Sudden cardiac arrest is a leading cause of death in developed countries and impacts over 300,000 patients in the United States per year.1 Despite initial resuscitation, 50% of arrest victims do not survive to discharge from the hospital. One third die from refractory cardiovascular shock or the cause of initial arrest. The remaining patients survive the initial insult only to later succumb due to organ dysfunction and neurologic injury stemming from the cardiac arrest. Among survivors, the burden of cardiac arrest persists with up to 30% of patients suffering permanent neurologic injury. These data underscore the impressive health care burden of sudden cardiac arrest.
The early post-arrest period has emerged as a critical window to impact the outcome of cardiac arrest victims. Improved morbidity and mortality achieved with therapeutic hypothermia prove the potential for treatments applied following return of spontaneous circulation (ROSC) to impact clinical outcome. As such, contemporary emergency care now emphasizes intensive support during this vulnerable and modifiable phase of illness. Priorities of the post-arrest period include stabilization of organ perfusion and oxygenation, identification and treatment of reversible causes of cardiac arrest, and initiation of neuroprotective therapy (Table 15-1). This chapter focuses on the immediate and early post-resuscitation phase of illness where timely interventions provide the greatest opportunity to achieve the goal of neurologically intact survival of cardiac arrest victims.
Table 15-1. Early Post-Resuscitation Priorities |Favorite Table|Download (.pdf)
Table 15-1. Early Post-Resuscitation Priorities
- Provide adequate oxygenation and ventilation
- Reverse shock and stabilize hemodynamics
- Identify and treat reversible cause of cardiac arrest
- Apply neuroprotective therapies—therapeutic hypothermia
- Correct metabolic disturbances
Post-resuscitation disease is a unique multiorgan illness2 (Table 15-2). Reperfusion following a period of whole-body ischemia and hypoxia ignites a complex systemic immunologic response. Proinflammatory cytokines, coagulation abnormalities, and endothelial dysfunction characterize a state of systemic inflammation analogous to that of severe infection.3,4 The clinical consequence of this immune activation is macrocirculatory and microcirculatory dysfunction manifested as hemodynamic instability and early organ dysfunction.
Table 15-2. Post-Cardiac Arrest Disease and Pathophysiology |Favorite Table|Download (.pdf)
Table 15-2. Post-Cardiac Arrest Disease and Pathophysiology
|Systemic ischemia–reperfusion injury|
- Systemic inflammatory response syndrome (SIRS)
- Inappropriate vasodilation
- Dysregulated coagulation
- Impaired microvascular function
- Early organ dysfunction
|Acute myocardial dysfunction|
- Myocardial stunning
- Acute coronary syndrome
- Anoxic brain insult
- Ischemic-reperfusion injury
- Impaired autoregulation
|Persistent arrest precipitating pathology|
Low and no-flow periods of cardiac arrest are invariably associated with global ischemia. However, adequate oxygen delivery is not restored with ROSC. A brief hyperdynamic cardiovascular response is common immediately following ROSC but is typically followed by early cardiovascular deterioration.5,6 The swiftness and degree of hemodynamic decline is inversely related to the period of cardiac arrest.7 Persistent shock should be anticipated and represents an important target of therapy.