The Physiology of Cardiopulmonary Resuscitation
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Society for Critical Care Anesthesiologists Section Editor: Avery Tung E REVIEW ARTICLE CME The Physiology of Cardiopulmonary Resuscitation Keith G. Lurie, MD, Edward C. Nemergut, MD, Demetris Yannopoulos, MD, and Michael Sweeney, MD * † ‡ § Outcomes after cardiac arrest remain poor more than a half a century after closed chest cardiopulmonary resuscitation (CPR) was first described. This review article is focused on recent insights into the physiology of blood flow to the heart and brain during CPR. Over the past 20 years, a greater understanding of heart–brain–lung interactions has resulted in novel resuscitation methods and technologies that significantly improve outcomes from cardiac arrest. This article highlights the importance of attention to CPR quality, recent approaches to regulate intrathoracic pressure to improve cerebral and systemic perfusion, and ongo- ing research related to the ways to mitigate reperfusion injury during CPR. Taken together, these new approaches in adult and pediatric patients provide an innovative, physiologically based road map to increase survival and quality of life after cardiac arrest. (Anesth Analg 2016;122:767–83) udden cardiac arrest remains a leading cause of pre- during CPR, and new approaches to reduce injury associ- hospital and in-hospital death.1 Efforts to resuscitate ated with reperfusion.3,5–8,10–48 Given the debate surrounding patients after cardiac arrest have preoccupied scien- what is known, what we think we know, and what remains S 1,2 tists and clinicians for decades. However, the majority unknown about resuscitation science, this article also pro- of patients are never successfully resuscitated.1,3–5 Based vides some contrarian and nihilistic points of view. on the published reports, the overall survival rates after When the cause of the arrest is reversible, the primary cardiac arrest are grim, ranging from 1% to <20% for out- treatment goal of sudden cardiac arrest is to fully restore of-hospital nontraumatic cardiac arrest and <40% for in- cardiac and brain function. The leading causes of cardiac hospital cardiac arrest.1,6 Of these, 10% to 50% have poor arrest, such as a primary or ischemia-induced arrhythmia, neurological function.1,7 Surprisingly, the physiologic pulmonary emboli, hemorrhage, trauma, or medication/ principles that underlie the life-saving process of car- drug overdose, all require emergent efforts to increase car- diopulmonary resuscitation (CPR) remain only partially diocerebral circulation.1,8 The critical first step to successful understood and are often controversial.1,8 Some would resuscitation is restoring blood flow with sufficient aortic argue that current approaches to cardiac arrest are fatally pressure. Understanding the complex physiology of cardio- flawed, and that is why the overall survival rates have cerebral perfusion during CPR is crucial to reducing mor- hovered around 7% for out-of-hospital cardiac arrest and bidity and mortality after cardiac arrest. Vital organ flow <30% for in-hospital cardiac arrest nationwide for a half enhancement is critical, but often by itself insufficient, to a century.9 fully restore life after cardiac arrest. This review article is primarily focused on recent advances There are multiple areas in resuscitation science where in the field of CPR, with primary focus on new ways to pro- significant knowledge gaps and unmet needs limit our abil- mote better perfusion to the heart and brain. There have been ity to consistently restore full life after cardiac arrest. First significant advances in our understanding of the physiology is the need for greater blood flow than the minimal amount produced by conventional closed chest cardiac massage, the of resuscitation over the past 2 decades, with new insights most commonly used method of CPR that has not changed into the physiologic mechanisms that regulate blood flow to for over a half a century.3,49,50 Second is the need for tools the vital organs, common errors in the delivery of CPR that that help provide better quality CPR.51–54 Third is the need often reduce its effectiveness, ways to enhance circulation to reduce the potential for brain injury associated with the simultaneous arterial and venous pressure compression waves focused toward the brain each time the chest is com- From the Department of Emergency and Internal Medicine, University 14 of Minnesota, Minneapolis, Minnesota; Department of Anesthesiology pressed. Fourth is to prevent reperfusion injury in the first and Neurological* Surgery, University of Virginia, Charlottesville, Virginia; seconds and minutes of reperfusion, especially after pro- Department of Internal Medicine Cardiovascular† Division, University of 37–43 Minnesota, Minneapolis, Minnesota; and Departments of Anesthesiology longed periods of no flow. The fifth large area where and‡ Pediatrics, University of Minnesota, Minneapolis, Minnesota. there are unmet clinical needs is in postresuscitation care, § Accepted for publication June 8, 2015. which is beyond the scope of this review.15–20,55–57 Funding: None. In what follows, we try to highlight some recent Conflict of Interest: See Disclosures at the end of the article. advances in resuscitation science aimed at addressing these Reprints will not be available from the authors. unmet needs and to discuss why some with doubts believe Address correspondence to Keith Lurie, MD, Department of Emergency that there is a lack of progress.9 We leave it to the reader Medicine, Hennepin County Medical Center, 701 Park Ave., Minneapolis, MN 55415. Address e-mail to [email protected]. to decide whether progress is being made, whether we are Copyright © 2016 International Anesthesia Research Society simply treading water, or whether the science of resuscita- DOI: 10.1213/ANE.0000000000000926 tion is actually regressing. March 2016 • Volume 122 • Number 3 www.anesthesia-analgesia.org 767 Copyright © 2015 International Anesthesia Research Society. Unauthorized reproduction of this article is prohibited. E REVIEW ARTICLE Figure 1. Representative pressure curve during 0° supine cardiopulmonary resuscitation (CPR), 30° head-up CPR, and −30° head-down CPR showing aortic pressure (Ao), right atrial pressure (RA), intracranial pressure (ICP), and cerebral perfusion pressure (CerPP). Pressure curves from a representative animal study in the experiments described by Debaty et al.14 CONVENTIONAL CPR PHYSIOLOGY that not enough attention is focused on understanding the The Compression Phase interactions among the changes in right-side cardiac pres- Conventional or standard (S)-CPR is performed with a pair sures, ICP, and the resultant cerebral and coronary perfusion of hands.1,49 With each chest compression, intrathoracic pres- pressures. sure is increased, and the heart is squeezed between the ster- num and the spine.49,58–62 With each compression, both the Common Errors During Chest Compression aortic and the right atrial pressures increase, with right atrial Preclinical and clinical studies support the American Heart pressure similar to, or sometimes higher than, left-sided pres- Association (AHA) recommendation that chest compres- sures.63–65 Blood is propelled forward from the nonbeating sions should be 5-cm deep.1,2 When the chest is compressed heart toward the brain, coronary arteries, and the rest of the too slowly, too rapidly, too much, or too little, clinical out- body because of the presence of the 1-way valves within the comes are adversely affected.8,71–76 Similarly, interruptions heart and pressure differences between the thorax and the in chest compressions are harmful.5,6,71,77 Obviously, with- nonthoracic regions.58,61,66 Within the past decade, there has out chest compressions, there is no forward blood flow. Too been renewed interest in the effect of increased intrathoracic often, rescue personnel stop chest compressions for over pressure on intracranial pressure (ICP) during the compres- a minute to intubate, feel for pulses, auscultate the chest, sion phase.4,67–69 During this phase, ICP is increased, which and/or check the underlying rhythm.78–81 In the heat of in turn increases resistance to cerebral perfusion.14,67 It is the moment, rescuers often forget to perform high-quality speculated that the increase and decrease of ICP during CPR CPR.7,8,74 These common errors significantly and adversely is secondary to changes in intrathoracic pressure transduced affect outcomes. through the paravertebral venous/epidural plexus and spi- A recent analysis of CPR quality during a large National nal fluid to the intracranial compartment.68 ICP increases Institutes of Health Resuscitation Outcomes Consortium with each positive pressure ventilation.67,68 The increase in Prehospital Resuscitation using an IMpedance valve and ICP and the simultaneous decrease in the calculated cere- Early versus Delayed (ROC PRIMED) trial demonstrated bral perfusion pressure (CerPP) are shown in Figure 1 (0° that these errors were common and harmful. Nearly half supine tracings). Right atrial, right ventricular, and pulmo- of the time, compressions were performed at rates and nary artery pressures increase in parallel with each compres- depths outside of the recommended range of the AHA 7,8,74 sion.65 During CPR, the coronary artery perfusion pressure is guidelines. At least one-third of the subjects had com- 8,74 generally calculated as the difference between the aortic and pression rates in excess of 120 per minute, and survival 8,30,a,74 the right-sided pressures.70 Thus, high right-sided pressures