeping like a baby.

    1. 4-7-8 breathing technique

    Here’s how to practice the 4-7-8 breathing technique:

    • Allow your lips to gently part.
    • Exhale completely, making a breathy whoosh sound as you do.
    • Press your lips together as you silently inhale through the nose for a count of 4 seconds.
    • Hold your breath for a count of 7.
    • Exhale again for a full 8 seconds, making a whooshing sound throughout.
    • Repeat 4 times when you first start. Eventually, work up to 8 repetitions.

    Dr. Andrew Weil developed this technique as a variation of pranayama, an ancient yogic technique that helps people relax as it replenishes oxygen in the body.

    2. Bhramari pranayama breathing exercise

    These steps will help you perform the original Bhramari pranayama breathing exercise:

    • Close your eyes and breathe deeply in and out.
    • Cover your ears with your hands.
    • Place your index fingers one each above your eyebrows and the rest of your fingers over your eyes.
    • Next, put gentle pressure to the sides of your nose and focus on your brow area.
    • Keep your mouth closed and breathe out slowly through your nose, making the humming “Om” sound.
    • Repeat the process 5 times.

    In clinical studies Bhramari pranayama has been shown to quickly reduce breathing and heart rate. This tends to be very calming and can prepare your body for sleep.

    3. Three-part breathing exercise

    To practice the three-part breathing exercise, follow these three steps:

    • Take a long, deep inhale.
    • Exhale fully while focusing intently on your body and how it feels.
    • After doing this a few times, slow down your exhale so that it’s twice as long as your inhale.

    4. Diaphragmatic breathing exercise

    To do diaphragmatic breathing exercises:

    • Lie on your back and either bend your knees over a pillow or sit in a chair.
    • Place one hand flat against your chest and the other on your stomach.
    • Take slow, deep breaths through your nose, keeping the hand on your chest still as the hand on your stomach rises and falls with your breaths.
    • Next, breathe slowly through pursed lips.
    • Eventually, you want to be able to breathe in and out without your chest moving.

    This technique slows your breathing and decreases your oxygen needs as it strengthens your diaphragm.

    5. Alternate nasal breathing exercise

    Here are the steps for the alternate nasal or alternate nostril breathing exercise, also called nadi shodhana pranayama:

    • Sit with your legs crossed.
    • Place your left hand on your knee and your right thumb against your nose.
    • Exhale fully and then close the right nostril.
    • Inhale through your left nostril.
    • Open your right nostril and exhale through it, while closing the left.
    • Continue this rotation for 5 minutes, finishing by exhaling through your left nostril.

    2013 study reported that people who tried nasal breathing exercises felt less stressed afterward.

    6. Buteyko breathing

    To practice buteyko breathing for sleep:

    • Sit in bed with your mouth gently closed (not pursed) and breathe through your nose at a natural pace for about 30 seconds.
    • Breathe a bit more intentionally in and out through your nose once.
    • Gently pinch your nose closed with your thumb and forefinger, keeping your mouth closed as well, until you feel that you need to take a breath again.
    • With your mouth still closed, take a deep breath in and out through your nose again.

    Many people don’t realize that they are hyperventilating. This exercise helps you to reset to a normal breathing rhythm.

    7. The Papworth method

    In the Papworth method, you focus on your diaphragm to breathe more naturally:

    • Sit up straight, perhaps in bed if using this to fall asleep.
    • Take deep, methodical breaths in and out, counting to 4 with each inhale — through your mouth or nose — and each exhale, which should be through your nose.
    • Focus on your abdomen rising and falling, and listen for your breath sounds to come from your stomach.

    This relaxing method is helpful for reducing habits of yawning and sighing.

    8. Kapalbhati breathing exercise

    Kapalbhati breathing involves a series and inhaling and exhaling exercises, involving these steps, as outlined by the Art of Living:

    • Sit in a comfortable position with your spine straight. Place your hands on your knees, palms facing the sky. You may choose to sit cross-legged on the floor, on a chair with feet flat on the floor, or in Virasana Pose (sitting on your heels with knees bent and shins tucked beneath the thighs).
    • Take a deep breath in.
    • As you exhale, contract your belly, forcing the breath out in a short burst. You may keep a hand on your stomach to feel your abdominal muscles contract.
    • As you quickly release your abdomen, your breath should flow into your lungs automatically.
    • Take 20 such breaths to complete one round of Kapalbhati pranayama.
    • After completing one round, relax with your eyes closed and observe the sensations in your body.
    • Do two more rounds to complete your practice.

    Kapalbhati breathing has been reported as helping open the sinuses and improving concentration. It’s considered an advanced breathing technique. It’s advisable to master other techniques, such as Bhramari pranayama, before attempting this one.

    9. Box breathing

    During box breathing, you want to focus intently on the oxygen you’re bringing in and pushing out:

    • Sit with your back straight, breathe in, and then try to push all the air out of your lungs as you exhale.
    • Inhale slowly through your nose and count to 4 in your head, filling your lungs with more air with each number.
    • Hold your breath and count to 4 in your head.
    • Slowly exhale through your mouth, focusing on getting all the oxygen out of your lungs.

    Box breathing is a common technique during meditation, a very popular method of finding mental focus and relaxing. Meditation has a variety of known benefits for your overall health.

    No matter which type of breathing exercise you prefer, the evidence is clear that breathing exercises can help you on relax, sleep, breathe more naturally and effectively

    With so many varieties to choose from, you may find yourself fast asleep before you know it.

    Breathing Exercises with COPD

    Chronic obstructive pulmonary disease (COPD) is a health condition that affects an individual’s ability to breathe well. It’s often associated with other conditions such as emphysema and chronic bronchitis.

    Symptoms include:

    • wheezing
    • chest tightness
    • shortness of breath
    • large amounts of mucus that collect in the lungs

    These can worsen with time, but practicing breathing exercises can help you manage them.

    When you practice regularly, breathing exercises can help you exert yourself less during daily activities. They can also potentially aid in your return to exercising, which can lead to you feeling more energetic overall.

    Read on to learn about these five exercises that can be especially useful for people with COPD

    • pursed-lip breathing
    • coordinated breathing
    • deep breathing
    • huff cough
    • diaphragmatic breathing

    Pursed lip breathing

    According to the Cleveland Clinic, pursed-lip breathing has a range of benefits:

    • It’s been shown to reduce how hard you have to work to breathe.
    • It helps release the air trapped in the lungs.
    • It promotes relaxation.
    • It reduces shortness of breath.

    Practicing this technique 4 to 5 times daily can help. Here’s how to practice pursed-lip breathing

    • While keeping your mouth closed, take a deep breath in through your nose, counting to 2. Follow this pattern by repeating in your head “inhale, 1, 2.” The breath doesn’t have to be deep. A typical inhale will do.
    • Put your lips together as if you’re starting to whistle or blow out candles on a birthday cake. This is known as “pursing” your lips.
    • While continuing to keep your lips pursed, slowly breathe out by counting to 4. Don’t try to force the air out, but instead breathe out slowly through your mouth.

    Exercise tip: Pursed lip breathing is best for performing strenuous activities, such as climbing stairs.

    Coordinated breathing

    Feeling short of breath can cause anxiety that makes you hold your breath. To prevent this from occurring, you can practice coordinated breathing using these two steps:

    • Inhale through your nose before beginning an exercise.
    • While pursuing your lips, breathe out through your mouth during the most strenuous part of the exercise. An example could be when curling upward on a bicep curl.

    Exercise tip: Coordinated breathing can be performed when you’re exercising or feeling anxious.

    Deep breathing

    Deep breathing prevents air from getting trapped in your lungs, which can cause you to feel short of breath. As a result, you can breathe in more fresh air.

    Here’s how to practice deep breathing

    • Sit or stand with your elbows slightly back. This allows your chest to expand more fully.
    • Inhale deeply through your nose.
    • Hold your breath as you count to 5.
    • Release the air via a slow, deep exhale, through your nose, until you feel your inhaled air has been released.

    Exercise tip: It’s best to do this exercise with other daily breathing exercises that can be performed for 10 minutes at a time, 3 to 4 times per day.

    Huff cough

    • When you have COPD, mucus can build up more easily in your lungs. The huff cough is a breathing exercise designed to help you cough up mucus effectively without making you feel too tired.

    Here’s how to practice the huff cough

    • Place yourself in a comfortable seated position. Inhale through your mouth, slightly deeper than you would when taking a normal breath.
    • Activate your stomach muscles to blow the air out in three even breaths while making the sounds “ha, ha, ha.” Imagine you’re blowing onto a mirror to cause it to steam.

    Exercise tip: A huff cough should be less tiring than a traditional cough, and it can keep you from feeling worn out when coughing up mucus.

    Diaphragmatic breathing

    • The diaphragm is an important muscle involved in the work of breathing.
    • People with COPD tend to rely more on the accessory muscles of the neck, shoulders, and back to breathe, rather than on the diaphragm.

    Diaphragmatic or abdominal breathing helps to retrain this muscle to work more effectively. Here’s how to do it

    • While sitting or lying down with your shoulders relaxed, put a hand on your chest and place the other hand on your stomach.
    • Take a breath in through your nose for 2 seconds, feeling your stomach move outward. You’re doing the activity correctly if your stomach moves more than your chest.
    • Purse your lips and breathe out slowly through your mouth, pressing lightly on your stomach. This will enhance your diaphragm’s ability to release air.
    • Repeat the exercise as you are able to.

    Exercise tip: This technique can be more complicated than the other exercises, so it’s best for a person with a little more practice under their belt. If you’re having difficulty, talk to your doctor or respiratory therapist.

    According to the American Academy of Family Physicians (AAFP), people with COPD who use breathing exercises experience greater improvements in exercise capacity than those who don’t.

    9 Home Treatments for Shortness of Breath (Dyspnea)

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    Shortness of breath, or dyspnea, is an uncomfortable condition that makes it difficult to fully get air into your lungs. Problems with your heart and lungs can harm your breathing.

    Some people may experience shortness of breath suddenly for short periods of time. Others may experience it over the long term — several weeks or more.

    In light of the 2020 COVID-19 pandemic, shortness of breath has become widely associated with this illness. Other common symptoms of COVID-19 include dry cough and fever.

    Most people who develop COVID-19 will only experience mild symptoms. However, seek emergency medical attention if you experience:

    • trouble breathing
    • persistent tightness in your chest
    • blue lips
    • mental confusion

    If your shortness of breath isn’t caused by a medical emergency, you could try several types of home treatments that are effective at helping alleviate this condition. Many simply involve changing position, which can help relax your body and airways.

    Here are nine home treatments you can use to alleviate your shortness of breath:

    1. Pursed-lip breathing

    • This is a simple way to control shortness of breath. It helps quickly slow your pace of breathing, which makes each breath deeper and more effective
    • It also helps release air that’s trapped in your lungs. It can be used any time you’re experiencing shortness of breath, especially during the difficult part of an activity, such as bending, lifting objects, or climbing stairs.

    To perform pursed-lip breathing

    • Relax your neck and shoulder muscles.
    • Slowly breathe in through your nose for two counts, keeping your mouth closed.
    • Purse your lips as if you’re about to whistle.
    • Breathe out slowly and gently through your pursed lips to the count of four.

    2. Sitting forward

    Resting while sitting can help relax your body and make breathing easier.

    • Sit in a chair with your feet flat on the floor, leaning your chest slightly forward.
    • Gently rest your elbows on your knees or hold your chin with your hands. Remember to keep your neck and shoulder muscles relaxed.

    3. Sitting forward supported by a table

    If you have both a chair and table to use, you may find this to be a slightly more comfortable sitting position in which to catch your breath.

    • Sit in a chair with your feet flat on the floor, facing a table.
    • Lean your chest slightly forward and rest your arms on the table.
    • Rest your head on your forearms or on a pillow.

    4. Standing with a supported back

    Standing can also help relax your body and airways.

    • Stand near a wall, facing away, and rest your hips on the wall.
    • Keep your feet shoulder-width apart and rest your hands on your thighs.
    • With your shoulders relaxed, lean slightly forward, and dangle your arms in front of you.

    5. Standing with supported arms

    • Stand near a table or other flat, sturdy piece of furniture that’s just below the height of your shoulder.
    • Rest your elbows or hands on the piece of furniture, keeping your neck relaxed.
    • Rest your head on your forearms and relax your shoulders.

    6. Sleeping in a relaxed position

    • Many people experience shortness of breath while they sleep. This can lead to waking up frequently, which can diminish the quality and duration of your sleep.
    • Try lying on your side with a pillow between your legs and your head elevated by pillows, keeping your back straight. Or lie on your back with your head elevated and your knees bent, with a pillow under your knees.
    • Both of these positions help your body and airways relax, making breathing easier. Have your doctor assess you for sleep apnea and use a CPAP machine if recommended.

    7. Diaphragmatic breathing

    Diaphragmatic breathing can also help your shortness of breath. To try this breathing style

    • Sit in a chair with bent knees and relaxed shoulders, head, and neck.
    • Place your hand on your belly.
    • Breathe in slowly through your nose. You should feel your belly moving under your hand.
    • As you exhale, tighten your muscles. You should feel your belly fall inward. Breathe out through your mouth with pursed lips.
    • Put more emphasis on the exhale than the inhale. Keep exhaling for longer than usual before slowly inhaling again.
    • Repeat for about 5 minutes.

    8. Using a fan

    • One study found that cool air can help relieve shortness of breath. Pointing a small handheld fan toward your face can help your symptoms.

    9. Drinking coffee

    • An early study indicated that caffeine relaxes the muscles in the airways of people with asthma. This can help improve lung function for up to four hours.

    Lifestyle changes to treat shortness of breath

    • There are many possible causes of shortness of breath, some of which are serious and require emergency medical care. Less serious cases can be treated at home.

    Lifestyle changes you can make to help keep shortness of breath at bay include

    • quitting smoking and avoiding tobacco smoke
    • avoiding exposure to pollutants, allergens, and environmental toxins
    • losing weight if you have obesity or overweight
    • avoiding exertion at high elevations
    • staying healthy by eating well, getting enough sleep, and seeing a doctor for any underlying medical issues
    • following the recommended treatment plan for any underlying illness such as asthma, COPD, or bronchitis

    Remember, only a doctor can properly diagnose the cause of your shortness of breath.

    Box Breathing

    Box breathing, also known as square breathing, is a technique used when taking slow, deep breaths. It can heighten performance and concentration while also being a powerful stress reliever. It’s also called four-square breathing.

    This technique can be beneficial to anyone, especially those who want to meditate or reduce stress. It’s used by everyone from athletes to U.S. Navy SEALs, police officers, and nurses.

    You may find it particularly helpful if you have a lung disease such as chronic obstructive pulmonary disease (COPD).

    Getting started with box breathing

    Before you get started, make sure that you’re seated upright in a comfortable chair with your feet flat on the floor. Try to be in a stress-free, quiet environment where you can focus on your breathing.

    Keeping your hands relaxed in your lap with your palms facing up, focus on your posture. You should be sitting up straight. This will help you take deep breaths.

    When you’re ready, start with step 1.

    • Step 1: Slowly exhale – Sitting upright, slowly exhale through your mouth, getting all the oxygen out of your lungs. Focus on this intention and be conscious of what you’re doing.
    • Step 2: Slowly inhale – Inhale slowly and deeply through your nose to the count of four. In this step, count to four very slowly in your head. Feel the air fill your lungs, one section at a time until your lungs are completely full and the air moves into your abdomen.
    • Step 3: Hold your breath – Hold your breath for another slow count of four.
    • Step 4: Exhale again – Exhale through your mouth for the same slow count of four, expelling the air from your lungs and abdomen, Be conscious of the feeling of the air leaving your lungs.
    • Step 5: Hold your breath again. Hold your breath for the same slow count of four before repeating this process.

    Benefits of box breathing

    According to the Mayo Clinic, there’s sufficient evidence that intentional deep breathing can actually calm and regulate the autonomic nervous system (ANS).

    • This system regulates involuntary body functions such as temperature. It can lower blood pressure and provide an almost immediate sense of calm.
    • The slow holding of breath allows CO2 to build up in the blood. An increased blood CO2 enhances the cardio-inhibitory response of the vagus nerve when you exhale and stimulates your parasympathetic system. This produces a calm and relaxed feeling in the mind and body.
    • Box breathing can reduce stress and improve your mood. That makes it an exceptional treatment for conditions such as generalized anxiety disorder (GAD), panic disorder, post-traumatic stress disorder (PTSD), and depression.
    • It can also help treat insomnia by allowing you to calm your nervous system at night before bed. Box breathing can even be efficient at helping with pain management.

    Tips for beginners

    • If you’re new to box breathing, it may be difficult to get the hang of it. You may get dizzy after a few rounds. This is normal. As you practice it more often, you’ll be able to go longer without dizziness. If you get dizzy, stay sitting for a minute and resume normal breathing.
    • To help you focus on your breathing, find a quiet, dimly lit environment to practice box breathing. This isn’t at all necessary to perform the technique, but it can help you focus on the practice if you’re new to it.
    • Ideally, you’ll want to repeat the box breathing cycle four times in one sitting.
    • Do box breathing several times a day as needed to calm your nerves and relieve stress

    5 Ways to Keep Your Lungs Healthy and Whole

    Most people want to get healthier. Rarely, though, do they think about protecting and maintaining the health of their lungs.

    It’s time to change that. According to the National Heart, Blood, and Lung InstituteTrusted Source, chronic lower respiratory diseases — including chronic obstructive pulmonary disease (COPD) and asthma — were the third leading cause of death in 2010. Lung diseases, excluding lung cancer, caused an estimated 235,000 deaths that year.

    Include lung cancer, and the numbers go up. The American Lung Association (ALA) states that lung cancer is the leading cause of cancer deaths in both men and women. An estimated 158,080 Americans were expected to die from it in 2016.

    The truth is that your lungs, just like your heart, joints, and other parts of your body, age with time. They can become less flexible and lose their strength, which can make it more difficult to breathe. But by adopting certain healthy habits, you can better maintain the health of your lungs, and keep them working optimally even into your senior years.

    1. Don’t smoke or stop smoking

    • You probably already know that smoking increases your risk of lung cancer. But that’s not the only disease it can cause. In fact, smoking is linked to most lung diseases, including COPD, idiopathic pulmonary fibrosis, and asthma. It also makes those diseases more severe. Smokers are 12 to 13 times more likely to die from COPD than nonsmokers, for example.
    • Every time you smoke a cigarette, you inhale thousands of chemicals into your lungs, including nicotine, carbon monoxide, and tar. These toxins damage your lungs. They increase mucus, make it more difficult for your lungs to clean themselves, and irritate and inflame tissues. Gradually, your airways narrow, making it more difficult to breathe.
    • Smoking also causes lungs to age more rapidly. Eventually, the chemicals can change lung cells from normal to cancerous.
    • According to the Centers for Disease Prevention and Control (CDC), more than 10 times as many U.S. citizens have died prematurely from cigarette smoking than have died in all the wars fought by the U.S. during its history. In addition, smoking causes about 90 percent of all lung cancer deaths in men and women. More women die from lung cancer each year than from breast cancer.
    • No matter how old you are or how long you’ve been a smoker, quitting can help. The ALA states that within just 12 hours of quitting, the carbon monoxide level in your blood drops to normal. Within a few months, your lung function begins to improve. Within a year, your risk of coronary heart disease is half that of a smoker’s. And it only gets better the longer you stay smoke-free.
    • Quitting usually takes several attempts. It’s not easy, but it’s worth it. Combining counseling and medication may be the best way to succeed, according to a report by the Agency for Healthcare Research and Quality.

    2. Exercise to breathe harder

    • Besides avoiding cigarettes, getting regular exercise is probably the most important thing you can do for the health of your lungs. Just as exercise keeps your body in shape, it keeps your lungs in shape too.
    • When you exercise, your heart beats faster and your lungs work harder. Your body needs more oxygen to fuel your muscles. Your lungs step up their activity to deliver that oxygen while expelling additional carbon dioxide.
    • According to a recent article, during exercise, your breathing increases from about 15 times a minute to about 40 to 60 times a minute. That’s why it’s important to regularly do aerobic exercise that gets you breathing hard.
    • This type of exercise provides the best workout for your lungs. The muscles between your ribs expand and contract, and the air sacs inside your lungs work quickly to exchange oxygen for carbon dioxide. The more you exercise, the more efficient your lungs become.
    • Creating strong, healthy lungs through exercise helps you to better resist aging and disease. Even if you do develop lung disease down the road, exercise helps to slow the progression and keeps you active longer.

    3. Avoid exposure to pollutants

    • Exposure to pollutants in the air can damage your lungs and accelerate aging. When they’re young and strong, your lungs can easily resist these toxins. As you get older, though, they lose some of that resistance and become more vulnerable to infections and disease.

    Give your lungs a break. Reduce your exposure as much as you can

    • Avoid secondhand smoke, and try not to go outside during peak air pollution times.
    • Avoid exercising near heavy traffic, as you can inhale the exhaust.
    • If you’re exposed to pollutants at work, be sure to take all possible safety precautions. Certain jobs in construction, mining, and waste management can increase the risk of exposure to airborne pollutants.

    The U.S. Consumer Product Safety Commission reports that indoor pollution is typically worse than outdoor. That, plus the fact that many spend most of their time indoors these days, increases exposure to indoor pollutants.

    Here are some tips for decreasing indoor pollutants

    • Make your home a smoke-free zone.
    • Dust the furniture and vacuum at least once a week.
    • Open a window frequently to increase indoor air ventilation.
    • Avoid synthetic air fresheners and candles that can expose you to additional chemicals like formaldehyde and benzene. Instead, use an aromatherapy diffuser and essential oils to more naturally scent the air.
    • Keep your home as clean as you can. Mold, dust, and pet dander can all get into your lungs and cause irritation.
    • Use natural cleaning products when possible, and open a window when using products that create fumes.
    • Make sure you have adequate fans, exhaust hoods, and other ventilation methods throughout your home.

    4. Prevent infections

    • Infections can be particularly dangerous for your lungs, especially as you age. Those who already have lung diseases like COPD are particularly at risk for infections. Even healthy seniors, though, can easily develop pneumonia if they’re not careful.
    • The best way to avoid lung infections is to keep your hands clean. Wash regularly with warm water and soap, and avoid touching your face as much as possible.
    • Drink plenty of water and eat lots of fruits and vegetables — they contain nutrients that help boost your immune system.
    • Stay up-to-date with your vaccinations. Get a flu shot each year, and if you’re 65 or older, get a pneumonia vaccination as well.

    5. Breathe deeply

    • If you’re like many people, you take shallow breaths from your chest area, using only a small portion of your lungs. Deep breathing helps clear the lungs and creates a full oxygen exchange.
    • In a small study published in the Indian Journal of Physiology and Pharmacology researchers had a group of 12 volunteers perform deep breathing exercises for 2, 5, and 10 minutes. They tested the volunteers’ lung function both before and after the exercises.
    • They found that there was a significant increase in vital capacity after 2 and 5 minutes of deep breathing exercise. Vital capacity is the maximum amount of air the volunteers could exhale from their lungs. The researchers concluded that deep breathing, even for just a few minutes, was beneficial for lung function.
    • The ALA agrees that breathing exercises can make your lungs more efficient. To try it yourself, sit somewhere quietly, and slowly breathe in through your nose alone. Then breathe out at least twice as long through your mouth. It may help to count your breaths. For example, as you inhale count 1-2-3-4. Then as you exhale, count 1-2-3-4-5-6-7-8.
    • Shallow breaths come from the chest, and deeper breaths come from the belly, where your diaphragm sits. Be aware of your belly rising and falling as you practice. When you do these exercises, you may also find you feel less stressed and more relaxed

    8 Deep Breathing Exercises to Reduce Anxiety

    Chest vs. Abdominal Breathing

    Most people aren’t really conscious of the way they’re breathing, but generally, there are two types of breathing patterns

    • Diaphragmatic (abdominal) breathing: This type of breathing is a type of deep, even breathing that engages your diaphragm, allowing your lungs to expand and creating negative pressure that drives air in through the nose and mouth, filling your lungs with air.3 This is the way newborn babies naturally breathe. You’re also probably using this pattern of breathing when you’re in a relaxed stage of sleep.
    • Thoracic (chest) breathing: This type of breathing comes from the chest and involves short, rapid breaths. When you’re anxious, you might not even be aware that you’re breathing this way. The easiest way to determine your breathing pattern is to put one hand on your upper abdomen near the waist and the other in the middle of your chest. As you breathe, notice which hand raises the most.

    If you’re breathing properly, your abdomen should expand and contract with each breath (and the hand on it should raise the most). It’s especially important to be aware of these differences during stressful and anxious times when you’re more likely to breathe from your chest.

    Breathing Exercises

    The next time you’re feeling anxious, there are a variety of deep breathing exercises to try.

    Alternate-Nostril Breathing

    Alternate-nostril breathing (nadi sodhana) involves blocking off one nostril at a time as you breathe through the other, alternating between nostrils in a regular pattern.4 It’s best to practice this type of breathing in a seated position in order to maintain your posture.

    • Position your right hand by bending your pointer and middle fingers into your palm, leaving your thumb, ring finger, and pinky extended. This is known as Vishnu mudra in yoga.
    • Close your eyes or softly gaze downward.
    • Inhale and exhale to begin.
    • Close off your right nostril with your thumb.
    • Inhale through your left nostril.
    • Close off your left nostril with your ring finger.
    • Open and exhale through your right nostril.
    • Inhale through your right nostril.
    • Close off your right nostril with your thumb.
    • Open and exhale through your left nostril.
    • Inhale through your left nostril.

    Do your best to work up to 10 rounds of this breathing pattern. If you begin to feel lightheaded, take a break. Release both nostrils and breathe normally.

    Belly Breathing

    According to The American Institute of Stress, 20 to 30 minutes of belly breathing each day will reduce anxiety and stress.5 Find a comfortable, quiet place to sit or lie down. For example, try sitting in a chair, sitting cross-legged, or lying on your back with a small pillow under your head and under your knees.

    • Place one hand on your upper chest and the other hand on your belly, below the ribcage.
    • Allow your belly to relax, without forcing it inward by squeezing or clenching your muscles.
    • Breathe in slowly through your nose. The air should move into your nose and downward so that you feel your stomach rise with your other hand and fall inward (toward your spine).
    • Exhale slowly through slightly pursed lips. Take note of the hand on your chest, which should remain relatively still.

    Although the sequence frequency will vary according to your health, most people begin by doing the exercise three times and working up to five to 10 minutes, one to four times a day.

    Box Breathing

    Also known as four-square breathing, box breathing is very simple to learn and practice. In fact, if you’ve ever noticed yourself inhaling and exhaling to the rhythm of a song, you’re already familiar with this type of paced breathing. It goes like this

    • Exhale to a count of four.
    • Hold your lungs empty for a four-count.
    • Inhale to a count of four.
    • Hold air in your lungs for a count of four.
    • Exhale and begin the pattern anew.

    4-7-8 Breathing

    The 4-7-8 breathing exercise, also called the relaxing breath, acts as a natural tranquilizer for the nervous system. At first, it’s best to perform the exercise seated with your back straight. Once you become more familiar with the breathing exercise, however, you can perform it while lying in bed:

    • Place and keep the tip of your tongue against the ridge of tissue behind your upper front teeth for the duration of the exercise.
    • Completely exhale through your mouth, making a whoosh sound.
    • Close your mouth and inhale quietly through your nose to a mental count of four.
    • Hold your breath for a count of seven.
    • Exhale completely through your mouth, making a whoosh sound to a count of eight.

    Lion’s Breath

    Lion’s breath, or simhasana in Sanskrit, during which you stick out your tongue and roar like a lion, is another helpful deep breathing practice. It can help relax the muscles in your face and jaw, alleviate stress, and improve cardiovascular functions.

    The exercise is best performed in a comfortable, seated position, leaning forward slightly with your hands on your knees or the floor.

    • Spread your fingers as wide as possible.
    • Inhale through your nose.
    • Open your mouth wide, stick out your tongue, and stretch it down toward your chin.
    • Exhale forcefully, carrying the breath across the root of your tongue.
    • While exhaling, make a “ha” sound that comes from deep within your abdomen.
    • Breathe normally for a few moments.
    • Repeat lion’s breath up to seven times.

    Mindful Breathing

    Mindfulness meditation involves focusing on your breathing and bringing your attention to the present without allowing your mind to drift off to the past or future.

    • Choose a calming focus, including a sound (“om”), positive word (“peace”), or phrase (“breathe in calm, breath out tension”) to repeat silently as you inhale or exhale.
    • Let go and relax. When you notice your mind has drifted, take a deep breath and gently return your attention to the present.

    Pursed-Lip Breathing

    Pursed-lip breathing is a simple breathing technique that will help make deep breaths slower and more intentional. This technique has been found to benefit people who have anxiety associated with lung conditions like emphysema and chronic obstructive pulmonary disease.

    • Sit in a comfortable position, with your neck and shoulders relaxed.
    • Keeping your mouth closed, inhale slowly through your nostrils for two seconds.
    • Exhale through your mouth for four seconds, puckering your mouth as if giving a kiss.
    • Keep your breath slow and steady while breathing out.

    To get the correct breathing pattern, experts recommend practicing pursed-lip breathing four to five times a day.

    Resonance Breathing

    Resonance breathing, or coherent breathing, can help you get into a relaxed state and reduce anxiety.

    • Lie down and close your eyes.
    • Gently breathe in through your nose, mouth closed, for a count of six seconds. Don’t fill your lungs too full of air.
    • Exhale for six seconds, allowing your breath to leave your body slowly and gently without forcing it.
    • Continue for up to 10 minutes.
    • Take a few additional minutes to be still and focus on how your body feels.

    Simple Breathing Exercise

    You can perform this exercise as often as needed. It can be done standing up, sitting down, or lying down. If you find this exercise difficult or believe it’s making you anxious or panicky, stop for now. Try it again in a day or so and build up the time gradually.

    • Inhale slowly and deeply through your nose. Keep your shoulders relaxed. Your abdomen should expand, and your chest should rise very little.
    • Exhale slowly through your mouth. As you blow air out, purse your lips slightly, but keep your jaw relaxed. You may hear a soft “whooshing” sound as you exhale.
    • Repeat this breathing exercise. Do it for several minutes until you start to feel better.

    Sometimes people with a panic disorder initially feel increased anxiety or panic while doing this exercise. This may be due to anxiety caused by focusing on your breathing, or you may be unable to do the exercise correctly without some practice.

    Benefits of Breathing Exercises

    • Improves immunity – Breathing exercises increase the amount of oxygen in the body and increases the release of toxins with carbon-di-oxide. Increased oxygen in the cells and tissues makes them healthier and helps them perform better. Healthier and proper functioning organs improve the immune system of the body as well. Clean blood full of oxygen fights better against infectious bacteria and viruses. Improved breathing will also help in better absorption of vitamins and minerals in the body.
    • Clams down anxiety – Psychologists swear by deep breathing exercises to tackle anxiety attacks and also as a long-term treatment practice. Deep breathing helps in bringing heart rate to normal and increases oxygen levels. This helps in giving the brain the signal to unwind. Regular deep breathing will help in balancing the hormones releasing endorphins in the body.
    • Increases sleep quality – A deep breathing exercise that entails complete exhalation of the air out provides better sleep. Breathing detoxifies the body and signals to calm down. A deep breathing exercise before bed can help even insomnia suffering people.
    • Decreases toxicity of the body – Stress, eating habits, and shallow exhalation turns the body acidic, and with deep breathing, all the toxins are released turning the body alkaline. It detoxifies the body. Deep breathing also helps in releasing the lymph around the body and removes strain from the body.
    • Improves digestive system – Deep breathing increases oxygen in the digestive organ and they perform better relieving from any gastrointestinal issues, constipation, indigestion, etc. proper digestion keeps the body energetic and healthy.
    • Good for cardiovascular health – Breathing exercises will help strengthen the cardiovascular muscles and improve blood pressure. Regular deep breathing also decreases the chances of stroke. Deep breathing stimulates the vagus nerve which reduces the ‘fight or flight response.
    • Improve concentration and cognitive properties – Regular breathing exercises can improve focus and concentration. It also improves memory and cognitive properties and brain functioning.
    • Gives healthy and glowing skin – Breathing exercises increase the oxygen concentration in cells giving skin a healthy and inner glow. It makes your skin healthy. Breathing exercises burn fat and help in balance hormones which results in less stress and clear skin.
    • Reduces inflammation in the body – Sheetali pranayama is one such breathing exercise that helps in cooling the body down. It triggers a powerful evaporating cooling effect which brings down inflamed agitated emotions and decreases inflammation in the digestive system which stresses the whole body.
    • Helps sinusitis – Yogic breathing practices can help in sinusitis as the vibrations produced in this exercise dislodge all mucous and drain sinusitis from the body.
    • Makes the body and joints strong – Breathing exercises increase the oxygen level in the cells and it affects joints in a good way. It makes joints and muscles strong. It helps in reducing the strain of physical exercise and the chances of wearing the muscles down. Body’s ability to handle intense physical movement increases
    • Strengthen lungs – Lifestyle habits have greatly affected the lungs and their lungs. Breathing exercise helps in increasing the air build-up in the lungs and diaphragm. It increases lung elasticity which gives more breathing space.
    • Natural painkiller – When you deep breathe, the body releases endorphins, which are the feel-good hormones and a natural pain killer created by the body itself.
    • Improves blood flow –  When we take deep breaths, the upward and downward movement of the diaphragm helps remove the toxins from the body promoting better blood flow. Deep breathing brings fresh oxygen and exhales out toxins and carbon dioxide. When the blood is oxygenated, it ensures the smoother functioning of your vital organs, including the immune system. A cleaner, toxin-free, and healthier blood supply help ward off infection-causing germs from the base and strengthens your immunity. Deep breathing also acts as a natural toxin reliever. It also benefits the absorption of vitamins and nutrients in the body, making sure you recover faster as well.
    • Calms down anxiety – Practising deep breathing is a hack a lot of experts and psychologists swear by to treat anxious thoughts and nervousness in a jiffy. Deep breathing slows down your heart rate, allows the body to take in more oxygen, and ultimately signals the brain to wind down. It also balances your hormones- lowering down cortisol levels, increasing the endorphin rush in the body.
    • Increases energy level  – Due to increased blood flow, we get more oxygen into our blood. Increased oxygen results in increased energy levels.

    • Improves posture – Believe it or not, bad posture is related to incorrect breathing. If you don’t believe it, try it yourself. Try to breathe deeply and notice how your body starts to straighten up during the process. When you fill your lungs with air, this automatically encourages you to straighten up your spine.
    • Reduces inflammation – A lot is said that diseases like cancer only thrive in bodies that are acidic in nature. Deep breathing is said to reduce the acidity in your body, thereby making it alkaline. Stress also increases the acidity level in the body. Breathing also reduces stress and thus acidity.
    • It detoxifies the body – Carbon dioxide is a natural toxic waste that comes out from our bodies only through breathing. But when our lungs are compromised by shallow breathing the other detoxification system starts working harder to expel this waste. This can make our body weaker and lead to illness.
    • Stimulates lymphatic system – As our breathing is what moves the lymph, shallow breathing can lead to a sluggish lymphatic system that will not detoxify properly. Deep breathing will help you get the lymph flowing properly so that your body can work more efficiently.
    • Improves digestion – Breathing deep supplies more oxygen to all our body parts including our digestive system, thus making it work more efficiently. The increased blood flow due to deep breathing also encourages intestinal action which further improves your overall digestion. In addition, deep breathing results in a calmer nervous system, which in turn also enhances optimal digestion.
    • Breathing relaxes mind and body – When you are angry, tensed, or scared, your muscles are tightened and your breathing becomes shallow. Your breathing constricts. At this time your body is not getting the amount of oxygen it requires. Long deep breathing reverses this process, allowing your body (and mind) to become calmer.

    References

    Hypertensive Retinopathy – Causes, Symptoms, Treatment

    Hypertensive retinopathy rarely causes significant visual loss. The retinal changes can be halted when hypertension is treated. However, arteriolar narrowing and AV changes persist. For untreated malignant hypertension, the mortality is high as 50% within 2 months of diagnosis and almost 90% by the end of 1 year. Vision loss in hypertensive retinopathy is because of either secondary optic atrophy after prolonged papilloedema or retinal pigmentary changes after exudative retinal detachment.

    Poorly controlled hypertension (HTN) affects several systems such as the cardiovascular, renal, cerebrovascular, and retina. The damage to these systems is known as target-organ damage (TOD). HTN affects the eye causing 3 types of ocular damage: choroidopathy, retinopathy, and optic neuropathy. Hypertensive retinopathy (HR) occurs when the retinal vessels get damaged due to elevated blood pressure. There has been significant evidence that hypertensive retinopathy acts as a predictor of systemic morbidity and mortality due to TOD. A study by Erden et al. showed that the increase in the incidence of retinopathy is related to the degree of severity and duration of HTN.

    Types of Hypertensive Retinopathy

    The following are classification systems for hypertensive retinopathy based on fundus examination with indirect ophthalmoscopy or +90 D lens.

    Keith-Wagner- Barker classification

    • Group 1: Slight constriction of retinal arterioles
    • Group 2: Group 1 + focal narrowing of retinal arterioles + AV nicking
    • Group 3: Group 2 + flame-shaped haemorrhages + cotton-wool spots + hard exudates
    • Group 4: Group 3 + optic disc swelling

    Scheie Classification

    For Hypertensive Retinopathy

    • Stage 0: No visible abnormalities
    • Stage 1: Diffuse arteriolar narrowing
    • Stage 2: Stage 1 + focal arteriolar constriction
    • Stage 3: Stage 2 + retinal hemorrhage
    • Stage 4:  Stage 3 + hard exudates + retinal edema+ optic disc swelling

    For Arteriosclerosis

    • Stage 0: Normal
    • Stage 1: Broadening of arteriolar light reflex
    • Stage 2: Stage 1 + AV crossing changes
    • Stage 3: Copper wiring of arterioles
    • Stage 4: Silver wiring of arterioles

    Causes of Hypertensive Retinopathy

    Apart from essential and secondary hypertension, there are other factors which play an important role in the development of hypertensive retinopathy. The prevalence of hypertensive retinopathy is more in Afro-Caribbean as compared to Europeans and more in women as compared to men. Genetic factors can also play a role with certain genotypes associated with an increased risk of hypertensive retinopathy. Pontremoli et al. studied the genetic factors linked to hypertensive retinopathy and found the deletion of the allele of the angiotensin-converting enzyme has a higher risk associated with the development of hypertensive retinopathy. Smoking is considered to have a strong association with severe or malignant hypertensive retinopathy as studied by Poulter et al. Renal dysfunction (persistent microalbuminuria and low creatinine clearance) in patients has shown to be a marker for hypertensive retinopathy and end-organ damage. Uckaya et al. found an association with plasma leptin. It was observed that plasma leptin levels were higher in patients with hypertensive retinopathy and postulated that it is associated with vascular endothelium damage.

    Retinal blood vessels have distinct features, which differentiate them from other blood vessels:

    •  The absence of sympathetic nerve supply
    •  Autoregulation of blood flow
    •  Presence of blood-retinal barrier

    Thus, an increase in blood pressure (BP) is transferred directly to the vessels which initially constrict. However, a further increase in BP overcomes this compensatory tone and damage to the muscle layer and endothelium ensues.

    Hypertensive retinopathy has the following phases:

    Vasoconstrictive Phase

    In this phase, the local autoregulatory mechanisms come into play. This causes vasospasm and retinal arteriole narrowing, which is evident by the decrease in the arteriole to venule ratio (Normal = 2:3). In older patients with arteriosclerosis, focal arteriolar narrowing develops, as affected vascular segments cannot undergo narrowing.

    Sclerotic Phase

    Persistent increase in BP causes certain changes in vessel wall:

    • Intima layer: Thickening
    • Media layer: Hyperplasia
    • Arteriolar wall: Hyaline degeneration

    This leads to a severe form of arteriolar narrowing, arteriovenous (AV) crossing changes, and widening and accentuation of light reflex (silver and copper wiring). AV crossing changes occur when a thickened arteriole crosses over a venule and subsequently compresses it as the vessels share a common adventitious sheath. The vein, in turn, appears dilated and torturous distal to the AV crossing.

    Exudative Phase

    Seen in patients with severely increased BP; characterized by the disruption of the blood-brain barrier and leakage of blood and plasma into the vessel wall disrupting the autoregulatory mechanisms. In this stage, retinal signs occur such as retinal hemorrhage (flame-shaped and dot blot), hard exudate formation, necrosis of smooth muscle cells and retinal ischemia (cotton-wool spots).

    Malignant Hypertension

    Severe intracranial hypertension leads to optic nerve ischemia and edema (papilledema). Also, fibrinoid necrosis of choroidal arterioles occurs leading to segmental infarction of choriocapillaries. This gives rise to:

    • Elschnig’s spots: Where the overlying retinal pigment epithelium (RPE) appears yellow
    • Siegrist’s streak: RPE hyperplasia over choroidal infarcts
    • Neurosensory RPE detachments

    These signs are termed as choroidopathy.

    The other conditions which present with optic disc swelling are

    • Diabetic allopathy
    • Central retinal vein occlusion
    • Anterior ischemic optic neuropathy
    • Neuroretinitis

    Conditions that mimic chronic hypertensive retinopathy are

    • Diabetic retinopathy
    • Retinal venous obstruction
    • Hyperviscosity syndrome
    • Ocular ischemic syndrome
    • Radiation retinopathy

    Symptoms and Signs of Hypertensive Retinopathy

    Signs of damage to the retina caused by hypertension include:

    • Arteriolar changes, such as generalized arteriolar narrowing, focal arteriolar narrowing, arteriovenous nicking, changes in the arteriolar wall (arteriosclerosis) and abnormalities at points where arterioles and venules cross. Manifestations of these changes include Copper wire arterioles where the central light reflex occupies most of the width of the arteriole and Silver wire arterioles where the central light reflex occupies all of the width of the arteriole, and “arterio-venular (AV) nicking” or “AV nipping”, due to venous constriction and banking.
    • advanced retinopathy lesions, such as microaneurysms, blot hemorrhages and/or flame hemorrhages, ischemic changes (e.g. “cotton wool spots”), hard exudates and in severe cases swelling of the optic disc (optic disc edema), a ring of exudates around the retina called a “macular star” and visual acuity loss, typically due to macular involvement.
    • Strongly modulated blood flow pulse in central and branch arteries can result from hypertension. Microangiography by laser Doppler imaging[rx] may reveal altered hemodynamics non-invasively.

    Mild signs of hypertensive retinopathy can be seen quite frequently in normal people (3–14% of adult individuals aged ≥40 years), even without hypertension.[rx] Hypertensive retinopathy is commonly considered a diagnostic feature of a hypertensive emergency although it is not invariably present.[rx]

    In the early stages, funduscopy identifies arteriolar constriction, with a decrease in the ratio of the width of the retinal arterioles to the retinal venules.

    Chronic, poorly controlled hypertension causes the following:

    • Permanent arterial narrowing
    • Arteriovenous crossing abnormalities (arteriovenous nicking)
    • Arteriosclerosis with moderate vascular wall changes (copper wiring) to more severe vascular wall hyperplasia and thickening (silver wiring)
    • Sometimes total vascular occlusion occurs. Arteriovenous nicking is a major predisposing factor to the development of a branch retinal vein occlusion.
    • Superficial flame-shaped hemorrhages
    • Small, white, superficial foci of retinal ischemia (cotton-wool spots)
    • Yellow hard exudates
    • Optic disk edema

    Diagnosis of Hypertensive Retinopathy

    Clinical Features

    Hypertensive retinopathy is usually asymptomatic and is diagnosed on fundoscopic features. The following are signs of hypertensive retinopathy.

    AV Crossing Changes

    • Salus’s sign: Deflection of retinal vein as it crosses the arteriole.
    • Gunn’s sign: Tapering of the retinal vein on either side of the AV crossing.
    • Bonnet’s sign: Banking of the retinal vein distal to the AV crossing.

    Arterial Changes

    • Decrease in the arteriovenous ratio to 1:3 ( the normal ratio is 2:3).
    • Change in the arteriolar light reflex (light reflex appears as copper and/or silver wiring)

    Retinal Changes

    • Retinal hemorrhages: 

      • Dot-blot hemorrhages: Bleeding in the inner retinal layer
      • Flame shaped hemorrhage: Bleeding is in the superficial retinal layer
    • Retinal exudates:

      • Hard exudates: Lipid deposits in the retina
      • Soft exudates: These are also known as cotton wool spots which appear due to ischemia of the nerve fibers

    Macular Changes

    Macular star formation due to deposition of hard exudates around the macula.

    Optic Nerve Changes

    Optic disk swelling (also known as hypertensive optic neuropathy)

    In a study by Wong et al., they identified certain retinal signs to be associated with increased risk for stroke. The signs are AV nicking, focal arteriolar narrowing (as this is associated with arteriosclerosis), microaneurysms, cotton wool spots, retinal hemorrhages (dot blot and flame-shaped), and decreased AV ratio.

    Clinical diagnosis

    The signs of malignant hypertension are well summarized by the Modified Scheie Classification of Hypertensive Retinopathy[rx]:

    • Grade 0: No changes
    • Grade 1: Barely detectable arterial narrowing
    • Grade 2: Obvious arterial narrowing with focal irregularities
    • Grade 3: Grade 2 plus retinal hemorrhages, exudates, cotton wool spots, or retinal edema
    • Grade 4: Grade 3 plus papilledema

    The signs of chronic arteriosclerotic hypertension are also summarized by the Scheie Classification[rx]:

    • Stage 1: Widening of the arteriole light reflex
    • Stage 2: Stage 1 + Arteriovenous crossing sign
    • Stage 3: Copper wiring of arterioles (copper colored arteriole light reflex)
    • Stage 4: Silver wiring of arterioles (silver colored arteriole light reflex).

    Another classification schema is the Keith-Wagner-Barker classification proposed in 1939.[rx]

    • Grade 1: Mild, generalized constriction of retinal arterioles
    • Grade 2: Definite focal narrowing of retinal arterioles + AV nicking
    • Grade 3: Grade 2 + flame-shaped hemorrhages + cotton-wool spots + hard exudates
    • Grade 4: Severe Grade 3 retinopathy + papilledema or retinal edema

    Of specific interest is the classification of hypertensive retinopathy by Wong and Mitchell (2004) in which the worsening grades of retinopathy were more strongly associated with systemic issues.[tx] The classification is as follows:

    • None: no detectable signs
    • Mild: one or more of the following: generalized arteriolar narrowing, focal arteriolar narrowing, arteriovenous nicking, opacity (“copper wiring”) of the arteriolar wall
    • Moderate: one or more of the following: retinal hemorrhage (blot, dot, or flame-shaped), microaneurysm, cotton-wool spot, hard exudate, or a combination of these signs
    • Severe: moderate retinopathy plus swelling of the optic disc

    A new classification has been proposed recently (2014) based on optical coherence tomography (OCT) features such as subretinal fluid (SRF). The study compared the grading system based on OCT findings to the Keith-Wagner-Barker grading system and found that the following classification was significantly correlated to final best-corrected visual acuity.[rx]

    • Mild-Moderate Retinopathy
    • Malignant Retinopathy w/o SRF
    • Malignant R w/ SRF

    Lab Test And Imaging

    • Ophthalmoscope – Your doctor will use a tool called an ophthalmoscope to examine your retina. This tool shines a light through your pupil to examine the back of your eye for signs of narrowing blood vessels or to see if any fluid is leaking from your blood vessels. This procedure is painless. It takes less than 10 minutes to complete.
    • Fluorescein angiography – In some cases, a special test called fluorescein angiography is performed to examine retinal blood flow. In this procedure, your doctor will apply special eye drops to dilate your pupils and then take pictures of your eye. After the first round of pictures, your doctor will inject a dye called fluorescein into a vein. They’ll typically do this on the inside of the elbow. Then, they’ll take more pictures as the dye moves into the blood vessels of your eye.

    Treatment of Hypertensive Retinopathy

    The main purpose of screening for hypertensive retinopathy is that retinal vessels are the only blood vessels visible on routine examination. The effects of chronically elevated HTN are easily visible in the eye as hypertensive retinopathy and choroidopathy, and this reflects the vascular changes occurring in other systems. Ophthalmologists and general physicians should work in collaboration to ensure that hypertensive patients are efficiently screened, and timely managed to reduce the risk of ocular and systemic morbidity and mortality. Henderson et al., however, noted that Hypertensive retinopathy is associated with an increased risk of stroke even after controlling BP and other vascular risk factors.

    The management of hypertensive retinopathy depends on the severity of the disease:

    • Mild hypertensive retinopathy: The treatment consists of controlling of BP with regular monitoring.
    • Moderate hypertensive retinopathy: Referral to a physician is essential to exclude other associated factors like diabetes mellitus and to check for any cardiovascular abnormalities. Routine care including BP control and monitoring is a must.
    • Severe hypertensive retinopathy: Requires urgent treatment and referral as it has the strongest association with mortality. Other systems such as renal, cardiovascular, and brain should be monitored for signs of TOD.

    Important to note is that BP should be lowered in a controlled fashion. This is crucial to prevent ischemic damage to vital organs such as optic nerve and brain.

    Blood Pressure Goals

    • SHEP and HYVET trials have shown significant benefits of antihypertensive treatment in patients with the goal of SBP <150 mmHg.
    • The VALsartan in Elderly Isolated Systolic Hypertension (VALISH) trial showed no significant difference in the primary outcome of sudden death, fatal or nonfatal myocardial infarction and stroke, heart failure death, or other cardiovascular death among patients with strict (< 140 mmHg) and moderate (140 to 150 mmHg) SBP control.
    • However, the VALISH trial was underpowered due to the low number of events.
    • Hence, the optimal SBP in patients with hypertensive disorder remained a controversial topic.
    • The most recent Systolic Blood Pressure Intervention Trial (SPRINT) has shown that intensive SBP target of < 120 mmHg improved the cardiovascular outcomes and the overall survival compared to the standard SBP target of 135 to 139 mmHg.
    • However, aggressive SBP lowering may be harmful in the elderly and incite more adverse effects such as hypotension, end-organ hypoperfusion (causing acute kidney injury, and intracranial hypoperfusion which may link to cognitive decline), and polypharmacy.
    • It is suggested that a goal blood pressure of < 130/80 mmHg is appropriate as long as the patient tolerates it.
    • Otherwise, < 140/90 mmHg is considered reasonable in patients who are in the elderly population and patients with labile blood pressure or polypharmacy.
    • Management strategies should always be patient-centered, with the aim of optimizing blood pressure control and avoiding polypharmacy, especially in the elderly.

    J-curve Phenomenon

    • Various studies have shown a J-curve association between blood pressure with risk of myocardial infarction and death.
    • Patients with isolated systolic hypertension who receive antihypertensive treatment may precipitously drop their DBP as well.
    • As myocardial perfusion occurs mainly during diastole, an excessive drop in DBP may increase the risk of cardiovascular disease and death.

    Complications of hypertensive retinopathy

    People with HR are at risk of developing complications related to the retina. These include the following:

    • Ischemic optic neuropathy, which occurs when high blood pressure blocks off normal blood flow in the eyes, damaging the optic nerve. The optic nerve carries images of what we see to the brain.
    • Retinal artery occlusion, which occurs when the arteries that carry blood to the retina become blocked by blood clots. When this happens, the retina doesn’t get enough oxygen or blood. This results in vision loss.
    • Retinal vein occlusion, which occurs when the veins that carry blood away from the retina become blocked by blood clots.
    • Nerve fiber layer ischemia, or damage to the nerve fibers, which may lead to cotton-wool spots, or fluffy white lesions on the retina.
    • Malignant hypertension, which is a rare condition that causes blood pressure to increase suddenly, interfering with vision and causing sudden vision loss. This is a potentially life threatening condition.
    • Retinal artery occlusion
    • Retinal vein occlusion
    • Macro aneurysm of retinal arteriole
    • Diabetic retinopathy (DR): Both hypertensive retinopathy and DR together in a patient is called as mixed retinopathy. HTN is also known to be a major risk factor for the progression of DR.
    • Anterior ischemic optic neuropathy
    • Age-related macular degeneration
    •  Glaucoma
    • Retinal arteriolar emboli
    • Epiretinal membrane formation
    • Cystoid macular edem

    People with HR are also at an increased risk of having a stroke or heart attack. One 2013 study of 2,907 people between the ages of 50 and 73 found that those with HR were more likely to have a stroke than people without the condition.

    This was true even in people with blood pressure controlled by treatment. A 2008 study of 5,500 people between the ages of 25 and 74 showed both an increased risk of stroke or cardiovascular disease in those with HR.

    Lifestyle changes

    You may also need to make some lifestyle changes as part of your ISH treatment plan. These can include:

    • Losing weight. This can help lower your blood pressure. In fact, for every two pounds you lose, you could lower your blood pressure by about 1 mm Hg.
    • Eating a heart-healthy diet. You should also aim to reduce the amount of sodium in your diet. Consider the DASH diet, which emphasizes eating:
      • vegetables
      •  whole grains
      •  low-fat dairy products
      •  fruits
    • Exercising. Not only can exercise help you lower your blood pressure, but it can help you control your weight and stress levels. Aim to perform some sort of aerobic exercise for at least 30 minutes most days of the week.
    • Decreasing alcohol consumption. Healthy alcohol intake is one drink per day for women and two per day for men.
    • Quitting smoking. Smoking can raise your blood pressure and also contribute to a variety of other health problems.
    • Managing stress. Stress can raise your blood pressure, so finding ways to relieve it are important. Examples of techniques to help lower stress are meditation and deep breathing exercises.
    • Eating a heart-healthy diet: Choose fruits, vegetables, grains and low-fat dairy foods.
    • Exercising regularly, at least 30 minutes a day of moderate activity, such as walking (check with your healthcare provider before starting an exercise program).
    • Keeping your weight under control: Check with your healthcare provider for a weight-loss program, if needed.
      Cutting back on alcoholic drinks.
    • Limiting caffeine intake.
    • Limiting sodium (salt) in your diet: Read nutrition labels on packaged foods to learn how much sodium is in one serving.
    • Reducing and avoiding stress when possible: Many people find that regular meditation or yoga helps.

    References

     

    Renal Hypertension – Causes, Symptoms, Diagnosis, Treatment

    Renal Hypertension/Renovascular hypertension is one of the most common causes of secondary hypertension. It is mostly due to the narrowing of blood vessels in the kidney. This activity reviews the evaluation and management of renovascular hypertension and highlights the role of the healthcare team in evaluating and treating patients with this condition.

    High blood pressure affects 75 million adults in the United States and accounts for 8.6% of all primary care visits. Renovascular hypertension is one of the most common causes of secondary hypertension and often leads to resistant hypertension. It is defined as systemic hypertension that manifests secondary to the compromised blood supply to the kidneys, usually due to an occlusive lesion in the main renal artery.

    Causes of Renal Hypertension

    The cause of renovascular hypertension is consistent with any narrowing/blockage of blood supply to the renal organ (renal artery stenosis). As a consequence of this action the renal organs release hormones that indicate to the body to maintain a higher amount of sodium and water, which in turn causes blood pressure to rise. Factors that may contribute are: diabetes, high cholesterol and advanced age,[rx] also of importance is that a unilateral condition is sufficient to cause renovascular hypertension.[rx]

    It is important to realize that any condition that compromises blood flow to the kidneys can contribute to renovascular hypertension. The most common causes of renovascular hypertension include:

    • Renal artery stenosis (RAS), mostly secondary to atherosclerosis
    • Fibromuscular dysplasia (FMD)
    • Arteritides such as Takayasu’s, Antiphospholipid Antibody (APLA) or Mid aortic syndrome
    • Extrinsic compression of a renal artery
    • Renal artery dissection or infarction
    • Radiation fibrosis
    • Obstruction from aortic endovascular grafts

    The underlying mechanism in renovascular hypertension involves decreased perfusion to the kidney and activation of the Renin-Angiotensin-Aldosterone (RAAS) pathway. This was first explained by Goldblatt et al. in the 1930s. His model studied the effect of decreased blood supply to the kidneys in dogs and found that ischemic kidneys contribute to persistent hypertension. He also proposed the presence of a substance that “may affect a pressor action like that of a hormone.” This hormone he was referring to was ‘renin,’ which is secreted by juxtaglomerular cells of the kidney. Renin secretion by the kidneys is stimulated by three main pathways,

    • 1) renal baroreceptors that sense decrease perfusion to the kidney,
    • 2) low sodium chloride levels detected by the macula densa and
    • 3) beta-adrenergic stimulation. Prolonged ischemia also increases the number of renin expressing cells in the kidney in a process called ‘JG recruitment.’ When renin is secreted into the blood, it acts on angiotensinogen (produced by the liver). Renin cleaves angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE) that is primarily found in the vascular endothelium of lungs and kidney. Angiotensin II raises blood pressure by multiple mechanisms, which include:
    • Vasoconstriction, mostly in the heart, kidney, and vascular smooth muscle
    • Sympathetic nervous stimulation causing a presynaptic release of norepinephrine
    • Stimulates secretion of aldosterone by the adrenal cortex, which in turn causes sodium and water retention, thereby raising blood pressure.
    • It also causes the increased synthesis of collagen type I and III in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis
    • It has been shown to have a growth effect on renal cells, which has been implicated in the development of glomerulosclerosis and tubulointerstitial fibrosis

    Though atherosclerotic renal artery stenosis (ARAS) and FMD are the two most common conditions causing this cascade, any pathology leading to decreased blood flow to the kidneys can essentially trigger this and lead to high blood pressure.

    Symptoms Of Renal Hypertension 

    The main symptoms of renovascular hypertension are rapidly increasing blood pressure of 180/120 or higher and signs of organ damage. Usually, the damage happens to the kidneys or the eyes.

    Other symptoms depend on how the rise in blood pressure affects your organs. A common symptom is bleeding and swelling in the tiny blood vessels in the retina. The retina is the layer of nerves that line the back of the eye. It senses light and sends signals to the brain through the optic nerve, which can also be affected by renovascular hypertension. When the eye is involved, can renovascular hypertension cause changes in vision.

    Other symptoms of malignant hypertension include

    • Pheochromocytoma – Sweating, increased frequency or force of heartbeats, headache, anxiety
    • Cushing’s syndrome – Weight gain, weakness, abnormal growth of body hair or loss of menstrual periods (in women), purple striations (lines) on the skin of the abdomen
    • Thyroid problems – Fatigue (tiredness), weight gain or weight loss, intolerance to heat or cold
    • Conn’s syndrome or primary aldosteronism – Weakness due to low levels of potassium in the body
    • Obstructive sleep apnea – excessive fatigue or sleepiness during daytime, snoring, pauses in breathing during sleep
    • High blood pressure at a young age
    • High blood pressure that suddenly gets worse or is hard to control
    • Kidneys that are not working well (this can start suddenly)
    • Narrowing of other arteries in the body, such as to the legs, the brain, the eyes and elsewhere
    • Sudden buildup of fluid in the air sacs of the lungs (pulmonary edema)
    • High blood pressure (early age)
    • Kidney dysfunction
    • Narrowing of arteries elsewhere in the body
    • Pulmonary edema
    • Change in mental status, such as anxiety, confusion, decreased alertness, decreased ability to concentrate, fatigue, restlessness, sleepiness, or stupor
    • Chest pain (feeling of crushing or pressure)
    • Cough
    • Headache
    • Nausea or vomiting
    • Numbness of the arms, legs, face, or other areas
    • Reduced urine output
    • Seizure
    • Shortness of breath
    • Weakness of the arms, legs, face, or other areas
    • Blurred vision
    • Chest pain (angina)
    • Difficulty breathing
    • Dizziness
    • Numbness in the arms, legs, and face
    • Severe headache
    • Shortness of breath

    In rare cases, renovascular hypertension can cause brain swelling, which leads to a dangerous condition called hypertensive encephalopathy. Symptoms include:

    • Changes in mental status
    • Coma
    • Confusion
    • Drowsiness
    • Headache that continues to get worse
    • Nausea and vomiting
    • Seizures

    Diagnosis of Renal Hypertension

    History and Physical

    Salient points in history that suggest the presence of renovascular hypertension include:

    • Resistant hypertension –  Uncontrolled blood pressure necessitating the use of 2 or 3 antihypertensive agents of different classes, one of which is a diuretic
    • Trial of multiple medications to control blood pressure
    • History of multiple hospital admissions for hypertensive crisis
    • Elevation in creatinine of more than 30% after starting an angiotensin-converting enzyme (ACE) inhibitor (ACEI)
    • Patients with renal artery stenosis secondary to atherosclerosis are usually older and might have the presence of other atherosclerotic diseases such as carotid artery stenosis, peripheral artery stenosis or coronary artery disease
    • A premenopausal female (15-50 years) with hypertension is most likely to have FMD
    • Long term history of smoking
    • Patients with systemic vasculitis can develop vasculitis of renal arteries and present with renovascular hypertension
    • Recurrent episodes of flash pulmonary edema and/or unexplained congestive heart failure
    • Unexplained Azotemia
    • Elevation in serum creatinine on starting ACE-I, which occurs due to interference with autoregulation and post glomerular arterial tone
    • Unexplained hypokalemia and metabolic alkalosis
    • Unilateral small or atrophic kidney.

    Physical examination may reveal an abdominal bruit, indicating the presence of renal artery stenosis.

    Lab Test

    Patients with renovascular hypertension often undergo an extensive evaluation to find a cause for uncontrolled hypertension.

    Laboratory tests

    • Urine analysis – to check for proteinuria, hematuria, and casts. The presence of proteinuria indicates the presence of renal parenchymal disorder, whereas the presence of hematuria or RBC casts indicates the presence of glomerulonephritis.
    • Blood urea nitrogen and serum creatinine – to assess baseline kidney function.
    • Basal metabolic profile: to assess for electrolyte disturbances and acid-base balance.
    • Complement levels and autoimmune profile – in suspected cases of autoimmune diseases affecting the renal vasculature.
    • Plasma free metanephrines or 24-hour urinary fractionated metanephrines and normetanephrine to rule out pheochromocytoma
    • Plasma renin-aldosterone ratio to rule out hyperaldosteronism
    • 24 hr urinary free cortisol or low dose dexamethasone suppression test to rule out Cushing’s syndrome

    Imaging

    • Catheter angiography  – There are multiple imaging modalities available to evaluate renovascular hypertension. Since the most common cause of renovascular hypertension is renal artery stenosis, renal arteriography remains the gold standard diagnostic test. However, catheter angiography is invasive, costly, time-consuming, and can lead to complications such as renal artery dissection or cholesterol embolization. Other imaging tests that can be done to evaluate the renal vessels include duplex ultrasonography, computed tomography with angiography (CTA), and magnetic resonance angiography (MRA). The type of imaging test used often depends on the suspicion for high-grade lesions, and the need for intervention.
    • Duplex ultrasonography – is the initial imaging test of choice to evaluate the renal arteries. It is relatively cheap, non-invasive, and does not involve the administration of contrast or exposure to radiation. A duplex scan has been shown to have an excellent correlation with contrast-enhanced angiography. Though there are several criteria to assess the presence of renal artery stenosis, the most important sign is peak systolic velocity (PSV). A PSV higher than 180 cm/s suggests the presence of stenosis of greater than 60%.
    • Ultrasonography – can also measure the resistive index (RI), which is calculated as ((PSV-End diastolic velocity)/PSV)). A value of more than 0.7 indicates the presence of pathological resistance to flow, and studies have shown that a value >0.8 predicts poor response to revascularization treatments. The most significant setbacks for duplex ultrasonography are its reduced sensitivity in obese patients, hindrance by overlying bowel gas and operator dependence.
    • CT angiography – involves the administration of intravenous contrast and acquiring detailed images of blood vessels or tissues by moving the beam in a helical manner across the area being studied. In a study by Wittenberg et al, the sensitivity and specificity for hemodynamically significant RAS (>50%) by CTA was found to be 96% and 99%. CTA also has a comparable negative predictive value to MRA in ruling out renal artery stenosis. It can also diagnose extrinsic compression of renal arteries, FMD, arterial dissection, and help in evaluating surrounding structures. However, CTA can only provide an anatomical assessment of the lesion and is not able to evaluate the degree of obstruction to renal blood flow. Exposure to radiation, allergy to contrast, and acute kidney injury are other downfalls of CTA.
    • MRA  – uses a powerful magnetic field, pulses of radio waves, and intravenous gadolinium to evaluate the renal blood vessels and surrounding structures. Several studies have shown the sensitivity and specificity of MRA to be around 97% and 92% in diagnosing renal artery. MRA does not involve radiation, and gadolinium contrast is less likely to cause an allergic reaction as compared to the iodine contrast used in CTA. However, MRA has been shown to overestimate the grade of stenosis and is often affected by motion artifacts or opacification of renal veins, leading to difficulty visualizing the renal arteries. Also, gadolinium has been shown to induce a rare, progressively fatal disease called nephrogenic systemic fibrosis (NSF).  NSF can affect the skin, joints, and multiple organs leading to progressive, irreversible fibrosis and eventual death. This occurs due to a transmetalation reaction that displaces gadolinium ion from its chelate, resulting in the deposition of gadolinium in the skin and soft tissues. The 1-year incidence of NSF has been reported to be around 4.6% and almost all cases occurred in patients with a glomerular filtration rate < 30 mL/min/1.73 m.
    • Nuclear medicine ACE-Inhibitor (ACE-I) renography – is another non-invasive, relatively safe imaging method that uses radioactive material, a special camera, and a computer to evaluate for renovascular hypertension. It involves the administration of an ACE-I to determine if the cause of hypertension is due to the narrowing of the renal arteries. The sensitivity and specificity of this test have shown to be variable, with values between 74% – 94% for sensitivity and 59% – 95% for specificity. It is a time-consuming procedure, and there is a risk of radiation exposure and irritation or pain from the injection of the radiotracer. The sensitivity of ultrasound has shown to be higher than captopril renography which makes it a better choice for an initial diagnostic test.
    • Magnetic resonance angiogram, or MRA – Images from this test show blood flow and organ function without using x-rays. Contrast medium may be injected into a vein in your arm to better see the structure of your arteries. You remain awake, although a muscle relaxer may be used, if necessary. You lie still on a table that slides into a tunnel-shaped device. There is no radiation exposure with this study. Claustrophobia can be an issue with MRAs as the tube is quite narrow.
    • Catheter angiogram – A special kind of x-ray in which a catheter, or a thin, flexible tube, is threaded through your large arteries into your renal artery. This often is from a small slit in the groin. The patient is usually awake, although a muscle relaxer may be given to lessen anxiety during the procedure. A contrast medium, or a colored dye, is injected through the catheter, so the renal artery shows up more clearly on the x-ray. The benefits of this study are that it is more accurate than the other tests and if a significant narrowing is seen, it can be dilated with a balloon (angioplasty) or stented (a tube-like cage that keeps the vessels open) at the same time. A catheter angiogram is an invasive procedure so this is usually reserved for patients who have a positive result of one of the other tests and plans are made to dilate the blood vessel.

    Catheter arteriography – is the gold standard test to evaluate for renovascular hypertension and provides the best temporal and spatial resolution. Catheter angiography has the added advantage of measuring translesional pressure gradients to assess the hemodynamic significance of anatomically severe lesions. It is most useful in:

    • Patients with a disparity between imaging modalities
    • Patients with a high index of suspicion and negative imaging findings
    • Patients anticipated having an intervention

    It can also evaluate anatomical abnormalities of the kidney, renal arteries, aorta, and can be followed by endovascular intervention for the treatment of significant lesions. Also, the surrounding tissues and bones can be removed or subtracted from the final image revealing only the arterial framework. This method is known as digital subtraction angiography (DSA). However, the radiation doses are higher than CTA, and because it is an invasive procedure, there are risks of complications such as arterial dissection, tear, rupture, or thromboembolic phenomenon.

    Treatment of Renal Hypertension

    The management of renovascular hypertension aims to treat the underlying cause. Several options are available, which include pharmacological and invasive therapy.

    Pharmacological therapy entails the use of antihypertensive medications to control blood pressure. The American College of Cardiology and the American Heart Association (ACC/AHA) advocates pharmacological therapy as the first-line treatment for renal artery stenosis. Since RAAS is the most prominent pathway contributing to hypertension in these disorders,

    • ACEI and angiotensin receptor blockers (ARBs) form the cornerstone of managing renovascular hypertension (Class 1a indication). Often more than one medication will be needed to control the blood pressure.
    • Calcium channel blockers, thiazides, beta-blockers, and hydralazine have been shown to be effective to control blood pressure in patients with RAS. Direct renin inhibitors such as aliskiren have been studied as monotherapy or in combination with ACEIs/ARBs to treat hypertension. Though it has been shown to be effective for the treatment of hypertension there is not enough data to prove its efficacy in treating renovascular hypertension.
    • ACEIs and ARBs inhibit the action of angiotensin II, thereby causing vasodilation and promote sodium and water excretion. However, these medications are contraindicated in patients with a single functioning kidney or bilateral lesions as they can cause efferent arteriolar vasodilatation leading to interruption in autoregulation and thereby decreasing glomerular filtration. While these medications are effective in controlling blood pressure, they can also lead to worsening renal function.
    • Percutaneous angioplasty is the treatment of choice for renovascular hypertension due to FMD and for patients with atherosclerotic renal artery stenosis that is not controlled with medications. The ACC/AHA guidelines recommend revascularization for renal artery disease in the following scenarios:
    • Patients with hemodynamically significant RAS and recurrent, unexplained congestive heart failure or sudden, unexplained pulmonary edema (class Ia)
    • Hemodynamically significant RAS and accelerated hypertension, resistant hypertension, malignant hypertension or hypertension with an unexplained unilateral small kidney, and hypertension with intolerance to medication (Class IIa)
    • Patients with bilateral RAS and progressive chronic kidney disease or a RAS to a solitary functioning kidney (Class IIa)
    • Patients with hemodynamically significant RAS and unstable angina (class IIa)
    • Asymptomatic bilateral or solitary viable kidney with hemodynamically significant RAS (Class IIb)
    • Patients with RAS and chronic renal insufficiency with unilateral RAS (class IIb)
    • In addition to angioplasty, renal stent placement is indicated for patients with ostial atherosclerotic lesions (Class I).
    • Patients with FMD and renovascular hypertension are also treated with percutaneous intervention with or without a stent. Multiple studies have shown a decrease in baseline blood pressure after intervention for FMD. However, there remains an ongoing debate about the benefit of revascularization when compared to medical management in patients with atherosclerotic renal artery stenosis (ARAS). Several studies have failed to show a significant decrease in blood pressure or the number of antihypertensive agents between angioplasty and medical treatment groups.
    A meta-analysis of 7 trials by Zhu et al. revealed that medical management is as effective as percutaneous revascularization in the treatment of RAS. Three recent trials ASTRAL, CORAL, and STAR found no difference between stenting and medical therapy in patients with atherosclerotic renal artery stenosis.  Thus it can be established that revascularization does not reverse renal damage or decrease blood pressure in patients with atherosclerotic renal artery stenosis.

    In the case of recurrent renal artery stenosis or blood pressure not controlled with medication and or/angioplasty, renal bypass surgery may be an option. In this procedure, the surgeon uses a vein or synthetic tube to connect the kidney to the aorta, to create an alternate route for blood to flow around the blocked artery into the kidney. This is a complex procedure and rarely used. The ACC/AHA guidelines recommend surgery for RAS in

    • Patients with RAS secondary to FMD, especially those with complex disease and/or those having microaneurysms
    • Patients with atherosclerotic RAS involving multiple vessels or involvement of early primary branch of the main renal artery
    • Patients with atherosclerotic RAS who require pararenal aortic reconstructions (such as with aortic aneurysms or severe aortoiliac obstruction).

    Several studies have also evaluated the role of unilateral nephrectomy in patients with renovascular hypertension and have shown improvement in blood pressure control, renal function, and decrease in the use of anti-hypertensives. However, this is an invasive procedure with inherent risks and long term consequences of such a procedure are unclear.

    Surgery

    • In terms of treatment for renovascular hypertension surgical revascularization versus medical therapy for atherosclerosis, it is not clear if one option is better than the other according to a 2014 Cochrane review; balloon angioplasty did show a small improvement in blood pressure .[rx]
    • Surgery can include percutaneous surgical revascularization, and also nephrectomy or autotransplantation, and the individual may be given beta-adrenergic blockers.[rx] Early therapeutic intervention is important if ischemic nephropathy is to be prevented. Inpatient care is necessary for the management of hypertensive urgencies, quick intervention is required to prevent further damage to the kidneys.[rx]

    Blood Pressure Goals

    • SHEP and HYVET trials have shown significant benefits of antihypertensive treatment in patients with the goal of SBP <150 mmHg.
    • The VALsartan in Elderly Isolated Systolic Hypertension (VALISH) trial showed no significant difference in the primary outcome of sudden death, fatal or nonfatal myocardial infarction and stroke, heart failure death, or other cardiovascular death among patients with strict (< 140 mmHg) and moderate (140 to 150 mmHg) SBP control.
    • However, the VALISH trial was underpowered due to the low number of events.
    • Hence, the optimal SBP in patients with hypertensive disorder remained a controversial topic.
    • The most recent Systolic Blood Pressure Intervention Trial (SPRINT) has shown that intensive SBP target of < 120 mmHg improved the cardiovascular outcomes and the overall survival compared to the standard SBP target of 135 to 139 mmHg.
    • However, aggressive SBP lowering may be harmful in the elderly and incite more adverse effects such as hypotension, end-organ hypoperfusion (causing acute kidney injury, and intracranial hypoperfusion which may link to cognitive decline), and polypharmacy.
    • It is suggested that a goal blood pressure of < 130/80 mmHg is appropriate as long as the patient tolerates it.
    • Otherwise, < 140/90 mmHg is considered reasonable in patients who are in the elderly population and patients with labile blood pressure or polypharmacy.
    • Management strategies should always be patient-centered, with the aim of optimizing blood pressure control and avoiding polypharmacy, especially in the elderly.

    J-curve Phenomenon

    • Various studies have shown a J-curve association between blood pressure with risk of myocardial infarction and death.
    • Patients with isolated systolic hypertension who receive antihypertensive treatment may precipitously drop their DBP as well.
    • As myocardial perfusion occurs mainly during diastole, an excessive drop in DBP may increase the risk of cardiovascular disease and death.

    Lifestyle changes

    You may also need to make some lifestyle changes as part of your ISH treatment plan. These can include:

    • Losing weight. This can help lower your blood pressure. In fact, for every two pounds you lose, you could lower your blood pressure by about 1 mm Hg.
    • Eating a heart-healthy diet. You should also aim to reduce the amount of sodium in your diet. Consider the DASH diet, which emphasizes eating:
      • vegetables
      •  whole grains
      •  low-fat dairy products
      •  fruits
    • Exercising. Not only can exercise help you lower your blood pressure, but it can help you control your weight and stress levels. Aim to perform some sort of aerobic exercise for at least 30 minutes most days of the week.
    • Decreasing alcohol consumption. Healthy alcohol intake is one drink per day for women and two per day for men.
    • Quitting smoking. Smoking can raise your blood pressure and also contribute to a variety of other health problems.
    • Managing stress. Stress can raise your blood pressure, so finding ways to relieve it are important. Examples of techniques to help lower stress are meditation and deep breathing exercises.
    • Eating a heart-healthy diet: Choose fruits, vegetables, grains and low-fat dairy foods.
    • Exercising regularly, at least 30 minutes a day of moderate activity, such as walking (check with your healthcare provider before starting an exercise program).
    • Keeping your weight under control: Check with your healthcare provider for a weight-loss program, if needed.
      Cutting back on alcoholic drinks.
    • Limiting caffeine intake.
    • Limiting sodium (salt) in your diet: Read nutrition labels on packaged foods to learn how much sodium is in one serving.
    • Reducing and avoiding stress when possible: Many people find that regular meditation or yoga helps.

    References

     

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