RT Book, Section A1 Otto, Charles W. A2 Longnecker, David E. A2 Mackey, Sean C. A2 Newman, Mark F. A2 Sandberg, Warren S. A2 Zapol, Warren M. SR Print(0) ID 1144135783 T1 Cardiopulmonary Resuscitation T2 Anesthesiology, 3e YR 2017 FD 2017 PB McGraw-Hill Education PP New York, NY SN 9780071848817 LK accessanesthesiology.mhmedical.com/content.aspx?aid=1144135783 RD 2024/04/18 AB KEY POINTSDuring many in- and out-of-hospital resuscitation attempts, less than half the time is devoted to chest compressions. Interrupting compressions reduces myocardial perfusion and is detrimental to the ultimate success of resuscitation. Maintaining uninterrupted chest compressions must be the first priority during cardiopulmonary resuscitation.The relative importance of chest compressions, ventilation, and defibrillation during resuscitation must be adjusted for the context of the rescue situation and the personnel available.When an arrest is witnessed, which is likely to be of cardiac (rather than respiratory) cause, and advanced care will be available within a short time, closed chest compressions alone may be as efficacious as compressions and mouth-to-mouth ventilation.Interrupting chest compressions is harmful, occurs frequently and reduces survival.Fluctuations in intrathoracic pressure play a significant role in blood flow during most resuscitations, and the cardiac pump mechanism contributes under some circumstances.The critical myocardial blood flow is associated with aortic diastolic pressure exceeding 40 mmHg.Cardiac output is severely depressed during cardiopulmonary resuscitation (CPR), ranging from 10% to 33% of prearrest values in experimental animals. Nearly all of the cardiac output is directed to organs above the diaphragm.During CPR, measurement of blood gases reveals an arterial respiratory alkalosis and a venous respiratory acidosis because the arterial Pco2 is reduced and the venous Pco2 is elevated.Exhaled end-tidal CO2 is an excellent noninvasive guide to the effectiveness of standard CPR.Defibrillation for VF arrest is most effective if applied within 4-5 minutes of collapse. Otherwise, a brief period of 2-3 minutes of chest compressions before defibrillation may improve survival.Amiodarone and lidocaine are used during cardiac arrest to aid defibrillation when ventricular fibrillation is refractory to electrical countershock therapy or when fibrillation recurs following successful conversion.It has been questioned whether any drug therapy improves outcome from cardiac arrest. In recent drug trials, if any effect was found, it was only short-term outcomes of improved return of spontaneous circulation or admission to hospital.Outcome studies prospectively comparing standard and high-dose epinephrine have not demonstrated conclusively that higher doses will improve survival.Evidence currently suggests that, like other potent vasopressors, vasopressin is equivalent to but not better than epinephrine for use during CPR.All resuscitated patients with ST elevation as well as those without ST elevation when an acute coronary event is suspected should undergo emergent coronary angiography regardless of their neurological status.In contrast to pharmacologic therapy, three randomized controlled trials (RCTs) demonstrate improved neurologic outcomes when targeted temperature management (maintaining a constant temperature between 32-36°C) is induced for 12-24 hours in cardiac arrest survivors who remained comatose after hospital admission.