Hypovolemic and distributive shock

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Hypovolemic and Distributive Shock

Introduction

Shock is a life-threatening state of circulatory failure in which tissue perfusion becomes inadequate to meet cellular metabolic demands. As a result, cells shift to anaerobic metabolism, producing lactic acidosis and progressive organ dysfunction. Among the major categories of shock, hypovolemic shock and distributive shock differ fundamentally in their underlying mechanisms. Hypovolemic shock arises from a significant reduction in circulating intravascular volume, leading to decreased venous return and reduced cardiac output. Distributive shock, in contrast, is characterized by profound peripheral vasodilation and loss of vascular tone, resulting in lowered systemic vascular resistance despite normal or increased cardiac output. Understanding these distinctions is essential because each type requires a different therapeutic strategy.

Hypovolemic Shock

Hypovolemic shock develops when intravascular volume falls to the point at which the heart can no longer maintain adequate stroke volume. With reduced preload, cardiac output declines, leading to systemic hypotension and impaired tissue perfusion. Hemorrhage is the most common cause and includes traumatic bleeding, gastrointestinal bleeding, ruptured aneurysms, or obstetric hemorrhage. Non-hemorrhagic causes include severe dehydration due to vomiting or diarrhea, large burns that cause plasma loss, excessive sweating, third-spacing of fluids in pancreatitis or peritonitis, and overuse of diuretics.

The fall in circulating volume triggers compensatory mechanisms involving the sympathetic nervous system and the renin–angiotensin–aldosterone system. Catecholamine release increases heart rate and peripheral vasoconstriction, while aldosterone and antidiuretic hormone promote salt and water retention. These mechanisms temporarily maintain perfusion but are insufficient if blood loss continues. As shock progresses, prolonged hypoperfusion leads to metabolic acidosis, endothelial damage, and eventual multiorgan failure.

Clinically, hypovolemic shock presents with tachycardia, hypotension, cool and clammy skin due to vasoconstriction, delayed capillary refill, oliguria, and often altered mental status in advanced stages. Laboratory findings may show hemoconcentration in dehydration, anemia in hemorrhage, elevated lactate, and metabolic acidosis. Diagnosis is largely clinical but may be supported by ultrasound showing a collapsed inferior vena cava or small cardiac chambers. Treatment centers on rapid restoration of intravascular volume using isotonic crystalloids, blood transfusions when hemorrhage is present, and prompt identification and control of the underlying cause.

Distributive Shock

Distributive shock results from an abnormal distribution of blood flow due to marked vasodilation and reduced systemic vascular resistance. A characteristic feature is that cardiac output may initially be normal or even elevated, yet perfusion remains inadequate because of excessive vascular capacity and impaired microcirculatory regulation. The most common form is septic shock, which arises from infection and the associated systemic inflammatory response. In sepsis, cytokines, nitric oxide, and other mediators induce vasodilation, capillary leakage, and mitochondrial dysfunction, together producing “cytopathic hypoxia.”

Other important types include anaphylactic shock, caused by IgE-mediated mast cell degranulation with release of histamine, leukotrienes, and prostaglandins, and neurogenic shock, which occurs after acute spinal cord injury when sympathetic outflow is lost, resulting in vasodilation and often bradycardia. Endocrine causes, such as adrenal insufficiency, may also produce distributive physiology.

Clinically, septic shock may initially present with warm, flushed skin due to vasodilation (“warm shock”), bounding pulses, tachycardia, fever, or hypothermia, followed later by cold extremities as perfusion deteriorates.

Anaphylactic shock features urticaria, airway edema, wheezing, and rapid cardiovascular collapse. Neurogenic shock is distinguished by hypotension with bradycardia and warm, dry skin. Diagnosis relies on identifying the underlying trigger and recognizing the hemodynamic pattern of low systemic vascular resistance. Elevated lactate levels reflect impaired tissue oxygenation.

Management focuses on restoring vascular tone and improving perfusion. Fluid resuscitation is essential but generally less effective alone than in hypovolemic shock because vasodilation persists. Norepinephrine is the first-line vasopressor for septic shock. Early broad-spectrum antibiotics and source control are critical. Anaphylactic shock requires immediate intramuscular epinephrine, followed by airway support and antihistamines. Neurogenic shock is managed with fluids and vasopressors, and bradycardia may require atropine.

Summary

Hypovolemic and distributive shock are two distinct forms of circulatory failure that differ in both cause and hemodynamic profile. Hypovolemic shock results from inadequate intravascular volume and leads to reduced preload and cardiac output, whereas distributive shock stems from profound vasodilation and inappropriate blood distribution despite preserved or increased cardiac output. Clinical recognition depends on understanding these mechanisms and the characteristic findings associated with each type. Early diagnosis and appropriate treatment—restoring volume in hypovolemic shock and restoring vascular tone while treating the underlying cause in distributive shock—are essential to prevent irreversible organ failure.

Sources

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Guyton and Hall Textbook of Medical Physiology, 14th edition.

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Pathophysiology: The Biologic Basis for Disease in Adults and Children, 8th edition.

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“Shock: Hypovolemic, Septic, Anaphylactic.” Accessed 2024.

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“Classification and Pathophysiology of Shock.” Accessed 2024.