Active compression-decompression resuscitation: A novel method of cardiopulmonary resuscitation

Active compression-decompression resuscitation: A hovel method of cardiopulmonary resuscitation

Chest compression is an important part of cardiopulmonary resuscitation (CPR), but it only aids circulation during a portion of the compression cycle and has been shown to only minimally increase blood flow to vital organs. The purpose of this study was to quantitate the short-term hemodynamic effects of CPR with a hand-held suction device that incorporates both active compression and decompression of the chest. The suction device was applied to the middle of the sternum and compared with standard manual CPR in eight nonventilated anesthetized dogs. Coronary perfusion pressure, systolic and diastolic aortic pressures, right atrial diastolic pressure, and the velocity time integral (an analog of cardiac output), which were obtained by means of transesophageal pulsed wave Doppler echocardiography from the main pulmonary artery, were measured every 30 seconds during CPR. Minute ventilation was measured over the last minute of each CPR technique. Both active compression-decompression CPR and standard CPR were sequentially performed for 2 minutes in random order 30 seconds after induced ventricular fibrillation. The CPR techniques consisted of 100 compressions per minute, with a compression depth of 1.5 to 2 inches and a 50% duty cycle. Coronary perfusion pressure, velocity time integral (cardiac output analog), minute ventilation, and systolic arterial pressure were all significantly improved by active compression-decompression CPR when compared with standard CPR. We conclude that active compression-decompression CPR is a simple technique that appears to improve coronary perfusion pressure, systolic arterial pressure, cardiac output, and minute ventilation in nonventilated animals when compared with standard CPR. Further research is necessary to determine the efficacy of this method in patients who are experiencing cardiac arrest. (AM HEART J 1992;124:1145.)

Todd J. Cohen, MD, Kelly J. Tucker, MD, Rita F. Redberg, MD, Keith G. Lurie, MD, Michael C. Chin, BS, John P. Dutton, BS, Melvin M. Scheinman, MD, Nelson B. Schiller, MD, and Michael L. Callaham, MD Sun Francisco, Calif.

Since the original description of manual cardiopulmonary resuscitation (CPR) by Kouwenhoven et al.’ in 1960, little has changed with regard to this technique. The American Heart Association currently recommends manual CPR, which consists of active chest compression to a depth of 1.5 to 2 inches at a rate of 80 to 100 compressions per minute and a 50% duty cycle with passive chest expansion.2 This technique is known to be inefficient, since it produces less than one third of the normal cardiac output.3 A

From the Department of Medicine and the Cardiovascular Research Insti- tute, University of California, San Francisco.

Received for publication Mar. 5, 1992; accepted May 1, 1992.

Reprint requests: Todd J. Cohen, MD, Director of Electrophysiology, Car- diology Division. North Shore University Hospital-Cornell University Medical College, 300 Community Dr., Manhasset, Long Island, NY 11030.

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large number of studies have been performed in an effort to find a better technique for CPR that would improve perfusion and chances of resuscitation.4-12 To date, none of these methods have gained wide- spread acceptance as a preferred method of CPR.

Lurie et a1.13 described an episode of cardiac arrest in an elderly man. His son, who was not trained in standard CPR, applied a plunger to his father’s chest and proceeded to resuscitate him. The authors hy- pothesized that this form of resuscitation effectively provided both active compression and relaxation (decompression) of the chest. In addition, they thought this method may have facilitated ventilation.

The purpose of this study was to quantitate the short-term hemodynamic effects of resuscitation with a hand-held suction device that incorporates both active compression and decompression of the chest.

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A

B

ml- ‘C I

STANDARD CPR

=-a ACDCPR Fig. 1. Right atria1 and ascending aortic pressure tracings during standard (panel A) and ACD CPR (panel B) in dog no. 1. Standard CPR resulted in a cardiac output of I.4 L/min, a systolic arterial pressure of 59 f 6 mm Hg, and no ventilation. ACD CPR produced a cardiac output of 3.2 L/min, a systolic arterial pressure of 85 mm Hg, and a minute ventilation of 5.3 L/min.

METHODS

This study was approved by the University of California, Committee on Animal Research and was performed in ac- cordance with the “Principles of Laboratory Animal Care” as formulated by the National Society of Medical Research and “Guide for Care and Use of Laboratory Animals,” which was prepared by the National Academy of Sciences and published by the National Institutes of Health (DHEW [NIH] Publication 85-23, revised 1985). The suction device was constructed from a rubber polymer and consisted of a large suction cup head (radius = 5.2 cm; height = 3 cm; thickness = 0.5 cm) and a handle.

For each experiment, the dogs were premeditated with fentanyl (0.04 mg/kg) and droperidol (2 mg/kg), anesthetized with pentobarbital sodium (7 to 12 mg/kg adminis- tered intravenously), and endotracheally intubated. The animals were not endotracheally ventilated during CPR, so that both ventilatory and hemodynamic effects of active compression-decompression (ACD) and standard CPR could be assessed. The long-haired dogs’ chests were shaved to provide a smooth surface for ACD suction-adhe- sion. Two micromanometer pressure transducers (model

no. 110-4, Camino Laboratories, San Diego, Calif.) were inserted through the femoral vein and artery and positioned with the use of fluoroscopy in the right atrium and ascending aorta to record ascending aortic and right atria1 pressures. Ventricular fibrillation was induced by applica- tion of alternating current to the right ventricular apex via a 6F right ventricular quadripolar catheter.

Coronary perfusion pressure was determined by the dif- ference between mean aortic pressure and mean right atria1 pressure in diastole. Pulsed wave Doppler tracings, which were continuously obtained from the main pulmonary artery, were used to determine the velocity time integral (VTI). The VT1 or stroke distance is an expression of the distance that an average red blood cell travels during each compression cycle. This is obtained by integrating the pulsed wave velocity profile over time.“-‘7 Cardiac output can be determined from the product of VTI, pulmonary arterial cross-sectional area, and compression rate. In a given animal, assuming that cross-sectional area and compression rates are constant, the VT1 represents an analog of cardiac output. The minute ventilation was determined by spirometry.

ACD resuscitation was performed with the suction cup placed in the middle or slightly to the right of the sternum (depending on the chest configuration). The CPR operator was positioned over the chest, on a stool, with hands on the handle of the ACD device. A downward force was applied to actively compress the suction cup head and the chest to the standard depth. Once the device and the chest were completely compressed, the operator pulled up on the handle, which pulled the chest back to a fully expanded position, without losing contact with the chest wall (chest decompression phase).

ACD CPR was compared with standard manual CPR in eight nonventilated anesthetized dogs (with weights of 10 to 30 kg). The first three animals were beagles with flat chests, such that when each animal was on its back, the suction cup could adhere directly to the middle of the sternum. In five mongrel dogs with keel-shaped chests, the suction cup surface area exceeded the small keel-shaped area, and thus CPR was performed slightly off center; the animal was secured with a V-shaped stoichiometric device. Each animal was randomized (with the use of a random numbers table) to receive ACD and standard CPR sequentially for 2 minutes each.

The first experiment (pilot study) was performed at the end of a 30.minute defibrillation protocol after the dog be- came asystolic. The remainder of the experiments were performed again in healthy, hemodynamically stable animals after 30 seconds of induced ventricular fibrillation. Each CPR method was performed at a rate of 100 compressions per minute. Compressions were synchronized to a metronome, and the depth and duty cycle were monitored by an American Heart Association Certified Advanced Cardiac Life Support instructor. The instructor gave con- tinuous feedback to the operator in an attempt to maintain a compression depth of 1.5 to 2 inches and a 509; duty cycle. After 2 minutes of use of the first technique, two transthoracic defibrillations were attempted (200 J and 400

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J). If successful, at least 5 minutes was allowed before re- induction of ventricular fibrillation and assessment of the second technique. If the defibrillation was unsuccessful, the second CPR technique was started immediately, and the recording of CPR data started 1 minute after the shock. This delay in recording hemodynamic data was created to minimize the immediate postshock effects of released en- dogenous catecholamines. Coronary perfusion pressure, systolic and diastolic aortic pressures, right atria1 diastolic pressures, and VT1 were recorded at 30, 60, 90, and 120 seconds of CPR. Hemodynamic measurements were obtained over a &second period before the measured time in- terval. Minute ventilation was determined between 60 and 120 seconds of CPR. In four dogs, arterial blood gases were obtained immediately after each CPR technique. In three dogs, end-tidal COs concentration was obtained at 30, 60, 90, and 120 seconds of each CPR technique (Nellcor PlOOO, Capnometer, Hayward, Calif.).

All data are presented as means + standard deviation. ACD CPR was compared with standard CPR with Stu- dent’s two-tailed t test. A p value of less than 0.05 was con- sidered statistically significant.

RESULTS

Fig. 1 shows the right atria1 and ascending aortic pressures that were obtained during standard and ACD CPR in animal no. 1. Fig. 2, A-F shows systolic and diastolic aortic pressures, right atria1 diastolic pressure, coronary perfusion pressure, minute ventilation, and VT1 for each technique in each dog. ACD CPR resulted in significant increases in each measured parameter, except diastolic aortic and right atria1 pressures, as compared with standard CPR. Specifically, when compared with standard CPR, ACD CPR increased coronary perfusion pressure (18 I 11 mm Hg during ACD CPR; 8 + 6 mm Hg during standard CPR; p < 0.02), VT1 (8.0 f 1.1 cm/ compression during ACD CPR; 4.4 + 1.4 cm/compression during standard CPR; p < O.OOOl), minute ventilation (4.2 + 1.4 L/min during ACD CPR; 2.0 + 1.2 L/min during standard CPR;p < 0.01); and systolic aortic pressure (58 k 19 mm Hg during ACD CPR; 44 +- 11 mm Hg during standard CPR; p < 0.01). Diastolic aortic and right atria1 pressures were not significantly different when the ACD technique was used. Arterial blood gases that were obtained immediately after CPR in four dogs (dogs nos. 1,3,7, and 8) demonstrated a pH of 7.30 +- 0.18, PCOZ of 38 -t 24 mm Hg, and PO:! of 81 f 18 mm Hg after standard CPR. Values that were obtained after ACD CPR were similar, with a pH of 7.37 + 0.22, POZ of 103 k 53. mm Hg, and PCOZ of 35 + 19 mm Hg (p = NS for all values). In the first three dogs end-tidal COs tended to be higher with ACD CPR, 17 i 8 mm Hg with ACD as compared with 13 + 7 mm Hg with standard CPR, but this trend was not

a)

Active compression-decompression CPR 1147

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31 STD ACD

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ST0 AC0

STD ACD

STD AkD

Fig. 2. Panels A-F show the systolic and diastolic aortic pressures, right atria1 diastolic pressures, coronary perfusion pressures, VTI, and minute ventilation in each dog for both ACD and standard CPR. Consistent increases were observed with systolic aortic pressure (p < O.Ol), coronary perfusion pressure (p < 0.02), VT1 (p < O.OOOl), and minute ventilation (p < 0.01) during ACD as compared with standard CPR.

statistically significant. In two of eight dogs (dogs nos. 2 and 8), ventricular fibrillation remained re- fractory to transthoracic defibrillation after standard CPR but converted spontaneously during ACD resuscitation (Fig. 3, A and B). There were no dogs in which the reverse was true. Autopsies were performed in all animals after completion of the CPR protocol. No evidence of myocardial contusion or rib

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STOP ACD CPR

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Fig. 3. Panels A and B show simultaneous recordings of the surface ECG and right atrial and ascending aortic pressure tracings during standard and ACD CPR in dog no. 8. After 2 minutes of standard CPR, 200 J and 300 J transthoracic shocks failed to terminate ventricular fibrillation, and ACD CPR was promptly instituted. Within the next 15 seconds, spontaneous ventricular activity was noted. After 1 minute, ACD CPR was stopped, and high-grade atrioventricular block was present but resolved shortly thereafter.

fracture was noted as a result of either CPR technique.

DISCUSSION

This is the first study to demonstrate improved coronary perfusion pressure, VT1 (an analog of cardiac output), minute ventilation, and systolic arterial pressure through the use of ACD resuscitation. This new method of CPR employs a suction device that adheres to the anterior chest and thus facilitates chest expansion and compression. We speculate that venous return and cardiac filling are improved by the negative intrathoracic pressure, which produces the significant increase in cardiac output that was observed in our study.

Previously, complicated devices have been applied to the abdomen and chest to assist in ventricular filling and CPR. In 1939, Eisenmenger described a large abdominal suction device called the “Biomotor” in an article entitled, “Suction and Air Pressure Over the Belly, Its Action and Applications.“” He demonstrated the circulation of India ink in a human ca- daver but was unable to successfully apply this device to patients who were experiencing cardiac arrest. Other devices such as the tank respirator or “iron

lung,” the cuirass, and the breathing jacket have been developed and implemented to assist ventilation in the patient with paresisI

Ohomoto et a1.20 described a method of CPR in which external cardiac massage and abdominal coun- termassage were applied by means of two machines in closed-chest dogs. Carotid and coronary flows were increased by 1.4 to 2 times with this method when compared with manual CPR. Recently manual abdominal counterpressure during CPR has been re- ported to improve survival after cardiac arrest in human beings. 21 However, the hemodynamic improvements that were attained with all of these methods have usually been marginal.4-‘”

Fig. 4 shows the Active Compression-Decompres- sion resuscitator (Cardiopump, Ambu, International, Copenhagen, Denmark), which has been developed for use in human beings during cardiac arrest. This device consists of a circular handle to ensure stabil- ity, a calibrated gauge to monitor performance, and a suction cup to permit chest decompression without dislodgment. This device is currently undergoing clinical investigation in the United States, as well as abroad.

Our study has several limitations. First, a trained

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Fig. 4. The Active Compression-Decompression (ACD) resuscitator, which has been developed for use during cardiac arrest in human beings. This device permits both active chest compression (A) and active chest expansion or decompression (BJ.

observer monitored compression depth and duty cycle during both CPR techniques. A mechanical method for controlling both force and displacement would have been preferable, but in our efforts to de- velop such a device we found that it limited the ease and effectiveness of the decompression phase, so we had to rely on the observer method of controlling the depth of chest compression. This problem is similar to that. of many prior studies of cardiac arrest, which relied on human (and thus not completely standard- ized and reproducible) compression of the chest or abdomen. A second limitation is that this study was designed to assess the immediate effects of ACD CPR on both ventilation and circulation, and therefore animals were not ventilated during CPR. This design did in fact demonstrate that ACD CPR provided su- perior and physiologic ventilation. We do not believe the lack of ventilation affected the hemodynamic variables that we measured because of the similarity of the blood gas values in both treatment groups and the fact that they were both within the expected range during experimental cardiac arrest. The effects of ACD CPR on nonintubated dogs require further investigation. A further limitation is that we measured hemodynamic variables, including coronary perfusion pressure, but did not directly measure coronary or cerebral perfusion or survival. Of note, end- tidal CO:! concentration has been shown to correlate well with coronary perfusion pressure and myocardial perfusion in cardiac arrest,22-26 and there was a trend toward increased end-tidal CO* concentration with the ACD technique. Future studies are necessary to determine the exact mechanism of augmented hemodynamics during ACD resuscitation and to measure to what degree this technique improves cerebral and myocardial perfusion, as well as survival.

The ACD CPR technique uses standard American Heart Association recommendations for CPR2 in conjunction with interposed active chest expansion. Use of the ACD device (Cardiopump) is a simple manual technique, which is easy to perform and requires no set-up time. Therefore it appears to be practical for first responders to apply this method during early CPR. This method also provides physiologic minute ventilation in intubated animals. We conclude that ACD CPR holds the promise of a much more effective method of CPR with a simple device that requires minimal training to use and that animal and human survival studies may be warranted.

ADDENDUM

After completion of this animal study, a study of similar design investigated ACD CPR in human beings late during cardiac arrest. This subsequent study confirmed that dramatic improvements in cardiopulmonary circulation occur with ACD CPR as compared with standard CPR.27 REFERENCES

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Active compression-decompression resuscitation: A novel method of cardiopulmonary resuscitation