From the Guidelines
Cardiac function is typically compromised immediately following cardiac arrest, with the onset of post–cardiac arrest myocardial dysfunction beginning within hours of the arrest. This condition is characterized by reduced contractility and decreased cardiac output, and is associated with early mortality despite successful initial resuscitation in children and adults 1. The heart may require supportive measures such as inotropic medications to maintain adequate circulation.
Key Points to Consider
- The severity of the myocardial dysfunction may be related to the duration of no-flow time during cardiac arrest 1.
- The pathophysiology contributing to this frequently reversible deterioration of cardiac function after cardiac arrest is not fully understood but is associated with cardiovascular ischemia/reperfusion 1.
- Healthcare providers will closely monitor hemodynamic parameters, often using tools like echocardiography to assess heart function and guide treatment during this critical recovery period.
Treatment and Management
- The initial objectives of post–cardiac arrest care are to optimize cardiopulmonary function and vital organ perfusion, and to identify and treat the precipitating causes of the arrest and prevent recurrent arrest 1.
- Supportive measures such as inotropic medications (like dobutamine or epinephrine) may be necessary to maintain adequate circulation.
- The dysfunction usually improves within 24-72 hours if the patient survives, with the onset of post–cardiac arrest myocardial dysfunction beginning within hours of the arrest, peaking at ≈8 hours, and typically resolving within 48 to 72 hours 1.
From the Research
Cardiac Function After Cardiac Arrest
- Cardiac arrest results in multiorgan ischemia until return of spontaneous circulation, often followed by a low-flow shock state 2.
- Post-cardiac arrest syndrome includes myocardial dysfunction, which can lead to low cardiac output or ventricular systolic or diastolic dysfunction 3.
- Impaired left ventricular systolic function is reported in nearly two-thirds of patients resuscitated after cardiac arrest, and hypotension and shock requiring vasopressor support are common 3.
- The pathophysiology of myocardial dysfunction and shock after cardiac arrest involves cardiovascular ischemia/reperfusion injury and cardiovascular toxicity from excessive levels of inflammatory cytokine activation and catecholamines 3.
Immediate Compromise of Cardiac Function
- Cardiac function can be compromised immediately following cardiac arrest due to the underlying cause of the arrest and the resulting ischemia/reperfusion injury 4, 5.
- Hemodynamic stabilization after resuscitation from cardiac arrest involves restoration of preload, vasopressors to support arterial pressure, and inotropic support if needed to reverse the effects of myocardial dysfunction and improve systemic perfusion 3.
- Early invasive approach to coronary reperfusion with percutaneous coronary intervention, together with active targeted temperature management and optimization of hemodynamic, ventilator, and metabolic parameters, may improve survival and neurologic outcomes in cardiac arrest survivors 5.
Management of Cardiac Function After Cardiac Arrest
- A structured approach to post-cardiac arrest care is needed, including minimizing CNS injury, managing cardiovascular dysfunction, reducing systemic ischemic/reperfusion injury, and identifying and treating the underlying cause of the arrest 4.
- Care after cardiac arrest includes controlled reoxygenation, therapeutic hypothermia for comatose survivors, percutaneous coronary intervention, circulatory support, and control of blood-glucose levels and seizures 6.
- Prognostication in comatose survivors of cardiac arrest needs a careful, multimodal approach using clinical and electrophysiological assessments after at least 72 h 6.