Clinical Findings in Cardiogenic Shock
Cardiogenic shock presents with the triad of persistent hypotension (systolic blood pressure <90 mmHg for >30 minutes or requiring vasopressors/inotropes), signs of end-organ hypoperfusion, and elevated cardiac filling pressures. 1
Hemodynamic Profile
The defining hemodynamic pattern distinguishes cardiogenic shock from other shock states:
- 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 1, 2
- Cardiac power output <0.6 W is the most critical threshold for identifying refractory shock 1
- Elevated pulmonary capillary wedge pressure (PCWP) >15 mmHg (often >20 mmHg), indicating left ventricular failure and pulmonary congestion 1, 2
- Increased systemic vascular resistance (SVR) as a compensatory mechanism attempting to maintain blood pressure despite falling cardiac output 1
- Elevated central venous pressure (CVP) >15 mmHg from right-sided filling pressures and backward failure 1
Clinical Manifestations of Hypoperfusion
Cardiovascular Signs
- Profound hypotension with systolic blood pressure <90 mmHg despite compensatory mechanisms 1
- Tachycardia as the body attempts to maintain cardiac output when stroke volume is reduced 1
- Decreased pulse pressure reflecting reduced stroke volume and increased arterial stiffness from vasoconstriction 1
- Cold, clammy extremities with peripheral cyanosis from peripheral vasoconstriction 1, 3
Pulmonary Findings
- Pulmonary edema with crackles on auscultation from elevated left ventricular filling pressures 1
- Jugular venous distension indicating elevated right-sided pressures 1
End-Organ Hypoperfusion Markers
Neurologic:
Renal:
- Oliguria with urine output <0.5 mL/kg/h indicating inadequate renal perfusion 1
- Acute kidney injury with rising creatinine 1
Hepatic:
- Elevated bilirubin ≥1.3 mg/dL independently predicts 180-day cardiac mortality 1
- Acute liver injury as part of multiorgan dysfunction 1
Metabolic:
- Elevated lactate >2 mmol/L indicating tissue hypoperfusion and anaerobic metabolism 2, 1
- Decreased mixed venous oxygen saturation (SvO2) <70% indicating inadequate oxygen delivery with increased tissue oxygen extraction 1
SCAI Classification Staging
The Society for Cardiovascular Angiography and Interventions provides a nuanced staging system that correlates with clinical findings 1:
- Stage A (At Risk): Normal hemodynamics, normotension, clear lungs, normal perfusion
- Stage B (Beginning Shock): Relative hypotension, tachycardia, early hypoperfusion signs
- Stage C (Classic Shock): Hypotension requiring intervention, hypoperfusion with oliguria, altered mental status
- Stage D (Deteriorating/Doom): Worsening despite initial interventions, requiring escalating support
- Stage E (Extremis): Cardiac arrest, refractory hypotension requiring CPR and/or ECMO 1
Phenotype-Specific Findings
Left Ventricular-Dominant Shock
Right Ventricular-Dominant Shock
- RA pressure >15 mmHg with PCWP <15 mmHg 2
- Jugular venous distension without pulmonary edema 2
- Clear lung fields despite shock state 2
Biventricular Shock
Critical Diagnostic Pitfalls
Avoid confusing late-stage septic shock with cardiogenic shock, as septic shock can develop myocardial depression but the primary hemodynamic pattern remains distributive with decreased SVR, not the elevated SVR seen in cardiogenic shock 1. The key distinguishing feature is that cardiogenic shock demonstrates elevated filling pressures (PCWP >15 mmHg, CVP >15 mmHg) while hypovolemic and distributive shock show decreased filling pressures 1.
Dynamic changes in hemodynamic parameters occur rapidly as shock progresses or responds to treatment, emphasizing the need for continuous monitoring rather than single-point assessment 1.