ON THE DIFFERENCES IN THE EFFECTS OF STIMULATION OF THE TWO VAGUS NERVES ON RATE AND CONDUCTION OF THE DOG'S HEART

It may be concluded from the results obtained in these experiments : 1. That stimulation of the right vagus nerve in the dog usually causes arrest of all the chambers of the heart. 2. That stimulation of the left vagus nerve exerts a moderate negative chronotropic effect on the auricles. 3. That stimulation of the left vagus nerve has a profound effect on the conduction of impulses over the auriculoventricular system. 4. That the degree of effect exercised on the auriculoventricular system by stimulation of the left vagus nerve varies. In some dogs conduction is depressed to an extent which causes only a delay in the conduction of impulses from auricles to ventricles (P-R time) ; in other dogs the conduction is depressed to a degree which results in incomplete heart-block; while in still other dogs conduction is so depressed that although the auricles continue to contract, no impulses pass from them to the ventricles. 5. That when stimulation of either the right or left vagus nerve causes asystole of nomotopic ventricular contractions, ectopic ventricular contractions may occur. 6. That the time which elapses before ectopic ventricular contractions occur depends upon the irritability of the ventricular muscle, and this may vary in different dogs. 7. That stimulation of the left vagus nerve may rarely cause sino-auricular block. Possibly stimulation of the right nerve may also produce this effect. 8. That there is consequently usually a great qualitative difference in the action of the two vagus nerves on the heart of the dog.     

STUDIES WITH THE ELECTROCARDIOGRAPH ON THE ACTION OF THE VAGUS NERVE ON THE HUMAN HEART : II. THE EFFECTS OF VAGUS STIMULATION ON THE HEARTS OF CHILDREN WITH CHRONIC VALVULAR DISEASE.

The electrocardiographic records taken during vagus stimulation by pressure from children suffering with chronic heart disease have shown that the stimulation of the vagi in these cases is strikingly effectual. In some of the cases, a definite difference was demonstrated between the action of the right and left vagi. The control of the rate of the heart-beat seemed to predominate usually in the right vagus nerve, while the control of stimulus conduction from auricles to ventricles apparently predominated usually in the left vagus. This difference in the two nerves probably exists on account of the difference in their anatomical distribution, the right vagus going especially to that part of the heart which controls the rate of contraction, the sinus node above the right auricle, and the left vagus going especially to that part in which the conducting mechanism is found. Each nerve, however, has to a lesser degree the function which predominates in the other. The whole heart seems to respond, as a rule, more promptly to right than to left vagus pressure, and fairly constant differences have been seen in the effects which stimulation of each nerve has on the various waves of the electrocardiograms. The stimulation of each vagus may influence directly the contractions of the ventricles, causing great diminution in their force. Right vagus stimulation was followed at times by a complete dissociation of auricles and ventricles. The auricular rhythm was slowed sufficiently at this time to allow the ventricles, whose inherent rhythmicity is apparently unaffected by right vagus stimulation, to take up their own independent rhythm. The heightened ventricular rhythmicity in these cases allowed this to take place after only moderate slowing of the auricles. The independent ventricular rhythm was sometimes established in the region of the node of Tawara, for no disturbance of the ventricular portion of the electrocardiogram occurred. At another time, some other point in the ventricles inaugurated the stimuli of the independent ventricular contractions and an abnormal electrocardiogram resulted. The resemblance of our curves, showing dissociation, to those obtained during right vagus and left accelerator stimulation in dogs is definite. That analogy, the clinical picture, and the form of the electrocardiograms of these cases have led us to the belief that an important feature in the pathological physiology of these cases is hypertonus of the cardiac accelerator nerves. This factor, as a cause of symptoms and as a hindrance to the establishment of cardiac rest, may prove of great importance, against which a new form of cardiac therapeutics must be directed.     

STUDIES WITH THE ELECTROCARDIOGRAPH ON THE ACTION OF THE VAGUS NERVE ON THE HUMAN HEART : I. THE EFFECT OF MECHANICAL STIMULATION OF THE VAGUS NERVE.

In hearts showing auricular fibrillation mechanical stimulation of the right vagus nerve causes, as a rule, marked slowing or stoppage of ventricular rhythm, without producing any appreciable effect in the electrocardiographic record of the auricular fibrillation. The ventricular pauses are apparently due to the blocking of stimuli from the auricles. The force of ventricular systole is distinctly weakened for several beats after vagus stimulation, and ectopic ventricular systoles have been seen in several instances, apparently the result of the vagus action. There may, in some cases, be lowered excitability of the ventricles, while no constant change is seen in the size of the electrical complexes representing ventricular systole.     

THE INFLUENCE OF THE VAGUS NERVES UPON CONDUCTION BETWEEN AURICLES AND VENTRICLES IN THE DOG DURING AURICULAR FIBRILLATION

The experiments that have been reported indicate that stimulation of either the right vagus or the left vagus nerve is equally effectual in blocking impulses from the auricles to the ventricles when auricular fibrillation is present. Stimulation of the left vagus nerve is as effectual in blocking impulses from the normally beating auricles as from the auricles when in a state of fibrillation, and the type of auricular activity has apparently no influence on the effect which stimulation of the left vagus has on auriculoventricular conduction.     

THE INFLUENCE OF THE VAGUS NERVES ON THE FARADIZED AURICLES IN THE DOG'S HEART

An abnormal auricular activity is produced by faradization of the right auricle of the dog, which frequently becomes established and continues for varying periods of time after faradization is discontinued. This auricular activity consists of a rapid auricular tachycardia coexisting with true auricular fibrillation. In some dogs the auricles are thrown into this abnormal activity more readily by faradization after the vagi have been cut than before. Cutting the nerves has little or no effect on the abnormal auricular activity, but the ventricular rate may be much increased if the vagi are cut after the abnormal auricular activity has been established, apparently because of an improvement in the auriculoventricular conductivity. Stimulation of the right vagus nerve changes the character of the activity of the faradized auricles by inhibiting the auricular tachycardia while the fibrillation is uninfluenced. Stimulation of the left vagus nerve has little or no apparent inhibitory effect on the auricular tachycardia, but has possibly an inhibitory effect on the auricular fibrillation. Vagus stimulation increases the susceptibility of the auricles to faradization. The abnormal activity set up by faradization may be established in hearts otherwise refractory by vagus stimulation of short duration following the faradization. Vagus stimulation usually holds the auricles in the abnormal activity set up by faradization as long as it is continued in hearts in which, without vagus stimulation, the sequential beat always returns as soon as faradization is stopped. The right vagus is more effectual in this respect than the left. In some hearts vagus stimulation alone is capable of initiating the same abnormal auricular activity which is caused by auricular faradization. The normal sequential beat is often restored by vagus stimulation. It replaces the abnormal auricular activity not during, but a few seconds after, the termination of vagus stimulation. Left vagus stimulation is somewhat more effectual in producing this result than right vagus stimulation.     

A STUDY WITH THE ELECTROCARDIOGRAPH OF THE MODE OF DEATH OF THE HUMAN HEART

In four of the seven cases the ventricles remained active from one and a half to eighteen minutes after the electrocardiograms failed to show evidence of auricular activity. In two cases the auricles outlasted the ventricles and in one case only did the auricles and ventricles stop apparently at the same time. Complete dissociation occurred three times. Some delay in the conduction time was seen in five of the seven cases. In two cases the auricles ceased to beat before evidence of impaired conduction appeared. There was always marked slowing; the slowest independent ventricular rates varied from 13.6 to 47.0. The slowest rates at which the auricles beat regularly varied from 20 to 65 per minute. There was never evidence of auricular fibrillation, although in two cases the electrocardiograms give fairly conclusive evidence that ventricular fibrillation occurred. The ventricles reëstablished a regular rhythm after a short period of ventricular fibrillation in one case, while in the other but one ventricular contraction occurred after the appearance of fibrillation. Characteristic changes in the ventricular complex of the electrocardiograms occurred in all the records. They consisted of a gradual fusion of the R- and T-waves, forming, when the fusion was complete, a large rounded or peaked wave. In some cases the identity of the two waves was not entirely lost. In spite of the marked change in shape of the ventricular complexes, there was often but little change in their duration. In some cases the ventricular systole was shortened at the end, while in others it was prolonged. The change in the form of the ventricular electrical complex indicates that the course of the stimulus and the manner of the contraction of the muscle were abnormal. The fact that the R-wave became gradually prolonged suggests that the conduction of the stimulus through the ventricular walls became delayed as the heart died. The fact that after death there is a continuation of cardiac muscular activity sufficient to cause a difference in electrical potential between the two sides of the body does not necessarily mean that a ventricular systole in the sense of muscular shortening takes place. It has been observed experimentally that well defined electrical complexes may be caused by cardiac activity which cannot be seen or recorded graphically. As the duration of the ventricular complexes characteristic of the dying heart usually does not differ markedly from the duration of the complexes before clinical death, it seems probable that the entire musculature of the ventricles participates in the contraction; as definite shortening, or at least a marked change in duration, would be expected if only a part of the ventricular musculature participated in the activity which produced the complex.     

THE EFFECT OF MORPHIN ON THE MECHANISM OF THE DOG'S HEART AFTER REMOVAL OF ONE VAGUS NERVE

The effect of injecting morphin in right vagus dogs is to slow or practically to stop auricular systoles, the circulation being maintained by ectopic, independent, ventricular contractions. The function of conduction is, relatively speaking, undisturbed. The fact that after morphin injections there is little or no disturbance of conduction in right vagus dogs and a profound one in left vagus dogs may be used as a factor in distinguishing between them, especially when there is a reduction in rate greater than usual in left vagus dogs. The effect on left vagus dogs is to slow the rate of the auricles moderately and to increase the length of conduction, so that partial auriculoventricular block or complete auriculoventricular dissociation results. These are precisely the results that have been obtained by faradic stimulation of one vagus nerve, the other being divided. There are slight differences in the results obtained between the two methods, but the explanation for these is probably to be found in the differences in the nature of the experiments. When faradic stimulation is employed, the stimulus is applied a short time only,—in our experiments for periods not longer than ten seconds. The occurrence of the maximum effect is sudden and does not provide for a gradual introduction of the ventricles to new conditions. In right vagus stimulation the ventricles usually stop beating. A gradual introduction is, however, not always necessary, as may be seen in figures 5 and 6 of the paper (4) already quoted, where idioventricular rhythms began without delay. Another difference between the two methods is found in the degree of effect produced on stimulating the left vagus; in the faradic method the change in conduction varies from mere lengthening to a condition so profound that complete dissociation results; these degrees have been described. The morphin method usually produces only incomplete dissociations. Twice only was complete dissociation produced. The similarity between the results of the two methods is sufficiently close to render it likely that in obtaining them an identical mechanism in the heart is involved. It may, therefore, be concluded that the inconstant action of the vagus resulting from morphin injections, called "ungleichartig" by Einthoven and Wieringa, appears so on account of the fact that the predominating effect of morphin may be exercised now on one and now on the opposite cardio-inhibitory system, and not, as was suggested, on account of a shifting of predominance from one to another of the fiber tracts in the vagi themselves. The explanation offered as the results of this series of experiments differs from theirs. The results obtained substantiate the conclusion reached in the former series, that the two vagi act differently. A fact relating to the mechanism of the right vagus nerve can now be added, from a consideration of the cardiac mechanism in right vagus dogs, namely, that derangements in conduction result, to a very slight extent only, as the effect of the influence of the right vagus nerve Although no solution of the production of the extreme grades of sinus irregularity seen in morphin intoxication is offered, the failure of this rhythm to be converted into a more profound irregularity may be explained. There seems little doubt that the occasion for the occurrence of an independent ventricular rhythm in these experiments was due to the slowness of the auricular rate resulting from morphin injection. But in the cases of sinus irregularity (Nos. 683, 685, and 700), the rate of the auricles was never sufficiently low for the ventricles to initiate an independent rhythm. The lowest rates recorded in them were 66.3 (No. 683), 85.7 (No. 685), and 91.4 (No. 700), and it appears that before an independent ventricular rhythm occurred in any of the experiments, the auricular rate had always fallen below 41 (Nos. 686, 688, 697, 698, 706, 715, and 721). On the other hand, the ventricular rates in the cases of sinus irregularity were higher than the highest idioventricular rates observed and no advantage could consequently have been gained by the onset of a new rhythm. No. 683 was an exception, but the rate in this case exceeded the idioventricular rates of all but Nos. 702 and 706 and was only 11.1 beats below that of the highest recorded. Whether sinus irregularity itself is a morphin irregularity the result of a sino-auricular block, in the sense of Eyster and Meek, has already been discussed.     

ON THE ACTION OF SUBSTANCES OF THE DIGITALIS SERIES ON THE CIRCULATION IN MAMMALS

In summing up the contents of the preceding pages it may be stated that the action of digitalis has been divided into two stages according to the changes evinced by the ventricles under its influence; of these the first is characterized by marked inhibitory action together with modification of the cardiac muscle, while in the second the inhibitory action is less marked and the muscular action becomes the more prominent feature. The inhibitory action is due to direct stimulation by this series of the pneumogastric centrally in the medulla oblongata and peripherally in the heart. The extent to which the inhibitory mechanism is stimulated varies in different animals and with different members of the digitalis series. The muscular action of small quantities betrays itself in a tendency to increase the extent of the contraction, while in some cases the degree of relaxation reached in diastole is also lessened by it. In larger quantities the series increases the irritability of the cardiac muscle very considerably, and the spontaneous rhythm of the ventricles therefore becomes developed. Through the interaction of these two factors in the first stage the rhythm of the whole heart is slowed, the contraction of the ventricle is more complete, and the diastolic relaxation is generally increased, although it may be unchanged or lessened. The systolic pressure is increased and the fall from maximum to minimum pressure is slower than normal owing to the increased completeness and longer duration of systole (Rolleston). The auricles generally contract with less force and may relax more completely than normally. Sometimes, however, their contractions also are more complete than before the injection of the drug. This latter condition generally precedes the diminution of the force of the auricular contraction. This variation of the effects of digitalis in the auricle explains the changes in intra-auricular pressure noted by Kaufmann. The contraction volume of the ventricles is always much increased, and the output per unit of time is generally augmented, and this together with the contraction of the peripheral arterioles causes an increase in the tension in the systemic circulation, an acceleration of the circulation, and possibly a temporary increase in the pressure in the great veins and in the auricle and ventricle in diastole (Kaufmann). The pressure in the pulmonary artery is practically unaffected by some members of the series, while by others it is considerably increased. This difference in the reaction of the pulmonary circulation is due to the varying extent to which these drugs act on the peripheral arteries and not to any difference in their action on the two sides of the heart. If the inhibitory action be very strongly marked the slowing of the heart may be extreme, the ventricles assuming their own spontaneous rhythm and all connection with the auricles being lost. While the contraction volume of the ventricle is still greater than normal, their output per unit of time may become less than normal, the aortic tension therefore fall and the rapidity of the circulation be lessened. The ventricles maintain their association throughout, and probably the rhythm of the two auricles also remains equal. The ventricular rhythm, however, becomes irregular owing to the variation in the duration of the diastolic pause. The auricles may cease altogether in diastole, or may continue to beat with a slower or faster rhythm than the ventricles. During the second stage the rhythm of the heart becomes accelerated owing to the increased irritability of the heart muscle. The ventricle tends to assume a rapid spontaneous rhythm, while the auricular rhythm is also quicker than in the first stage. When these two rhythms interfere by the passage of impulses across the auriculo-ventricular boundary in either direction, irregularity of the heart is produced, generally bearing a distinctly periodic character. The ventricles continue to maintain their common rhythm, while the auricles and ventricles may contract at quite different rates. The two ventricles, however, do not necessarily contract with equal force, and the contractions of one may present periodic variations in strength, while those of the other may be almost perfectly uniform. The contractions of the auricles vary in the same way as regards each other and the ventricles. The inhibitory nerves are no longer able to slow the ventricular rhythm, but may affect the completeness of systole and diastole in the ordinary way. The auricular contractions can still be lessened in force and possibly be abolished by their stimulation, and the impulses passing between the auricle and ventricle may therefore be blocked and regularity of the heart produced by powerful inhibition. The irregularity of the contractions is therefore due indirectly to the increased irritability of the cardiac muscle and the acceleration must be attributed to the same cause. An extreme phase of this stage produced by the interference of the rhythms is a temporary standstill of one of the chambers, generally the auricle. The irregularity leads to a lessened efficiency of the work of the heart. The output varies extremely in successive observations and the contraction volume of every individual beat may differ. The various chambers often show a tendency to dilate during this stage. The blood pressure in the systemic arteries at first remains high, in fact may be higher than in the first stage owing to the increased rapidity of the heart rhythm, but afterwards falls continuously as the periodic variations become shorter in duration. The auricles generally cease contracting before the ventricles, but not invariably. There is no fixed order in the cessation of the ventricles or auricles. Each division comes to a standstill in a position somewhat nearer diastole than systole and then passes into delirium and dilates to the fullest extent.     

THE RELATION OF THE AURICULAR ACTIVITY FOLLOWING FARADIZATION OF THE DOG'S AURICLE TO ABNORMAL AURICULAR ACTIVITY IN MAN

The tumultuous auricular activity which follows faradization of the auricles of mammals and which has been variously described, could be distinctly seen to consist almost constantly in our experiments on dogs of true fibrillatory movements of the separate muscle fibers coëxisting with a rapid auricular tachycardia. During peripheral stimulation of the right vagus nerve the true fibrillation alone existed, the tachycardia being inhibited. A comparison of the electrocardiograms from dogs with this abnormal auricular activity with those from patients with the type of cardiac arhythmia which has been attributed to auricular fibrillation, and from patients with so called auricular flutter, indicates that the auricular activity in patients with either of these conditions differs somewhat from that usually seen in the faradized auricles of the dog in our experiments. The auricular activity of the cases of cardiac arhythmia is apparently true fibrillation, similar to that seen in the faradized auricles of the dog during right vagus stimulation. The electrocardiograms from cases of so called auricular flutter usually give no evidence of auricular fibrillation, and the auricular activity seems to consist of tachycardia alone. Fibrillation may apparently coëxist with the tachycardia in some cases, when the auricular activity seems to resemble closely that usually seen in the dog after auricular faradization. During peripheral stimulation of the left vagus nerve, the electrocardiograms obtained after auricular faradization show changes which render them more nearly similar to those obtained from patients with auricular flutter. The facts that the auricular activity of the faradized auricles of the dog may apparently pass spontaneously into that closely resembling auricular flutter in man, that it may be changed into true fibrillation by right vagus stimulation, and that the abnormal auricular activity in man passes from a state of flutter to that of fibrillation in a similar manner, may be taken as evidence for the belief that auricular fibrillation and auricular flutter in man are closely allied cardiac disorders.     

SINUS STIMULATION AS A FACTOR IN THE RESUSCITATION OF THE HEART

The four series of experiments described above indicate clearly that tetanic stimulation of the sinus region of the auricles is of material assistance to massage in the resuscitation of the heart. It causes the auricles to generate impulses, either rhythmical or irregular, to which the ventricles, when susceptible, respond. When massage administered for brief periods has failed to resuscitate the heart, the same period of massage combined with tetanic stimulation of the sinus has usually brought the circulation back to normal. In some instances massage alone when continued over long periods has been without effect, and to all appearances would have continued to be without effect, whereas at such a time massage combined with stimulation of the sinus has effected recovery. Whether the stimulus causes the auricles to beat normally or to fibrillate seems to make no essential difference in the end result. Not infrequently conductivity and irritability are lowered to such an extent by the cessation of the circulation, that impulses generated in an auricle started by stimulation can at first manifest no effect upon the ventricles. Under such circumstances massage alone or, more frequently, massage plus stimulation may cause the ventricles to beat with their inherent slow rate. Often then the force of the ventricular contractions is insufficient for the maintenance of an effective circulation. In such cases, however, with the gradual improvement in the condition of the heart, the auricular impulses, as a rule, soon begin to reach the ventricles, with the result that the latter immediately begin to beat more rapidly and effectively. The beneficial results of stimulation of the auricles, therefore, manifest themselves relatively late, but none the less effectively. It has been found that even after the heart has begun to beat, stimulation of the sinus region may still be of some assistance, though in another direction. It not infrequently happens that after resuscitation of the heart the blood pressure fails to rise above a certain low and insufficient level. In such cases repeated tetanic stimulation of the sinus may accelerate the rise of blood pressure and so hasten recovery (protocol of experiment 12, series II, and text-figure 5). No attempt has been made to determine the mechanism of this effect.     

AN EXPERIMENTAL CONTRIBUTION TO THE STUDY OF CARDIAC HYPERTROPHY

1. Hypertrophy induced by the production of aortic insufficiency involves all the chambers of the heart. The greatest absolute increase in weight is in the left ventricle. The remaining segments, arranged in the order of decreasing increments are septum, right ventricle, and auricles. The greatest relative increase is also in the left ventricle, but the auricles show a relative hypertrophy greater than that of the septum or right ventricle. 2. The co-hypertrophy of the auricles is not due to an altered venous pressure, but results from an increased force of auricular systole. 3. The heart shows an increase in weight within one week after the production of aortic insufficiency. The increase in weight is due only in part to an increased water content.     

THE EXTENT OF THE CAPILLARY BED OF THE HEART

By means of injections made into the coronary arteries of beating hearts it has been possible to determine the number of capillaries in the normal heart muscle. This study has shown a very rich blood supply with an average of approximately one capillary for each muscle fibre in the ventricular walls and papillary muscles, and a less abundant supply in the auricular muscle and Purkinje system. The number of capillaries per sq. mm. of ventricular wall or papillary muscle is about twice that found by Krogh in skeletal muscle. Capillaries were not found constantly in the valves of hearts in which there was apparently a complete injection of the capillary bed. The method described for injecting the capillaries of the heart also provides a means of studying the blood supply to the muscle, valves and aortic wall in pathological hearts.     

Long-Term Clinical Outcome of Right Bundle Branch Radiofrequency Catheter Ablation for Treatment of Bundle Branch Reentrant Ventricular Tachycardia

This study assessed the long-term outcome of patients undergoing radiofrequency ablation of the right bundle for bundle branch reentrant ventricular tachycardia. Bundle branch reentrant tachycardia was diagnosed in 16 patients (ejection fraction 31%± 15%) who underwent electrophysiology study in our laboratory. All patients had His-Purkinje system conduction delay with mean HV interval of 68 ± 8 ms. After ablation, right bundle branch block developed in 15 patients. One patient developed complete heart block, which was anticipated. One patient died of heart failure 9 months after ablation. Two patients were successfully bridged to heart transplantation 0.5 and 13 months, respectively, after ablation. Two patients received implantable defibrillators for other ventricular tachycardias. One patient had syncope 11 months after ablation, but there was no evidence of ventricular tachycardia or heart block in repeat electrophysiology study. This patient died suddenly 29 months after ablation. The remaining nine patients were alive and well for a mean follow-up of 19 ± 10 months. Radiofrequency ablation of the right bundle branch is an effective therapy for treatment of bundle branch reentrant ventricular tachycardia. Survival is excellent provided that other types of ventricular tachycardia, when present, are treated as well. This technique maybe helpful in management of patients who have unacceptable frequent shocks from their implanted defibrillators and may be helpful in avoiding implantation of such a device completely in others. In some patients with terminal heart failure and incessant ventricular tachycardia, this procedure can function as a bridge to cardiac transplantation.     

Inadvertent Catheter-Induced Right Bundle Branch Block in a Patient with Preexistent Left Bundle Branch Block and Recurrent Macroreentrant Ventricular Tachycardia

This article describes the inadvertent, catheter-induced induction of right bundle branch block resulting not only in transient complete infra-His heart block but also in temporary interruption of the macroreentry circuit of ventricular tachycardia. A patient with preexistent left bundle branch block and spontaneous ventricular tachycardia based upon the bundle branch reentry mechanism underwent electrophysiological testing for the evaluation of sotalol drug efficacy. In search of an optimal His-bundle recording, the manipulation of a 6 Fr quadripolar catheter caused a right bundle branch block, thus advancing the preexistent left bundle branch block to complete heart block. Retrograde ventriculoatrial conduction remained unaffected. The macroreentrant tachycardia with left bundle branch block configuration was no longer inducible. While the patient continued on unchanged sotalol medication (320 mg/d) he required temporary pacing for 16 hours until the block subsided. A subsequent induction attempt demonstrated initiation of the tachycardia. Finally, guided by invasive testing, the patient successfully received amiodarone therapy (300 mg/d). The patient completed an uneventful follow up of 27 months. No progression of conduction delay was observed. This case suggests that the inadvertent induction of right bundle branch block prevents the initiation of ventricular tachycardias relying on bundle branch reentry. Therefore, missed diagnosis or misinterpretation of antiarrhythmic drug efficacy might occur if there is no electrophysiological reevaluation after right bundle branch recovery.     

Termination of "ventricular" arrhythmias from digoxin by selective production of complete atrioventricular block with physostigmine in the dog

In previous studies we have come to doubt that ventricular rhythms of an automatic nature will arise spontaneously from the peripheral Purkinje system. In 20 anesthetized dogs, digoxin was administered i.v. (0.1-1.0 mg/kg) and in 12 dogs by selectively perfusing the atrioventricular (AV) node artery (2 ml; 40 microgram/ml). We obtained the following results. First, selective pharmacological production of complete AV block (acetylcholine or physostigmine) interrupts the "ventricular" arrhythmias considered characteristic of digitalis intoxication.Second, digitalis arrhythmias are difficult to produce when this type of complete heart block had been previously established. Third, abolition of ventricular arrhythmias by selective pharmacological production of heart block can be reversed (i.e., the arrhythmia restored) with atropine. Fourth, rapid pacing of the ventricles during complete heart block in dogs poisoned with digitalis can eventually induce ventricular arrhythmias, but not quickly. We interpret that these digitalis arrhythmias originated within the acetylcholine-sensitive portion of the AV node-His bundle region.     

超声诊断复杂心脏畸形心室襻及心室手型

目的 分析不同类型复杂先天性心脏病(先心病)心室襻的图像特征,探讨应用超声心动图判定心室襻或心室手型的方法学及价值。方法 回顾性分析45例复杂先心病患者的超声图像,包括右心室双出口7例,完全型大动脉转位5例,矫正型大动脉转位11例,解剖矫正型大动脉异位2例,单心室15例,十字交叉心4例和楼上楼下心室1例。全部病例均由外科手术或CT检查证实。结果 7例右心室双出口中,心室右襻4例,心室左襻3例。5例完全型大动脉转位均为心室右襻。11例矫正型大动脉转位患者中,心室右襻1例,心室左襻10例。2例解剖矫正型大动脉异位患者均为心室右襻。15例单心室患者中,心室右襻8例,心室左襻4例,心室不定襻3例。4例十字交叉心和1例楼上楼下心室中,右手型心室3例,左手型心室2例。结论 超声心动图对复杂先心病的心室襻或手型定位具有重要价值,超声判定心室手型可以帮助分析复杂的心室构型。     

THE REFRACTORY PERIOD OF THE NORMALLY-BEATING DOG'S AURICLE; WITH A NOTE ON THE OCCURRENCE OF AURICULAR FIBRILLATION FOLLOWING A SINGLE STIMULUS

1. A method is described for determining the refractory period of the dog''s auricle during the normal sinus rhythm. The advantages of the method are: (a) The total stimulating effects of repeated induction shocks are avoided. (b) The action current is recorded from a point one millimeter or less from the point of stimulation. (c) Alterations in the spontaneous rate of the auricle do not interfere with the accurate determination of the refractory period. 2. The values obtained for the normal refractory period and the changes produced by atropine and by stimulation of the vagus agree closely with those of previous observers. 3. The automatic features of the method make possible the determination of the refractory period under adrenalin. This drug brings about a distinct shortening of the refractory period but less than that produced by stimulation of the vagus. 4. During vagal stimulation a single induction shock, introduced soon after the end of the refractory period, frequently produces auricular fibrillation. The cause of this irregularity is discussed and its relation to clinical auricular fibrillation is suggested.     

心脏增大临床常用诊断方法比较

本文以220例先心病和风心病术中发现的心脏房或室增大的所见为基础,与术前心电图、胸部 x 光片及二维超声心动图的结果进行对照结果:超声心动图对左室增大诊断正确率最好为92.3%;胸片对右室增大诊断正确率最好为83.6%;两者对左房增大诊断正确率相近,分别为86.4%及86.8%。三种方法对右房增大诊断正确率均在75.2%以下。而心电图是三种方法诊断房室增大比较最不敏感者。     

Traumatic tricuspid insufficiency: a case report with a review of the literature.

Traumatic tricuspid insufficiency, a rare complication of blunt chest trauma, has been reported with increasing frequency during the last 40 years. Automobile accidents are the leading cause of traumatic tricuspid valve regurgitation. The most frequently reported injury is chordal rupture, followed by rupture of the anterior papillary muscle and leaflet tear, primarily of the anterior leaflet. In the acute phase of the injury, the traumatic lesion may go undetected. In the chronic phase many patients remain asymptomatic and others exhibit symptoms and signs of moderate to severe right heart failure. Clinically overt right heart failure has been the traditional indication for surgery, which usually consisted of tricuspid valve replacement. More recently, a more aggressive strategy, with surgical repair of the valve performed before deterioration of the right ventricular function occurs, has been advocated.     

上下心的超声心动图表现及诊断

目的 观察上下心的超声心动图特征及诊断方法,并探讨上下心与十字交叉心的关系.方法 回顾性分析14例确诊上下心患者的二维超声心动图和彩色血流多普勒特征,探讨其诊断要点及诊断方法.结果 14例患者右心室及左心室均呈上下排列,其中9例为十字交叉心,5例为三尖瓣闭锁伴右心室发育不良及心室大动脉连接异常;12例为心房正位,13例房室连接关系一致,7例伴有完全性大动脉转位,7例伴有右室双出口,14例全部伴有室间隔缺损.结论 超声心动图能够清晰显示室间隔定位,对上下心进行明确诊断;上下心不等同于十字交叉心,也可存在于其他复杂先天性心脏畸形之中.