Circulatory Shock – Anatomy, Types, Mechanism, Functions

Types of Shock

Circulatory shock is a life-threatening medical condition that occurs due to inadequate substrate for aerobic cellular respiration.

Circulatory shock, commonly known simply as shock, is a life-threatening medical condition that occurs due to inadequate substrates for aerobic cellular respiration. In the early stages, this is generally caused by an inadequate tissue level of oxygen. The typical signs of shock are low blood pressure, a rapid heartbeat, and signs of poor end-organ perfusion or decompensation (such as low urine output, confusion, or loss of consciousness). In some people with circulatory shock, blood pressure remains stable.

The presentation of shock is variable with some people having only minimal symptoms such as confusion and weakness. While the general signs for all types of shock are low blood pressure, decreased urine output, and confusion, these may not always be present. Specific subtypes of shock may have additional symptoms.

Hypovolemic Shock

Hypovolemic shock, the most common type, is caused by insufficient circulating volume, typically from hemorrhage although severe vomiting and diarrhea are also potential causes.

Hypovolemic shock is graded on a four-point scale depending on the severity of symptoms and level of blood loss. Typical symptoms include a rapid, weak pulse due to decreased blood flow combined with tachycardia, cool, clammy skin, and rapid and shallow breathing.

Cardiogenic Shock

Cardiogenic shock is caused by a failure of the heart to pump correctly, either due to damage to the heart muscle through myocardial infarction or through cardiac valve problems, congestive heart failure, or dysrhythmia.

Obstructive Shock

Obstructive shock is caused by an obstruction of blood flow outside of the heart. This typically occurs due to a reduction in venous return, but may also be caused by blockage of the aorta.

Distributive Shock

Distributive shock is caused by an abnormal distribution of blood to tissues and organs and includes septic, anaphylactic, and neurogenic causes.

Septic

Septic shock is the most common cause of distributive shock and is caused by an overwhelming systemic infection that cannot be cleared by the immune system, resulting in vasodilation and hypotension.

Anaphylactic

Anaphylactic shock is caused by a severe reaction to an allergen, leading to the release of histamine that causes widespread vasodilation and hypotension.

Neurogenic

Neurogenic shock arises due to damage to the central nervous system, which impairs cardiac function by reducing heart rate and loosening the blood vessel tone, resulting in severe hypotension.

or

1. Distributive Shock

Characterized by peripheral vasodilatation.

Types of distributive shock include:

Septic Shock

Sepsis is defined as life-threatening organ dysfunction resulting from dysregulated host response to infection.[2] Septic shock is a subset of sepsis with severe circulatory, cellular, and metabolic abnormalities resulting in tissue hypoperfusion manifested as hypotension which requires vasopressor therapy and elevated lactate levels (more than 2 mmol/L)

The most common pathogens associated with sepsis and septic shock in the United States are gram-positive bacteria, including streptococcal pneumonia and Enterococcus.

Systemic Inflammatory Response Syndrome

Systemic inflammatory response syndrome (SIRS) is a clinical syndrome of the vigorous inflammatory response caused by either infectious or noninfectious causes. Infectious causes include pathogens such as gram-positive (most common) and gram-negative bacteria, fungi, viral infections (e.g., respiratory viruses), parasitic (e.g., malaria), rickettsial infections. Noninfectious causes of SIRS include but are not limited to pancreatitis, burns, fat embolism, air embolism, and amniotic fluid embolism

Anaphylactic Shock

Anaphylactic shock is a clinical syndrome of severe hypersensitivity reaction mediated by immunoglobulin E (Ig-E), resulting in cardiovascular collapse and respiratory distress due to bronchospasm. The immediate hypersensitivity reactions can occur within seconds to minutes after the presentation of the inciting antigen. Common allergens include drugs (e.g., antibiotics, NSAIDs), food, insect stings, and latex.

Neurogenic Shock

Neurogenic shock can occur in the setting of trauma to the spinal cord or the brain. The underlying mechanism is the disruption of the autonomic pathway resulting in decreased vascular resistance and changes in vagal tone.

Endocrine Shock

Due to underlying endocrine etiologies such as adrenal failure (Addisonian crisis) and myxedema.

2. Hypovolemic Shock

Hypovolemic shock is characterized by decreased intravascular volume and increased systemic venous assistance (compensatory the mechanism to maintain perfusion in the early stages of shock). In the later stages of shock due to progressive volume depletion, cardiac output also decreases and manifest as hypotension. Hypovolemic shock divides into two broad subtypes: hemorrhagic and non-hemorrhagic.

Common causes of hemorrhagic hypovolemic shock include

• Gastrointestinal bleed (both upper and lower gastrointestinal bleed (e.g., variceal bleed, portal hypertensive gastropathy bleed, peptic ulcer, diverticulosis) trauma
• Vascular etiologies (e.g., aortoenteric fistula, ruptured abdominal aortic aneurysm, tumor eroding into a major blood vessel)
• Spontaneous bleeding in the setting of anticoagulant use (in the setting of supratherapeutic INR from drug interactions)

Common causes of non-hemorrhagic hypovolemic shock include:

• GI losses – the setting of vomiting, diarrhea, NG suction, or drains.
• Renal losses – medication-induced diuresis, endocrine disorders such as hypoaldosteronism.
• Skin losses/insensible losses – burns, Stevens-Johnson syndrome, Toxic epidermal necrolysis, heatstroke, pyrexia.
• Third-space loss – in the setting of pancreatitis, cirrhosis, intestinal obstruction, trauma.

3. Cardiogenic Shock

Due to intracardiac causes leading to decreased cardiac output and systemic hypoperfusion. Different subtypes of etiologies contributing to cardiogenic shock include:

• Cardiomyopathies – include acute myocardial infarction affecting more than 40% of the left ventricle, acute myocardial infarction in the setting of multi-vessel coronary artery disease, right ventricular myocardial infarction, fulminant dilated cardiomyopathy, cardiac arrest (due to myocardial stunning), myocarditis.
• Arrhythmias – both tachy- and bradyarrhythmias
• Mechanical – severe aortic insufficiency, severe mitral insufficiency, rupture of papillary muscles, or chordae tendinae trauma rupture of ventricular free wall aneurysm.

4. Obstructive Shock

Mostly due to extracardiac causes leading to a decrease in the left ventricular cardiac output

• Pulmonary vascular – due to impaired blood flow from the right heart to the left heart. Examples include hemodynamically significant pulmonary embolism, severe pulmonary hypertension.[3]
• Mechanical – impaired filling of right heart or due to decreased venous return to the right heart due to extrinsic compression. Examples include tension pneumothorax, pericardial tamponade, restrictive cardiomyopathy, constrictive pericarditis.

Homeostatic Responses to Shock

An organism responds with numerous reactions during each of the four stages of shock in an attempt to maintain cellular homeostasis.

Circulatory shock, commonly known simply as shock, is a life-threatening medical condition that occurs due to inadequate substrate for aerobic cellular respiration. In the early stages this is generally an inadequate level of oxygen in the tissues.

There are four stages of shock. As it is a complex and continuous condition there is no sudden transition from one stage to the next.

Initial Stage

During the initial stage, the state of hypoperfusion causes hypoxia. Due to the lack of oxygen, the cells perform anaerobic respiration. Since oxygen is not abundant, the Kreb’s cycle is slowed, resulting in lactic acidosis (the accumulation of lactate).

Compensatory Stage

The compensatory stage is characterized by the employment of neural, hormonal, and biochemical mechanisms in the body’s attempt to reverse the lactic acidosis. The increase in acidity will initiate the Cushing reflex, generating the classic symptoms of shock. The individual will begin to hyperventilate to rid the body of carbon dioxide to raise the blood pH (lower the acidity). As a result, the baroreceptors in the arteries detect the hypotension and initiate the release of epinephrine and norepinephrine to increase heart rate and blood pressure.

Progressive Stage

Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage, in which the compensatory mechanisms begin to fail. As anaerobic metabolism continues, increasing the body’s metabolic acidosis, the arteriolar smooth muscle and precapillary sphincters relax. Blood remains in the capillaries, leading to leakage of fluid and protein into the surrounding tissues. As fluid is lost, blood concentration and viscosity increase, causing blockage of the microcirculation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion. If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the additional complication of endotoxic shock.

Refractory Stage

At the refractory stage, the vital organs have failed and shock can no longer be reversed. Brain damage and cell death are occurring, and death is imminent. Shock is irreversible at this point since a large amount of cellular ATP has been degraded into adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation, and then is transformed into uric acid. Because cells can only produce adenosine at a rate of about 2% of the cell’s total need per hour, even restoring oxygen is futile at this point because there is no adenosine to phosphorylate into ATP.

Signs and Symptoms of Shock

The clinical manifestation of shock varies depending on the type of shock and the individual, but there are some general symptoms.

The presentation of shock varies. Some people presenting only minimal symptoms, such as confusion and weakness. Typical symptoms of shock include elevated but weak heart rate, low blood pressure, and poor organ function, typically observed as low urine output, confusion or loss of consciousness.

While a fast heart rate is common, those on beta blockers and those who are athletic may have a normal or slow heart rate. This also occurs in 30% of cases of shock caused by abdominal bleeding. Specific subtypes of shock may have additional symptoms.

Hypovolemic shock results from the direct loss of effective circulating blood volume. This leads to a rapid, weak pulse due to decreased blood flow combined with tachycardia, stimulation of vasoconstriction, and cool, clammy skin. It also presents with acidosis as well as rapid, shallow breathing due to sympathetic nervous system stimulation. Hypothermia due to decreased perfusion and evaporation of sweat, and thirst and dry mouth due to fluid depletion, may also be present.