Vasodilatory Shock: Definition and Clinical Characteristics
Vasodilatory shock is a life-threatening circulatory failure characterized by pathological peripheral vasodilation leading to severely decreased systemic vascular resistance (SVR), resulting in profound hypotension and tissue hypoperfusion despite normal or elevated cardiac output. 1, 2
Pathophysiology
The fundamental hemodynamic abnormality in vasodilatory shock is uncontrolled vasodilation and vascular hyporesponsiveness to endogenous vasoconstrictors, causing failure of physiologic vasoregulatory mechanisms 2. This creates a state of relative hypovolemia where blood volume is insufficient to fill the pathologically dilated vascular space 1.
Key pathophysiological features include:
- Decreased systemic vascular resistance as the hallmark finding, distinguishing it from cardiogenic shock where SVR is elevated 3, 1
- Normal or elevated cardiac output in early stages, contrasting with the reduced cardiac output seen in cardiogenic and hypovolemic shock 3, 4
- Abnormal distribution of microvascular blood flow resulting in metabolic distress despite potentially adequate cardiac output 1
- Vasopressin deficiency appears to play a significant role in the pathophysiology 5
Common Etiologies
Vasodilatory shock occurs in multiple critical illness contexts:
- Septic shock - the most common cause and leading etiology of critical illness-related mortality 3, 5
- Anaphylaxis 1
- Neurogenic shock (from spinal cord injury) 6
- Severe pancreatitis 1
- Major burns 1
- Post-cardiotomy shock 7
Hemodynamic Profile
The characteristic hemodynamic pattern that distinguishes vasodilatory shock includes:
- Low systemic vascular resistance (opposite of cardiogenic shock) 3
- High or normal cardiac index (>3.3 L/min/m² or normal range) 3, 4
- Normal or decreased central venous pressure (not elevated as in cardiogenic shock) 4
- Normal or decreased pulmonary capillary wedge pressure 3
- Hypotension refractory to fluid administration as the cardinal feature 1
Clinical Presentation
Patients with vasodilatory shock typically present with:
- Profound hypotension (systolic BP <90 mmHg or MAP <65 mmHg) despite fluid resuscitation 3, 1
- Warm extremities (in contrast to the cool extremities of cardiogenic shock) 3
- Tachycardia as a compensatory mechanism 1
- Altered mental status from cerebral hypoperfusion 1
- Decreased urine output (<0.5 mL/kg/h) reflecting renal hypoperfusion 1
- Elevated serum lactate (>2 mmol/L) indicating tissue hypoxia and anaerobic metabolism 3, 1
Important Clinical Distinction
Vasodilatory shock with high cardiac output and low SVR must be distinguished from cardiogenic shock, which presents with low cardiac output, high SVR, and elevated filling pressures 3, 4. This distinction is critical because treatment strategies differ fundamentally - vasodilatory shock requires vasopressors to restore vascular tone, while cardiogenic shock may require afterload reduction 3.
Myocardial Depression Complication
Up to one-third of patients with vasodilatory shock, particularly septic shock, develop myocardial depression with reduced cardiac output despite the primary vasodilatory pathophysiology 3, 1. When this occurs, the hemodynamic profile shifts to low cardiac output with low SVR 3, requiring addition of inotropic support alongside vasopressors 3.
Refractory Vasodilatory Shock
Approximately 7% of critically ill patients develop refractory vasodilatory shock, defined as inadequate hemodynamic response to high doses of vasopressor medications, with short-term mortality exceeding 50% 2. This represents the most severe manifestation requiring aggressive multimodal vasopressor therapy 2, 8.