A Preliminary Study of Cardiopulmonary Resuscitation by Circumferential Compression of the Chest with Use of a Pneumatic Vest

Peter Belfer Cardiac Mechanics Laboratory, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD 21205.
New England Journal of Medicine (Impact Factor: 55.87). 09/1993; 329(11):762-8. DOI: 10.1056/NEJM199309093291104
Source: PubMed


More than 300,000 people die each year of cardiac arrest. Studies have shown that raising vascular pressures during cardiopulmonary resuscitation (CPR) can improve survival and that vascular pressures can be raised by increasing intrathoracic pressure.
To produce periodic increases in intrathoracic pressure, we developed a pneumatically cycled circumferential thoracic vest system and compared the results of the use of this system in CPR (vest CPR) with those of manual CPR. In phase 1 of the study, aortic and right-atrial pressures were measured during both vest CPR (60 inflations per minute) and manual CPR in 15 patients in whom a mean (+/- SD) of 42 +/- 16 minutes of initial manual CPR had been unsuccessful. Vest CPR was also carried out on 14 other patients in whom pressure measurements were not made. In phase 2 of the study, short-term survival was assessed in 34 additional patients randomly assigned to undergo vest CPR (17 patients) or continued manual CPR (17 patients) after initial manual CPR (duration, 11 +/- 4 minutes) had been unsuccessful.
In phase 1 of the study, vest CPR increased the peak aortic pressure from 78 +/- 26 mm Hg to 138 +/- 28 mm Hg (P < 0.001) and the coronary perfusion pressure from 15 +/- 8 mm Hg to 23 +/- 11 mm Hg (P < 0.003). Despite prolonged unsuccessful manual CPR, spontaneous circulation returned with vest CPR in 4 of the 29 patients. In phase 2 of the study, spontaneous circulation returned in 8 of the 17 patients who underwent vest CPR as compared with only 3 of the 17 patients who received continued manual CPR (P = 0.14). More patients in the vest-CPR group than in the manual-CPR group were alive 6 hours after attempted resuscitation (6 of 17 vs. 1 of 17) and 24 hours after attempted resuscitation (3 of 17 vs. 1 of 17), but none survived to leave the hospital.
In this preliminary study, vest CPR, despite its late application, successfully increased aortic pressure and coronary perfusion pressure, and there was an insignificant trend toward a greater likelihood of the return of spontaneous circulation with vest CPR than with continued manual CPR. The effect of vest CPR on survival, however, is currently unknown and will require further study.

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    • "The snakes accomplish this by encircling their prey with loops of their bodies; pressure is then generated when this coil is reduced in diameter (Greene and Burghardt, 1978;Mehta and Burghardt, 2008). We believe that this circumferential compression generated by snake constriction is especially effective because of the efficiency of energy transfer from this geometric shape change (Halperin et al., 1993). When significant constriction pressure was placed on the rat's thoracic or abdominal region, CVP increased and PAP decreased almost immediately, presumably due to increased thoracic and/or abdominal pressures. "
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    ABSTRACT: As legless predators, snakes are unique in their ability to immobilize and kill their prey through the process of constriction, and yet how this pressure incapacitates and ultimately kills the prey remains unknown. In this study, we examined the cardiovascular function of anesthetized rats before, during and after being constricted by boas (Boa constrictor) to examine the effect of constriction on the prey's circulatory function. The results demonstrate that within 6 s of being constricted, peripheral arterial blood pressure (PBP) at the femoral artery dropped to 1/2 of baseline values while central venous pressure (CVP) increased 6-fold from baseline during the same time. Electrocardiographic recordings from the anesthetized rat's heart revealed profound bradycardia as heart rate (fH) dropped to nearly half of baseline within 60 s of being constricted, and QRS duration nearly doubled over the same time period. By the end of constriction (mean 6.5±1 min), rat PBP dropped 2.9-fold, fH dropped 3.9-fold, systemic perfusion pressure (SPP=PBP-CVP) dropped 5.7-fold, and 91% of rats (10 of 11) had evidence of cardiac electrical dysfunction. Blood drawn immediately after constriction revealed that, relative to baseline, rats were hyperkalemic (serum potassium levels nearly doubled) and acidotic (blood pH dropped from 7.4 to 7.0). These results are the first to document the physiological response of prey to constriction and support the hypothesis that snake constriction induces rapid prey death due to circulatory arrest. © 2015. Published by The Company of Biologists Ltd.
    Preview · Article · Jul 2015 · Journal of Experimental Biology
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    • "Indeed, standard CPR only provides 10–20% of normal blood flow to the heart and 20–30% of normal blood flow to the brain [1] [2] [3]. Many have tried to develop new CPR techniques [4] [5] [6] [7] [8] [9]. Most efforts have focused on means to increase systemic pressures directly during the compression phase of CPR. "
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    ABSTRACT: The purpose of this multicentre clinical randomized controlled blinded prospective trial was to determine whether an inspiratory impedance threshold device (ITD), when used in combination with active compression-decompression (ACD) cardiopulmonary resuscitation (CPR), would improve survival rates in patients with out-of-hospital cardiac arrest. Patients were randomized to receive either a sham (n = 200) or an active impedance threshold device (n = 200) during advanced cardiac life support performed with active compression-decompression cardiopulmonary resuscitation. The primary endpoint of this study was 24 h survival. The 24 h survival rates were 44/200 (22%) with the sham valve and 64/200 (32%) with the active valve (P = 0.02). The number of patients who had a return of spontaneous circulation (ROSC), intensive care unit (ICU) admission, and hospital discharge rates was 77 (39%), 57 (29%), and 8 (4%) in the sham valve group versus 96 (48%) (P = 0.05), 79 (40%) (P = 0.02), and 10 (5%) (P = 0.6) in the active valve group. Six out of ten survivors in the active valve group and 1/8 survivors in the sham group had normal neurological function at hospital discharge (P = 0.1). The use of an impedance valve in patients receiving active compression-decompression cardiopulmonary resuscitation for out-of-hospital cardiac arrest significantly improved 24 h survival rates.
    Full-text · Article · Jul 2004 · Resuscitation
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    • "Newer promising techniques, which require skilled users, include manual chest compression with active decompression [19] [20], and the use of a valve to impede airflow during chest decompression to increase negative intrathoracic pressure [20] [21]. Circumferential thoracic vest inflation techniques can improve pressures substantially [3] [22], but the size, weight, and power requirements of the vest system make it logistically difficult to use. "
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    ABSTRACT: The purpose of this pilot clinical study was to determine if a novel chest compression device would improve hemodynamics when compared to manual chest compression during cardiopulmonary resuscitation (CPR) in humans. The device is an automated self-adjusting electromechanical chest compressor based on AutoPulse technology (Revivant Corporation) that uses a load distributing compression band (A-CPR) to compress the anterior chest. A total of 31 sequential subjects with in-hospital sudden cardiac arrest were screened with institutional review board approval. All subjects had received prior treatment for cardiac disease and most had co-morbidities. Subjects were included following 10 min of failed standard advanced life support (ALS) protocol. Fluid-filled catheters were advanced into the thoracic aorta and the right atrium and placement was confirmed by pressure waveforms and chest radiograph. The coronary perfusion pressure (CPP) was measured as the difference between the aortic and right atrial pressure during the chest compression's decompressed state. Following 10 min of failed ALS and catheter placement, subjects received alternating manual and A-CPR chest compressions for 90 s each. Chest compressions were administered without ventilation pauses at 100 compressions/min for manual CPR and 60 compressions/min for A-CPR. All subjects were intubated and ventilated by bag-valve at 12 breaths/min between compressions. Epinephrine (adrenaline) (1mg i.v. bolus) was given at the request of the attending physician at 3-5 min intervals. Usable pressure signals were present in 16 patients (68 +/- 6 years, 5 female), and data are reported from those patients only. A-CPR chest compressions increased peak aortic pressure when compared to manual chest compression (153 +/- 28 mmHg versus 115 +/- 42 mmHg, P < 0.0001, mean +/- S.D.). Similarly, A-CPR increased peak right atrial pressure when compared to manual chest compression (129 +/- 32 mmHg versus 83 +/- 40 mmHg, P < 0.0001). Furthermore, A-CPR increased CPP over manual chest compression (20 +/- 12 mmHg versus 15 +/- 11 mmHg, P < 0.015). Manual chest compressions were of consistent high quality (51 +/- 20 kg) and in all cases met or exceeded American Heart Association guidelines for depth of compression. Previous research has shown that increased CPP is correlated to increased coronary blood flow and increased rates of restored native circulation from sudden cardiac arrest. The A-CPR system using AutoPulse technology demonstrated increased coronary perfusion pressure over manual chest compression during CPR in this terminally ill patient population.
    Full-text · Article · Jun 2004 · Resuscitation
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