Collapse of circulation, circulatory shock - classification and phases of shock

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Circulatory shock

Scheme of Symptoms of Circulatory Shock

Definition of Shock

Shock is a life-threatening state of circulatory failure characterized by inadequate tissue perfusion and cellular hypoxia. This could be a result from a reduction in effective circulating blood volume, insufficient cardiac output, decrease in systemic vascular resistance or obstruction of blood flow. If not promptly corrected, shock could lead to to cellular dysfunction, organ failure, and death.

Classification of Shock

Shock is broadly classified into four major types, based on the underlying pathophysiological mechanism:

1. Distributive (Vasodilatory) shock
2. Hypovolemic shock
3. Cardiogenic shock
4. Obstructive shock

1. Distributive Shock

Distributive shock is characterized by systemic vasodilation, leading to a marked reduction in systemic vascular resistance (SVR), causing hypotension despite a normal or increased cardiac output in early stages.

Types of Distributive Shock

a) Septic Shock

Septic shock results from a host response to infection, most commonly bacterial. Microbial products (for example, endotoxins) and host inflammatory mediators (TNF-α, IL-1, nitric oxide) cause widespread vasodilation, increased capillary permeability, and endothelial dysfunction, leading to hypotension and impaired tissue perfusion.

b) Anaphylactic Shock

Anaphylactic shock is caused by an IgE-mediated type I hypersensitivity reaction. Antigen exposure leads to mast cell and basophil degranulation, releasing histamine, resulting in severe vasodilation, increased vascular permeability, and bronchoconstriction.

c) Neurogenic Shock

Neurogenic shock occurs due to loss of sympathetic vascular tone, usually following spinal cord injury or brainstem injury. This leads to unopposed parasympathetic activity, causing vasodilation, hypotension, and often bradycardia, distinguishing it from other forms of shock.

2. Hypovolemic Shock

Hypovolemic shock results from a reduction in intravascular volume, leading to decreased venous return, reduced preload, diminished cardiac output, and impaired tissue perfusion. Hypovolemic shock typically develops when 15–20% or more of total blood volume is lost (approximately 750–1000 mL in adults).

Causes of Hypovolemic Shock

1. Hemorrhagic shock
2. Traumatic shock
3. Surgical shock
4. Burns (due to plasma leakage from damaged capillaries)
5. Vomiting or Diarrhea (leads to fluid loss)

3. Cardiogenic Shock

Cardiogenic shock is caused by primary failure of the heart as a pump, resulting in inadequate cardiac output despite adequate intravascular volume.

The most common cause is acute myocardial infarction involving the left ventricle, but other causes include:

• Severe heart failure
• Life-threatening arrhythmias
• Acute valvular dysfunction
• Myocarditis

Cardiogenic shock is characterized by pulmonary and visceral congestions, reduced organ perfusion, and hypotension.

4. Obstructive Shock

Obstructive shock results from mechanical obstruction to cardiac filling or outflow, leading to reduced cardiac output. Although myocardial function may be intrinsically normal, cardiac performance is impaired by the obstruction.

Causes include:

• Pulmonary embolism
• Cardiac tamponade
• Tension pneumothorax
• Severe pulmonary hypertension

Clinically, obstructive shock can resemble cardiogenic shock, with signs of systemic congestion and reduced cardiac output.

Phases of Shock

Shock progresses through three phases, reflecting worsening circulatory and cellular dysfunction.

1. Compensated (Reversible) Shock

In the compensated phase, compensatory mechanisms maintain perfusion of vital organs, particularly the brain, heart, adrenal glands, and kidneys.

Key compensatory mechanisms include:

• Activation of the sympathetic nervous system, leading to tachycardia and peripheral vasoconstriction
• Release of catecholamines (epinephrine and norepinephrine)
• Activation of the renin–angiotensin–aldosterone system (RAAS), increasing sodium and water retention
• Secretion of antidiuretic hormone (ADH), enhancing water reabsorption

Blood flow is redistributed away from less vital tissues (skin, skeletal muscle, gastrointestinal tract).

2. Decompensated (Progressive) Shock

In this phase, compensatory mechanisms become insufficient to maintain adequate tissue perfusion.

Prolonged hypoperfusion leads to:

• Cellular hypoxia and anaerobic glycolysis
• Lactic acidosis
• Failure of ATP-dependent ion pumps
• Endothelial injury and increased capillary permeability

Fluid leakage into interstitial spaces worsens hypovolemia, while acidosis and hypoxia cause loss of vasomotor tone, leading to forced vasodilation, further exacerbating hypotension. Reperfusion injury may occur due to the generation of reactive oxygen species (ROS).

Scheme of symptoms of Irreversible Shock

3. Irreversible (Refractory) Shock

The irreversible phase is characterized by cellular and organ injury, leading to multiple organ dysfunction syndrome (MODS).

At this stage, cell death and organ failure progress despite restoration of hemodynamic parameters, and shock is irreversible.

References

1. Robbins and Cotran Pathologic Basis of Disease, 10th Edition Kumar V, Abbas AK, Aster JC. Elsevier – Chapter: Hemodynamic Disorders, Thromboembolic Disease, and Shock
2. Pathophysiology of Disease: An Introduction to Clinical Medicine, 8th Edition McPhee SJ, Hammer GD. McGraw-Hill – Chapter: Shock
3. Pathophysiology of Disease: An Introduction to Clinical Medicine 7th ed.  McPhee SJ, Hammer GD. New York: McGraw-Hill Education; 2014.
4. Ganong’s Review of Medical Physiology, 26th Edition Barrett KE et al. McGraw-Hill – Circulatory regulation and shock mechanisms
5. Harrison’s Principles of Internal Medicine, 21st Edition Jameson JL et al. McGraw-Hill – Sections on shock and critical illness