Resuscitation 82 (2011) 14751476

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Resuscitation
journal homepage: www.elsevier.com/locate/resuscitation

Editorial

During CPR, push hard and fast and please do not stop!

Over one million people worldwide suffer sudden cardiac arrest each year. Survival has remained disappointingly low, varying from 1 to 12% after out-of-hospital cardiac arrest.1 In addition, the survival rates for patients that present in asystole or pulseless electrical activity (PEA) are substantially worse that those with arrests from ventricular brillation (VF) or ventricular tachycardia (VT). Despite a huge annual loss of human lives, many fundamental questions in the science of cardiopulmonary resuscitation (CPR) remain unanswered. We are still practicing cardiopulmonary resuscitation based on science that was developed more than 50 years ago. In 1889, Prevost and Battelli applied alternating and direct current shocks to brillate dog ventricles, and discovered that a countershock could debrillate the ventricles.2 Epinephrine was rst discovered in 1894, and was rst introduced into human cardiopulmonary resuscitation in 1922.3 In 1960, Knickerbocker et al. observed while studying debrillation that when electrodes were pressed rmly to the chest, there was a simultaneous rise in arterial pressure. This latter discovery led to the development of modern day cardiopulmonary resuscitation with the combination of chest compressions and debrillation.4 The importance of those three therapeutic interventions is obvious since they remain the core components of current CPR efforts. Although early debrillation is a very important element for successful outcomes, the prevalence of shockable rhythms at the time of arrival of emergency medical services on the scene is low, and is generally below 30% in most published studies. Debrillation is less likely, therefore, to be the primary therapy in most arrests. The importance of chest compressions has been documented from its rst conception in the 1960s, and has reemerged as an important factor in recent years. In the absence of a beating heart, chest compressions generate forward blood ow that is critical in maintaining viability of the heart and brain. Forward blood ow is generated by changes in the intrathoracic pressures, and some degree of mechanical cardiac compression, along with intact valvular structures.5 The generated blood ow is related to compression rate that is optimized between 80 and 120 min1 , and to the force of compression that translates into sternal displacement during standard CPR.6,7 In addition, a very important parameter recently recognized is the chest compression fraction (CCF); which is the actual fraction of time that compressions are delivered, taking into account pauses for pulse checks, debrillation, ventilations, and any other interruptions. Substantial evidence exists that outcomes improve when chest compression are not interrupted frequently. First, studies have shown that when compression to ventilation ratios increased, there was a direct increase in cardiac output during CPR, related to

the increased number of compressions delivered over a minute (30:2 versus15:2 and versus 15:1). In addition, continuous chest compression, with asynchronous ventilations, have been shown to provide similar or superior outcomes to the standard compression:ventilation ratio of 30:2 or 15:2.8 Finally, studies have correlated limiting ventilation, and thereby minimizing compression interruption (increasing compression fraction), with similar or superior outcomes in patients, especially in patients with ventricular brillation.9 Superior methods of CPR, with their improved blood ow, can increase neurological intact survival rates both in animals and humans, especially when resuscitation efforts are prolonged.10,11 The benet observed is associated with higher ow rates and better tissue supply/demand coupling. In addition, animal studies have shown that low ow during CPR leads to a decreased chance for successful debrillation, and less return of spontaneous circulation.12 It becomes obvious, therefore, that the chest compression fraction during CPR efforts, with its resulting effect on blood ow, should have an important effect on resuscitation efforts. In this issue of Resuscitation, Vaillancourt and the Resuscitation Outcomes Consortium (ROC) investigators13 showed that a high chest compression fraction was associated favorably (but not statistically signicantly) with achieving return of spontaneous circulation (ROSC) in 2103 patients presenting with non-VF/VT cardiac arrest. Analysis of this very large database is a substantial contribution. This is the rst time that an analysis showed an association (independent from other factors) between time spent in compression and hard endpoints in patients with asystole and PEA. The authors very nicely presented an association between chest compression fraction and the probability of achieving ROSC. They provided further evidence that efforts should be made to improve the chest compression fraction, and optimize it closer to 80%, where the probability for successful ROSC is >50%, compared with a CCF of 50% or less. The message from this study is entirely aligned with the 2010 American Heart Association recommendation: push hard and push fast. We should add to that recommendation, and emphasize: and minimize interruption.7 The authors noted, however, that there was no association between chest compression fractions greater than 80% and better outcomes. They suggested that this lack of improvement could be due to fatigue, and thereby less forceful compressions, affecting the outcomes, a hypothesis that could not be tested based on the data collected from ROC investigators. A way to study whether improving the CCF beyond 80% would improve outcomes would be to consider automated CPR devices as the chest

0300-9572/$ see front matter 2011 Published by Elsevier Ireland Ltd. doi:10.1016/j.resuscitation.2011.08.026

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Editorial / Resuscitation 82 (2011) 14751476 6. Feneley MP, Maier GW, Kern KB, et al. Inuence of compression rate on initial success of resuscitation and 24 hour survival after prolonged manual cardiopulmonary resuscitation in dogs. Circulation 1988;77:24050. 7. Berg RA, Hemphill R, Abella BS, et al. Part 5: adult basic life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122:S685705. 8. Yannopoulos D, Aufderheide TP, Gabrielli A, et al. Clinical and hemodynamic comparison of 15:2 and 30:2 compression-to-ventilation ratios for cardiopulmonary resuscitation. Crit Care Med 2006;34:14449. 9. Svensson L, Bohm K, Castren M, et al. Compression-only CPR or standard CPR in out-of-hospital cardiac arrest. N Engl J Med 2010;363:43442. 10. Yannopoulos D, Matsuura T, Schultz J, et al. Sodium nitroprusside enhanced cardiopulmonary resuscitation improves survival with good neurological function in a porcine model of prolonged cardiac arrest. Crit Care Med 2011;39:126974. 11. Aufderheide TP, Frascone RJ, Wayne MA, et al. Standard cardiopulmonary resuscitation versus active compression-decompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-ofhospital cardiac arrest: a randomised trial. Lancet 2011;377:30111. 12. Halperin HR, Lee K, Zviman M, et al. Outcomes from low versus high-ow cardiopulmonary resuscitation in a swine model of cardiac arrest. Am J Emerg Med 2010;28:195202. 13. Vaillancourt C, Siobhan Everson-Stewart S, Christenson J. The impact of increased chest compression fraction on return of spontaneous circulation for out-of-hospital cardiac arrest patients not in ventricular brillation. Resuscitation 2011;81:15017.

compression delivery system, since they would not be prone to fatigue. Retrospective analysis of data, of course, is complicated by the fact that only associations can be made. The observed differences in outcomes could alternatively be explained by the fact that the higher CCF group had a 10% higher rate of bystander CPR (a known predictor of outcomes) compared with the lower CCF group (27% in the 040% CCF versus 37% in the 6080% CCF p = 0.0032). Adjustment corrections made to take these difference into account may be based on assumptions that are likely a best guess of the effect of a confounding factor. In conclusion, basic science and clinical circumstantial evidence supports the importance of achieving a higher chest compression fraction during cardiopulmonary resuscitation. Caution should be taken, however, for generalization of these ndings in the clinical setting, since any action may have unintended consequences. Conict of interest statement Dr Yannopoulos None. Dr Halperin Consultant and grant support from Zoll Medical. References
1. Nichol G, Thomas E, Callaway CW, et al. Regional variation in out-of-hospital cardiac arrest incidence and outcome. JAMA 2008;300:142331. 2. Prevost JL, Battelli F. La mort par les courants electriques-courants alternatifs a haute tension. J Physiol Pathol 1899;1:427. 3. Crile D. Resuscitation, intracardiac injections. Surg Gynecol Obstet 1922;35:7725. 4. Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed-chest cardiac massage. JAMA 1960;173:10647. 5. Halperin HR, Tsitlik JE, Guerci AD, et al. Determinants of blood ow to vital organs during cardiopulmonary resuscitation in dogs. Circulation 1986;73:53950.

Demetris Yannopoulos Henry R. Halperin The Johns Hopkins Hospital, Division of Cardiology, 600 North Wolfe Street, Blalock Room 524, Baltimore, MD 21205, United States
Corresponding author. E-mail address: hhalper@jhmi.edu (H.R. Halperin)

17 August 2011