The physiologic basis for cardiac resuscitation from ventricular fibrillation—Method for serial defibrillation

Abstract A number of procedures which can be credited with a measure of success in defibrillating the ventricles of dogs and in restoring normal, vigorous beats are reviewed. The physiologic conditions which seem to determine success or failure are analyzed and, based upon this, a modification of the countershock method, called serial defibrillation, which appears to be more uniformly successful, is described. In dogs with exposed hearts, fibrillation can be stopped and coordinated beats re-established by passing strong alternating currents for brief intervals (0.1 to 5 sec.) through the ventricles, provided such countershock is applied within approximately two minutes. It has been estimated that, in order to achieve similar results in man by applying electrodes to the chest, 2,000 to 3,000 volts yielding currents of twentyseven to thirty amperes might be needed; so much current would be dangerous to both operator and patient. Hearts of dogs which have fibrillated for five to fifteen minutes may likewise be revived, provided the ventricles are rhythmically compressed by hand for about one minute previous to the application of the countershock. Frequent inability to revive the ventricles by these procedures is the result of one or more factors: (1) Failure to abolish every trace of fibrillation, (2) failure of natural pacemakers, or conduction, to survive (3) depression of muscle fractions as a result of anoxia, so that they cannot respond with sufficiently vigorous contractions after defibrillation, and (4) the reawakening of too many pacemakers, which cause a reversion to fibrillation through conflicting excitations. As regards the first difficulty, our recent experimental work indicates that fibrillation can be more certainly abolished in every portion of the ventricle, and by the use of weaker currents, if, instead of one shock, three to seven shocks are applied at intervals of about one or two seconds. Each consecutive shock causes a coarser type of fibrillation, involving larger masses of muscle, until the final shock arrests the fibrillation completely. It is apparently not necessary for such currents to traverse the entire myocardium in order to bring about complete defibrillation. We call the procedure serial defibrillation . It is preferable to the use of drugs, such as quinidine, procaine, etc.; the adjuvant defibrillating action of these drugs has not yet been crucially demonstrated, but the fact that they exert a depressing action on contractility is well established. As regards the second and third difficulties, it has been shown that the viability of pacemakers and of contracting myocardium can be assured by efficient massage which raises arterial pressure, restores coronary flow, and relieves the anoxia. Incidentally, the viability of the central nervous system tends to be maintained. The use of stimulating drugs, such as epinephrine, calcium salts, etc., cannot be expected to benefit an anoxic mammalian heart, and, after reoxygenation, usually sets up multiple pacemakers which tend to cause reversion to fibrillation. The difficulties of meeting the conditions necessary for the revival of human fibrillating hearts are analyzed. The conclusion is reached that, although such an achievement is not impossible, we cannot anticipate remarkable results in the present state of our knowledge. For the present, it seems most profitable to attempt to discover, through methodical research, means of rendering the ventricles less sensitive to agents which cause fibrillation, or, even better, wholly refractory to them.