Cardiogenic Shock with Acute Pulmonary Edema
The correct answer is C: Increase systemic vascular resistance. This patient presents with classic cardiogenic shock (known heart disease, hypotension, tachycardia) and acute pulmonary edema (productive cough with pink frothy sputum, crackles), which is characterized by elevated systemic vascular resistance as a compensatory mechanism to maintain blood pressure despite falling cardiac output. 1
Hemodynamic Profile of Cardiogenic Shock
The clinical presentation described—hypotension, tachycardia, productive cough with pink sputum, and crackles—represents the Killip Stage III-IV classification of acute heart failure with cardiogenic shock. 2 This hemodynamic state is defined by specific physiologic derangements:
Why Systemic Vascular Resistance Increases (Answer C)
Compensatory vasoconstriction is the hallmark of cardiogenic shock. 1 When the damaged myocardium cannot generate adequate cardiac output, the body activates neurohormonal mechanisms that trigger systemic vasoconstriction to maintain perfusion pressure, thereby increasing systemic vascular resistance (SVR). 1 This creates a vicious cycle where the increased afterload further impairs the already failing heart. 1
- The European Society of Cardiology confirms that cardiogenic shock is characterized by peripheral vasoconstriction manifesting as cold, clammy skin and peripheral cyanosis. 2
- Hemodynamic measurements in cardiogenic shock consistently show elevated SVR as the body attempts to maintain blood pressure despite reduced cardiac output. 1
Why the Other Options Are Incorrect
A. Cardiac Output is DECREASED, not increased: 1
- Cardiogenic shock is defined by cardiac index <2.2 L/min/m² (normal 2.2-4.0 L/min/m²). 1
- The failing myocardium cannot generate adequate output despite elevated filling pressures. 1
- This patient's hypotension and signs of hypoperfusion (tachycardia) indicate severely reduced cardiac output. 2
B. Pulmonary Wedge Pressure is INCREASED, not decreased: 1
- Cardiogenic shock is characterized by pulmonary capillary wedge pressure (PCWP) >15 mmHg, often >20 mmHg. 2, 1
- The crackles and pink frothy sputum indicate pulmonary edema from elevated left ventricular filling pressures transmitted backward to the pulmonary circulation. 2
- The Forrester classification specifically defines cardiogenic shock as having elevated PCWP (>18 mmHg) combined with depressed cardiac index. 2
D. Central Venous Pressure is INCREASED, not decreased: 1
- Cardiogenic shock demonstrates elevated CVP (>15 mmHg) resulting from elevated right-sided filling pressures and backward failure. 1
- This is the opposite of hypovolemic shock, where CVP would be decreased. 1
- The distinction between cardiogenic and hypovolemic shock hinges on ventricular filling pressures: cardiogenic shock has elevated pressures despite poor output. 1
Clinical Correlation and Diagnostic Approach
The hemodynamic pattern in this patient follows a predictable sequence:
- Primary cardiac dysfunction → Decreased cardiac output and cardiac index <2.2 L/min/m². 1
- Compensatory mechanisms activate → Increased SVR through systemic vasoconstriction to maintain blood pressure. 1
- Backward failure develops → Elevated PCWP (>15-20 mmHg) causing pulmonary edema with pink frothy sputum and crackles. 2
- Right heart involvement → Elevated CVP from biventricular failure or isolated RV dysfunction. 1
Critical pitfall to avoid: Do not confuse late-stage septic shock with cardiogenic shock. While septic shock can develop myocardial depression, the primary hemodynamic pattern remains distributive with decreased SVR, which is the opposite of cardiogenic shock. 1
Point-of-care ultrasound would confirm decreased left ventricular contractility, dilated ventricles, and B-lines indicating pulmonary edema. 1 Invasive monitoring via pulmonary artery catheter would definitively show the classic cardiogenic shock profile: cardiac index <2.2 L/min/m², PCWP >15 mmHg, elevated SVR, and elevated CVP. 2, 1