What is the pathophysiology of cardiogenic shock?

Pathophysiology of Cardiogenic Shock

Cardiogenic shock is a state of inadequate cardiac output resulting from primary myocardial dysfunction, triggering a cascade of maladaptive compensatory mechanisms that perpetuate systemic hypoperfusion, end-organ ischemia, and progressive multiorgan failure. 1

Central Hemodynamic Derangement

The fundamental pathophysiologic defect is marked reduction in cardiac output (cardiac index <2.2 L/min/m²) caused by loss of myocardial contractility, which initiates a vicious cycle of progressive deterioration. 1, 2 This occurs when:

• At least 40% of left ventricular myocardium is lost or dysfunctional, either from extensive myocardial necrosis or stunned but viable myocardium following acute myocardial infarction. 3, 1
• The failing myocardium cannot generate adequate stroke volume despite elevated filling pressures (PCWP >15 mmHg, CVP >15 mmHg). 1, 2

The Maladaptive Spiral: Key Pathophysiologic Mechanisms

Impaired Coronary Perfusion and Progressive Myocardial Dysfunction

Progressive diastolic dysfunction raises ventricular end-diastolic pressures, which directly diminishes coronary perfusion pressure, further impairing myocardial contractility and stroke volume in a self-perpetuating cycle. 1 This creates ongoing myocardial ischemia even after initial revascularization in AMI-related shock.

Compensatory Vasoconstriction and Increased Afterload

The body responds to falling cardiac output by activating neurohormonal pathways that trigger systemic vasoconstriction, manifesting as increased systemic vascular resistance (SVR) in an attempt to maintain blood pressure. 1, 2 However, this compensatory mechanism backfires—the increased afterload further impairs the already failing heart, worsening cardiac output and perpetuating the shock state. 2

Inflammatory Cascade and Systemic Vasodilation

Inflammatory mediators released during shock further impair tissue metabolism and stimulate nitric oxide production, causing paradoxical systemic vasodilation that exacerbates hypotension despite the initial vasoconstriction. 1 This inflammatory response contributes to:

• Progressive endothelial dysfunction
• Microvascular thrombosis
• Worsening tissue hypoxia

Pulmonary Dysfunction and Right Ventricular Afterload

Hypoxia and pulmonary inflammation provoke pulmonary vasoconstriction, which increases biventricular afterload and myocardial oxygen demand, further compromising cardiac performance. 1 This mechanism is particularly important in:

• Right ventricular infarction (most commonly associated with inferior AMI) 3, 1
• Biventricular shock phenotypes where both RA pressure >15 mmHg and PCWP >15 mmHg 2

Volume Overload from Renal Compensation

Renal hypoperfusion activates sodium reabsorption and the renin-angiotensin-aldosterone system, leading to additional volume overload that worsens ventricular filling pressures and pulmonary congestion. 1 Simultaneously, sympathetically mediated splanchnic vasoconstriction redistributes approximately 50% of total blood volume back into the central circulation, further exacerbating volume overload and compromising cardiac performance. 1

Phenotype-Specific Pathophysiology

Left Ventricular-Dominant Shock

• PCWP >15 mmHg with RA <15 mmHg produces prominent pulmonary congestion and pulmonary edema from backward failure. 2
• Manifests with decreased LV ejection fraction, regional wall motion abnormalities, and decreased stroke volume. 3
• Secondary mitral regurgitation frequently develops, which is a major predictor of mortality. 3

Right Ventricular-Dominant Shock

• RA pressure >15 mmHg with PCWP <15 mmHg leads to jugular venous distension but relatively clear lung fields. 2
• Echocardiography demonstrates RV dyssynergy, dilatation, paradoxical septal motion, McConnell sign, and decreased TAPSE. 3
• Critical pitfall: When right-ventricular assist devices are used, the increased volume delivered to the LV may unmask significant underlying LV dysfunction. 3

Biventricular Shock

• Both RA >15 mmHg and PCWP >15 mmHg reflecting combined left- and right-heart failure with the worst prognosis. 2

Mechanical Complications with Distinct Pathophysiology

Ventricular Septal Rupture

Creates acute left-to-right shunting with rapid hemodynamic deterioration and volume overload of the right ventricle. 1, 4

Papillary Muscle Rupture

Produces acute severe mitral regurgitation, dramatically reducing forward cardiac output while increasing left atrial and pulmonary pressures. 1, 4

Free Wall Rupture

The most serious complication following AMI, presenting along a spectrum from acute catastrophic collapse with electromechanical dissociation to insidious pericardial effusion with tamponade physiology. 3, 1

End-Organ Consequences

The inadequate cardiac output and systemic hypoperfusion result in:

• Elevated lactate (>2 mmol/L) from anaerobic metabolism 2
• Oliguria (<0.5 mL/kg/h) from renal hypoperfusion 4
• Altered mental status from cerebral hypoperfusion 4
• Cool extremities from peripheral vasoconstriction 4
• Hepatic dysfunction with elevated bilirubin (≥1.3 mg/dL independently predicting 180-day cardiac mortality) 2

Common Diagnostic Pitfall

Avoid confusing late-stage septic shock with cardiogenic shock—septic shock can develop myocardial depression, but the primary hemodynamic pattern remains distributive with decreased SVR, whereas cardiogenic shock demonstrates elevated SVR as a compensatory mechanism. 4, 2 Invasive hemodynamic monitoring with pulmonary artery catheterization provides definitive differentiation when diagnosis remains unclear. 4, 2