What is cardiogenic shock?

What is Cardiogenic Shock?

Cardiogenic shock is a life-threatening state of inadequate cardiac output and tissue hypoperfusion caused by primary cardiac failure, defined by systolic blood pressure <90 mmHg for at least 30 minutes despite adequate filling status, combined with clinical signs of end-organ hypoperfusion including oliguria, altered mental status, cool extremities, and elevated lactate >2 mmol/L. 1, 2

Core Hemodynamic Definition

The hemodynamic hallmarks that distinguish cardiogenic shock from other shock states include: 2

• Cardiac index <2.2 L/min/m² (often <1.8 L/min/m² in severe cases) reflecting the failing myocardium's inability to generate adequate output 2, 3
• Elevated filling pressures: Pulmonary capillary wedge pressure (PCWP) >15 mmHg indicating left ventricular failure and backward congestion 1, 2
• Increased systemic vascular resistance (SVR) as a compensatory mechanism—the body attempts to maintain blood pressure through vasoconstriction despite falling cardiac output 2, 3
• Elevated central venous pressure (CVP) >15 mmHg from right-sided failure 2

Clinical Presentation

Patients present with a constellation of findings that reflect both pump failure and compensatory mechanisms: 1, 2

• Hypotension: Systolic BP <90 mmHg or requiring vasopressors/inotropes to maintain BP >90 mmHg 1, 2
• Signs of hypoperfusion: Cold, clammy extremities with peripheral cyanosis from vasoconstriction, oliguria (<0.5 mL/kg/h for ≥6 hours), altered mental status 1, 2
• Metabolic derangements: Lactate >2 mmol/L indicating anaerobic metabolism, metabolic acidosis, mixed venous oxygen saturation (SvO₂) <65% 1, 2
• Pulmonary congestion: Dyspnea, pulmonary edema, jugular venous distension from elevated filling pressures 1, 4

Most Common Causes

Acute myocardial infarction is the leading cause, complicating 7-10% of AMI cases and typically requiring loss of ≥40% of left ventricular myocardium to precipitate shock. 3, 4 The 30-day mortality remains 40-45% despite contemporary treatment advances. 2, 4

Other important etiologies include: 3, 4

• Mechanical complications of AMI: Ventricular septal rupture, papillary muscle rupture causing acute severe mitral regurgitation, free-wall rupture (most catastrophic), right ventricular infarction 3, 4
• Acute decompensated heart failure in patients with pre-existing cardiomyopathy—follows a more indolent course and more commonly requires biventricular support compared to AMI-related shock 3, 4
• Severe valvular disease, myocarditis, severe arrhythmias (atrial fibrillation present in nearly 20% of CS patients) 3, 4

Pathophysiology: The Vicious Cycle

The central derangement is marked reduction in cardiac output, which triggers maladaptive compensatory mechanisms that worsen the shock state: 3

• Impaired coronary perfusion: Elevated ventricular end-diastolic pressures reduce coronary perfusion pressure, further diminishing myocardial contractility and stroke volume 3
• Inflammatory cascade: Release of inflammatory mediators impairs tissue metabolism, stimulates nitric oxide production causing paradoxical vasodilation, and promotes microvascular thrombosis 3
• Increased afterload: Pulmonary vasoconstriction from hypoxia and inflammation increases biventricular afterload and myocardial oxygen demand 3
• Volume overload: Renal hypoperfusion activates sodium reabsorption and the renin-angiotensin-aldosterone system; sympathetic splanchnic vasoconstriction redistributes ~50% of total blood volume back into central circulation 3

SCAI Staging System

The Society for Cardiovascular Angiography and Interventions classification provides standardized severity staging: 2

• Stage A (At Risk): Normal hemodynamics but at risk for developing shock 2
• Stage B (Beginning Shock): Relative hypotension without hypoperfusion 2
• Stage C (Classic Shock): Hypotension requiring pharmacologic support with clinical hypoperfusion (oliguria, altered mental status) 2
• Stage D (Deteriorating/Doom): Worsening despite initial therapy, requiring escalation to mechanical circulatory support 2
• Stage E (Extremis): Cardiac arrest, refractory hypotension requiring CPR and/or ECMO 2

Mortality increases stepwise with progression through stages A to E. 2

Hemodynamic Phenotypes

Recognizing the specific phenotype guides device selection for mechanical circulatory support: 2

• Left ventricular-dominant shock: PCWP >15 mmHg with right atrial (RA) pressure <15 mmHg—presents with prominent pulmonary congestion, reduced LV ejection fraction, regional wall motion abnormalities 2, 3
• Right ventricular-dominant shock: RA pressure >15 mmHg with PCWP <15 mmHg—presents with jugular venous distension but clear lung fields, RV dyssynchrony, dilatation, paradoxical septal motion, reduced TAPSE 2, 3
• Biventricular shock: Both RA >15 mmHg and PCWP >15 mmHg—combined left and right heart failure 2

Critical Distinguishing Feature from Other Shock Types

The key differentiator is elevated filling pressures (PCWP >15 mmHg, CVP >15 mmHg) combined with increased SVR—the failing heart cannot generate adequate output despite elevated preload. 2 This contrasts sharply with:

• Hypovolemic shock: Decreased filling pressures (low PCWP, low CVP), increased SVR, decreased cardiac index 2
• Distributive shock: Normal or decreased filling pressures, decreased SVR (opposite of cardiogenic), normal or increased cardiac index in early stages 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. 2, 4 When diagnosis is unclear, invasive hemodynamic monitoring with pulmonary artery catheterization provides definitive measurements. 2, 4

Immediate Assessment Requirements

When cardiogenic shock is suspected: 1, 2

• 12-lead ECG immediately to identify acute coronary syndrome 2
• Transthoracic echocardiography immediately to assess ventricular function, detect mechanical complications, confirm diagnosis, and identify specific cause 2, 4
• Invasive arterial line monitoring for accurate blood pressure measurement 1, 2
• Lactate measurement as a marker of tissue hypoperfusion and treatment response 2

Refractory Cardiogenic Shock

Refractory shock is defined by persistent tissue hypoperfusion despite adequate doses of two vasoactive medications and treatment of the underlying etiology, with specific hemodynamic criteria: 2, 5

• Cardiac power output <0.6 W (most critical threshold, more predictive than cardiac index alone) 2
• Cardiac index <2.2 L/min/m² despite maximal medical therapy 2
• Systolic BP <80 mmHg despite maximal treatment or requiring high-dose vasopressors 2