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(Circulation. 1997;95:1335-1340.)
© 1997 American Heart Association, Inc.

Articles

Phased Chest and Abdominal Compression-Decompression

A New Option for Cardiopulmonary Resuscitation

Wanchun Tang, MD; Max Harry Weil, MD, PhD; Robert B. Schock, PhD; Yoji Sato, MD; John Lucas, ME; Shijie Sun, MD; Joe Bisera, MSEE

the Institute of Critical Care Medicine (W.T., M.H.W., Y.S., S.S., J.B.), Palm Springs, Calif; the University of Southern California School of Medicine (W.T., M.H.W., S.S., J.B.); and the Cardiac Assist Division, Datascope Corp (R.B.S., J.L.), Fairfield, NJ.

	Abstract

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Background We describe a new manual method of phased chest and abdominal compression-decompression with a Lifestick resuscitator for cardiopulmonary resuscitation (CPR).

Methods and Results Ventricular fibrillation (VF) was induced in 20 domestic pigs. After either 5 or 7 minutes of untreated VF, either phased chest and abdominal compression-decompression (Lifestick resuscitator) or precordial compression was initiated. Defibrillation was attempted at 2 minutes after the start of CPR. For the animals in which VF was untreated for 7 minutes, epinephrine was administered in doses of 20 µg/kg at 2 minutes after start of CPR. The coronary perfusion pressure generated by the Lifestick resuscitator was more than twofold greater (P<.01) than that generated by conventional precordial compression. Of 5 control animals, none were resuscitated after 5 minutes of VF. However, each of 5 animals treated with the Lifestick resuscitator was resuscitated (P<.01) and survived after 48 hours (P<.01). When untreated VF was prolonged to 7 minutes and epinephrine was administered, only 2 of the 5 control animals were resuscitated, and none of them survived for more than 4 hours. However, each of the Lifestick-treated animals was resuscitated and survived for more than 48 hours (P<.01).

Conclusions Phased chest and abdominal compression-decompression substantially increased hemodynamic efficacy of CPR and outcome in terms of successful resuscitation, 48-hour survival, and cerebral recovery.

Key Words: cardiopulmonary resuscitation • fibrillation • heart arrest • defibrillation • death, sudden

	Introduction

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It is estimated that in the United States alone, each year more than 500 000 otherwise functional individuals will die suddenly of cardiac causes. Fewer than 3% of these victims are likely to be successfully resuscitated to the extent that they are restored to productive lives.^{1 2}

During cardiac arrest, myocardial ischemia prompts maximal relaxation of coronary vessels, and coronary blood flow becomes essentially pressure dependent.^{3 4} Coronary blood flow is therefore remarkably well correlated with the CPP. The CPP is defined as the pressure gradient established between the aorta and the right atrium during the relaxation phase of precordial compression. Both in animal models and in human victims of cardiac arrest, CPP has served as the most reliable single predictor of the success of resuscitation.^{5 6 7}

External precordial compression as described in the landmark report by Kouwenhoven et al⁸ more than 30 years ago remains the standard intervention for sustaining organ perfusion during cardiac arrest. However, the coronary perfusion so generated rarely exceeds >30% of normal.^{9 10} Consequently, it fails to meet the metabolic requirements of the fibrillating heart. Global myocardial ischemia therefore persists during the conventional resuscitation effort.^{11 12}

The disappointing outcomes with conventional CPR during the past 35 years have prompted researchers to examine alternative methods by which blood flow produced by precordial compression may be increased. Interposed abdominal compression,¹³ active compression-decompression,^{14 15} and circumferential chest compression¹⁶ represent such alternative methods. In addition, intermittent ascending aortic balloon occlusion⁶ and extracorporeal circulation¹⁷ represent more invasive options. The newer noninvasive methods have yielded only moderate increases in CPP. The more invasive options provide for consistently greater CPP and improvements in outcome. However, their use is constrained by the time-consuming strategies that are required for assembling the devices and for vascular cannulation within the very small time window of resuscitability. Accordingly, there is as yet no persuasive evidence that these new methods have improved the ultimate outcome of CPR in human victims.

The concept of phased chest and abdominal compression-decompression and the development of the Lifestick resuscitator were based in part on the modeling study of Lin et al.¹⁸ These authors evaluated the efficacies of diverse mechanical methods of chest compression with a computer-based analog model presented by Babbs et al.¹⁹ The iterations of this model pointed to active compression and decompression of both the thorax and abdomen with a phase shift of 180° as optimal for coronary and cerebral perfusion. Subsequent in vivo trials by two of us (R.B.S., J.L.) suggested that a phase shift of 240° would further augment coronary and cerebral perfusion pressures. This option was adopted for the present study, in which the outcomes between conventional precordial compression and phased chest and abdominal compression-decompression were compared. Two levels of severity were selected. In the first group, VF was untreated for 5 minutes before compression was begun. In the second group, VF was untreated for 7 minutes, and epinephrine was administered in conjunction with compression. We further postulated that any improvement in outcomes of CPR on these established porcine models^{6 11 12 20} would be reflected in greater hemodynamic efficiency and especially greater CPP and increased PETCO₂.

	Methods

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Procedures
The protocol of studies was approved by our Institutional Animal Care and Use Committee. 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 (NIH publication 86-33, revised 1985).

Twenty domestic pigs 5 to 7 months old and weighing between 40 and 50 kg were investigated. The animals were fasted overnight except for free access to water. Anesthesia was initiated by injection of ketamine (20 mg/kg IM) and completed by ear vein injection of sodium pentobarbital 30 mg/kg. Our previous studies have demonstrated that in this porcine model, no significant difference in hemodynamic measurements during or after CPR or in outcomes occurred when the animals were anesthetized with either pentobarbital or an inhalant anesthetic agent, isoflurane.²¹ After tracheal intubation, the animals were mechanically ventilated with a Puritan Bennett MA-1 ventilator with a tidal volume of 15 mL/kg, peak flow of 40 L/min, and FIO₂ of 0.21. Respiratory rate was adjusted to maintain PaCO₂ between 35 and 40 mm Hg. PETCO₂ was monitored with an infrared analyzer (model 601 POET, Crit Care System). Anesthesia was maintained with bolus injections of 8 mg/kg pentobarbital IV, typically at 30-minute intervals.

Two 8F angiographic catheters (model 5441, Bard Inc) were surgically inserted into the left and right femoral arteries and advanced into the thoracic and abdominal aortas, respectively. These served for simultaneous measurement of thoracic and abdominal aortic pressures. For measurements of pulmonary artery pressure, right atrial pressure, blood temperature, and cardiac output, a balloon-tipped pentalumen thermodilution catheter (41216-01, Abbott) was flow-directed from the right femoral vein into the pulmonary artery. For measurement of intrathoracic pressure, a balloon-tipped catheter (model 4378, Ackrad Laboratories) was advanced from the incisor teeth into the esophagus for a distance of 35 cm. To induce VF, a 4F pacing catheter was advanced through the right cephalic vein into the right ventricle guided by the endocardial electrogram until a current of injury was recorded. Positions of the catheters were confirmed by characteristic pressure morphology and/or with fluoroscopy. Blood temperature was continuously measured in the pulmonary artery and maintained at 38±0.5°C with surface heating or cooling.

Measurements
Dynamic data, including lead II ECGs, intravascular pressures, intrathoracic pressures, PETCO₂, tidal volumes, and blood temperatures processed with conventional amplifiers were recorded with a PC-based data acquisition system supported by CODAS software. The frequency response of the system was 35 Hz with optimal damping. The CPP was digitally computed and displayed in real time. It represented the difference between the middiastolic aortic pressure and simultaneously measured mid–right atrial pressure, as previously described.^{6 11 12} The values for each beat were averaged within each preceding minute. Cardiac output was measured in the pulmonary artery by the bolus thermodilution method. A quantitative neurological alertness score based on the modifications of quantitative neurological deficit score proposed by Bircher and Safar²² was used for evaluating neurological recovery. Alertness was scored from 0 (unarousable coma) to 100 (fully alert). The alertness score is based on objective grading of level of consciousness, respiration, posture, and food and water intake. In earlier studies, the alertness score was highly correlated with the neurological deficit score (r=.97).

Blood was sampled from the thoracic aorta and pulmonary artery for measurement of blood gases with an automated blood gas analyzer (model 1301, Instrumentation Laboratories) and spectrophotometric oximeter (model 362 Co-oximeter, Instrumentation Laboratories) adapted for porcine blood. Blood lactate was measured with a lactic acid analyzer (model 23L, Yellow Springs Instruments).

Experimental Procedure
In the first study of 10 animals, immediately before VF was induced, animals were randomized to one of two groups. VF was induced by an alternating current delivered to the right ventricular endocardium. Mechanical ventilation was stopped. After 5 minutes of untreated VF, conventional precordial compression was initiated with precordial compression with a Thumper (model 1000, Michigan Instruments) or with phased compression-decompression of both the thorax and the abdomen, with the Lifestick resuscitator (Datascope Corp). In the animals that were randomized to conventional CPR, the chest was compressed at a rate of 80 cpm with equal compression-relaxation intervals as previously described.⁶ The force of chest compression was adjusted to decrease the anterior-posterior diameter of the chest by 25% to 30%. This corresponded to a Thumper force ranging from 140 to 160 lb (64 to 73 kg).

The prototype Lifestick was designed as a manually powered, noninvasive cardiac assist device (Fig 1). The device was constructed from a single rigid frame to which nonsterile adhesive-backed elastomeric pads were attached, one for adhesion to the chest and the other for adhesion to the abdomen. The chest pad, which measured 8x7 in (20x18 cm), was centered at the midsternum. The abdominal pad, which measured 10x15 in (25x38 cm), extended from a point immediately caudal to the xiphoid cartilage to the epigastrium. The pads were affixed to the shaved skin with medical-grade hydrogel adhesive. The frame incorporated handles through which appropriate forces were transmitted alternately to the chest and abdomen (Fig 1). The device was operated in seesaw fashion (Fig 2) with the operator standing on the left side of the animal.

View larger version (92K): [in this window] [in a new window]   Figure 1. Lifestick resuscitator.

View larger version (16K): [in this window] [in a new window]   Figure 2. Sequencing compression-decompression with the Lifestick resuscitator. The subject's head is on the right. Chest compression (A) is coincident with abdominal decompression (B). This is followed by chest decompression (C) and abdominal compression (D).

The operator's arms were extended and hands firmly applied to the handles of the resuscitator. This arrangement provided stability of the device, mechanical advantage, and minimal operator fatigue. The compressive forces applied to the chest and abdomen were 120 lb (55 kg) and 50 lb (23 kg), respectively. They were monitored with the aid of load cells (ELF-1000/26 Flatline Series Load Cells, Entran Devices, Inc) mounted to the frame assembly at the connection to the chest and abdominal pads. The output from the load cells was displayed to the operator, who was trained to maintain the force of chest and abdominal compression within 5 lb of the specified compressive force.

Compression at a frequency of 60 cpm was prompted by a metronome. An analog output of the applied forces was continuously recorded. The force gauge of the mechanical thumper and the load cells of the Lifestick were calibrated before each experiment. Immediately before attempted defibrillation, the operator removed his hands from the resuscitator. The transthoracic defibrillatory shock was delivered through conventional paddles applied to the lateral recesses of the chest pads.

For the control group, mechanical ventilation with oxygen was synchronized with the Thumper to provide a compression-to-ventilation ratio of 5:1. With the Lifestick resuscitator, two breaths of oxygen were delivered with a valved bag after each 15 cycles of phased chest and abdominal compression.

Defibrillation was attempted after 2 minutes of compression with a 200-J DC countershock. If VF was not reversed, compression-decompression was continued for an additional 60 seconds, after which a second 200-J countershock was delivered. Sequences were repeated for a maximum of 6 minutes. When the electrical shock produced a pulseless rhythm (electromechanical dissociation), compressions were continued but no additional electrical countershocks were delivered. Restoration of spontaneous circulation was defined as a return of a spontaneous supraventricular rhythm that generated a mean aortic pressure of 60 mm Hg for a minimum duration of 5 minutes.

Resuscitated animals were observed under intensive care conditions until they had recovered from the effects of anesthesia. The animals were then returned to their cages. Alertness in survivors was scored at 12-hour intervals for 48 hours. The animals were then euthanized by injection of 150 mg/kg pentobarbital IV. Autopsy was performed for documentation of injuries to the bony thorax and the thoracic and abdominal viscera.

In an additional 10 animals, the protocol was the same in every respect except that the duration of untreated VF was prolonged to 7 minutes and epinephrine in doses of 20 µg/kg bolus was injected into the right atrium after 2 minutes of precordial compression and repeated at 3-minute intervals thereafter.

Statistical Analyses
All data are presented as mean±SD. Resuscitability and 48-hour survival were analyzed with Fisher's exact test. Differences in the alertness scores were analyzed by ANOVA and multiple comparison procedures. Alertness was scored as zero for animals that died before the 12th hour after return of spontaneous circulation.

Differences of hemodynamic and metabolic measurements between groups were analyzed by ANOVA using the Scheffe method for multiple comparison. A value of P<.05 was regarded as significant.

	Results

Top Abstract Introduction Methods Results Discussion References

 
Twenty studies were performed and completed. Baseline measurements, which included measurements of aortic pressure, pulmonary artery pressure, CPP, and PETCO₂, did not differ between groups (Tables 1 and 2). After 5 minutes of untreated VF, none of the 5 animals were successfully resuscitated by conventional precordial compression in the absence of epinephrine. In contrast, all 5 animals were successfully resuscitated with phased chest and abdominal compression-decompression without administration of epinephrine. These animals demonstrated normal alertness at both 24 and 48 hours (Table 3). A significantly lower number of rib fractures was observed in the first group of animals resuscitated with the Lifestick resuscitator. When the duration of untreated VF was prolonged to 7 minutes and epinephrine was injected, each of the 5 animals was successfully resuscitated with phased chest and abdominal compression-decompression, and each survived for more than 48 hours. This contrasted with conventional chest compression, after which 2 of the 5 animals were resuscitated but none survived for more than 4 hours (Table 4). No significant injuries to the thoracic or abdominal viscera were observed, although a greater number of rib fractures followed conventional precordial compression.

View this table: [in this window] [in a new window]   Table 1. Effects of Lifestick Resuscitator After 5 Minutes of Untreated Cardiac Arrest

View this table: [in this window] [in a new window]   Table 3. Outcomes of Lifestick Resuscitator After 5 Minutes of Untreated Cardiac Arrest

View this table: [in this window] [in a new window]   Table 4. Outcomes of Lifestick Resuscitator in Combination With Epinephrine After 7 Minutes of Untreated Cardiac Arrest

CPP, aortic pressure, and PETCO₂ generated with the Lifestick resuscitator were significantly greater than those produced by conventional chest compression (Table 1). Representative tracings of CPPs, aortic pressure, and PETCO₂ generated by the Lifestick resuscitator are compared with those from conventional precordial compression (Fig 3). We also observed progressive increases in VF ECG voltage during phased chest and abdominal compression-decompression but only a transient increase in conventionally treated animals (Table 1). Both positive and negative thoracic pressures were significantly greater with the Lifestick resuscitator (Table 1). The greater hemodynamic efficacy of phased chest and abdominal compression-decompression was also observed after cardiac arrest was prolonged to 7 minutes and treatment included administration of epinephrine (Table 2).

View larger version (107K): [in this window] [in a new window]   Figure 3. Representative analog record of a control animal and a Lifestick-treated animal after 5 minutes of untreated VF. CPP, aortic pressure (AP), and PETCO2 are shown at 3 minutes after start of compression. Arrow labeled A indicates onset of chest compression and abdominal decompression. Arrow labeled B indicates onset of chest decompression and abdominal compression.

View this table: [in this window] [in a new window]   Table 2. Effects of Lifestick Resuscitator in Conjunction With Epinephrine After 7 Minutes of Untreated Cardiac Arrest

	Discussion

Top Abstract Introduction Methods Results Discussion References

 
The present study in a porcine model of cardiac arrest and resuscitation documented that phased chest and abdominal compression-decompression significantly improved immediate resuscitability, 48-hour survival, and neurological recovery compared with conventional precordial compression. This applied to group 1, in which VF was untreated for 5 minutes, and to group 2, in which VF was untreated for 7 minutes and the resuscitation protocol included epinephrine.

Striking improvements in outcomes with phased chest and abdominal compression-decompression were associated with corresponding increases in CPP. During global myocardial ischemia of cardiac arrest, myocardial blood flow becomes essentially pressure dependent.³ Both experimental and clinical studies have demonstrated that CPP is remarkably well correlated with both myocardial blood flow^{3 4} and the likelihood of successful resuscitation.⁶ CPPs above the threshold value of 15 mm Hg are associated with proportionately greater rates of survival in both animal models and human patients.^{23 24 25} CPP was consistently >30 mm Hg with the Lifestick resuscitator, a level more than twofold greater than with conventional precordial compression.

The impressively greater PETCO₂ provided further evidence that the Lifestick method of phased chest and abdominal compression-decompression maintained substantially greater pulmonary and therefore systemic blood flow, and it also produced greater minute ventilation.^{26 27}

Finally, phased chest and abdominal compression-decompression yielded greater VF voltages. This is additional evidence that myocardial perfusion was improved. Greater VF voltages are associated with significantly greater likelihood of initial resuscitation and postresuscitation survival; this also applies to human victims.²⁸

The greater hemodynamic efficacy of phased chest and abdominal compression-decompression is likely to be due to a combination of effects. As demonstrated in the present study, active thoracic decompression increases negative intrathoracic pressure, and this could account for increases in venous return and forward blood flow.^{29 30} Abdominal compression is also likely to augment venous return. Accordingly, it is likely to result in greater coronary and cerebral blood flows. Decompression of the abdomen coincident with chest compression might be likely to reduce ventricular afterload, and this would favor increased stroke volumes. These are the mechanical advantages that may explain the improved outcomes that we observed with the new technique of phased chest and abdominal compression-decompression.

Finally, our experience in the experimental setting demonstrated that the Lifestick technique of phased chest and abdominal compression-decompression was learned with only 15 minutes of training. Equally important, one rescuer effectively operated this device for up to 20 minutes without loss of efficiency or limitation due to operator fatigue. The technique is therefore likely to be applicable to both in-hospital and out-of-hospital settings of cardiac resuscitation.

	Selected Abbreviations and Acronyms

 

CPP = coronary perfusion pressure CPR = cardiopulmonary resuscitation PETCO2 = end-tidal PCO2 VF = ventricular fibrillation

	Acknowledgments

 
This study was supported in part by the Datascope Corporation; Mr and Mrs Jack Samuelson of La Canada, Calif; the Laerdal Foundation of Stavanger, Norway; and the Mary Pickford Foundation of Beverly Hills, Calif.

	Footnotes

 
Reprint requests to Max Harry Weil, MD, PhD, The Institute of Critical Care Medicine, 1695 Sunrise Way, Bldg 3, Palm Springs, CA 92262-5309. E-mail weilm@aol.com.

Received June 27, 1996; revision received October 25, 1996; accepted October 28, 1996.

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