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Resuscitation from ischemic ventricular fibrillation is more difficult than electrical ventricular fibrillation and is characterized by greater time to restoration of spontaneous circulation, frequent refibrillation, greater number of countershocks, higher epinephrine dose during resuscitation efforts, profound cardiac dysfunction, and a short-term survival rate approaching clinical experience. Ischemically induced ventricular fibrillation is a more clinically relevant model for the evaluation of resuscitation interventions.

A B S T R A C T Electrical ventricular defibrillation of heavy subjects (over 100 kg body weight) is uncommon for the human or any animal species. This paper reports trans-chest ventricular defibrillation of subjects ranging in weight from 2.3 to 340 kg using conventional defibrillation current (heavily damped sine wave) of 0.3-30 ms duration. It was found that a body weight-toelectrical-shock strength relationship exists and can be expressed in terms of either electrical energy or peak current. For the duration of current pulse used clinically (3-10 ms), the relationship between energy requirement and body weight is expressed by the equation U = 0.73 W"52, where U is the energy in W s and W is the body weight in kilograms. The current relationship is I = 1.87 W0 M where I is the peak current in amperes and W is the body weight in kilograms. The energy dose is somewhat more species and weight dependent and ranges from 0.5 to 10 W s/kg (0.23-4.5 W s/lb). The data obtained indicate that the peak current dose is virtually species and weight independent and is therefore a better indicator than energy for electrical defibrillation with precordial electrodes. In the duration range of 3-10

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SUMMARY Cardiopulmonary resuscitation (CPR) has been thought to produce blood flow by compression of the heart between the sternum and spine, termed "external cardiac massage," but there has been-no direct experimental documentation of this proposed mechanism.Micromanometric pressure recordings were synchronized with cineangiograms during mechanical CPR in 17 dogs with induced ventricular fibrillation. Chest compression produced equivalent pressure increases in the aorta (Ao) and right atrium (RA) (Ao 32 + 14 mm Hg, RA 30 ± 14 mm Hg; NS), a linear relationship between aortic and intrapleural pressures (r = 0.87, p < 0.001) over a wide range of induced pressures, cineangiographic blood flow through both left-heart chambers, and a pressure gradient (21 ± 14 mm Hg) between all intrathoracic cardiovascular compartments and the jugular veins that resulted from closure of venous valves at the thoracic inlets. Simultaneous chest compression and lung inflation significantly increased all intrathoracic vascular pressures, the aortojugular venous gradient (42 ± 13 mm Hg, p < 0.05 vs chest compression alone), electromagnetically determined carotid arterial blood flow (1.75 ± 0.81 ml/min/kg vs 0.51 ± 0.27 mI/min/kg during chest compression alone, p < 0.005), and angiographic left-heart flow.We conclude that blood flow during CPR results principally from an increased intrathoracic pressure and that there is selective flow to the brachiocephalic vascular bed because of the arteriovepous gradient produced by venous valves at the thoracic inlets. Greater intrathoracic pressure resulting from simultaneous inflation and compression improves left-heart flow. The left heart is therefore a conduit, not a pump, during CPR.THE ABILITY of closed-chest cardiopulmonary resuscitation (CPR) to produce an arterial pulse and perfuse vital organs in the arrested circulation was demonstrated experimentally and clinically in 1960 and termed "external cardiac massage."' As the name implied, the technique was thought to produce selective ventricular compression between the sternum and spine, propelling blood forward through the systemic vasculature. The technique was quickly accepted and its efficacy documented in clinical reports.2However, early hemodynamic observations during experimental CPR by Weale and Rothwell-Jackson' showed that chest compression resulted in an equal increase in arterial and venous pressures recorded in the iliac vessels, and the absence of a significant pressure gradient was believed to argue against antegrade flow. right atrium and arterial bed could result in retrograde flow or reflux into the extrathoracic venous bed. Rudikoff and co-workers" showed the absence of a significant net aortic-central venous pressure gradient during chest compression and documented that the pressures in all cardiac chambers and in the thoracic aorta increase proportionately with the increase in intrapleural pressure. These findings suggest that vascular pressures and flow recorded during chest compression are dependent upon the generated i...

We examined the rate of fall of arterial O2 saturation (dSao2/dt) after apnea onset in four spontaneously breathing adult male baboons. We postulated that a lower mixed venous O2 saturation (Svo2) would steepen dSao2/dt by more rapid depletion of alveolar O2. Single isolated (NREP) and five or more sequential repetitive apneas (REP) were created by clamping an indwelling cuffed endotracheal tube at end expiration. Fiberoptic catheters were used for continuous monitoring of Sao2, Svo2, and cardiac output. The mean dSao2/dt for all duration NREP apneas was 0.60%/s. Mean dSao2/dt increased above base line for each consecutive REP apnea and was higher in 60 s than in 45 and 30 s REP apnea series. The increase in dSao2/dt corresponded closely with the fall in preapneic Svo2. Preapneic arterial O2 content fell during successive REP apneas but the maximal decrement from base line (1.3 ml/dl) was much less than the maximal decrement in preapneic mixed venous O2 content of 5.1 ml/dl. Preapneic cardiac output for NREP apneas and nadir cardiac output for REP apneas remained constant. Nadir cardiac output for NREP apneas showed higher values for longer duration apneas. We concluded that dSao2/dt is inversely related to preapneic Svo2.

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