Carl J. Wiggers

The mechanism and nature of ventricular fibrillation

Abstract Ventricular fibrillation, which is a common cause of sudden death following anesthesia, coronary occlusion, electric shock, etc., cannot be adequately described as an asynchronous, incoordinate contraction of ultimate cardiac fractions. The process is an evolution of changes from the moment of its inception until it ceases completely, which is within thirty to forty-five minutes. The visible spread of waves and punctate unipolar electrocardiograms are reviewed. The available evidence favors the conclusion that, after a single premature systole, the phenomenon is caused by re-entry of circulating wave fronts which involve smaller and smaller blocks of myocardium, each of which develops an independent excitation. As a result of the anoxia which develops progressively after the cessation of coronary flow, conduction is slowed and the vigor of fractionate contractions decreased. The resultant of these changes causes, in succession, the undulatory, convulsive, tremulous, and atonic stages of its evolution. The theory which best explains these sequential changes and the initiation of fibrillation by the application of a brief, strong, localized shock during the vulnerable period of late systole may be stated briefly as follows: In order to initiate fibrillation, an electrical stimulus or noxious influences with a “fibrillation threshold” must be applied during the vulnerable period of late systole, at which time certain elements have passed out of the refractory phase. Such a stimulus excites impulses in a number of nonrefractory fractions. These weave their way slowly through local, nonrefractory tissue to form a small wave front, from which a massive excitation wave sweeps over comparatively large portions of the myocardium in sequential order. This constitutes the first premature systole. If the wave front is large enough, and the mode of spread favorable for re-entry at, or near, the point of excitation, several circuits are formed through the ventricles; this is the undulatory stage. In some way—possibly by collision of different excitation fronts, combined with slow conduction-these masses of myocardium are broken into smaller and smaller ones, in which divided waves reenter more frequently. Thus the process passes successively into the convulsive and tremulous stages; during the latter there are innumerable avenues of re-entry. The atonic stage is characterized by progressive enfeeblement of contraction and gradual failure of conduction, which are the result of anoxia caused by cessation of the coronary circulation. This theory is obviously incomplete in many details and can be expanded only through the development of more perfect methods for following the spread of impulses over the cardiac surface.

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.

Studies of ventricular fibrillation caused by electric shock

Abstract 1. 1. The natural course of events from the onset of fibrillation following faradic excitation to complete diastolic rest was studied by recording electrocardiograms and moving pictures simultaneously. In addition, intraventricular pressure curves were optically recorded during a number of experiments. The changes taking place when fibrillation was inhibited by intraventricular injections of 5 per cent KCl and the process of recovery following similar injections of 5 per cent CaCl2 solutions combined with massage, were investigated by the same means. 2. 2. Fibrillation induced by faradic stimulation continues naturally for fifteen to fifty minutes and may be divided into 4 stages, on the basis of surface changes, electrocardiographic deflections and intraventricular pressure variations. 3. 3. The initial stage of tachysystole lasts less than one second and is characterized by the spread of rapidly recurring but coordinated contraction waves, by large electrocardiographic deflections with steep gradients and by definite if small intraventricular pressure variations. 4. 4. The second stage of convulsive incoordination ordinarily lasts fifteen to forty seconds and is characterized by rapid irregular localized contractions which spread short and variable distances over the heart. They are accompanied by large electrical deflections, 600 or more per minute, which vary considerably in size, amplitude and contour. 5. 5. The third stage of tremulous incoordination ordinarily continues two or three minutes and is characterized by multitudes of irregular yet forceful shivering or trembling motions, each speading very short distances and with highly variable frequencies over different surface regions. They give rise to small irregular electrocardiographic oscillations having frequencies between 1100 and 1700 per minute, and are capable of increasing the intraventricular pressure level slightly. 6. 6. The fourth stage of atonic incoordination is characterized by feeble wavelets of contraction spreading irregularly and at slow rates over small areas until more and more areas become quiescent, and finally the very slightest movements remain in a few areas only. The electrical deflections perhaps become slightly more regular in contour and spacing, but their amplitude becomes progressively smaller, and their frequency is gradually reduced to 400 per minute or less. 7. 7. Potassium chloride injected into both ventricular cavities does not modify the stages through which fibrillation naturally passes; it merely hastens the process so that fibrillation stops within an average period of 2.4 minutes. 8. 8. Intraventricular injections of CaCl2 after potassium inhibition combined with massage, first inaugurate a coordinated idioventricular rhythm, characterized by slow waves of contraction sweeping over the two ventricles asynchronously but in coordinated fashion. After a short interval, a supraventricular rhythm is reestablished, the electrocardiogram regaining all its normal characteristics.

The Interplay of Coronary Vascular Resistance and Myocardial Compression in Regulating Coronary Flow

By integrating phasic coronary sinus flow curves in such a way that volume flow during systole plus isometric contraction and that during the remainder of diastole can be compared, the relative contribution of ventricular compression and coronary resistance to mean coronary flow can be assessed. It was found that anoxia, adenylic acid, compression of the aorta or pulmonary artery reduces coronary vascular resistance while epinephrine increases it. The augmentation in coronary mean flow following epinephrine is due solely to the greater force of ventricular contractions. On the basis of such evidence a revival of the “massaging theory” in modified form is suggested. Evidence was incidentally obtained which supports a former conclusion that the coronary sinus drains territories supplied by the right as well as the left coronary artery.

The Henry Jackson Memorial Lecture Dynamics of Ventricular Contraction under Abnormal Conditions

This lecture reviewed selected types of experiments carried out in our laboratory which are relevant to the interpretation of clinical disorders. From an analysis of ventricular pressure pulses, inferences were drawn as to basic determinants of cardiac performance in experimental conditions simulating those which arise clinically. The analysis included alterations in ventricular contraction patterns produced by pericardial effusion, hypervolemia, oligemia, arterial hypertension of peripheral origin and that due to coarctation of the aorta, aortic and pulmonary stenosis, idioventricular rhythms, ventricular alternation, coronary occlusion and myocardial ischemia, aortic regurgitation, and mitral insufficiency.

Myocardial depression in shock: A survey of cardiodynamic studies☆☆☆

The question as to whether myocardial depression occurs in hemorrhagic shock and, if so, its importance was reinvestigated. For this purpose the cardiodynamic changes which occur after simple hemorrhage, during prolonged hypotension (50 to 30 mm. Hg), during reinfusion of all the withdrawn blood, and during spontaneous circulatory failure following infusion, were studied in the same animal. In different series of experiments in which the same standard technique was used, we studied changes in calibrated arterial pressure pulses, cardiac output by a modified Stewart method, alterations in effective venous pressure, ventricular volume and pressure curves, inferior vena cava flow, and electrocardiograms by standard and chest leads. Following simple hemorrhage sufficient to reduce mean arterial pressure to 50 mm. Hg, the changes in ventricular action are all secondary to reduction in venous return and decrease in effective central venous pressure. Electrocardiograms reveal no significant changes. Changes in the contour of the central arterial pulse consist in abridgement of the period of systolic ejection and development of a primary spike followed by a peaked summit, and this is followed by a deep incisura. As a result of decreased venous pressure, ventricular filling is slower, initial tensions decrease in both ventricles, and their diastolic size is smaller. Pressure and volume curves indicate that the ventricles expel their diminished volumes with good velocity. If severe posthemorrhagic hypotension is prolonged for 135 minutes, death results from an oligemic type of failure unless blood is reinfused. However, such reinfusion is of only temporary benefit; a slow spontaneous circulatory failure and eventually death follow. Irreversibility develops during the period of prolonged hypotension. This includes depression of the myocardium, for while venous return continues to decrease slightly, effective venous and initial ventricular pressures return to or above control levels and the diastolic size of the ventricles augment. Nevertheless, the stroke volume and cardiac output decrease. Myocardial depression is further indicated by a subminimal stroke volume when venous pressures are elevated to normal levels and by development of S-T depression in electrocardiograms. Reinfusion of blood restores arterial pressures and pulses as well as cardiac output to normal, but in order to do so the ventricles are required to operate under supernormal conditions of high venous pressure and initial tensions. As soon as these re-establish at normal levels, cardiac output decreases, and the ventricles pump less efficiently due to a depressed state of the myocardium. As arterial pressure declines to ca. 70 mm. Hg, reduction in venous return becomes so great that the myocardial depression is obscured but is detectable by special tests. A progressive circulatory failure develops despite the fact that blood volumes are not significantly decreased. This represents a form of normovolemic shock due solely to default of the peripheral circulation and of the myocardium. The preduction of venous return is of paramount importance, but circulatory failure is hastened by coexistent myocardial depression. Since the functional state of the myocardium and the capacity of the coronary responses at the time of shock-producing catastrophies may often be below par, myocardial depression may play as significant a subsidiary role in some cases of human shock as it did in our animals submitted to a particular type of hemorrhage and shock. The problem deserves further careful exploration by cardiologists.

Basic hemodynamic changes produced by aortic coarctation of different degrees.

Basic hemodynamic studies on experimental coarctation of the aorta just beyond the left subclavian artery have revealed that hitherto unsuspected physical and physiologic factors are involved in creation of hypertension above a coarctation and in changes of pressure pulses below such a lesion. The effects are by no means explained by an increased resistance at the coarctation, as is generally believed. This communication analyzes the roles that changes in capacity and distensibility of the aortic compression chamber and increase in systolic discharge of the left ventricle play in the production of aortic hypertension, and discusses the physiologic compensations in blood flow by which an adequate return to the right heart is maintained despite extreme reduction in flow through the inferior cava. This communication also deals with the ways in which the pressure relations in the lower aorta and femoral artery are altered from the normal, emphasizing the relative shares that damping of the pulse wave and reduced input into the lower aorta play with different degrees of coarctation. The changing characteristics of the murmurs with progressive aortic constriction are also analyzed. The conclusion is reached that all the dynamic changes found in experimental and human coarctation are adequately explained without the assumption of accessory vasoconstriction through reflex or humoral agencies.

THE FUNCTIONAL CONSEQUENCES OF CORONARY OCCLUSION

Excerpt The symptomatology of acute coronary occlusion is too well-known to require detailed redescription. Let it suffice for our purpose to recall three outstanding phenomena, so serious for the ...

The functional importance of coronary collaterals.

T HE PHYSICIAN attending a patient with a recent coronary occlusion is confronted with many questions of prognostic importance: How long will muscles in the ischemic area remain viable? What will determine the size, shape, and depth of the infarct? What are the chances that collateral blood supply will limit its extent, promote healing, and prevent subsequent aneurysmal dilatation? Are drugs likely to be helpful? Careful clinical observations followed by necropsy control can suggest answers to these questions; basic knowledge derived from experimental studies helps to establish the correctness of the answers.

CARDIAC ADAPTATIONS IN ACUTE PROGRESSIVE ANOXIA

Excerpt CIRCULATORY REACTIONS IN MAN The reactions of the cardiovascular system in man to progressively diminishing oxygen have been repeatedly described, among others by Whitney,1Schneider,2Schnei...