Background-Current versions of automated external defibrillators (AEDs) require frequent stopping of chest compression for rhythm analyses and capacity charging. The present study was undertaken to evaluate the effects of these interruptions during the operation of AEDs. Methods and Results-Ventricular fibrillation was electrically induced in 20 male domestic swine weighing between 37. 5 and 43 kg that were untreated for 7 minutes before CPR was started. Defibrillation was attempted with up to 3 sequential 150-J biphasic shocks, but each was preceded by 3-, 10-, 15-, or 20-second interruptions of chest compression. The interruptions corresponded to those that were mandated by commercially marketed AEDs for rhythm analyses and capacitor charge. The sequence of up to 3 electrical shocks and delays were repeated at 1-minute intervals until the animals were successfully resuscitated or for a total of 15 minutes. Spontaneous circulation was restored in each of 5 animals in which precordial compression was delayed for 3 seconds before the delivery of the first and subsequent shocks but in none of the animals in which the delay was Ͼ15 seconds before the delivery of the first and subsequent shocks. Longer intervals of CPR interventions were required, and there was correspondingly greater failure of resuscitation in close relationship to increasing delays. The durations of interruptions were inversely related to the durations of subthreshold levels of coronary perfusion pressure. Postresuscitation arterial pressure and left ventricular ejection fraction were more severely impaired with increasing delays. Key Words: cardiopulmonary resuscitation Ⅲ fibrillation Ⅲ defibrillation Ⅲ compression Ⅲ myocardium A utomated external defibrillators (AEDs) provide the single best option for improving the currently poor outcomes of out-of-hospital cardiopulmonary resuscitation (CPR) performed by bystanders. Fundamental to the operation of AEDs is the capability of automated ECG rhythm analyses, during which CPR is interrupted. Previous experimental studies had demonstrated both decreased resuscitability and greater impairment of postresuscitation myocardial function and survival when precordial compression was interrupted for 20 seconds in small animals. 1-3 Because current versions of AEDs prompt "hands-off" intervals of Ͼ10 seconds for rhythm analyses before advising the rescuer to deliver an electrical shock, as documented below, we hypothesized that such interruptions would adversely affect the outcomes of CPR. Conclusions-InterruptionsThreshold levels of coronary perfusion pressure (CPP) are identified as major determinants of successful cardiac resuscitation. 4 -7 Interruptions in precordial compression predictably result in declines in CPP and therefore delays in restoring threshold values of CPP. 5,6 We therefore anticipated that increasing the length of intervals of interrupted chest compression results in corresponding decreases in the success of CPR and greater severity of postresuscitation myocardial dysfunction.These co...

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The severity of postresuscitation myocardial dysfunction is related, at least in part, to the magnitude of the electrical energy of the delivered shock.

End-tidal CO2 concentration (ETCO2) may serve as a simple noninvasive measurement of the blood flow generated by precordial compression during cardiopulmonary resuscitation (CPR). In a mechanically ventilated porcine preparation of ventricular fibrillation, onset of fibrillation was associated with a rapid decrease in ETCO2 from 4.0 + 0.2% to less than 0.7 + 0.2%. With precordial compression, it increased to 1.9 + 0.3%. Animals that were successfully defibrillated after 12 min of CPR demonstrated an immediate increase in ETCO2. The ETCO2 increased from 1.9 + 0.3% to 4.9 + 0.3% over an interval of between 30 and 60 sec. These changes in ETCO2 were closely related to proportionally similar decreases and increases in cardiac output (CO), and a close correlation between ETCO2 and CO was demonstrated (r = .92). A similar highly significant correlation between ETCO2 and CO was also demonstrated during open-chest cardiac massage (r = .95). ETCO2 therefore serves as a noninvasive measure of pulmonary blood flow and therefore CO. In 17 successfully resuscitated animals, ETCO2 during precordial compression averaged 1.7 + 0.2%, whereas it was only 0.5 ± 0. 1% in five animals in whom resuscitation procedures were unsuccessful (p<.001). Accordingly, ETCO2 prognosticates outcome during CPR and immediately identifies restoration of spontaneous circulation. Circulation 77, No. 1, 234-239, 1988. PRIMARY INTERVENTIONS during cardiopulmonary resuscitation (CPR) include external ventilation after establishing airway patency, and precordial compression.t It is precordial compression that maintains forward flow of blood in amounts that temporarily sustain the viability of major organs and especially the heart and the brain. The cardiac output measured during experimental closed-chest cardiac massage has ranged between 17% and 27% of prearrest values.2-5 Except for arterial or intracardiac pressure measurements, there are currently no reliable options for continuously monitoring the efficacy of precordial compression in terms of the blood flow that is generated. We therefore searched for practical, and preferably noninvasive, options with which the efficacy of precordial compression could be quantitatively monitored. Received Aug. 12, 1987; accepted Sept. 24, 1987. 234 In prior studies in a porcine preparation of cardiac arrest and subsequently on human patients, measurements of arterial blood gases demonstrated hypercarbia in mixed venous blood and hypocarbia in arterial blood during CPR.6-9 There was venous acidemia and arterial alkalemia. A large venoarterial Pco2 gradient was associated with decreases in end-tidal CO2 concentration (ETCO2). We hypothesized that this was related to a critical reduction in pulmonary blood flow during CPR accounting for a critical curtailment of CO2 excretion.10 11 In the present study, we observed a close relationship between ETCO2 and cardiac output. We further demonstrated the potential usefulness of ETCO2 as a prognosticator of resuscitability. Moreover, ETCO2 was an immediate in...

Lower-energy biphasic waveform shocks were as effective as conventional higher energy monophasic waveform shocks for restoration of spontaneous circulation after 4 and 7 min of untreated VF. Significantly better postresuscitation myocardial function was observed after biphasic waveform defibrillation.

A standardized method of cardiopulmonary resuscitation in rodents has been developed for anesthetized, mechanically ventilated rats. Ventricular fibrillation was induced and maintained by an alternating current delivered to the right ventricular endocardium. After 4 min of ventricular fibrillation, the chest was compressed with a pneumatic piston device. Eight of 14 animals were successfully resuscitated with DC countershock after 6 min of cardiac arrest. In confirmation of earlier studies from our laboratories in dogs, pigs, and human patients, this rodent model of cardiopulmonary resuscitation demonstrated large venoarterial [H+] and PCO2 gradients associated with reduced pulmonary excretion of CO2 during the low-flow state. Mean aortic pressure, coronary perfusion pressure, and end-tidal CO2 during chest compression were predictive of successful resuscitation.

AMSA has the potential for guiding more optimal timing of defibrillation without adverse interruption of cardiopulmonary resuscitation or the delivery of unsuccessful high energy electrical shocks that contribute to postresuscitation myocardial injury.

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