Cardiogenic Shock
The hemodynamic profile described—increased CVP, decreased cardiac output (COP), and increased vascular resistance—is pathognomonic for cardiogenic shock (Answer B).
Hemodynamic Differentiation
The key to identifying cardiogenic shock lies in understanding the compensatory mechanisms that occur when the heart fails as a pump:
Cardiogenic Shock Hemodynamics
- Decreased cardiac output/cardiac index (<2.2 L/min/m²) occurs due to primary myocardial dysfunction and impaired contractility 1
- Increased CVP (>15 mmHg) results from elevated right-sided filling pressures and backward failure 1, 2
- Increased systemic vascular resistance (SVR) develops as a compensatory mechanism—the body attempts to maintain blood pressure despite falling cardiac output through systemic vasoconstriction 1, 2
- Elevated pulmonary capillary wedge pressure (PCWP >15 mmHg) reflects left ventricular failure and volume overload 1, 2
Why Not the Other Options?
Hypovolemic shock (Option A) presents with the opposite pattern:
- Decreased CVP (not increased) due to intravascular volume depletion 2, 3
- Increased SVR (similar to cardiogenic) as a compensatory response 2
- Decreased cardiac output, but with low filling pressures 3, 4
Distributive/Neurogenic shock (Options C & D) shows:
- Normal or decreased CVP 2
- Decreased SVR (the opposite of what's described)—this is the hallmark of distributive shock with pathological vasodilation 1, 2
- Normal or increased cardiac output in early stages 1, 5
- Warm extremities due to vasodilation (Option D mentions this correctly for neurogenic shock, but the hemodynamics don't match the question) 1
Clinical Context
The pathophysiology makes sense when you understand the failing heart:
- The damaged myocardium cannot generate adequate cardiac output 1
- Blood backs up into the venous system, elevating CVP and PCWP 1, 6
- Compensatory neurohormonal activation triggers systemic vasoconstriction to maintain perfusion pressure, increasing SVR 1
- This increased afterload further impairs the already failing heart, creating a vicious cycle 1
Critical Pitfall
Do not confuse late-stage septic shock with cardiogenic shock. Septic shock can develop myocardial depression, but the primary hemodynamic pattern remains distributive with decreased SVR 1. The question specifically states increased vascular resistance, which excludes distributive etiologies 2.
The elevated CVP in cardiogenic shock is particularly important—it predicts higher mortality and may indicate subclinical right ventricular failure 6. A CVP >12 mmHg identifies patients at significantly higher risk for in-hospital mortality (65% vs 45%, p=0.02) 6.