Post-Cardiac Arrest Myocardial Dysfunction

Post-cardiac arrest myocardial dysfunction is reversible global left and right ventricular systolic and diastolic dysfunction after return of spontaneous circulation, with reduced cardiac output, hypotension and arrhythmia. It is a component of post-cardiac arrest syndrome that is distinct from the cause of the arrest.

Epidemiology. It occurs in about 50 to 70% of resuscitated patients, begins within minutes to hours, usually peaks at around 8 hours and recovers over 24 to 72 hours. Persistent shock is an independent predictor of death.

Contributors. Duration of arrest and resuscitation, number and energy of shocks, adrenaline dose, underlying infarction, cardiomyopathy and sepsis, and the ischaemia reperfusion response.

Pathophysiology. Myocardial stunning follows global ischaemia, with calcium overload, oxidative stress, mitochondrial injury and catecholamine toxicity. Cytokine release causes vasodilation, so low output and low vascular tone coexist.

Presentation is hypotension, tachycardia or arrhythmia, cool peripheries, raised lactate, pulmonary oedema and oliguria. Right ventricular failure may produce raised venous pressure.

Red flags.

• Mean arterial pressure under 65 mmHg despite vasopressor.
• Lactate rising after 6 hours, or low central venous oxygen saturation.
• Recurrent ventricular arrhythmia or ST elevation.

Echocardiography as soon as feasible (ventricular function, regional abnormalities, valve disease, tamponade, right ventricular size, left ventricular outflow obstruction), 12-lead ECG, troponin (interpret in context), lactate, central venous oxygen saturation, natriuretic peptide, gas and electrolytes. Add pulmonary artery catheter or other cardiac output monitoring for refractory shock. Coronary angiography when ischaemia is suspected.

Differential diagnosis. Acute coronary occlusion, pulmonary embolism, tamponade, tension pneumothorax, haemorrhage, sepsis, stress cardiomyopathy and drug effect.

Treat causes. Revascularise culprit coronary lesions, treat pulmonary embolism, drain tamponade, and manage sepsis and bleeding.

Haemodynamic targets. Mean arterial pressure at least 65 mmHg, lactate falling, urine output over 0.5 mL/kg/h, central venous oxygen saturation over 65 to 70%.

Fluid. Give 250 to 500 mL balanced crystalloid boluses only if echocardiography or dynamic indices suggest responsiveness. Avoid overload, which worsens pulmonary oedema.

Vasopressor and inotrope.

• Noradrenaline 0.05 to 0.5 microgram/kg/min first line.
• Dobutamine 2.5 to 10 microgram/kg/min (maximum 20 microgram/kg/min) for low output, with attention to arrhythmia and hypotension.
• Adrenaline 0.05 to 0.3 microgram/kg/min when both effects are needed. Use the lowest effective dose.
• Milrinone 0.25 to 0.5 microgram/kg/min (reduce in renal impairment) or levosimendan 0.05 to 0.2 microgram/kg/min for specialist use.
• Vasopressin 0.03 units/min to spare catecholamine.

Mechanical circulatory support. Intra-aortic balloon pump, percutaneous ventricular assist device or venoarterial ECMO for refractory cardiogenic shock after revascularisation, as a bridge to recovery.

Rhythm. Correct potassium and magnesium, and treat arrhythmia. Amiodarone 150 mg IV, then 1 mg/min for 6 hours, then 0.5 mg/min for recurrent ventricular arrhythmia.

Avoid negative inotropes, excessive hyperoxia and hypocapnia, and fever.

Monitoring. Arterial pressure, lactate every 2 hours, echocardiography every 24 hours, urine output, and ECG.

Referral and escalation. Cardiology and intensive care, with a mechanical support centre for persistent shock.

Special groups. In renal impairment, reduce milrinone. In right ventricular failure, avoid high airway pressure and hypoxia.