What is cardiomyopathic shock, its etiology, signs, diagnosis, treatment, and potential complications?

Cardiomyopathic Shock: Definition, Etiology, Diagnosis, and Management

Cardiomyopathic shock is a life-threatening condition characterized by inadequate cardiac output resulting in systemic hypoperfusion and end-organ damage due to underlying cardiomyopathy, with mortality rates exceeding 40% despite advances in treatment. 1

Definition & Pathophysiology

• Cardiomyopathic shock is clinically defined as persistent hypotension (systolic BP <90 mmHg for >30 minutes) despite adequate filling status with signs of hypoperfusion 1
• Hemodynamically defined as systolic BP <90 mmHg with central filling pressure >20 mmHg, or cardiac index <1.8 L/min/m² 1
• The central pathophysiologic derangement is diminished cardiac output leading to systemic hypoperfusion and maladaptive cycles of ischemia, inflammation, vasoconstriction, and volume overload 2
• This creates a vicious cycle where tissue ischemia triggers inflammatory mediators that induce nitric oxide production, causing systemic vasodilation and exacerbating hypotension 2
• Renal hypoperfusion activates the renin-angiotensin-aldosterone system, resulting in further volume overload and compromised diuretic effectiveness 2

Etiology

• Acute myocardial infarction (AMI) is the most common cause, complicating 5-12% of AMIs 1
• AMI-related shock typically occurs with >40% loss of left ventricular myocardium 2, 1
• Mechanical complications of AMI including free wall rupture, ventricular septal defect, and papillary muscle rupture 2
• Acute decompensated heart failure with cardiogenic shock (ADHF-CS) due to longstanding ventricular dysfunction 2
• Post-cardiotomy cardiogenic shock complicating 0.1% to 0.5% of cardiac surgeries 2
• Dilated cardiomyopathy characterized by progressive decrease in cardiac contractility, no increase in peripheral vascular resistance, and high pulmonary hypertension 3
• Other causes include severe valvular heart disease, myocarditis, myocardial contusion, and acute aortic dissection 2

Signs & Symptoms

• Hypotension (systolic BP <90 mmHg) despite adequate filling status 1, 4
• Clinical signs of tissue hypoperfusion: cold extremities, decreased urine output, altered mental status 1
• Elevated lactate levels (>2 mmol/L) indicating tissue hypoperfusion 4
• Pulmonary congestion with respiratory distress (respiratory rate >25 breaths/min, SaO2 <90%) 4
• Elevated jugular venous pressure and peripheral edema indicating right heart failure 2
• Decreased cardiac output and cardiac index (<1.8 L/min/m²) 1

Diagnosis & Evaluation

• Immediate Doppler echocardiography is essential to assess ventricular and valvular functions, loading conditions, and detect mechanical complications 4
• Echocardiography shows depressed LV global (ejection fraction) and regional function, decreased stroke volume and cardiac output, elevated LV filling and pulmonary pressures with or without secondary mitral regurgitation 2
• Laboratory evaluation should include cardiac biomarkers, lactate levels, and organ function tests 4
• Early invasive hemodynamic assessment using pulmonary artery catheter is recommended to identify the CS phenotype and guide tailored therapy 2
• The Society for Cardiovascular Angiography and Interventions (SCAI) has developed a 5-stage (A-E) classification system for cardiogenic shock severity that correlates with in-hospital and cardiac intensive care unit mortality 2

Interventions & Treatments

Immediate Management

• Immediate revascularization with percutaneous coronary intervention (PCI) is the standard of care for AMI-related shock 1, 4
• Norepinephrine is the preferred first-line vasopressor to maintain mean arterial pressure 1, 4
• Dobutamine (2-20 μg/kg/min) is the first-line inotropic agent to increase cardiac output when signs of low cardiac output persist 4
• Intravenous inotropes should be used in the lowest possible doses for the shortest duration due to their propensity to increase myocardial oxygen demand and arrhythmias 2

Advanced Support Measures

• Consider short-term mechanical circulatory support in patients with refractory shock 4
• Options include intra-aortic balloon pump (IABP), percutaneous ventricular assist devices, and extracorporeal membrane oxygenation (ECMO) 1
• For patients with heart failure and pulmonary congestion but adequate blood pressure (SBP >90 mmHg), consider dobutamine or levosimendan 4
• Milrinone and levosimendan may be considered for patients on beta-blockers due to their mechanism of action independent of beta-adrenergic receptors 2
• Ultrafiltration may be considered for patients with refractory congestion who fail to respond to diuretic-based strategies 4

Team-Based Approach

• Implement a multidisciplinary shock team approach for complex cases 4
• Transfer patients with cardiogenic shock to a tertiary care center with 24/7 cardiac catheterization capability and mechanical circulatory support availability 4
• In patients with SCAI stage E or end-stage CS in whom aggressive therapies may be futile, palliative care consultation and discussions regarding goals of care may be warranted 2

Potential Complications

• Multiorgan system failure is associated with nearly 50% in-hospital mortality 1
• Acute kidney injury, acute liver injury, respiratory failure, coagulopathy, and metabolic acidosis 1
• Malignant arrhythmias due to myocardial ischemia and inotropic therapy 2
• More than 50% of AMI-CS patients suffer concomitant cardiac arrest, either preceding or as a consequence of CS 2
• Survivors face impaired quality of life with higher rates of immobility, depression, and chronic anxiety 2

Relevant Red Flags & CVICU Tips

• Avoid routine use of intra-aortic balloon pump as it has not shown mortality benefit 4
• In RV infarction, avoid volume overload as it might worsen hemodynamics 4
• Do not delay diagnosis - cardiogenic shock has high mortality despite advances in treatment 4
• For patients with SCAI stage C or D CS, initial stabilization using vasopressor therapy and mechanical ventilation may be necessary before catheterization, but without significantly delaying reperfusion 2
• Target hemodynamic parameters include wedge pressure <20 mmHg and cardiac index >2 L/min/m² 4
• Complete revascularization during the index procedure should be considered in patients presenting with cardiogenic shock 4