The Quality of Chest Compressions During Cardiopulmonary Resuscitation Overrides Importance of Timing of Defibrillation

Original Research CRITICAL CARE MEDICINE

The Quality of Chest Compressions During Cardiopulmonary Resuscitation Overrides Importance of Timing of Defibrillation* Giuseppe Ristagno, MD; Wanchun Tang, MD, FCCP; Yun-Te Chang, MD; Dawn B. Jorgenson, PhD; James K. Russell, PhD; Lei Huang, MD; Tong Wang, MD; Shijie Sun, MD; and Max Harry Weil, MD, PhD, Master FCCP

Background: We address the quality of chest compressions and the impact on initial defibrillation or initial chest compressions after sudden death. Methods: Ventricular fibrillation was induced by occlusion of the left anterior descending coronary artery in 24 domestic pigs with a mean (ⴞ SD) weight of 40 ⴞ 2 kg. Cardiac arrest was left untreated for 5 min. Animals were then randomized to receive chest compressions-first or defibrillation-first and were further randomized to “optimal” or “conventional” chest compressions. A total of four groups of animals were investigated using a factorial design. For optimal chest compressions, the anterior posterior diameter of the chest was reduced by 25%, representing approximately 6 cm. Only 70% of this depth, or approximately 4.2 cm, represented conventional chest compressions. Chest compressions were delivered with a mechanical chest compressor. Defibrillation was attempted with a single biphasic 150-J shock. Postresuscitation myocardial function was echocardiographically assessed. Results: Coronary perfusion pressures and end-tidal PCO2 were significantly lower with conventional chest compressions. With optimal chest compressions, either as an initial intervention or after defibrillation, each animal was successfully resuscitated. Fewer shocks were required prior to the return of spontaneous circulation after initial optimal chest compressions. No animals were resuscitated when conventional chest compressions preceded the defibrillation attempt. When defibrillation was attempted as the initial intervention followed by conventional chest compressions, two of six animals were resuscitated. Conclusions: In this animal model of cardiac arrest, it was the quality of the chest compressions, rather then the priority of either initial defibrillation or initial chest compressions, that was the predominant determinant of successful resuscitation. (CHEST 2007; 132:70 –75) Key words: cardiac arrest; cardiopulmonary resuscitation; chest compression; defibrillation; survival; ventricular fibrillation Abbreviations: CPP ⫽ coronary perfusion pressure; CPR ⫽ cardiopulmonary resuscitation; EF ⫽ ejection fraction; EtPco2 ⫽ end-tidal Pco2; FAC ⫽ fractional area change; LAD ⫽ left anterior descending coronary; MAP ⫽ mean aortic pressure; MPAP ⫽ mean pulmonary arterial pressure; RAP ⫽ right atrial pressure; ROSC ⫽ return of spontaneous circulation; SV ⫽ stroke volume; VF ⫽ ventricular fibrillation

evidence is secure that the quality of chest T hecompressions is a major determinant of successful resuscitation.1–3 Yet, there is also persuasive evidence that conventional manual chest compressions are often performed ineffectively.4,5 In settings of both in-hospital and out-of-hospital cardiac arrest, 70

chest compressions are typically performed such that the compression depth was only 70% of that recommended in the current American Heart Association guidelines.4 – 6 In addition, “early defibrillation” may not be the optimal initial intervention, especially after unwitOriginal Research

nessed cardiac arrest.7–10 Accordingly, the effectiveness of chest compressions in relation to the timing of defibrillation has been a subject of major interest. Both animal and human studies1,9 –12 have more recently diminished enthusiasm for initial defibrillation in favor of initial chest compressions, especially when the duration of untreated cardiac arrest exceeds 4 min. Nevertheless, a randomized study including 256 persons who experienced out-of-hospital cardiac arrest yielded no differences in outcomes when one intervention preceded the other.13 We therefore sought to compare outcomes between the quality of chest compressions and early or delayed defibrillation under controlled conditions in an established animal model. We hypothesized that if chest compressions are delivered effectively in an animal model simulating “sudden death,” defibrillation may be delayed without the compromise of outcomes. However, with less effective chest compressions, we anticipated that initial defibrillation would provide better outcomes.

Methods and Materials Experiments were performed in an established swine model of cardiac arrest14 –18 which was recently modified so as to induce ventricular fibrillation (VF) by transient coronary artery occlusion.19 All animals received humane care in compliance with the “Principles of Laboratory Animal Care” formulated by the National Society for Medical Research and the Guide for the Care and Use of Laboratory Animals prepared by the Institute of Laboratory Animal Resources and published by the National Institutes of Health (NIH publication 86 –32, revised 1985). The protocol was approved by the Institutional Animal Care and Use Committee of the Weil Institute of Critical Care Medicine. The animal laboratories of the Weil Institute are fully accredited by the American Association for Accreditation of Laboratory Animal Care International.

Animal Preparation Twenty-four male Yorkshire-cross domestic pigs (Sus scrofa) with a mean (⫾ SD) weight of 40 ⫾ 2 kg were fasted overnight except for free access to water. Anesthesia was initiated by the IM injection of ketamine (20 mg/kg) and was completed by ear vein injection of sodium pentobarbital (30 mg/kg). Additional doses of sodium pentobarbital (8 mg/kg) were injected at intervals of approximately 1 h to maintain anesthesia. A cuffed endotracheal tube was advanced into the trachea, and animals were mechanically ventilated with a volume-controlled ventilator (model MA-1; Puritan-Bennett; Carlsbad, CA) using a tidal volume of 15 mL/kg, a peak flow of 40 L/min, and a fraction of inspired oxygen of 0.21. End-tidal Pco2 (EtPco2) was monitored with an infrared capnometer (model NPB-75; Nellcor Puritan Bennett Inc; Pleasanton, CA). Respiratory frequency was adjusted to maintain EtPco2 between 35 and 40 mm Hg prior to inducing cardiac arrest and after the restoration of spontaneous circulation (ROSC). For the measurement of left ventricular function, a transesophageal echocardiographic transducer was advanced from the incisor teeth into the esophagus for a distance of approximately 35 cm. For the measurement of mean aortic pressure (MAP), a fluid-filled 8F angiographic catheter (model 6523; USCI, C.R. Bard, Inc; Salt Lake City, UT) was advanced from the right femoral artery into the thoracic aorta. For the measurement of right atrial pressure (RAP), mean pulmonary artery pressure (MPAP), and thermodilution cardiac output, a 7F, pentalumen, thermodilution-tipped catheter (No. 41216; Abbott Critical Care Systems; North Chicago, IL) was advanced from the right femoral vein and flow-directed into the pulmonary artery. Conventional external pressure transducers were used (Transpac IV; Abbott Critical Care Systems). VF was induced in this closedchest preparation after intraluminal occlusion of the left anterior descending (LAD) coronary artery between the first and second diagonal branches, with the aid of a 7F balloon tipped catheter (No. 41216; Abbott Critical Care) inserted from the right common carotid artery.19 After confirmation of the LAD coronary artery site with contrast medium (Renografin-76; Squibb Diagnostics; New Brunswick, NJ), the balloon of the catheter was inflated with 0.5 mL of air to occlude flow. Heparin (2,500 UI) was injected distal to the occluding balloon. ECG was recorded with adhesive electrodes that were applied to the shaved skin of the upper and lower limbs. Experimental Procedures

*From the Weil Institute of Critical Care Medicine (Drs. Ristagno, Tang, Chang, Huang, Wang, and Sun), Rancho Mirage, CA; and Philips Medical Systems (Drs. Jorgenson and Russell), Seattle, WA. Presented in part by Dr. Ristagno, who was the recipient of a “Young Investigator” Award for this work, at the 2005 AHA Resuscitation Science Symposium. This study was supported, in part, by Philips Medical Systems, Seattle, WA Drs. Russell and Jorgenson are employed by Philips Medical Systems. The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. Manuscript received December 21, 2006; revision accepted April 15, 2007. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml). Correspondence to: Wanchun Tang, MD, FCCP, Weil Institute of Critical Care Medicine, 35100 Bob Hope Dr, Rancho Mirage, CA 92270; e-mail: [email protected] DOI: 10.1378/chest.06-3065 www.chestjournal.org

Fifteen min prior to inducing cardiac arrest, the animals were randomized to the following four groups: (1) defibrillation-first or (2) chest compressions-first; and (3) “optimal” chest compression or (4) “conventional” chest compression. For optimal chest compressions, the anterior-posterior diameter of the chest was reduced by 25%, representing approximately 6 cm. Preliminary studies20,21 indicated that coronary perfusion pressure (CPP) was thereby increased to levels that exceeded the threshold of 15 mm Hg that was predictive of ROSC for this model. Only 70% of this depth (approximately 4.2 cm) represented conventional chest compressions.4,5 VF was induced, and mechanical ventilation was discontinued. At the end of a 5-min interval of untreated VF, the LAD coronary artery balloon was deflated, the catheter was withdrawn, and the resuscitation procedure was started in accordance with the four algorithms, as follows: (1) 3 min of optimal chest compressions followed by a single defibrillation attempt; (2) 3 min of conventional chest compressions followed by a single defibrillation attempt; (3) an initial defibrillation attempt followed by 3 min of optimal chest compressions; and (4) an initial defibrillation attempt followed by 3 min of conventional chest CHEST / 132 / 1 / JULY, 2007

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compressions. If ROSC was not achieved, each resuscitation sequence was immediately restarted and defibrillation was repeated every 3 min, if needed. The resuscitation procedures were continued until ROSC or for a maximum of 15 min. No vasopressor and, more specifically, no epinephrine was administered during cardiopulmonary resuscitation (CPR) to avoid the additional variables, including the detrimental ␤-adrenergic effects of epinephrine on postmyocardial function.22 ROSC was defined as the restoration of an organized cardiac rhythm with a MAP of ⬎ 60 mm Hg that persisted for an interval of ⱖ 5 min. Precordial compressions were performed with a mechanical chest compressor (Thumper, model 1000; MI Instruments; Grand Rapids, MI) at 100 compressions per min. The compression pad was centered at the junction of the middle and lower third of the sternum. The depth of compressions was visually confirmed during CPR on the scale corresponding to the distance of descent of the piston in the chest compressor (Thumper). Coincident with the start of precordial compressions, the animals were mechanically ventilated with a tidal volume of 15 mL/kg and a fraction of inspired oxygen of 1.0. Chest compressions were synchronized to provide a compression/ventilation ratio of 15:2 with equal compression-relaxation intervals. Electrical defibrillation was attempted with a single biphasic 150-J electrical shock, which was delivered between the conventional right infraclavicular electrode and the apical electrode (Heartstart XL defibrillator; Philips Medical Systems; Andover, MA). Each defibrillation was preceded by a 10-s interval for visual ECG rhythm confirmation of VF. After successful resuscitation, anesthesia was maintained and the animals were monitored for an additional 4 h. Catheters were then removed, wounds were surgically repaired, and the animals were extubated and then returned to their cages. Analgesia with butorphanol (0.1 mg/kg) was administered by IM injection as needed over the following 72 h. The animals were then observed for an additional 68 h. At the end of the 72-h postresuscitation observation interval, animals were reanesthetized with ketamine and pentobarbital. Echo-Doppler measurements of myocardial functions were then repeated. Animals were then euthanized with an IV injection of 150 mg/kg pentobarbital. Autopsy was routinely performed for the documentation of potential injuries to the thoracic and abdominal viscera during CPR or due to obfuscating disease. Measurements Hemodynamic data, EtPco2, and ECG were continuously measured and recorded on a personal computer-based data acquisition system using appropriate hardware/software (CODAS; Computer Data Acquisition System; Cambridge, MA), as previously described.21 The CPP was digitally computed from the differences in time-coincident diastolic aortic pressure and RAP was displayed in real time. Arterial and mixed venous blood gas, hemoglobin, and oxyhemoglobin levels were measured on 200-␮L aliquots of blood with a stat profile analyzer (ULTRA C; Nova Biomedical Corporation; Waltham, MA), which was adapted for porcine blood. Arterial and mixed-venous blood lactate levels were measured with a lactic acid analyzer (model 23L; Yellow Springs Instruments; Yellow Springs, OH). These measurements were obtained 15 min prior to inducing cardiac arrest, and at 60 min and 240 min following ROSC. Cardiac output was measured by conventional thermodilution techniques after the injection of 5 mL of saline solution maintained at a temperature between 0 and 2°C. Echocardiographic measurements were obtained with the aid of a 5.5/7.5 Hz biplane Doppler transesophageal echocardiographic transducer with four-way flexure (model 21363A; Hewlett-Packard Co; Andover, MA). Left ventricular end-systolic and end-diastolic volumes were 72

calculated by the method of discs, as previously described.21 From these, stroke volumes (SVs), ejection fractions (EFs), and fractional area changes (FACs) were computed. Measurements were obtained at baseline and at hourly intervals thereafter for a total of 4 h. These measurements were repeated at 72 h following resuscitation. A neurologic alertness score, which was developed by our group,20 was used for evaluating neurologic recovery at 24, 48, and 72 h. Statistical Analysis The independent variables were the quality of chest compressions (optimal or conventional) and the priority of treatment (ie, chest compressions-first or defibrillation-first). The dependent variables included the following: arterial blood gas measurements; heart rate; MAP; RAP; MPAP; EtPco2; thermodilution cardiac output; initial resuscitation; numbers of shocks delivered prior to ROSC; incidence of recurrent VF; the duration of CPR; postresuscitation myocardial function, including left ventricular SVs, EFs and FACs; duration of survival; and postresuscitation neurologic recovery. Analyses were performed with a statistical software package (Statistica, version 6.1 for analyses of variance; StatSoft Inc; Tulsa, OK). Analysis of variance was used for continuous variables. Binomial responses were evaluated with a Fisher exact test. A p value of ⬍ 0.05 was regarded as being statistically significant.

Results There were no differences in the weight of the animals and in the baseline values of blood gas or lactate measurements, ECG heart rate, MAP, EtPco2, RAP, MPAP, thermodilution CO, and echocardiographically measured myocardial function among groups prior to inducing cardiac arrest or at hourly intervals for 4 h in resuscitated animals. CPP and EtPco2, during the first 3 min of CPR, were significantly greater in the groups that received optimal chest compressions compared to those that received conventional chest compressions (Fig 1). The quality of chest compressions was the major determinant of ROSC (p ⫽ 0.0004). After optimal chest compressions, each animal was successfully resuscitated. As shown in Table 1, this contrasted with the situation in animals after conventional chest compressions, of which only 2 of 12 had ROSC (p ⬍ 0.0001). Regardless of the order of initiating CPR with either defibrillation-first or chest compressions-first, the only differences in outcome were related to the quality of the chest compressions. The first shock terminated VF only when optimal chest compressions preceded defibrillation. There were no significant differences in the duration of CPR prior to ROSC or in the number of episodes of recurrent VF among resuscitated animals (Table 1). Each resuscitated animal survived for ⬎ 72 h with full neurologic recovery (Table 1). As anticipated, SV, EF, and FAC were significantly reduced in each resuscitated animal during the 4-h interval after Original Research

Figure 1. CPP and EtPco2 during the first 3 min of precordial compressions (PCs). CPP and EtPco2 were significantly greater during optimal chest compressions. * ⫽ p ⬍ 0.05, ** ⫽ p ⬍ 0.01, † ⫽ p ⬍ 0.0001 vs conventional chest compressions groups.

ROSC, but these measures had normalized at 72 h in each instance (Table 2). Autopsy revealed no evidence of CPR-related injury. Discussion The timing of defibrillation, whether before or after an interval of chest compressions, in this model

of ischemically induced cardiac arrest had no significant effects on ROSC or on postresuscitation outcomes. This contrasted with the dominant role of chest compression depth. Initial defibrillation prior to chest compressions required a larger number of shocks prior to ROSC. Though suboptimal chest compressions after an initial electrical shock yielded a minority of survivors, the ultimate benefit of a shock-first protocol was contingent on the performance of optimal chest compressions. This more limited benefit of a shock-first protocol was consistent with clinical experience.23,24 The primary determinant of initial resuscitation and survival was the efficacy of the chest compressions. The priority of the role of chest compressions was documented in human victims by Wik et al1 under the theme of “good bystander CPR.” Whereas 23% of victims were resuscitated after what Wik et al1 defined as “good CPR,” only 1% were resuscitated with “not good CPR.” In both in-hospital and outof-hospital settings, the quality of CPR, and specifically chest compressions, was also the major determinant of the ROSC. Based on 176 victims of out-of-hospital cardiac arrest, only 28% of rescuers performed competent chest compressions in which the anterior-posterior diameter was decreased by approximately 5 cm so as to conform to the international guidelines.5,6 Abella et al4 also observed an inadequate depth of chest compressions based on 67 instances of in-hospital cardiac arrest. CPP values generated during CPR are directly related to the depth of the chest compressions.25 Threshold levels of CPP have also been identified as the leading predictor of the success of CPR.14,26 –29 Our study supports these earlier findings. In fact, optimal chest compressions resulted in both greater CPP and greater EtPco2. EtPco2 has also emerged as an indicator of the effectiveness of chest compressions; it is in fact an indirect measurement of

Table 1—Outcomes* Optimal CC Outcomes Resuscitated Shocks prior to ROSC, No. Duration of CPR prior to ROSC, s Episodes of recurrent VF, No. 72-h survival Total

Conventional CC

CCs First

Shock First

CCs First

Shock First

6/6 1⫾0 190 ⫾ 1 1.3 ⫾ 2.8 6/6

6/6 2 ⫾ 0.6§ 220 ⫾ 106 1.5 ⫾ 1.4 6/6

0/6†

2/6‡ 1.5 ⫾ 0.7 396 ⫾ 330 0⫾0 2/6‡

12/12

0/6† 2/12㛳

*CC ⫽ chest compression. †p 0.001 vs optimal-CC groups. ‡p 0.025, vs optimal-CC groups. §p 0.05 vs optimal-CC first. 㛳p ⱕ 0.0001 vs optimal-CC groups. www.chestjournal.org

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Table 2—Echocardiographically Measured Myocardial Function* Optimal CC Variables SV, mL BL PR 1 h PR 2 h PR 3 h PR 4 h PR 72 h EF, % BL PR 1 h PR 2 h PR 3 h PR 4 h PR 72 h FAC, % BL PR 1 h PR 2 h PR 3 h PR 4 h PR 72 h

Conventional CC

CC First

Shock First

CC First

Shock First

26 ⫾ 3 20.8 ⫾ 4 19.2 ⫾ 1.7 20.9 ⫾ 3 21.3 ⫾ 1.2 22 ⫾ 3.3

26 ⫾ 3 19.3 ⫾ 4.2 20 ⫾ 3.7 22 ⫾ 4.4 21.5 ⫾ 5.5 26.7 ⫾ 6.9

23 ⫾ 3

25 ⫾ 3 20.6 ⫾ 5.2 20.5 ⫾ 6.4 22.6 ⫾ 6.1 18.8 ⫾ 0.9 25 ⫾ 3.9

61 ⫾ 2 54.5 ⫾ 4.6 55.3 ⫾ 3.4 54.5 ⫾ 3.9 54.8 ⫾ 3.7 57.7 ⫾ 3.4

59 ⫾ 3 47.7 ⫾ 8.2 48.8 ⫾ 5.3 48.3 ⫾ 5.4 50 ⫾ 5.7 59 ⫾ 2.1

61 ⫾ 3

61 ⫾ 3 47.5 ⫾ 6.4 49 ⫾ 2.8 50 ⫾ 4.2 50 ⫾ 4.2 54.5 ⫾ 4.9

46 ⫾ 2 41.5 ⫾ 6.6 42.3 ⫾ 3.4 40 ⫾ 5.3 39.7 ⫾ 3 45.2 ⫾ 3.3

47 ⫾ 4 35.2 ⫾ 7.6 39.7 ⫾ 4 36.3 ⫾ 6.3 35.3 ⫾ 7 47.7 ⫾ 4.4

44 ⫾ 5

46 ⫾ 5 33 ⫾ 14.1 33.5 ⫾ 9.2 34.5 ⫾ 4.9 32 ⫾ 11.3 38 ⫾ 7.1

*Values are given as the mean ⫾ SD. BL ⫽ baseline; PR ⫽ postresuscitation. See Table 1 for abbreviation not used in the text. None of the differences between categories were statistically significant.

pulmonary blood flow during CPR and therefore of cardiac output produced by chest compressions.30,31 EtPco2 continuously exceeded the threshold level of approximately 15 mm Hg only during optimal chest compressions, values that are predictive of successful resuscitation.32,33 These greater EtPco2 values observed during optimal chest compressions are explained through the greater cardiac outputs and therefore greater systemic and pulmonary blood flows generated by the more effective chest compressions, in contrast to those produced by conventional chest compressions. Improvements in rates of survival to hospital discharge among persons who had experienced prolonged cardiac arrest from 24 to 30% were reported by Cobb et al,9 as was more favorable neurologic recovery, from 17 to 23%, when 90 s of CPR preceded the defibrillation attempt. In a separate clinical trial,10 including 200 victims of cardiac arrest, there was better 1-year survival when chest compressions preceded defibrillation. The present study therefore supports the benefit of chest compressions, providing that they are optimal, as the initial intervention. When optimal chest compressions preceded attempted defibrillation, a smaller number of electrical shocks was required for the ROSC. We recognize limitations in the present study and in the interpretation of the results. First, our study was performed on young and healthy anesthetized 74

animals that were free of underlying disease, under conditions of optimal airway control and mechanical ventilation, conditions that are not likely to prevail in most out-of-hospital settings. Moreover, the direct applicability of our experimental findings to clinical practice cannot be assumed. Though the experimental protocol in the present study provided for a 5-min interval of untreated VF, clinical settings typically present with variable durations of untreated cardiac arrest. These limitations notwithstanding, this controlled experiment demonstrated that the quality of chest compressions, and specifically the depth of chest compressions, was primarily responsible for outcomes after an interval of 5 min of untreated cardiac arrest. Survival was assured in this model when chest compressions were optimal and poor when chest compressions were suboptimal. The priority of shock-first or compressions-first had a much less important role. References 1 Wik L, Steen PA, Bircher NG. Quality of bystander cardiopulmonary resuscitation influences outcome after prehospital cardiac arrest. Resuscitation 1994; 28:195–203 2 Gallagher EJ, Lombardi G, Gennis P. Effectiveness of bystander cardiopulmonary resuscitation and survival following out-of-hospital cardiac arrest. JAMA 1995; 274:1922–1925 3 Van Hoeyweghen RJ, Bossaert LL, Mullie A, et al. Quality and efficiency of bystander CPR: Belgian Cerebral ResusciOriginal Research

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