Biomedical subjects
Publications and source records attributed to R R Hope.
A patient with lithium intoxication and Q-T prolongation is described. As serum lithium levels fell with therapy, serial electrocardiograms (ECGs) demonstrated T wave changes more commonly associated with lithium. All changes were ultimately reversible.
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The effect of lidocaine on His-Purkinje conduction in dogs with ischemic damage to the His bundle was compared with the effect of lidocaine in normal dogs. The anterior septal artery was ligated in 14 dogs, and 30 minutes later atrial pacing was performed to increase residual ischemic damage. Four to 6 days later, His bundle recordings were obtained during sinus rhythm and atrial pacing before and after the administration of lidocaine in a dose of 2 mg/kg and a total dose of 4 mg/kg. His bundle recordings were also obtained in nine control animals beofre and after the administration of lidocaine. Lidocaine significantly increased the H-V time in the animals with ischemic damage during sinus rhythm and at all packing rates. It also resulted in advanced His-Purkinje conduction defects including His bundle block and right bundle branch block in these animals. In contrast, the effect of lidocaine in the normal animals was negligible. It is concluded that lidocaine significantly depresses His-Purkinje conduction in the setting of preexisting ischemic damage. These results suggest that lidocaine may be used as a diagnostic tool to unmask latent His-Purkinje conduction defects due to ischemia.
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Fractionated His bundle potentials were induced by ischemia or trauma in 30 anesthetized dogs, in vivo. Functional dissociation, i.e., alteration of the activation sequence of portions of these His bundle potentials was demonstrated in vivo as well as in 10 in vitro preparations of the His-Purkinje system. In vivo, plunge wire and electrode catheters were utilized to record from portions of the His bundle. During vagal-induced slowing of the heart rate, atrial pacing or His bundle pacing, His-Purkinje conduction as measured by the H-V interval was constant over a wide range of heart rates, 50-300/min. One or two hours after anterior septal artery ligation, His bundle damage manifested as split His bundle potentials (H, H'). Atrial pacing or proximal His bundle pacing induced H-H' delays with concomitant right or left bundle branch block patterns in ECG leads. However, distal His bundle pacing at comparable or even higher rates produced normal QRS complexes. In other cases, during atrial pacing or with progressive ischemia at a constant rate, H' progressively delayed during the H-V interval or even disappeared into the QRS complex with a concomitant occurrence of right or left bundle branch block. In vitro, a dissected septal preparation was studied containing the His bundle, proximal and distal right bundle and left bundle branches. Normal conduction throughout the His-Purkinje system was observed at pacing rates of 30-220/min. Punctate lesions, anatomically placed above the branching His bundle caused tachycardia-dependent, complete bundle branch blocked with concurrent temporal reversal of proximal and distal His bundle action potentials. These data suggest that ischemic or traumatic lesions in the His bundle may manifest on the electrocardiogram as bundle branch block patterns. From a clinical point of view, a critical site of lesion would markedly increase the liability for A-V blocked although the electrocardiogram alone would not indicate the actual site of lesion. Predestination of fiber tracts and alternative proposals to the pedestination theory are considered to explain QRS aberration due to exclusive His bundle lesions.
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Twenty dogs were studied 3 to 9 days after myocardial infarction. None had ventricular arrhythmias during sinus rhythm, and ventricular automaticity (as revealed by sinus nodal crush procedure or vagal stimulation, or both) was within the normal range. With regular atrial pacing or pacing with long-short cycle sequences it was possible to induce ventricular arrhythmias in all animals. Quadrigeminal and pentageminal rhythms (19 of 20 dogs) and trigeminal (17 of 20) and bigeminal ventricular rhythms (8 of 20) were observed. These rhythms which were manifest or partially or entirely concealed were always associated with delayed and fractionated electrical activity within the "infarcted" subepicardium. Continuous electrical activity (electrical activity that bridged the interval between two or more successive beats) was recorded from the infarct zone. Such activity either was manifest as ventricular arrhythmia during atrial pacing or remained concealed until atrial pacing was stopped and then was manifest as ventricular tachycardia.
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Dogs 3-7 days following ligation of the anterior descending coronary artery representing a remarkably stable model for re-entrant ventricular arrhythmias (RVA) and allowed detailed electrophysiologic studies of the re-entrant mechanism. In these dogs, we could regularly illustrate the presence of continuous electrical activity originating from the infarction zone (IZ) and bridging the diastolic interval between the initiating and re-entrant beats as well as between consecutive re-entrant beats. Conduction in the IZ was highly complex, with multiple potentially re-entrant pathways, functionally dissociated areas, and areas of localized ventricular fibrillation. Conduction disorders in ischemic myocardium were consistently tachycardia-dependent with the spontaneous onset of RVA specifically associated with a Wenckebach-like conduction pattern in a potentially re-entrant pathway. Both manifest and concealed re-entry, as well as re-entrant beats with regular extrasystolic grouping, constant or variable coupling, uniform multiform and bidirectional QRS configurations, were related to characteristic conduction patterns in the IZ. In summary, the study provides the first direct in vivo evidence of ventricular re-entry and demonstrates propensity for RVA and sudden death in the late myocardial infarction period.
The electrophysiologic mechanisms for the initiation and termination of re-entrant ventricular arrhythmias (RVA) were critically analyzed in dogs 3-7 days following ligation of the anterior descending coronary artery, utilizing direct recordings of the re-entrant pathway (RP) from the epicardial surface of the infarction zone. Re-entry could occur during a regular cardiac rhythm if the heart rate is within the narrow critical range during which conduction in a potentially RP exhibits a Wenckebach-like (W) pattern with a beat-to-beat increment of conduction delay until the activation waveform is sufficiently delayed to re-excite normal myocardium. If a regular cardiac rhythm is associated with limited conduction delay in a potentially RP, premature beats within a critical range of coupling intervals could result in sufficient conduction delay to induce re-entry. Re-entrant ventricular arrhythmias may be unmasked on abrupt termination of a critical fast rate of cardiac pacing only if pacing was terminated during those beats of a W pattern associated with marked conduction delay in a RP. RVA could be ended by one or more properly timed premature beats that would pre-excite part of the RP. An electrophysiologic mechanism for R-on-T and its relationship to onset of ventricular fibrillation was shown, based on markedly delayed RP conduction of the beat prior to the one apparently coupled to the premature beat.
Re-entrant beats with regular extrasystolic grouping were seen in 44- of dogs 3--7 days following ligation of the anterior descending coronary artery. Utilizing direct recording of the re-entrant pathway (RP) from the epicardial surface of the infarction zone, we found extrasystolic grouping to be based on the infarction tachycardia-dependent conduction disorders in a potentially RP. Trigeminy and quadrigeminy were related, respectively, to a 3:2 and 4:3 Wenckebach-like conduction cycle in a RP. However, quadrigeminy could also be due to an underlying bigeminal rhythm with concealment of alternate re-entrant beats, i.e., concealed bigeminy. A bigeminal rhythm was the result of a 2:1 conduction pattern in a re-entrant pathway with a sufficient degree of conduction delay during the conducted beat of the 2:1 cycle to result in re-entry. A trigeminal or quadrigeminal rhythm could change to a bigeminal rhythm on critical shortening of the cardiac cycle. Fixed and variable coupling were related, respectively, to stable and changing conduction pattern in a re-entrant pathway. On the other hand, extrasystolic grouping could be concealed due to either block in the re-entrant pathway or entrapment in a small area of the closely bordering normal zone.
The effect of lidocaine on re-entrant ventricular arrhythmias (RVA) was studied in dogs 3-7 days following ligation of the anterior descending coronary artery; direct recordings were made of the re-entrant pathway (RP) from the epicardial surface of the infarction zone (IZ). Lidocaine in a therapeutic dose consistently prolonged refractoriness of potentially RP(s) in the IZ and produced a higher degree of conduction block at a constant heart rate. Conduction in the adjacent normal zone was not affected. The impairment of conduction induced by lidocaine in the RP was directly related to its ability to abolish re-entrant ventricular beats and tachycardia. Gradual slowing of conduction in the RP consistently developed before abolition: lengthening of coupling of extrasystolic beats in surface leads and gradual slowing of ventricular tachycardia rate occurred. The termination of re-entry was characteristically associated with complete block in the RP. A "selectivity hypothesis" for the antiarrhythmic action of lidocaine is proposed.
Recent studies emphasize the importance of heart rate in the genesis of ventricular arrhythmias during myocardial ischemia. The role of alterations in rhythm has not previously been systematically investigated. In 20 dogs subjected to acute myocardial ischemia and crushing of the sinus node, standard electrocardiographic leads were recorded, as well as His bundle and epicardial electrograms from the normal and ischemic areas. Abrupt pauses in regular atrial pacing did not cause arrhythmias prior to the onset of ischemia; however, during ischemia, atrial pacing with intermittent abrupt pauses resulted in the induction of ventricular arrhythmias beginning after the second conducted beat following each pause (ventricular premature beats, 20/20; ventricular tachycardia, 19/20; and ventricular fibrillation, 8/20). Onset of the arrhythmia was associated with increased delay in activation of ischemic epicardium and fractionation of the electrogram potential of the second conducted impulse. Typical Gouaux-Ashman phenomenon was an incidental observation. Unlike the Gouaux-Ashman phenomenon, which is restricted to the His-Purkinje system, the phenomenon we observed orginated within ischemic myocardium. In vitro studies indicate that the underlying mechanism may be related to postrepolarization refractoriness induced by ischemia.
A case of giant haemangioma with disseminated intravascular coagulation (Kasabach-Merritt) syndrome) is presented. Death occurred despite therapy and postmortem evidence of clinically unrecognised gram negative bacteraemia was seen.
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