Cardiogenic shock

Definition

Shock is a state of organ hypoperfusion with inadequate oxygen delivery to tissues and resulting cellular damage. Cardiogenic shock is a relative or absolute reduction in cardiac output due to a primary cardiac disorder, such as myocardial infarction or arrhythmia. It is distinguished from obstructive shock caused by mechanical interference with filling or emptying (e.g. cardiac tamponade, tension pneumothorax, pulmonary embolism).

Classification

SCAI shock stages

• A – At risk: no signs of shock yet but at risk, e.g. large acute myocardial infarction or acute or acute-on-chronic heart failure; normal perfusion and normal lactate.
• B – Beginning: hemodynamic instability with relative hypotension (systolic below 90 mmHg, mean arterial pressure below 60 mmHg or a fall of more than 30 mmHg) or tachycardia of 100/min or more, but without hypoperfusion.
• C – Classic: hypoperfusion, e.g. cold, mottled extremities, delayed capillary refill, altered mental status, urine output below 30 ml/h, lactate of 2 mmol/l or more; invasively cardiac index below 2.2 l/min/m² and pulmonary capillary wedge pressure above 15 mmHg.
• D – Deteriorating: as C, but with worsening hypoperfusion despite initial support, with rising lactate persistently above 2 mmol/l and worsening organ dysfunction.
• E – Extremis: actual or impending circulatory collapse, e.g. lactate of 8 mmol/l or more, severe acidosis with pH below 7.2.

Aetiopathogenesis

• Impaired contractility: myocardial ischemia or myocardial infarction, myocarditis, drugs.
• Arrhythmias: tachycardia, bradycardia.
• Structural disorders: acute mitral or aortic regurgitation, ruptured interventricular septum, prosthetic valve malfunction.
• Pathophysiology: in myocardial infarction the ischemic or infarcted myocardium does not contract normally; stroke volume and cardiac output fall. When oxygen delivery is inadequate, cells shift to anaerobic metabolism and lactate rises; if shock persists, irreversible cell damage occurs.

Common constellations

• Acute coronary syndrome with large LV injury: most common cause (~80 % of all cardiogenic shocks).
• Mechanical post-MI complications: papillary muscle rupture → acute mitral regurgitation.

Clinical features

• altered mental status (lethargy, confusion, somnolence)
• pale, cool, clammy, often cyanotic hands and feet, as well as earlobes, nose and nail beds; capillary refill time prolonged beyond 2 seconds
• weak, rapid peripheral pulses; often only femoral or carotid pulses palpable
• oliguria
• frequently heart rate above 100/min, respiratory rate above 22/min, systolic blood pressure below 90 mmHg or a fall of 30 mmHg from baseline
• depending on the cause signs of congestion (crackles, raised jugular venous pressure), a new systolic murmur (ventricular septal rupture or mitral regurgitation after infarction) or a diastolic murmur (aortic regurgitation in dissection)

Diagnosis

• Lactate: above 2 mmol/l indicates tissue hypoperfusion.
• Further laboratory tests: renal and liver function, electrolytes, blood count, coagulation, blood gases; cardiac biomarkers.
• ECG and chest X-ray.
• Echocardiography (bedside or transesophageal) as a less invasive alternative to the pulmonary artery catheter.
• Invasive measurement: central venous pressure, pulmonary artery occlusion pressure and cardiac output via a pulmonary artery catheter in shock of uncertain or mixed cause or in severe shock.

Hemodynamic patterns

• Low CO + high PCWP: cardiogenic shock (Forrester IV).
• Low CO + low PCWP: hypovolemic shock.
• High CO + low SVR: septic/anaphylactic.

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Further reading (open access)

1. MSD Manual Professional: Shock
2. SCAI SHOCK Stage Classification Expert Consensus Update (2022)
3. StatPearls: Cardiogenic Shock
4. Cardiogenic Shock (Review), J Am Heart Assoc 2019

Cross-references