What are the different types of shock that a critically ill adult with severe hypotension or septic shock may develop?

Types of Shock in Critically Ill Adults

Critically ill adults can develop four main categories of shock: distributive (including septic shock), hypovolemic, cardiogenic, and obstructive shock, with distributive/septic shock being by far the most common type encountered in intensive care settings. 1, 2, 3

Classification of Shock States

Distributive Shock

• Septic shock is the most prevalent form of distributive shock and the most common shock state overall in critically ill patients 1, 3
• Defined as persistent hypotension (MAP <65 mmHg or SBP <90 mmHg) despite adequate fluid resuscitation (at least 30 mL/kg of crystalloids) in the presence of documented or suspected infection 4, 5
• Characterized by profound vasodilation with low systemic vascular resistance, resulting in inadequate tissue perfusion despite often normal or elevated cardiac output 2
• Other causes of distributive shock include anaphylaxis, neurogenic shock, and toxic shock syndrome 4, 1

Hypovolemic Shock

• Results from acute reduction in intravascular volume due to hemorrhage, severe dehydration, or fluid losses 2, 3
• Characterized by decreased preload, low cardiac output, and compensatory vasoconstriction 1, 2
• Responds to volume replacement as the primary therapeutic intervention 3

Cardiogenic Shock

• Caused by primary myocardial dysfunction with inability to maintain adequate cardiac output 1, 2
• Results from acute myocardial infarction, severe heart failure, arrhythmias, or valvular emergencies 3
• Characterized by elevated filling pressures (CVP), low cardiac output, and elevated systemic vascular resistance 1, 2
• Requires inotropic support and cautious fluid management to avoid pulmonary edema 3

Obstructive Shock

• Caused by mechanical obstruction to cardiac output despite adequate intravascular volume and myocardial function 1, 2
• Common causes include massive pulmonary embolism, tension pneumothorax, cardiac tamponade, and severe intra-abdominal hypertension 4, 1
• Requires immediate intervention to relieve the mechanical obstruction 2, 3

Pathophysiologic Mechanisms

Common Final Pathway

• All shock states result in acute widespread reduction in effective tissue perfusion 2
• This creates an imbalance between oxygen supply and demand, leading to anaerobic metabolism and lactic acidosis 2
• Prolonged shock causes cellular and organ dysfunction, metabolic abnormalities, and if untreated, irreversible damage and death 2

Hemodynamic Distinctions

• Shock results from changes in one or combination of: intravascular volume, myocardial function, systemic vascular resistance, or distribution of blood flow 2
• Septic shock specifically involves profound vasodilation (low diastolic blood pressure ≤40 mmHg or diastolic shock index ≥3), increased capillary permeability, and often myocardial depression in 10-20% of cases 4, 6
• Hypovolemic and cardiogenic shock both present with low cardiac output but differ in filling pressures (low vs. high CVP respectively) 1, 2

Clinical Recognition

Critical Diagnostic Thresholds for Septic Shock

• SBP <90 mmHg or reduction ≥40 mmHg from baseline 5
• MAP <65 mmHg despite initial fluid resuscitation of 30 mL/kg crystalloids 4, 5
• Heart rate ≥90 bpm with signs of tissue hypoperfusion 5
• Lactate ≥1 mmol/L (some recommend >2 mmol/L cutoff for defining shock) 5
• Oliguria ≤0.5 mL/kg/h for at least 2 hours despite adequate fluids 5
• Altered mental status, confusion, or apathy 5
• Reduced capillary refill or skin mottling indicating peripheral vasoconstriction 5

Differentiating Shock Types

• Point-of-care ultrasound helps evaluate undifferentiated shock and determine fluid responsiveness 3
• Clinical history, physical examination, and hemodynamic monitoring are essential to differentiate shock states 1
• Critical pitfall: One shock state may convert to another (e.g., septic shock developing cardiogenic component), requiring continual reassessment 1

Management Implications by Shock Type

Septic/Distributive Shock

• Norepinephrine is the first-choice vasopressor, targeting MAP ≥65 mmHg 4, 7, 5
• Early vasopressor initiation (within first hour) may reduce mortality and fluid overload, particularly when diastolic BP ≤40 mmHg or diastolic shock index ≥3 7, 6, 8
• Add vasopressin 0.03 units/min when norepinephrine requirements are moderate-to-high 4, 7
• Hydrocortisone 200 mg/day when hemodynamic stability cannot be achieved with fluids and vasopressors 4, 7, 5

Hypovolemic Shock

• Aggressive fluid resuscitation is the primary intervention 3
• Vasopressors are generally not indicated until volume is restored 2

Cardiogenic Shock

• Inotropic support (dobutamine) for persistent hypoperfusion with low cardiac output 4, 7
• Norepinephrine may be required in profound cardiogenic shock with severe hypotension 3
• Cautious fluid administration to avoid worsening pulmonary edema 3

Obstructive Shock

• Immediate intervention to relieve mechanical obstruction (needle decompression for tension pneumothorax, pericardiocentesis for tamponade, thrombolysis/embolectomy for massive PE) 4, 1

Critical Pitfalls to Avoid

• Do not delay vasopressor initiation in septic shock patients with profound hypotension (diastolic BP ≤40 mmHg) while waiting for additional fluid boluses 7, 6, 8
• Do not continue aggressive fluid resuscitation when CVP is already elevated (≥13 mmHg), as this risks pulmonary edema without improving perfusion 7
• Do not use dopamine as first-line therapy in septic shock; reserve only for highly selected patients with bradycardia and low arrhythmia risk 4, 7
• Do not assume a single shock mechanism—patients may have mixed shock states requiring continual reassessment 1
• Do not abruptly stop hydrocortisone once started, as this can cause hemodynamic deterioration and rebound inflammation 5