Return of spontaneous circulation is not the end of resuscitation. After cardiac arrest, the brain and heart remain vulnerable to secondary injury. Blood pressure management is one piece of that post-arrest physiology.
The post-arrest circulation is often unstable. Myocardial stunning can reduce cardiac output. Vasoplegia may develop from ischemia-reperfusion physiology and systemic inflammation. Sedation, temperature management, and arrhythmias can further alter hemodynamics. The brain needs adequate perfusion pressure, but more pressure is not automatically better.
Excessive vasoconstriction may increase afterload and myocardial oxygen demand. Too little pressure may worsen cerebral and coronary perfusion. This creates a difficult balance. The BOX trial compared two mean arterial pressure targets, approximately 63 mm Hg and 77 mm Hg, in comatose survivors of out-of-hospital cardiac arrest of presumed cardiac cause.