ByRx Harun

Lung Ventilation – Indications, Contraindications

Lung Ventilation involves ventilating one lung and letting the other collapse for providing surgical exposure in the thoracic cavity or isolating ventilation to one lung. The protective role of the single lung ventilation involves protecting one lung from the ill effects of fluid from the other lung – which may be blood, lavage fluid, malignant or purulent secretions. Thus it is prudent to ensure perfect placement of the tube as a misplaced tube defeats the goals of lung isolation or differential ventilation. This is ensured by bronchoscopy done after tube placement and after any position changes thereafter. This activity reviews the technique, indications, contraindications and highlights the role of the interprofessional team in the preoperative workup of patients undergoing lung resection.

Single lung ventilation, also known as ‘One Lung’ ventilation, is a method of ventilation which was first conceptualized by physiologists Eduard Pflüger and Claude Bernard who studied gas exchange in dogs using a lung isolation catheter.[rx] Wolffberg isolated the two lungs using the catheter in 1871 which is the first reported concept of an endobronchial single-lumen tube. The first instance of clinical use in humans was by Loewy and von Schrotter with lower lobe bronchus catheterized under fluoroscopic control. Head designed the first double-lumen tube in 1889 which had two tracheal cannulas – one short tracheal and one longer endobronchial one. Gale and Walters in 1932 advanced Head’s design and created the prototype for the modern-day double-lumen tubes. Double lumen tubes paved the way for one-lung ventilation offering better control of ventilation and more efficient separation of the two lungs.

Single lung ventilation involves ventilating one lung and letting the other collapse for providing surgical exposure in the thoracic cavity or isolating ventilation to one lung. The protective role of the single lung ventilation involves protecting one lung from the ill effects of fluid from the other lung – which may be blood, lavage fluid, malignant or purulent secretions. Thus it is prudent to ensure perfect placement of the tube as a misplaced tube defeats the goals of lung isolation or differential ventilation. This is ensured by bronchoscopy done after tube placement and after any position changes thereafter. One lung ventilation is used to facilitate a wide variety of procedures on ipsilateral thoracic or mediastinal structures as well as to provide lung isolation; this is made possible by the use of double-lumen tubes, bronchial blockers, and endobronchial tubes. Familiarity with the use of these instruments and the physiology of one-lung ventilation is essential to the performance of safe anesthesia.

Anatomy and Physiology

A good understanding of airway anatomy and the tracheobronchial tree is essential to performing safe one-lung ventilation. The fiberoptic bronchoscopy enables a good visualization of the airway anatomy. The first branching point in the airway is the carina – which marks the bifurcation of the trachea into the two mainstem bronchi at the level of the sternal angle – left and right main bronchus. The trachea is about 10 to 13 cm long and has 12 concentric cartilaginous rings. These rings are deficient in their posterior aspect and thus for C-shaped rings as seen on a cross-section. The trachea divides in an area known as the carina which marks the division into left and right main bronchus.

The left main bronchus (LMB) continues for about 5 cms after which it branches into left lower lobe bronchus (LLLB) and left upper lobe bronchus (LULB). The right main bronchus (RMB) is shorter than the left side, but it is also wider and more vertical than the left side. The right main bronchus gives off the right upper lobe bronchus and then continues further as the bronchus intermedius. The take-off of the right upper lobe bronchus is about 2.0cm in adult men and about 1.6 cm in adult females. A knowledge of tracheal anatomy helps the anesthesiologist to position the double-lumen tube for selectively isolating one lung for ventilation. This anatomy must undergo careful observation once the double-lumen tube is in place and the fiberoptic scope is inserted to check the cuff position and verify correct tube placement.

Indications

The indications of single-lung ventilation aim at facilitating surgical exposure by isolating the lung away from the field of surgery or preventing further lung trauma by providing selective ventilation as well as preventing infection or secretions from entering the healthy lung.

Surgical Exposure

Video-assisted thoracoscopic surgery including pneumonectomy, wedge resections
Pulmonary resections including pneumectomies and lobectomies
Mediastinal surgery
Thoracic vascular surgery
Esophageal surgery
Spine surgery

Lung Isolation

For protective isolation:

Massive pulmonary hemorrhage
Infection/purulent secretions

For control of ventilation:

Tracheobronchial trauma
Broncho-pleural/Broncho-cutaneous fistula

Contraindications

These are some of the relative contraindications for single lung ventilation.

Patient unable to tolerate OLV/Dependence on bilateral ventilation
Intraluminal airway masses (making DLT placement difficult)
Hemodynamic instability
Severe hypoxia
Severe COPD
Severe pulmonary hypertension
Known or suspected difficult intubation

Equipment

Single lung ventilation is achieved with the use of special airway devices such as double-lumen tubes (DLT) and bronchial blockers (BB) which selectively direct the airflow to one lung. They are used to collapse one lung selectively for surgery on the ipsilateral side.

Double Lumen Tubes: The most common design of the double-lumen tube used in the present practice of thoracic anesthesia is the Robertshaw design. It is available in left and right-sided types, and varying sizes from 26 Fr to 41 Fr. The size denotes the external diameter of the tube in cms. The Robertshaw design of the DLT comprises two semicircles placed back to back to form two independent lumens that can be ventilated independently of each other. The lumens have different openings depending on which sided DLT is present. The right-sided DLT has a curve to the right, and similarly, the left-sided DLT has a curve to the left. The double-lumen tube cuffs are high volume and low-pressure cuffs.[rx][rx]
Connector: The connector is an important component of the Double lumen tube as it provides the user with an opportunity to selectively block either lumen or ventilate bilaterally. The connector piece is composed of a Y-shaped piece which has two openings – one each for the connection to the bronchial and tracheal lumen respectively and a common portion that fits into the anesthesia circuit. The connector usually has tracheal and bronchial lumen parts made of different colors for ease of use. Universally the blue color is used by manufacturers to denote the endobronchial lumen/cuff. The cuffs are colored similarly to the connector tubes to maintain uniformity in identification. This safety mechanism ensures correct side lung collapse and ventilation achieved by clamping the side on which lung needs to collapse temporarily.
Bronchial Blockers: Bronchial blockers are used to achieve single lung ventilation by blocking either left or right primary bronchus. Several manufacturers produce bronchial blockers with different designs. However, their basis is on a simple design comprising an inflatable low pressure, high volume cuff at the end of a catheter. The advantages offered by a bronchial blocker over a DLT include the ability to place through an existing endotracheal tube, ability to use in patients with airway trauma and the ability to perform selective lobar blockade if needed. Bronchial blockers are not without their own disadvantages. They require a minimum of 7.5 endotracheal tubes in place for introduction into the airway. They allow the slower collapse of the lung. Owing to the variable take-off of the right upper lobe, bronchial blockers are often difficult to position to seal off the right upper lobe. They are also much more prone to dislodgement when compared to Double lumen tubes.[rx]
Fiber-optic Bronchoscope: A fiberoptic scope is mandatory when attempting to place a double-lumen tube; this is because accurate positioning is essential to achieving a good seal and lung isolation. Malpositioned tubes are avoided by checking the tube position after the patient is in place in the final position for the procedure.
Endobronchial Tubes: Endotracheal tubes may be placed in the endobronchial to provide one-sided ventilation. The major disadvantage of such a technique is the inability to have access to the non-intubated lung. Endobronchial tubes are preferred in specific clinical scenarios to a DLT, such as patients with previous neck or oral surgery who present with a difficult airway and require adequate lung separation. The placement of a DLT is more challenging than that of an endobronchial SLT. DLT placement has higher chances for airway injury and bleeding. Endobronchial tubes may be mandatory in patients requiring lung isolation who have a short or long-term tracheostomy present before the procedure.[rx][rx][rx]

Preparation

Anesthetic Considerations[rx]

Patients usually undergoing single lung ventilation for a variety of procedures have underlying pulmonary disease. Patients should be evaluated comprehensively for their primary disease prior to performing the surgical procedure. Echocardiography may be useful in patients with cor pulmonale and may provide information about baseline cardiac function and reserve.

A review of the relevant radiological anatomy on a case-to-case basis may help plan anesthetic management for single lung ventilation. This review will also allow proper preparation for patients who require specialized airway management. Presence of decreased baseline function due to large effusions, consolidations and atelectasis predispose patients to hypoxemia during the procedure, which may obviate the need to use higher fractions of inspired oxygen during the procedure. The presence of any bullae on the non-operative lung may provide clues to patients more likely to develop a pneumothorax in the perioperative period. Tumors need to be evaluated for the presence of any paraneoplastic syndromes as their presence may guide anesthetic management.

Special considerations need to be placed on patients age as it is an independent risk factor which decides complication rates in patients undergoing pulmonary resection using single lung ventilation. Elderly patients have been found to have higher morbidity and mortality from pulmonary resections. Patients undergoing lung resections need additional testing to predict the risks involved in lung resection besides age. The most common tests used for such an assessment are FEV1 (forced expiratory volume-one second) and DLCO (diffusing capacity of the lungs for carbon monoxide).

FEV1 is a predictor of postoperative complications including death that may arise from undergoing pulmonary resection. A reduced preoperative FEV1 (less than 60 percent predicted) was found to be the strongest predictor of postoperative complications by multiple authors.[rx][rx]

DLCO has been studied as a factor that decides postoperative morbidity as well. DLCO measured as a percent of the predicted value and predicted postoperative DLCO is considered the most valuable predictors of mortality & postoperative complications in pulmonary resections.[rx] The current ACCP guidelines do not provide numerical cutoffs for DLCO below which pulmonary resections should not be performed on patients. Instead, they give importance in determining the predicted postoperative (PPO) values. Assessment of the postoperative predicted values is the deciding factor in such cases and predicts the success of single lung ventilation. The interpretation of postoperative values are as follows:

Patients who have both PPO FEV1 and PPO DLCO are greater than 60 percent do not need any further testing to undergo pulmonary resection.
Patients who have either PPO FEV1 or PPO DLCO less than 60 percent, however, have both values greater than 30 percent need additional testing with stair climbing or a shuttle walk test.
If both values are less than 30 percent, patients should undergo cardiopulmonary exercise testing with additional measurement of the maximal oxygen consumption.

The cut-off for the stair climb test is 22 meters. Incremental shuttle walk test distance greater than 400 meters denotes a maximal oxygen uptake of (VO max) greater than or equal to 15 mL/kg per minute. Such information may help the physician interpret the procedural risks and better clinical outcomes for patients undergoing single lung ventilation.

Technique

The most commonly used DLT is the left-sided DLT irrespective of which side requires the isolation; this is because placing a left-sided DLT is less challenging than the right-sided one. This comparative ease is in part due to the short take-off of the right upper bronchus which leads to higher chances of dislodgement and or impaired ventilation of the right upper bronchus.

DLT placement technique: After inducing the patient with general anesthesia and confirming complete neuromuscular blockade, the following steps are taken to place a Left-sided DLT

A direct laryngoscopy using a Macintosh blade is used for laryngoscopy as the DLT is a large tube and this technique provides the maximum space for its insertion.
The double-lumen tube is introduced with a rigid stylet with the endobronchial curvature facing anteriorly.
The rigid style ensures passage through the vocal cords. After the DLT passes through the vocal cords, the style is removed.
The tube is then rotated by a 90 degrees angle anticlockwise to the left until the blue bronchial lumen faces left and tracheal lumen faces right.
The next step involves either advancing the tube further until we meet resistance or using a fibreoptic bronchoscope to guide further placement. At this moment the tracheal cuff may be inflated and the connector attached to start ventilation.
The shape of the left-sided DLT facilitates the bronchial cuff to be positioned in the left bronchus when advanced, but the DLT position should be confirmed with a fibreoptic bronchoscope to make sure that the tracheal lumen opening is above the carina and bronchial lumen is in the left bronchus. The bronchial cuff can now be inflated with 1 to 2 ml of air.
Bilateral ventilation confirmation is by auscultation. Air entry should be audible in bilateral lungs at this point.
Next, lung isolation is confirmed with selective clamping of the tracheal and bronchial lumens.
When ventilation through the bronchial lumen completes, only the left lung should be inflated.
When clamping the bronchial lumen and ventilating through the tracheal lumen, only the right lung should inflate.

Inability to perform a direct laryngoscopy is a contraindication to use of a DLT. In such a situation a bronchial blocker may be a suitable alternative.

Complications

Management of Hypoxemia[rx]

During single lung ventilation, the ventilation to one of the lungs is interrupted. However, the perfusion is still present in the non-ventilated lung, which leads to an intrapulmonary shunt in the form of wasted perfusion to the non-ventilated lung. Protective mechanisms like hypoxic pulmonary vasoconstriction can counteract hypoxia to a certain degree. However, it is mandatory for the anesthesiologist to have measures in place for hypoxemia that may arise during single lung ventilation. Ventilation and perfusion (V- Q) matching plays a significant role in the management of oxygenation in patients on single lung ventilation. Some authors note that oxygenation is much better in the lateral decubitus position when compared to the supine position.

Classically, an inspired oxygen fraction (FiO2) of 1.0 has been advocated while performing one-lung ventilation. The rationale behind using a higher inspired fraction of oxygen is to have a safety margin. Higher Fio2 also leads to vasodilatation, and this may help increase the blood to the ventilated lung. Oxygenation at FiO2 of 1.0 can lead to atelectasis, so it is advisable to initiate with a Fio2 less than 1.0 and increase if needed.

If hypoxia develops during the performance of one lung ventilation the following step s must take place :

Check the position of the double-lumen tube/endobronchial tube/bronchial blocker. Changes in position may occur due to surgical manipulation. A repeat fiberoptic bronchoscopy through the tracheal lumen is useful in clinching the diagnosis. Additional steps involve suctioning the lumens of the tube to clear secretions which may also contribute to hypoxia.
FiO2 is increased to 1.0 to improve the amount of oxygen delivered.
Recruitment maneuvers are employed on the ventilated lung which is in the dependent position; this is done to overcome any atelectasis and thus help in oxygenation. PEEP may be applied to this lung to eliminate atelectasis, resulting in a decrease in the shunt thereby improving oxygenation
CPAP to the operative lung may be applied to decrease shunting and thus improve oxygenation. However, this does make the surgical procedure challenging to the surgeon, and should only be an option when other measures have not resulted in any improvement.
If the hypoxemia is severe and does not resolve with the abovementioned steps, the next best step is to revert to two lung ventilation.
Severe hypoxemia should alert the anesthesiologist to look for causes like pneumothorax on the dependent lung. Chronic obstructive lung disease patients are more likely to experience such a complication. Intraoperative development of pneumothorax mandates aborting the surgical procedure and immediate insertion of a chest tube on the side of the pneumothorax.

ByRx Harun

Invasive Mechanical Ventilation – Indications, Contraindications

Invasive mechanical ventilation is an intervention that is frequently used in acutely ill patients requiring either respiratory support or airway protection. The ventilator allows gas exchange to be maintained while other treatments are given to improve the clinical condition. This activity reviews the indications, contraindications, management and possible complications of invasive mechanical ventilation and highlights the importance of the interprofessional team in managing the care of patients requiring ventilatory support.

The need for mechanical ventilation is one of the most common causes of admission to the intensive care unit.[rx][rx][rx]

It is imperative to understand some basic terms to understand mechanical ventilation.

Ventilation: Exchange of air between the lungs and the air (ambient or delivered by a ventilator), in other words, it is the process of moving air in and out of the lungs. Its most important effect is the removal of carbon dioxide (CO2) from the body, not on increasing blood oxygen content. Ventilation is measured as minute ventilation in the clinical setting, and it is calculated as respiratory rate (RR) times tidal volume (Vt). In a mechanically ventilated patient, the CO2 content of the blood can be modified by changing the tidal volume or the respiratory rate.
Oxygenation: Interventions that provide greater oxygen supply to the lungs, thus the circulation. In a mechanically ventilated patient, this can be achieved by increasing the fraction of inspired oxygen (FiO 2%) or the positive end-expiratory pressure (PEEP).
PEEP: The positive pressure that will remain in the airways at the end of the respiratory cycle (end of exhalation) is greater than the atmospheric pressure in mechanically ventilated patients. For a full description of the use of PEEP, please review the article titled “Positive End-Expiratory Pressure (PEEP).”
Tidal volume: Volume of air moved in and outside the lungs in each respiratory cycle.
FiO2: Percentage of oxygen in the air mixture that is delivered to the patient.
Flow: Speed in liters per minute at which the ventilator delivers breaths.
Compliance: Change in volume divided by change in pressure. In respiratory physiology, total compliance is a mix of lung and chest wall compliance as these two factors cannot be separated in a patient.

Since having a patient on mechanical ventilation allows a practitioner to modify the patient’s ventilation and oxygenation, it has an important role in acute hypoxic and hypercapnic respiratory failure as well as in severe metabolic acidosis or alkalosis.[rx][rx]

Physiology of Mechanical Ventilation

Mechanical ventilation has several effects on lung mechanics. Normal respiratory physiology works as a negative pressure system. When the diaphragm pushes down during inspiration, negative pressure in the pleural cavity is generated, this, in turn, creates 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 inferior vena cava (IVC), increasing venous return. The application of positive pressure ventilation changes this physiology. The positive pressure generated by the ventilator transmits to the upper airways and finally to the alveoli, this, in turn, is transmitted to the alveolar space and thoracic cavity, creating positive pressure (or at least less negative pressure) in the pleural space. The increased RA pressure and decreased venous return generate a decrease in preload. This has a double effect in decreasing cardiac output: Less blood in the right ventricle means less blood reaching the left ventricle and less blood that can be pumped out, decreasing cardiac output. Less 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, which will result 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 consideration in patients who may not be able to increase their SVR, like in patients with distributive shock (septic, neurogenic, or anaphylactic shock).

On the other hand, mechanical ventilation with positive pressure can significantly decrease the work of breathing. This, in turn, decreases blood flow to respiratory muscles and redistributes it to more critical organs. Reducing the work from respiratory muscles also reduces the generation of CO2 and lactate from these muscles, helping improve acidosis.

The effects of mechanical ventilation with positive pressure on the venous return may be beneficial when used in patients with cardiogenic pulmonary edema. In these patients with volume overload, decreasing venous return will directly decrease the amount of pulmonary edema being generated, by decreasing right cardiac output. At the same time, the decreased return may improve overdistension in the left ventricle, placing it at a more advantageous point in the Frank-Starling curve and possibly improving cardiac output.

Proper management of mechanical ventilation also requires an understanding of lung pressures and lung compliance. Normal lung compliance is around 100 ml/cmH20. This means that in a normal lung the administration of 500 ml of air via positive pressure ventilation will increase the alveolar pressure by 5 cm H2O. Conversely, the administration of positive pressure of 5 cm H2O will generate an increase in lung volume of 500 mL. When working with abnormal lungs, compliance may be much higher or much lower. Any disease that destroys lung parenchyma like emphysema will increase compliance, any disease that generates stiffer lungs (ARDS, pneumonia, pulmonary edema, pulmonary fibrosis) will decrease lung compliance.

The problem with stiff lungs is that small increases in volume can generate large increases in pressure and cause barotrauma. This generates a problem in patients with hypercapnia or acidosis as there may be a need to increase minute ventilation to correct these problems. Increasing respiratory rate may manage this increase in minute ventilation, but if this is not feasible, increasing the tidal volume can increase plateau pressures and create barotrauma.

There are two important pressures in the system to be aware of when mechanically ventilating a patient:

Peak pressure is the pressure achieved during inspiration when the air is being pushed into the lungs and is a measure of airway resistance.
Plateau pressure is the static pressure achieved at the end of a full inspiration. To measure plateau pressure, we need to perform an inspiratory hold on the ventilator to permit for the pressure to equalize through the system. Plateau pressure is a measure of alveolar pressure and lung compliance. Normal plateau pressure is below 30 cm H20, and higher pressure can generate barotrauma.

Issues of Concern

Indications for Mechanical Ventilation

The most common indication for intubation and mechanical ventilation is in cases of acute respiratory failure, either hypoxic or hypercapnic.
Other important indications include a decreased level of consciousness with an inability to protect the airway, respiratory distress that failed non-invasive positive pressure ventilation, cases of massive hemoptysis, severe angioedema, or any case of airway compromise such as airway burns, cardiac arrest, and shock.
Common elective indications for mechanical ventilation are surgical procedures and neuromuscular disorders.

Contraindications

There are no direct contraindications for mechanical ventilation as it is a life-saving measure in a critically ill patient, and all patients should be offered the opportunity to benefit from this if needed.
The only absolute contraindication for mechanical ventilation is if it is against the patient’s stated wishes for artificial life-sustaining measures.
The only relative contraindication is if non-invasive ventilation is available and its use is expected to resolve the need for mechanical ventilation. This should be started first as it has fewer complications than mechanical ventilation.

Preparation

In order to initiate mechanical ventilation, certain measures should be taken. Proper placement of the endotracheal tube must be verified. This may be done by end-tidal capnography or a combination of clinical and radiological findings.
Proper cardiovascular support should be ensured with fluids or vasopressors as indicated on a case by case basis.
Ensure that proper sedation and analgesia are available. The plastic tube in the patient’s throat is painful and uncomfortable, and if the patient is restless or fighting the tube or the vent, it will make it much more difficult to control the different ventilation and oxygenation parameters.

Modes of Ventilation

After intubating a patient and connecting to the ventilator, it is time to select the mode of ventilation to be used. Several principles need to be grasped in order to do this consistently for the patient’s benefit.
As mentioned, compliance is the change in volume divided by the change in pressure. When mechanically ventilating a patient, one can select how the ventilator will deliver the breaths. The ventilator can be set up to either deliver a set amount of volume or a set amount of pressure, and it is up to the clinician to decide which would be more beneficial for the patient. When selecting what the ventilator will deliver, you are selecting which will be the dependent and which will be the independent variable in the lung compliance equation.
If we select to start the patient on volume-controlled ventilation, the ventilator will always deliver the same amount of volume (independent variable), and the generated pressure will be dependent on compliance. If compliance is poor, the pressure will be high, and barotrauma could ensue.
If on the other hand, we decide to start the patient on pressure-controlled ventilation, the ventilator will always deliver the same pressure during the respiratory cycle. However, the tidal volume will depend on lung compliance, and in cases where compliance frequently changes (like in asthma) this will generate unreliable tidal volumes and may cause hypercapnia or hyperventilation.
After selecting how the breath is delivered (by pressure or volume) the clinician has to decide which mode of ventilation to use. This means selecting if the ventilator will assist all the patient’s breaths, some patient’s breaths, or none of them and also selecting if the ventilator will deliver breaths even if the patient is not breathing on its own.
Other parameters that should be considered are how fast the breath is delivered (flow), what will be the waveform of that flow (decelerating waveform mimics physiological breaths and is more comfortable for the patient, while square waveforms in which the flow is given at full speed during all inhalation, are more uncomfortable for the patient but deliver quicker inspiratory times), and at what rate will breaths be delivered. All these parameters should be adjusted to achieve patient comfort, desired blood gasses, and prevent air trapping.
There are many different modes of ventilation that vary minimally between each other. In this review, we will focus on the most common modes of ventilation and their clinical use. The mode of ventilation includes assist control (AC), pressure support (PS), synchronized intermittent mandatory ventilation (SIMV), and airway pressure release ventilation (APRV).

Assist Control Ventilation (AC)

Assist control is when the ventilator will assist the patient by delivering support for every breath the patient takes (that is the assist part), and the ventilator will have control over the respiratory rate if it goes below the set rate (control part). In assist control, if the rate is set at 12 and the patient breathes at 18, the ventilator will assist with the 18 breaths, but if the rate drops to 8, the ventilator will take over control of the respiratory rate and deliver 12 breaths in a minute.

In assist control ventilation, the breath can be delivered by either giving volume or giving pressure. This is termed volume-assist control or pressure-assist control ventilation. In order to maintain simplicity, and understanding that given that ventilation is commonly a major problem than pressure and that volume control is used overwhelmingly more commonly than pressure control, the focus for the remainder of this review will use the term “volume control” interchangeably when discussing assist control.

Assist control (volume control) is the mode of choice used in the majority of intensive care units throughout the United States because it is easy to use. Four settings can be easily adjusted in the ventilator (respiratory rate, tidal volume, FiO2, and PEEP). The volume delivered by the ventilator in each breath in assist control will always be the same, regardless of the breath being initiated by the patient or the ventilator, and regardless of compliance, peak, or plateau pressures in the lungs.

Each breath can be time-triggered (if the patient’s respiratory rate is below the set ventilator rate, the machine will deliver breaths at a set interval of time) or patient-triggered if the patient initiates a breath on its own. This makes assist control a very comfortable mode for the patient as each of his or her efforts will be supplemented by the ventilator.

After making changes on the vent or after starting a patient on mechanical ventilation, careful consideration of checking arterial blood gases should be made and the oxygen saturation on the monitor should be followed to determine if further changes should be made to the ventilator.

The advantages of AC mode are increased comfort, easy corrections for respiratory acidosis/alkalosis, and low work breathing for the patient. Some disadvantages include that being a volume-cycled mode, pressures cannot be directly controlled which may cause barotrauma, the patient can develop hyperventilation with breath stacking, auto-PEEP, and respiratory alkalosis.[rx]

Synchronized Intermittent Mandatory Ventilation (SIMV)

SIMV is another frequently used mode of ventilation, although its use had been falling out of favor given its less reliable tidal volumes and failure to show better outcomes when compared to AC.

“Synchronized” means that the ventilator will adjust the delivery of its breaths with the patient’s efforts. “Intermittent” means that not all breaths are necessarily supported, and “mandatory ventilation” means that, as with AC, a set rate is selected and the ventilator will deliver these mandatory breaths each minute regardless of the patient’s respiratory efforts. The mandatory breaths can be triggered by the patient or by time if the patient’s RR is slower than the ventilator RR (as with AC). The difference from AC is that in SIMV the ventilator only will deliver the breaths that the rate is set up to deliver, any breath taken by the patient above this rate will not receive a full tidal volume or pressure support. This means that for each breath the patient takes above the set RR, the tidal volume pulled by the patient will depend solely on lung compliance and patient effort. This has been proposed as a method of “training” the diaphragm in order to maintain the muscular tone and wean off patients from the ventilator faster. Nonetheless, multiple studies have failed to show any advantages to SIMV. Furthermore, SIMV generates higher work of breathing than AC, which negatively impacts outcomes as well as generates respiratory fatigue. A general rule to go by is that the patient will be liberated from the ventilator when he or she is ready, and no specific mode of ventilation will make this faster. In the meantime, it is better to keep the patient as comfortable as possible and SIMV may not be the best mode to achieve this.

Pressure Support Ventilation (PSV)

PSV is a ventilator mode that relies completely on patient-triggered breaths. As the name implies it is a pressure-driven mode of ventilation. In this setting all breaths are patient-triggered as the ventilator has no backup rate, so each breath has to be started by the patient. In this mode, the ventilator will cycle between two different pressures (PEEP and pressure support). PEEP will be the remaining pressure at the end of exhalation, and pressure support is the pressure above the PEEP that the ventilator will administer during each breath for support of ventilation. This means that if a patient is set up in PSV 10/5, the patient will receive 5 cm H2O of PEEP, and during inhalation, he will receive 15 cm H2O of support (10 PS above PEEP).

Because there is no backup rate, this mode is not for use in patients with decreased consciousness, shock, or cardiac arrest. The tidal volumes will depend solely on the patient’s effort and lung compliance.

PSV often is used for ventilator weaning as it only augments patients breathing efforts but does not deliver a set tidal volume or respiratory rate.

The biggest drawback of PSV is its unreliable tidal volumes that may generate CO2 retention and acidosis as well as the higher work of breathing which can lead to respiratory fatigue.

To address this concern, a new algorithm for PSV was created called volume support ventilation (VSV). VSV is a similar mode to PSV, but in this mode, the tidal volume is used as feedback control, as the pressure support given to the patient will be constantly adjusted to the tidal volume. In this setting, if the tidal volume is decreasing, the ventilator will increase the pressure support to decrease the tidal volume and if the tidal volume increases the pressure support will decrease in order to keep the tidal volume close to the desired minute ventilation. There is some evidence suggesting that the use of VSV may decrease assisted ventilation time, total weaning time, and total T-piece time as well as a decreased need for sedation.

Airway Pressure Release Ventilation (APRV)

As the name suggests, in APRV mode the ventilator will deliver a constant high airway pressure that will deliver oxygenation, and ventilation will be served by releasing that pressure.

This mode has recently gained popularity as an alternative for difficult-to-oxygenate patients with ARDS in whom other modes of ventilation fail to reach the set targets. APRV has been described as a continuous positive airway pressure (CPAP) with an intermittent release phase. What this means is that the ventilator applies a continuous high pressure (P high) for a set amount of time (T high) and then releases that pressure, usually going back to zero (P low) for a much shorter period of time (T low).

The idea behind this is that during T high (which covers 80% to 95% of the cycle), there is constant alveolar recruitment, which improves oxygenation as the time maintained on high pressure is much longer than in other types of ventilation (open lung strategy). This reduces the repetitive inflation and deflation of the lungs that happens with other ventilator modes, preventing ventilator-induced lung injury. During this time (T high) the patient is free to breathe spontaneously (which makes it comfortable) but he will be pulling low tidal volumes as exhaling against such pressure is harder. Then, when T high is reached, the pressure in the ventilator will go down to P low (usually zero). This allows for air to be rushed out of the airways allowing for passive exhalation until T low is reached and the vent delivers another breath. To prevent airway collapse during this time the T low is set short, usually around 0.4-0.8 seconds. What happens here is that when the ventilator pressure goes to zero, the elastic recoil of the lungs pushes air out, but the time is not enough for all the air to leave the lungs, so the alveolar and airway pressure does not reach zero and there is no airway collapse. This time is usually set up so that T low ends when the exhalation flow drops to 50% of the initial flow.

Minute ventilation, then, will depend on T low and the patient’s tidal volumes during T high.

Indications for the use of APRV:

ARDS that is difficult to oxygenate with AC
Acute lung injury
Postoperative atelectasis.

Advantages of APRV:

APRV is a good mode for lung protection ventilation. The ability to set the P high means that the operator has control over the plateau pressure which can significantly lower the incidence of barotrauma
Because the patient initiates his respiratory efforts, there is better gas distribution secondary to improved V/Q matching.
Constant high pressure means more recruitment (open lung strategy)
APRV may improve oxygenation in ARDS patients who are difficult to oxygenate on AC
APRV may reduce the need for sedation and neuromuscular blocking agents as the patient may be more comfortable than with other modes.

Disadvantages and contraindications:

Given that spontaneous breathing is an important aspect of APRV, it is not ideal for heavily sedated patients
No data for APRV use in neuromuscular disorders or obstructive lung disease and its use should be avoided in these patient populations
Theoretically, constant high intrathoracic pressure could generate high pulmonary artery pressure and worsen intracardiac shunts in patients with Eisenmenger physiology
Strong clinical reasoning should be employed when selecting APRV as the mode of ventilation over more conventional modes such as AC.

Further information on the details of the different modes of ventilation and their setup can be found in the articles related to each specific mode of ventilation.

Clinical Significance for Invasive mechanical ventilation

Using the Ventilator

The initial ventilator setting can vary greatly depending on the cause for intubation and the scope of this review. Nonetheless, there are some basic settings for the majority of cases.

The most common ventilator mode to use in a newly intubated patient is AC. The AC mode provides good comfort and easy control of some of the most important physiologic parameters.

It is started with a FiO2 of 100% and titrated down guided by pulse oximetry or ABG, depending on the case.

Low tidal volume ventilation has been shown to be lung protective not only in ARDS but in other types of diseases. Starting the patient on a low tidal volume (6 to 8 mL/Kg of ideal body weight) will reduce the incidence of ventilator-induced lung injury (VILI). Always use a lung-protective strategy as there are not many advantages for higher tidal volumes and they will increase shear stress in the alveoli and may induce lung injury.

Initial RR should be comfortable for the patient 10-12 bpm should suffice. A very important caveat on this is for patients with severe metabolic acidosis. For these patients, the minute ventilation should at least be matched to their pre-intubation ventilation as failure to do so will worsen acidosis and can precipitate complications such as cardiac arrest.

Flow should be initiated at or above 60 L/min to prevent auto-PEEP.

Start with a low PEEP of 5 cm H2O and titrate up as tolerated by the patient to the goal for oxygenation. Pay close attention to blood pressure and patient comfort while doing this.

An ABG should be obtained 30 minutes after intubation and changes to the ventilator settings should be made in accordance with ABG findings.

Peak and plateau pressures should be checked on the vent to assure there are no problems with airway resistance or alveolar pressure in order to prevent ventilator-induced lung injury.

Attention should be given to the volume curves in the ventilator display as a reading showing that the curve is not coming back to zero at the time of exhalation is indicative of incomplete exhalation and development of auto-PEEP and corrections to the vent should be made immediately.[rx][rx]

Troubleshooting the Ventilator

With a good understanding of the concepts discussed, managing ventilator complications and solving problems should come as second nature.

The most common corrections that have to be done with the ventilator are to solve hypoxemia and hypercapnia or hyperventilation:

Hypoxia: Oxygenation depends on the FiO2 and the PEEP (T high and P high for APRV). To correct for hypoxia increasing any of these parameters should raise the oxygenation. Special attention should be paid to the possible adverse effects of raising PEEP which can cause barotrauma and hypotension. Raising FiO2 does not come without its concerns as high FiO2 can cause oxidative damage in the alveoli. Another important aspect of managing oxygen content is to define a goal for oxygenation. In general, there is little benefit from keeping oxygen saturation above 92-94% except for cases of carbon monoxide poisoning for example. A sudden drop in oxygen saturation should raise suspicion for tube misplacement, pulmonary embolism, pneumothorax, pulmonary edema, atelectasis, or the development of mucus plugs.
Hypercapnia: To modify CO2 content in blood one needs to modify alveolar ventilation. To do this, the tidal volume or the respiratory rate may be tampered with (T low and P Low in APRV). Raising the rate or the tidal volume, as well as increasing T low, will increase ventilation and decrease CO2. Consideration has to be made while increasing the rate, as this will also increase the amount of dead space and might not be as effective as tidal volume. While increasing volume or rate special attention should be paid to the flow-volume loop to prevent the development of auto-PEEP.
Elevated pressures: Two pressures are important in the system: peak and plateau. The peak pressure is a measure of airway resistance as well as compliance and includes the tubing and bronchial tree. Plateau pressures are a reflection of alveolar pressure and thus of lung compliance. If there is an increase in peak pressure, the first step to take is to do an inspiratory hold and check the plateau. Elevated peak pressure and normal plateau pressure: high airway resistance and normal compliance.

Possible causes: (1) Kinked ET tube – The solution is to unkink the tube; use a bite lock if the patient is biting on the tube, (2) Mucus plug – The solution is to suction the patient, (3) Bronchospasm – The solution is to give bronchodilators.

Elevated Peak and Elevated Plateau: Compliance Problems

Possible causes include:

Mainstem intubation: The solution is to retract the ET tube. For diagnosis, you will find a patient with unilateral breath sounds and a dull contralateral lung (atelectatic lung).
Pneumothorax: Diagnosis will be made by hearing breath sounds unilaterally and finding a hyper-resonant contralateral lung. In intubated patients, placement of a chest tube is imperative as the positive pressure will only worsen the pneumothorax.
Atelectasis: Initial management consists of chest percussions and recruitment maneuvers. Bronchoscopy may be used in resistant cases
Pulmonary edema: Diuresis, inotropes, high PEEP
ARDS: Use low tidal volume, high PEEP ventilation

Dynamic hyperinflation or auto-PEEP

This is a process in which some of the inhaled air is not fully exhaled at the end of the respiratory cycle. The accumulation of trapped air will increase pulmonary pressures and cause barotrauma and hypotension. The patient will be difficult to ventilate. To prevent and resolve auto-PEEP, enough time should be given for the air to leave the lungs during exhalation. The goal in management is to decrease the inspiratory to expiratory ratio, this can be achieved by decreasing respiratory rate, decreasing tidal volume (higher volume will require a longer time to leave the lungs), and increasing inspiratory flow (if the air is delivered quickly the inspiratory time is less and the expiratory time will be longer at any given respiratory rate). The same effect can be achieved by using a square waveform for inspiratory flow, what this means is that we can set the ventilator to deliver the full flow from beginning to end of inhalation. Other techniques that can be implemented are to assure adequate sedation to prevent patient hyperventilating and the use of bronchodilators and steroids to decrease airway obstruction. If auto-PEEP is severe causing hypotension, disconnecting the patient from the vent and letting time for all the air to be exhaled may be a life-saving measure. For a full description of the management of auto-PEEP please review the article titled “Positive End-Expiratory Pressure (PEEP)”

Another common problem found in mechanically ventilated patients is patient-ventilator dyssynchrony, usually termed as the patient “fighting the vent”. Important causes include hypoxia, auto-PEEP, not satisfying the patient’s oxygenation or ventilation demands, pain, and discomfort. After ruling out important causes as pneumothorax or atelectasis, patient comfort should be considered and proper sedation and analgesia should be assured. Consider changing the ventilator mode as some patients may respond better to different modes of ventilation.

Special Circumstances in Invasive mechanical ventilation

Special attention to vent settings should be taken in the following circumstances:

COPD – is a special case, as lungs in pure COPD have high compliance which causes a high tendency for dynamic airflow obstruction due to airway collapse and air trapping, making COPD patients very prone to developing auto-PEEP. Using a preventive ventilation strategy with high flow and low respiratory rate may help prevent auto-PEEP. Another important aspect to consider in chronic hypercapnic respiratory failure (due to COPD or another reason) is that there is no need to correct the CO2 back to normal, as these patients usually have a metabolic compensation for their respiratory problems. If a patient is ventilated to normal CO2 levels, his bicarbonate will decrease, and when a patient is extubated he will quickly go to respiratory acidosis as his kidneys cannot respond as fast as his lungs and his CO2 will go back to his baseline, causing respiratory failure and reintubation. To prevent this, CO2 goals should be determined based on pH and previously known or calculated baseline.
Asthma – As with COPD patients with asthma are very prone to air trapping, although the reason is pathophysiologically different. In asthma, air trapping is caused by inflammation, bronchospasm, and mucus plugs, not airway collapse. The strategy to prevent auto-PEEP is similar to the strategy used in COPD.
Cardiogenic pulmonary edema – High PEEP may decrease venous return and help resolve pulmonary edema as well as aid in cardiac output. The concern should be to make sure the patient is adequately diuresed before extubating, as the removal of the positive pressure may precipitate new pulmonary edema.
ARDS – is a type of non-cardiogenic pulmonary edema. An open lung strategy with high PEEP and low tidal volume has been shown to improve mortality.
Pulmonary embolism – is a difficult situation. These patients are very preload-dependent secondary to the acute increase in right atrial pressure. Intubating these patients will increase RA pressure and further decrease venous return, which may precipitate shock. If there is no way to prevent intubation, careful attention to blood pressure and initiation of vasopressors should be done promptly.
Severe pure metabolic acidosis – is a concern. When intubating these patients, careful attention should be paid to their pre-intubation minute ventilation. If this ventilation is not provided when starting mechanical support, pH will drop further possibly precipitating cardiac arrest.

Weaning from Mechanical Ventilation

Mechanical ventilation can be a lifesaving intervention and has impacted millions of lives since its invention, but it is not without complications. Shortening the ventilator time has shown to reduce ventilation-related complications like pneumonia, so actively pursuing liberation from mechanical ventilation (the so-called ventilation weaning) is imperative in every ventilated patient.

There are simple criteria that should be satisfied before a patient is determined to be ready for extubation:

The indication for intubation and mechanical ventilation must be resolved
The patient has to be able to maintain adequate gas exchange on its own without the help of positive pressure ventilation
There must be no auto-PEEP
The patient must have an adequate cardiovascular reserve (for example, in heart failure patients in which removing the vent can precipitate new pulmonary edema)
There should not be copious amounts of secretions in the ET tube that could generate high airway resistance and obstruction after extubation
The patient must be able to protect his or her airway.

After these criteria have been satisfied it is time to perform a spontaneous breathing trial (SBT). Two processes have to be completed to perform this:

A sedation holiday should be done daily to assess readiness for extubation with appropriate mental status and ability to protect the airway as well as to permit spontaneous breathing. This is usually protocolized in all intensive care units (ICU) and should be performed in every patient who is stable and in whom the indication for mechanical ventilation has resolved. During these daily trials, sedation is reduced to a minimum or completely eliminated until the patient is awake and cooperative but comfortable.
The second parameter is the SBT itself. To perform this, ventilator support should be reduced to a minimum. This can be done either via T-piece or pressure support. CPAP has been used in the past although it has been suggested to be inferior to the other two methods. A recent Cochrane review (2014) concluded that there are no major differences between T piece or pressure support trials on extubation success, reintubation, ICU mortality, or ICU length of stay. Nevertheless, pressure support was found to be superior for performing spontaneous breathing trials among patients with simple weaning (meaning patients successfully weaned in the first attempt) as it was shown to have a shorter weaning time.

SBT should be performed for 30 to 120 minutes, and the patient should be monitored closely for any signs of respiratory distress. If these signs are found, the patient should be placed back on his or her prior ventilator settings. If after this time patient meets criteria for successful SBT (RR < 35bpm; no signs of distress; HR <140/min and HR variability less than 20%; O2 sat greater than 90% or PaO2 greater than 60 mmHg on FiO2 less than 0.4; SBP greater than 80 and less than 180 mmHg or greater than 20% change from baseline), then the assessment for airway removal should be done by performing a cuff leak test when indicated.

If the patient is determined to be ready, the ETT should be removed and the patient should be monitored closely. In patients with high risk for reintubation (failure of two or more SBTs, CHF, CO2 greater than 45 after extubation, weak cough, pneumonia as a cause of respiratory failure), the use of noninvasive positive pressure ventilation after extubation as a bridge to ventilator free-breathing, has been shown to reduce ICU mortality and lower risk of intubation. This effect was not seen if the patient had already developed respiratory distress. High flow nasal cannula has also shown reduced reintubation rates, although no effect on mortality has been seen.

ByRx Harun

Pulmonary Ventilation and Its Effects, Mechanism

Pulmonary ventilation is commonly referred to as breathing. It is the process of air flowing into the lungs during inspiration (inhalation) and out of the lungs during expiration (exhalation). Air flows because of pressure differences between the atmosphere and the gases inside the lungs.

Pulmonary Ventilation Pressure Relationships

Inspiration (or inhalation) and expiration (or exhalation) are dependent on the differences in pressure between the atmosphere and the lungs. In a gas, pressure is a force created by the movement of gas molecules that are confined. For example, a certain number of gas molecules in a two-liter container has more room than the same number of gas molecules in a one-liter container. In this case, the force exerted by the movement of the gas molecules against the walls of the two-liter container is lower than the force exerted by the gas molecules in the one-liter container. Therefore, the pressure is lower in the two-liter container and higher in the one-liter container. At a constant temperature, changing the volume occupied by the gas changes the pressure, as does changing the number of gas molecules. Boyle’s law describes the relationship between volume and pressure in a gas at a constant temperature. Boyle discovered that the pressure of a gas is inversely proportional to its volume: If volume increases, pressure decreases. Likewise, if volume decreases, pressure increases. Pressure and volume are inversely related (P = k/V). Therefore, the pressure in the one-liter container (one-half the volume of the two-liter container) would be twice the pressure in the two-liter container. Boyle’s law is expressed by the following formula:

P 1 V 1 = P 2 V 2

In this formula, P₁ represents the initial pressure and V₁ represents the initial volume, whereas the final pressure and volume are represented by P₂ and V_2,respectively. If the two- and one-liter containers were connected by a tube and the volume of one of the containers were changed, then the gases would move from higher pressure (lower volume) to lower pressure (higher volume).

Pulmonary ventilation is dependent on three types of pressure: atmospheric, intra-alveolar, and intrapleural. Atmospheric pressure is the amount of force that is exerted by gases in the air surrounding any given surface, such as the body. Atmospheric pressure can be expressed in terms of the unit atmosphere, abbreviated atm, or in millimeters of mercury (mm Hg). One atm is equal to 760 mm Hg, which is the atmospheric pressure at sea level. Typically, for respiration, other pressure values are discussed in relation to atmospheric pressure. Therefore, negative pressure is pressure lower than the atmospheric pressure, whereas positive pressure is the pressure that it is greater than the atmospheric pressure. A pressure that is equal to the atmospheric pressure is expressed as zero.

Intra-alveolar pressure (intrapulmonary pressure) is the pressure of the air within the alveoli, which changes during the different phases of breathing. Because the alveoli are connected to the atmosphere via the tubing of the airways (similar to the two- and one-liter containers in the example above), the intrapulmonary pressure of the alveoli always equalizes with the atmospheric pressure.

This diagram shows the lungs and the air pressure in different regions.

Figure 22.16 Intrapulmonary and Intrapleural Pressure Relationships intra-alveolar pressure changes during the different phases of the cycle. It equalizes at 760 mm Hg but does not remain at 760 mm Hg.

Intrapleural pressure is the pressure of the air within the pleural cavity, between the visceral and parietal pleurae. Similar to intra-alveolar pressure, intrapleural pressure also changes during the different phases of breathing. However, due to certain characteristics of the lungs, the intrapleural pressure is always lower than, or negative to, the intra-alveolar pressure (and therefore also to atmospheric pressure). Although it fluctuates during inspiration and expiration, intrapleural pressure remains approximately –4 mm Hg throughout the breathing cycle.

Competing forces within the thorax cause the formation of negative intrapleural pressure. One of these forces relates to the elasticity of the lungs themselves—elastic tissue pulls the lungs inward, away from the thoracic wall. The surface tension of the alveolar fluid, which is mostly water, also creates an inward pull of the lung tissue. This inward tension from the lungs is countered by opposing forces from the pleural fluid and thoracic wall. Surface tension within the pleural cavity pulls the lungs outward. Too much or too little pleural fluid would hinder the creation of the negative intrapleural pressure; therefore, the level must be closely monitored by the mesothelial cells and drained by the lymphatic system. Since the parietal pleura is attached to the thoracic wall, the natural elasticity of the chest wall opposes the inward pull of the lungs. Ultimately, the outward pull is slightly greater than the inward pull, creating the –4 mm Hg intrapleural pressure relative to the intra-alveolar pressure.

Transpulmonary pressure is the difference between the intrapleural and intra-alveolar pressures, and it determines the size of the lungs. A higher transpulmonary pressure corresponds to a larger lung.

Factors Affecting Pulmonary Ventilation: Surface Tension of Alveolar Fluid

The surface tension of alveolar fluid is regulated by pulmonary surfactant, allowing efficient respiration.

Key Points

Type II avleolar epithelial cells secrete pulmonary surfactant to lower the surface tension of water, which helps prevent airway collapse.

Reinflation of the alveoli following exhalation is made easier by pulmonary surfactant.

The surfactant reduces surface tension within all alveoli through hydrophilic and hydrophobic forces.

Insufficient pulmonary surfactant in the alveoli can contribute to atelectasis (collapse of part or all of the lung ).

Premature infants often don’t have the capacity to produce enough surfactant to survive on their own.

Key Terms

atelectasis: The collapse of a part of or the whole lung caused by inner factors, rather than a pneumothorax.
surfactant: A lipoprotein in the tissues of the lung that reduces surface tension and permits more efficient gas transport.
Surface tension: The inward force created by films of molecules that can reduce the area of a surface.

EXAMPLES

Elective cesarean sections are becoming more common. One unfortunate consequence of this is that many of the infants delivered by this method are actually slightly physiologically premature. They lack sufficient surfactant to initiate proper breathing, and therefore, go into respiratory distress.

The alveoli are highly elastic structures in the parenchyma of the lungs that are the functional site of gas exchange. As the alveoli fill with air during inhalation they expand, and as air leaves the lung with exhalation, the alvoli return to their non-inflated size. The reason for the elasticity of the alveoli is a protein found in the extracellular matrix of the alveoli, called elastin, as well as the surface tension of water molecules on the alveoli themselves.

Surface Tension in the Lung

Surface tension is the force exerted by water molecules on the surface of the lung tissue as those water molecules pull together. Water (H₂O) is a highly polar molecule, so it forms strong covalent bonds with other water molecules. The force of these covalent bonds effectively creates an inward force on surfaces, such as lung tissue, with the effect of lowering the surface area of that surface as the tissue is pulled together. As the air inside the lungs is moist, there is considerable surface tension within the tissue of the lungs. Because the alveoli of the lungs are highly elastic, they do not resist surface tension on their own, which allows the force of that surface tension to deflate the alveoli as air is forced out during exhalation by the contraction of the pleural cavity.

Pulmonary Surfactant

The force of surface tension in the lungs is so great that without something to reduce the surface tension, the airways would collapse after exhalation, making re-inflation during inhalation much more difficult and less effective. The collapse of the lungs is called atelectasis. Fortunately, the type II epithelial cells of the alveoli continually secrete a molecule called surfactant that solves this problem.

A surfactant is a lipoprotein molecule that reduces the force of surface tension from water molecules on the lung tissue. The main reason that surfactant has this function is due to a lipid called dipalmitoylphosphatidylcholine (DPPC) which contains hydrophilic and hydrophobic ends. The hydrophilic ends are water-soluble and attach to the water molecules on the surface of the lungs. The hydrophilic ends are water-insoluble and face towards the air and pull away from the water. The net result is that the surface tension of the lungs from water is reduced so that the lungs can still inflate and deflate properly without the possibility of collapse from surface tension alone.

As unborn humans grow and develop in the womb, they receive oxygen from the mother, so their lungs aren’t fully functional right away. Of particular importance is the fact that they don’t produce surfactants until 24 weeks of development and usually don’t have enough built-up to prevent lung collapse until 35 weeks of development. Therefore prematurely born infants are at a high risk of respiratory distress syndrome from airway collapse, which can cause death if untreated. It is treated through pulmonary surfactant replacement therapy and mechanical ventilator treatment until the infant’s lungs are old enough to secrete enough surfactant to survive on their own. Other diseases may cause atelectasis, such as COPD, or any sort of lung trauma and inflammation that involves extensive damage to the pleural cavity or the lung parenchyma.

Diagram of an Alveoli: An alveoli with both cross-section and external views

Factors Affecting Pulmonary Ventilation: Compliance of the Lungs

Lung compliance refers to the magnitude of change in lung volume as a result of the change in pulmonary pressure.

Key Points

Low lung compliance would mean that the lungs would need a greater-than-average change in intrapleural pressure to change the volume of the lungs.

High lung compliance would indicate that little pressure difference in intrapleural pressure is needed to change the volume of the lungs.

Persons with low lung compliance due to obstructive lung diseases tend to take rapid shallow breaths and sit hunched over to make exhalation less difficult.

Persons with high lung compliance due to restrictive lung diseases tend to have difficulty expanding and deflating the lungs.

Two factors determine lung compliance: elasticity of the lung tissue and surface tensions at air-water interfaces.

Two factors determine lung compliance – elasticity of the lung tissue and surface tensions at air-water interfaces.

Key Terms

Lung compliance: The ability of the lungs and pleural cavity to change in volume based on changes in pressure.

EXAMPLES

Low lung compliance can be the result of interstitial lung diseases resulting from the inhalation of particulate substances such as asbestos (asbestosis) and silicon (silicosis).

Compliance is the ability of the lungs and pleural cavity to expand and contract based on changes in pressure. Lung compliance is defined as the volume change per unit of pressure change across the lung and is an important indicator of lung health and function. Measurements of lung volumes differ at the same pressure between inhalation and exhalation, meaning that lung compliance differs between inhalation and exhalation. Lung compliance can either be measured as static or dynamic based on whether only volume and pressure (static) are measured or if their changes over time are measured as well (dynamic).

Compliance and Elastic Recoil of the Lung

Compliance depends on the elasticity and surface tension of the lungs. Compliance is inversely related to the elastic recoil of the lungs, so thickening of lung tissue will decrease lung compliance. The lungs must also be able to overcome the force of surface tension from water on lung tissue during inflation in order to be compliant, and greater surface tension causes lower lung compliance. Therefore, surfactant secreted by type II epithelial cells increases lung compliance by reducing the force of surface tension.

A low lung compliance means that the lungs are “stiff” and have a higher than normal level of elastic recoil. A stiff lung would need a greater-than-average change in pleural pressure to change the volume of the lungs, and breathing becomes more difficult as a result. Low lung compliance is commonly seen in people with restrictive lung diseases, such as pulmonary fibrosis, in which scar tissue deposits in the lung making it much more difficult for the lungs to expand and deflate, and gas exchange is impaired. Pulmonary fibrosis is caused by many different types of inhalation exposures, such as silica dust.

Pulmonary Fibrosis: Pulmonary fibrosis stiffens the lungs through deposits of scar tissue, decreasing low compliance and making it more difficult for the lungs to inflate and deflate.

A high lung compliance means that the lungs are too pliable and have a lower than normal level of elastic recoil. This indicates that little pressure difference in pleural pressure is needed to change the volume of the lungs. Exhalation of air also becomes much more difficult because the loss of elastic recoil reduces the passive ability of the lungs to deflate during exhalation. High lung compliance is commonly seen in those with obstructive diseases, such of emphysema, in which destruction of the elastic tissue of the lungs from cigarette smoke exposure causes a loss of elastic recoil of the lung. Those with emphysema have considerable difficulty with exhaling breaths and tend to take fast shallow breaths and tend to sit in a hunched-over position in order to make exhalation easier.

Factors Affecting Pulmonary Ventilation: Airway Resistance

Airway resistance refers to resistance in the respiratory tract to airflow.

Key Points

Airway resistance is a concept in respiratory physiology that describes the resistance of the respiratory tract to airflow during inspiration and expiration.

Airway resistance can be indirectly measured with body plethysmography.

A two-fold change in the radius/diameter of an airway causes a 16-fold change in air resistance in the opposite direction (an inverse relationship).

Diseases affecting the respiratory tract can increase airway resistance.

Laminar flow is orderly and has low resistance while turbulent flow is disorganized and has high resistance.

Key Terms

Airway resistance: Airway Resistance is a concept in respiratory physiology that describes the resistance of the respiratory tract to airflow during inspiration and expiration.
plethysmography: The diagnostic use of a plethysmograph to measure changes in volume within an organ or whole body.
Turbulent flow: Air with disorganized layers that have higher resistance. It is often located in areas where the airways branch or diverge.

EXAMPLES

Airway resistance can change over time, especially during an asthma attack when the airways constrict causing an increase in airway resistance.

Airway Resistance

Airway resistance is the resistance to the flow of air caused by friction with the airways, which includes the conducting zone for air, such as the trachea, bronchi, and bronchioles. The main determinants of airway resistance are the size of the airway and the properties of the flow of air itself.

Size of the Airway

Resistance in an airway is inversely proportional to the radius of the airway. However, the ratio for this relationship is not 1:1. Below is the equation for calculating airway resistance (R).

$R = \frac{8 (Length \times Gas Viscosity)}{(π r^{4})}$

The most important part of this formula is the radius of the airway (r). A common example is that if one were to double the diameter of an airway (thus doubling the radius as well) the resistance of the airway would drop by a factor of 16. This mathematical property between radius and resistance is consistent for all tubes and is often applied to the blood vessels in the cardiovascular system.

The radius of the airways of the conducting zone becomes smaller as air goes deeper into the lungs. Therefore the resistance to air in the bronchi is greater than the resistance to air in the trachea. The number of airways also plays a large role in the resistance to air, with more airways reducing resistance because there are more paths for the air to flow into. Therefore, despite the fact that the terminal bronchioles are the smallest airway in terms of radius, their high number compared to the larger airways means that the bronchi actually have greater resistance because there are fewer of them compared to the terminal bronchioles. Another important fact is that airway resistance is inversely related to lung volumes because the airways expand a bit as they inflate, so the airways in a fully inflated lung will have lower resistance than a lung after exhalation.

Airway resistance can be indirectly measured with body plethysmography, which is an instrument used for measuring changes in volume within a structure, such as the airways. The resistance of the airways is an important indicator of lung health and function and can be used to diagnose lung diseases.

The size of the airways, and thus the resistance can change based on the health and conditions of the lungs. Most lung diseases increase airway resistance in many different ways. For example, in asthma attacks the bronchioles spasm and constrict, which increases resistance. Emphysema also increases airway resistance because the lung tissue becomes too pliable and it the airways become more difficult to hold open by the flow of air.

Flow of Air

The air that flows through the lungs varies considerably in the properties of the flow of air. The airflow can either be turbulent, transitional, or laminar based on the airway. Laminar flow involves an orderly and concentric distribution of layers of air particles and tends to occur in smaller airways, and has lower resistance. Turbulent flow is the disorganized distribution of the layers of air and tends to occur in larger airways and places where the airways branch, and has a higher resistance. Transitional flow occurs in places that branch within smaller airways, in which the airflow becomes in between laminar and turbulent flow and has moderate resistance. The relationship between resistance and type of airflow is difficult to measure and apply, but some mathematical models (such as Reynold’s number) can provide a rough estimate.

Laminar and Turbulent Flow: Laminar flow (a) has orderly layers and low resistance. Turbulent flow (b) has disorganized layers and high resistance.

ByRx Harun

Mechanics of Breathing – Anatomy, Types, Structure

Mechanics of Breathing/The processes of inspiration (breathing in) and expiration (breathing out) are vital for providing oxygen to tissues and removing carbon dioxide from the body. Inspiration occurs via active contraction of muscles – such as the diaphragm – whereas expiration tends to be passive unless it is forced.

The Lungs and Breathing

The space between the outer surface of the lungs and the inner thoracic wall is known as the pleural space. This is usually filled with pleural fluid, forming a seal that holds the lungs against the thoracic wall by the force of surface tension. This seal ensures that when the thoracic cavity expands or reduces, the lungs undergo expansion or reduction in size accordingly.

During breathing, the contraction and relaxation of muscles act to change the volume of the thoracic cavity. As the thoracic cavity and lungs move together, this changes the volume of the lungs, in turn changing the pressure inside the lungs.

Boyle’s law states that the volume of gas is inversely proportional to pressure (when the temperature is constant). Therefore:

When the volume of the thoracic cavity increases – the volume of the lungs increases and the pressure within the lungs decreases.
When the volume of the thoracic cavity decreases – the volume of the lungs decreases and the pressure within the lungs increases.

Process of Inspiration

Inspiration is the phase of ventilation in which air enters the lungs. It is initiated by the contraction of the inspiratory muscles:

Diaphragm – flattens, extending the superior/inferior dimension of the thoracic cavity.
External intercostal muscles – elevates the ribs and sternum, extending the anterior/posterior dimension of the thoracic cavity.

The action of the inspiratory muscles results in an increase in the volume of the thoracic cavity. As the lungs are held against the inner thoracic wall by the pleural seal, they also undergo an increase in volume.

As per Boyle’s law, an increase in lung volume results in a decrease in the pressure within the lungs. The pressure of the environment external to the lungs is now greater than the environment within the lungs, meaning air moves into the lungs down the pressure gradient.

Process of Passive Expiration

Expiration is the phase of ventilation in which air is expelled from the lungs. It is initiated by the relaxation of the inspiratory muscles:

Diaphragm – relaxes to return to its resting position, reducing the superior/inferior dimension of the thoracic cavity.
External intercostal muscles – relax to depress the ribs and sternum, reducing the anterior/posterior dimension of the thoracic cavity.

The relaxation of the inspiratory muscles results in a decrease in the volume of the thoracic cavity. The elastic recoil of the previously expanded lung tissue allows them to return to their original size.

As per Boyle’s law, a decrease in lung volume results in an increase in the pressure within the lungs. The pressure inside the lungs is now greater than in the external environment, meaning air moves out of the lungs down the pressure gradient.

Forced Breathing

Forced breathing is an active mode of breathing that utilizes additional muscles to rapidly expand and contract the thoracic cavity volume. It most commonly occurs during exercise.

Active Inspiration

Active inspiration involves the contraction of the accessory muscles of breathing (in addition to those of quiet inspiration, the diaphragm, and external intercostals). All of these muscles act to increase the volume of the thoracic cavity:

Scalenes – elevates the upper ribs.
Sternocleidomastoid – elevates the sternum.
Pectoralis major and minor – pulls ribs outwards.
Serratus anterior – elevates the ribs (when the scapulae are fixed).
Latissimus dorsi – elevates the lower ribs.

Active Expiration

Active expiration utilizes the contraction of several thoracic and abdominal muscles. These muscles act to decrease the volume of the thoracic cavity:

Anterolateral abdominal wall – increases the intra-abdominal pressure, pushing the diaphragm further upwards into the thoracic cavity.
Internal intercostal – depress the ribs.
Innermost intercostal – depress the ribs.

Pressure Changes During Pulmonary Ventilation

Ventilation is the rate at which gas enters or leaves the lung.

Key Points

Ventilation is the rate at which gas enters or leaves the lung.

The three types of ventilation are minute ventilation, alveolar ventilation, and dead space ventilation.

The alveolar ventilation rate changes according to the frequency of breath, tidal volume, and amount of dead space.

PA refers to the alveolar partial pressure of a gas, while Pa refers to the partial pressure of that gas in arterial blood.

Gas exchange occurs from passive diffusion because PAO2 is greater than PaO2 in deoxygenated blood.

Key Terms

ventilation: The bodily process of breathing, the inhalation of air to provide oxygen, and the exhalation of spent air to remove carbon dioxide.
partial pressure: The pressure exerted by a gas, either in air or dissolved, that indicates the concentration of that gas.

The Types of Ventilation Rates

In respiratory physiology, the ventilation rate is the rate at which gas enters or leaves the lung. Ventilation is generally expressed as volume of air times a respiratory rate.

The volume of air can refer to tidal volume (the amount inhaled in an average breath) or something more specific, such as the volume of dead space in the airways. The three main types of ventilation rates used in respiratory physiology are:

Minute ventilation (VE): The amount of air entering the lungs per minute. It can be defined as $VE = Tidal Volume \times Breaths Per Minute$
Alveolar ventilation (VA): The amount of gas per unit of time that reaches the alveoli and becomes involved in gas exchange. It is defined as $VA = (Tidal Volume - Dead Space Volume) \times Respiratory Rate$
Dead space ventilation (VD): The amount of air per unit of time that is not involved in gas exchange, such as the air that remains in the conducting zones. It is defined as $VD = Dead Space Volume \times Respiratory Rate$ .

Additionally, minute ventilation can be described as the sum of alveolar and dead space ventilation, provided that the respiratory rate used to derive them is in terms of breaths per minute.

The three types of ventilation are mathematically linked to one another, so changes in one ventilation rate can cause the change of the other. This is most apparent in changes of the dead space volume. Breathing through a snorkeling tube and having a pulmonary embolism both increase the amount of dead space volume (through anatomical versus alveolar dead space respectively), which will reduce alveolar ventilation.

Alveolar ventilation is the most important type of ventilation for measuring how much oxygen actually gets into the body, which can initiate negative feedback mechanisms to try and increase alveolar ventilation despite the increase in dead space. In particular, the body will generally attempt to combat increased dead space by raising the frequency of breaths to try and maintain sufficient levels of alveolar ventilation.

Partial Pressure of Gasses

This is a diagram of gas exchange in the lungs. It shows the aveoli removing carbon dioxide from the blood and then adding oxygen to the blood.

Gaseous Exchange in the Lungs: Diagram of gas exchange in the lungs.

When gasses dissolve in the bloodstream during ventilation, they are generally described by the partial pressure of the gasses. Partial pressure more specifically refers to the relative concentration of those gasses by the pressure they exert in a dissolved state.

In respiratory physiology, PAO₂ and PACO_2,refer to the partial pressures of oxygen and carbon dioxide in the alveoli.

PaO₂ and PaCO₂ refer to the partial pressures of oxygen and carbon dioxide within arterial blood. Differences in partial pressures of gasses between the alveolar air and the bloodstream are the reason that gas exchange occurs by passive diffusion.

Under normal conditions, PAO₂ is about 100 mmHg, while PaO₂ is 80–100 mmHg in systemic arteries, but 40–50 mmHg in the deoxygenated blood of the pulmonary artery going to the lungs.

Recall that gasses travel from areas of high pressure to areas of low pressure, so the greater pressure of oxygen in the alveoli compared to that of the deoxygenated blood explains why oxygen can passively diffuse into the bloodstream during gas exchange.

Conversely, PACO₂ is 35 mmHg, while PaCO₂ is about 40–45 mmHG in systemic arteries and 50 mmHg in the pulmonary artery. The partial pressure, and thus the concentration of carbon dioxide, is greater in the capillaries of the alveoli compared to the alveolar air, so carbon dioxide will passively diffuse from the bloodstream into the alveoli during gas exchange.

Additionally, because PaCO₂ is an indicator of the concentration of carbon dioxide in arterial blood, it can be used to measure blood pH and identify cases of respiratory acidosis and alkalosis.

Inspiration

Inhalation is the flow of air into an organism that is due to a pressure difference between the atmosphere and alveolus.

Key Points

In humans, inspiration is the flow of air into an organism from the external environment, through the airways, and into the alveoli.

Inhalation begins with the onset of a contraction of the diaphragm, which results in expansion of the thoracic and pleural cavities and a decrease in pressure (also called an increase in negative pressure).

There are many accessory muscles involved in inhalation—such as external intercostal muscles, scalene muscles, the sternocleidomastoid muscle, and the trapezius muscle.

Breathing only with the accessory muscles instead of the diaphragm is considered inefficient, and provides much less air during inhalation.

The negative pressure in the pleural cavity is enough to hold the lungs open in spite of the inherent elasticity of the tissue. The thoracic cavity increases in volume causing a drop in the pressure (a partial vacuum) within the lung itself.

As long as the pressure within the alveoli is lower than atmospheric pressure, air will continue to move inwardly, but as soon as the pressure is stabilized air movement stops.

Key Terms

inspiration: The drawing of air into the lungs, accomplished in mammals by elevation of the chest walls and flattening of the diaphragm.
accessory muscles: Muscles that help expand small parts of the thoracic cavity, either working in addition to the diaphragm or substituting for it if the diaphragm becomes injured.
intrapleural pressure: The pressure inside the pleural cavity, which is negative compared to outside air and becomes even more negative during inspiration.

Inspiration refers to inhalation—it is the flow of the respiratory current into an organism. In humans, it is the movement of ambient air through the airways and into the alveoli of the lungs.

The Process of Inspiration

Inspiration begins with the contraction of the diaphragm, which results in the expansion of the thoracic cavity and the pleural cavity. The pleural cavity normally has a lower pressure compared to ambient air (–3 mmHg normally and typically –6 mmHg during inspiration), so when it expands, the pressure inside the lungs drops.

Pressure and volume are inversely related to each other, so the drop in pressure inside the lung increases the volume of air inside the lung by drawing outside air into the lung. As the volume of air inside the lung increases, the lung pushes back against the expanded pleural cavity as a result of the drop in intrapleural pressure (pressure inside the pleural cavity).

The force of the intrapleural pressure is even enough to hold the lungs open during inpiration despite the natural elastic recoil of the lung. The alveolar sacs also expand as a result of being filled with air during inspiration, which contributes to the expansion inside the lung.

Eventually, the pressure inside the lung becomes less negative as the volume inside the lung increases and, when pressure and volume stabilize, air movement stops, inspiration ends, and expiration (exhalation) will begin. Deeper breaths have higher tidal volumes and require a greater drop in intrapleural pressure compared to shallower breaths.

This is a schematic drawing of the entire respiratory tract, include inner details such as the aveoli. It illustrates the respiratory tract as a complex, connected system where resistance in any part of it can cause problems.

Respiratory System: Resistance in any part of the respiratory tract can cause problems.

Accessory Muscles of Inspiration

The diaphragm is the primary muscle involved in breathing, however, several other muscles play a role in certain circumstances. These muscles are referred to as accessory muscles of inhalation.

External intercostal muscles: Muscles located between the ribs that help the thoracic cavity and pleural cavity expand during quiet and forced inspiration.
Scalene muscles: Muscles in the neck that lift the upper ribs (and the thoracic cavity around the upper ribs) to help with breathing. They provide a mechanism for inspiration when the diaphragm is injured and can’t contract normally.
Sternocleidomastoid muscle: Muscles that connect the sternum to the neck and allow for rotation and turning of the head. They can lift the upper ribs as the scalene muscles can.
Trapezius muscle: Muscles in the shoulders that retract the scapula and expand the upper part of the thoracic cavity.

The accessory muscles assist breathing by expanding the thoracic cavity in a similar way to the diaphragm. However, they expand a much smaller part of the thoracic cavity compared to diaphragm. Therefore they should not be used as the primary mechanism of inhalation, because they take in much less air compared to the diaphragm resulting in a much lower tidal volume.

For example, singers need a lot of air to support the powerful voice production needed for singing. A common problem in novice singers is breathing with the accessory muscles of the neck, shoulder, and ribs instead of the diaphragm, which gives them a much smaller air supply than what is needed to sing properly.

Expiration

Exhalation (or expiration) is the flow of the respiratory current out of the organism.

Key Points

In humans, exhalation is the movement of air out of the bronchial tubes, through the airways, to the external environment during breathing.

Exhalation is a passive process because of the elastic properties of the lungs.

During forced exhalation, internal intercostal muscles lower the rib cage and decrease the thoracic volume while the abdominal muscles push up on the diaphragm which causes the thoracic cavity to contract.

Relaxation of the thoracic diaphragm causes contraction of the pleural cavity which puts pressure on the lungs to expel the air.

Brain control of exhalation can be broken down into voluntary control and involuntary control.

Key Terms

Intercostal muscles: Intercostal muscles are several groups of muscles that run between the ribs, and help form and move the chest wall.
exhalation: The act or process of exhaling, or sending forth in the form of steam or vapor; evaporation.

Expiration, also called exhalation, is the flow of the respiratory current out of the organism. The purpose of exhalation is to remove metabolic waste, primarily carbon dioxide from the body from gas exchange. The pathway for exhalation is the movement of air out of the conducting zone, to the external environment during breathing.

Respiratory System: As the diaphragm relaxes, the pleural cavity contracts, which exerts pressure on the lungs, which reduces the volume of the lungs as air is passively pushed out of the lungs.

The Process of Expiration

Expiration is typically a passive process that happens from the relaxation of the diaphragm muscle (that contracted during inspiration). The primary reason that expiration is passive is due to the elastic recoil of the lungs. The elasticity of the lungs is due to molecules called elastins in the extracellular matrix of lung tissues and is maintained by surfactant, a chemical that prevents the elasticity of the lungs from becoming too great by reducing surface tension from water. Without surfactant the lungs would collapse at the end of expiration, making it much more difficult to inhale again. Because the lung is elastic, it will automatically return to its smaller size as air leaves the lung.

Exhalation begins when inhalation ends. Just as the pleural cavity’s increased negative pressure leads to air uptake during inhalation, the pleural cavity will contract during the exhalation (due to relaxation of the diaphragm), which exerts pressure on the lungs and causes the pressure inside the cavity to be less negative. An increase in pressure leads to a decrease in volume inside the lung, and the air is pushed out into the airways as the lung returns to its smaller size. The pleural cavity is so important to breathing because its pressure changes the volume of the lungs, and it provides a frictionless space for the lung to expand and contract during breathing.

While expiration is generally a passive process, it can also be an active and forced process. There are two groups of muscles that are involved in forced exhalation.

Internal Intercostal Muscles: Muscles of the ribcage that help lower the ribcage, which pushes down on the thoracic cavity, causing forced exhalation. Note that these are not the same as the external intercostal muscles involved in inspiration.
Abdominal Muscles: Any number of muscles in the abdomen that exert pressure on the diaphragm from below to expand it, which in turn contracts the thoracic cavity, causing forced exhalation.

This happens due to the elastic properties of the lungs, as well as the internal intercostal muscles that lower the rib cage and decrease thoracic volume. As the thoracic diaphragm relaxes during exhalation it causes the tissue it has depressed to rise superiorly and put pressure on the lungs to expel the air.

Control of Expiration

Expiration can be either voluntary or involuntary in order to serve different purposes for the body. These two types of expiration are controlled by different centers within the body.

Voluntary expiration is actively controlled. It is generally defined by holding air in the lungs and releasing it at a fixed rate, which enables control over when and how much air to exhale. It is required for voice production during speech or singing, which requires very specific control over air, or even simpler activities, like blowing out a candle on one’s birthday. The nervous system component that controls voluntary expiration is the motor cortex (the ascending respiratory pathway), because it controls muscle movements, but this pathway isn’t fully understood, and there are many other possible sites in the brain that may also be involved.

Involuntary expiration is not under conscious control and is an important component of metabolic function. Examples include breathing during sleep or meditation. Changes in breathing patterns may also occur for metabolic reasons, such as through increased breathing rate in people with acidosis from negative feedback. The principal neural control center for involuntary expiration consists of the medulla oblongata and the pons, which are located in the brainstem directly beneath the brain. While these two structures are involved in neural respiratory control, they also have other metabolic regulatory functions for other body systems, such as the cardiovascular system.

Breathing Patterns

Breathing is an autonomic process that moves air in and out of the lungs.

Key Points

Breathing patterns consist of tidal volume and respiratory rate in an individual.

An average breathing pattern is 12 breaths per minute and 500 mL per breath.

Eupnea is normal breathing at rest.

There are types of altered breathing patterns that are symptoms of many diseases.

Altered breathing patterns refer to changes in respiratory rate or amount of air exchanged during breathing, and do not always indicate changes in alveolar ventilation.

The mechanism of generation of the ventilatory pattern involves the integration of neural signals by respiratory control centers in the medulla and pons.

Key Terms

altered breathing patterns: Abnormal breathing patterns that indicate typically indicate either too fast or too slow respiratory rate or too much or too little tidal volume.
tidal volume: The amount of air displaced or exchanged in a single breath.

Breathing patterns refer to the respiratory rate, which is defined as the frequency of breaths over a period of time, as well as the amount of air cycled during breathing (tidal volume). Breathing patterns are important diagnostic criteria for many diseases, including some which involve more than the respiratory system itself.

Characteristics of the Breathing Patterns

The respiratory rate is the frequency of breaths over time. The time period is variable but usually expressed in breaths per minute because that time period allows for the estimation of minute ventilation. During normal breathing, the volume of air cycled through inhalation and exhalation is called tidal volume (VT), and is the amount of air exchanged in a single breath. Tidal volume multiplied by the respiratory rate is minute ventilation, which is one of the most important indicators of lung function. In an average human adult, the average respiratory rate is 12 breaths per minute, with a tidal volume of .5 liters and minute ventilation of 6 liters per minute, though these numbers vary from person to person. Infants and children have considerably higher respiratory rates than adults.

Spirometry curve: The normal respiratory rate refers to the cyclical inhalation and exhalation of tidal volume (VT).

The respiratory rate is controlled by involuntary processes of the autonomic nervous system. In particular, the respiratory centers of the medulla and the pons control the overall respiratory rate based on a variety of chemical stimuli from within the body. The hypothalamus can also influence the respiratory rate during emotional and stress responses.

Assessment points

System	Effect	Assessment by Hx	PE	Test
HEENT	Difficult airway Intracranial bleed ROP	Assoc with common difficult airway syndromes, Hx in NICU Intracranial hemorrhage	Morphology of airway esp. jaw, evaluation of breathing mechanics (stridor) Fontanel Ophthalmology exam	Not typically required unless obvious abn, x-ray, head and neck CT, MRI Cranial USOptho exam under anesthesia
RESP	RDS/ BPD Resp failure Pneumonia Pneumothorax	Risk factors, use of supplemental O₂ Hx/frequency of apnea Intubated and/or ventilated Fever curves, increasing O2 requirement	Resp rate (>60 abn) Intercostal retractions Grunting Rales or rhonchi Absent/decreased breath sounds, SubQ emphysema	CXR Blood gases
CVS	Hypovolemia Hypervolemia PDA CHF	Vital signs chart Wt chart UO Inotropes infusing	HR (120–160), murmur Bounding pulses (PDA), BP normal Liver enlarged (CHF), edema: feet or eyelids	ECG, ECHO CXR
HEME	Anemia Sepsis Coagulopathy	Precipitous delivery, placental bleeding Perinatal exposures Birth asphyxia (low factors) Vitamin K given Bleeding	Tachycardia, hypotension, poor growth rate A recent change in physiologic status-activity, resp function, CV stability, peripheral perfusion Purpura, occult bleeding	CBC, retic count WBC and differential Plt count PT, INR, fibrinogen
METAB	↑ or ↓ glucose, ↑ Temp Hypocalcemia, hypomagnesemia Hyperbilirubinemia Na⁺ or K⁺ disturbance	Review charts and reports	Twitching Seizures Hypotension	Serum electrolytes, Ca²⁺, Mg²⁺ Blood glucose, indirect bilirubin levels

Key Reference: Henderson-Smart DJ, Steer P. Postoperative caffeine for preventing apnea in preterm infants. Cochrane Database Syst Rev. 2000; CD000048.

Normal and Altered Breathing Patterns

Eupnea is the term for the normal respiratory rate of an individual at rest. Several other terms describe abnormal breathing patterns that are indicative of symptoms of many diseases, many of which aren’t mainly respiratory diseases. Some of the more common terms for altered breathing patterns include:

Dyspnea: commonly called shortness of breath. It describes dramatically decreased tidal volume and sometimes increased respiratory rate, leading to a sensation of breathlessness. It is a common symptom of anxiety attacks, pulmonary embolisms, heart attacks, and emphysema, among other things.
Hypernea: refers to increased volume of air cycled to meet the body’s metabolic needs, which may or may not involve a change in frequency of breathing. It is a symptom of exercise and adjustment to high altitude, which are generally not problematic but can also be seen in those with anemia or septic shock, which is problematic.
Tachypnea: describes increased respiratory rate. Often a symptom of carbon monoxide poisoning or pneumonia.
Bradypnea: describes decreased respiratory rate. Often a symptom of hypertension, heart arrhythmias, or slow metabolic rate from hypothyroidism.
Apnea: Transient stopped breathing that begins again soon afterward. It is the main symptom of sleep apnea, in which breathing temporarily stops during sleep.

These terms all describe an altered breathing pattern through increased or decreased (or stopped) tidal volume or respiratory rate. It is important to distinguish these terms from hyperventilation and hypoventilation, which refer to abnormalities in alveolar gas exchange (and thus blood pH) instead of an altered breathing pattern, but they may be associated with an altered breathing pattern. For example, dyspnea or tachypnea often occurs together with hyperventilation during anxiety attacks, though not always.

References

ByRx Harun

Ventilation – Anatomy, Types, Functions, Exercise

Ventilation/Breathing (or ventilation) is the process of moving air out and in the lungs to facilitate gas exchange with the internal environment, mostly to flush out carbon dioxide and bring in oxygen. All aerobic creatures need oxygen for cellular respiration, which uses the oxygen to break down foods for energy and produces carbon dioxide as a waste product. Breathing, or “external respiration”, brings air into the lungs where gas exchange takes place in the alveoli through diffusion. The body’s circulatory system transports these gases to and from the cells, where “cellular respiration” takes place.^[rx]^[rx]

Inhaled air is by volume 78% nitrogen, 20.95% oxygen and small amounts of other gases including argon, carbon dioxide, neon, helium, and hydrogen.^[rx]

The gas exhaled is 4% to 5% by volume of carbon dioxide, about a 100 fold increase over the inhaled amount. The volume of oxygen is reduced by a small amount, 4% to 5%, compared to the oxygen inhaled. The typical composition is:^[17]

5.0–6.3% water vapor
79% nitrogen ^[rx]
13.6–16.0% oxygen
4.0–5.3% carbon dioxide
1% argon
parts per million (ppm) of hydrogen, from the metabolic activity of microorganisms in the large intestine.^[19]
ppm of carbon monoxide from the degradation of heme proteins.
1 ppm of ammonia.
Trace many hundreds of volatile organic compounds especially isoprene and acetone. The presence of certain organic compounds indicates disease.^[rx]^[rx]

In addition to air, underwater divers practicing technical diving may breathe oxygen-rich, oxygen-depleted or helium-rich breathing gas mixtures. Oxygen and analgesic gases are sometimes given to patients under medical care. The atmosphere in space suits is pure oxygen. However, this is kept at around 20% of Earthbound atmospheric pressure to regulate the rate of inspiration.

Pressure Changes During Pulmonary Ventilation

Ventilation is the rate at which gas enters or leaves the lung.

Key Points

Ventilation is the rate at which gas enters or leaves the lung.

The three types of ventilation are minute ventilation, alveolar ventilation, and dead space ventilation.

The alveolar ventilation rate changes according to the frequency of breath, tidal volume, and amount of dead space.

PA refers to the alveolar partial pressure of a gas, while Pa refers to the partial pressure of that gas in arterial blood.

Gas exchange occurs from passive diffusion because PAO2 is greater than PaO2 in deoxygenated blood.

Key Terms

ventilation: The bodily process of breathing, the inhalation of air to provide oxygen, and the exhalation of spent air to remove carbon dioxide.
partial pressure: The pressure exerted by a gas, either in air or dissolved, that indicates the concentration of that gas.

The Types of Ventilation Rates

In respiratory physiology, the ventilation rate is the rate at which gas enters or leaves the lung. Ventilation is generally expressed as volume of air times a respiratory rate.

The volume of air can refer to tidal volume (the amount inhaled in an average breath) or something more specific, such as the volume of dead space in the airways. The three main types of ventilation rates used in respiratory physiology are:

Minute ventilation (VE): The amount of air entering the lungs per minute. It can be defined as $VE = Tidal Volume \times Breaths Per Minute$
Alveolar ventilation (VA): The amount of gas per unit of time that reaches the alveoli and becomes involved in gas exchange. It is defined as $VA = (Tidal Volume - Dead Space Volume) \times Respiratory Rate$
Dead space ventilation (VD): The amount of air per unit of time that is not involved in gas exchange, such as the air that remains in the conducting zones. It is defined as $VD = Dead Space Volume \times Respiratory Rate$ .

Additionally, minute ventilation can be described as the sum of alveolar and dead space ventilation, provided that the respiratory rate used to derive them is in terms of breaths per minute.

The three types of ventilation are mathematically linked to one another, so changes in one ventilation rate can cause the change of the other. This is most apparent in changes of the dead space volume. Breathing through a snorkeling tube and having a pulmonary embolism both increase the amount of dead space volume (through anatomical versus alveolar dead space respectively), which will reduce alveolar ventilation.

Alveolar ventilation is the most important type of ventilation for measuring how much oxygen actually gets into the body, which can initiate negative feedback mechanisms to try and increase alveolar ventilation despite the increase in dead space. In particular, the body will generally attempt to combat increased dead space by raising the frequency of breaths to try and maintain sufficient levels of alveolar ventilation.

Partial Pressure of Gasses

This is a diagram of gas exchange in the lungs. It shows the aveoli removing carbon dioxide from the blood and then adding oxygen to the blood.