His-bundle Electrocardiography Research Articles

Role of concealed conduction and allied phenomena in the genesis, maintenance, and termination of cardiac arrhythmias

Concealed conduction is a common electrocardiographic phenomenon whereby a series of events may occur as a result of incomplete propagation of an impulse. The occurrence, maintenance, and resolution (termination) of several events such as functional block and cardiac arrhythmias are linked to concealed conduction. This phenomenon should be suspected on the surface electrocardiogram whenever an arrhythmic event occurs unexpectedly. Several electrophysiological concepts such as transseptal conduction and linking phenomenon are close allies of concealed conduction. His-bundle electrocardiography and comprehensive electrophysiology may be needed to verify this phenomenon.

Atrioventricular conduction during adenosine-induced hypotension in dogs anaesthetized with sevoflurane

We have studied the effects of adenosine-induced hypotension on A-H interval (atrioventricular (AV) nodal conduction time during sinus rhythm), St-H interval (intra-atrial plus AV nodal conduction time during atrial pacing), H-V interval (His-Purkinje conduction time) and H-S interval (total ventricular conduction time) by His-bundle electrocardiography in addition to surface electrocardiogram during both sinus rhythm and atrial pacing in nine dogs anaesthetized with 1 MAC of sevoflurane. Stepwise increases in infusion rates of adenosine to 0.1, 0.3, 0.5 and 1.0 mg kg-1 min-1 produced a dose-related decrease in mean arterial pressure from 91 (6) to 38 (2) mm Hg. Adenosine significantly increased the A-H interval at infusion rates of 0.5 mg kg-1 min-1 and above, and the St-H interval at 1.0 mg kg-1 min-1. The H-V and H-S intervals remained unchanged. Heart rate decreased significantly only at 1.0 mg kg-1 min-1 with a significant increase in the PR interval. Adenosine-induced hypotension did not have deleterious effects on AV conduction times and the surface electrocardiogram in dogs anaesthetized with 1 MAC of sevoflurane. This may indicate that the effects of adenosine on AV conduction were small and therefore are unlikely to be a contraindication to the use of adenosine for inducing hypotension in patients with initially normal conduction during sevoflurane anaesthesia.

Comparison of the Effects of Halothane, Isoflurane, and Sevoflurane on Atrioventricular Conduction Times in Pentobarbital-Anesthetized Dogs

It is not known how sevoflurane affects the cardiac conduction system.We compared the effects of halothane, isoflurane, and sevoflurane on specialized atrioventricular (AV) conduction times in eight pentobarbital-anesthetized dogs. AV conduction times with three inhaled anesthetics at end-tidal concentrations of 1 and 2 minimum alveolar anesthetic concentration (MAC), were measured by His-bundle electrocardiography during both sinus rhythm and right atrial pacing at a slightly higher rate than sinus one. Heart rate and arterial pressure were simultaneously recorded. Halothane prolonged AV nodal conduction time during sinus rhythm (A-H interval) at 2 MAC compared with the control value, whereas isoflurane and sevoflurane did not alter the A-H interval, His-Purkinje conduction time (H-V interval), and ventricular conduction time (H-S interval) during sinus rhythm at 1 and 2 MAC. All three inhaled anesthetics did not change AV conduction times during right atrial pacing. No significant difference in AV conduction times was observed between isoflurane and sevoflurane. Heart rate during sinus rhythm remained unchanged despite a decrease in arterial pressure with three inhaled anesthetics. The property of sevoflurane and isoflurane which does not affect the cardiac conduction system may be important in the stability of the cardiac rhythm during anesthesia with these drugs. (Anesth Analg 1995;81:249-53)

Effects of halothane and calcium entry blockers on atrioventricular conduction-a comparative study of verapamil, diltiazem, and nifedipine.

The effects of halothane on AV nodal function were evaluated in dogs with verapamil, diltiazem, or nifedipine during atrial pacing using the technique of His-bundle electrocardiography. Fifty-one mongrel dogs were divided into six groups. Anesthesia was induced with ketamine 100 mg im. and thiamylal 25 mg/kg iv. The animals were intubated and mechanically ventilated at normocapneic levels. Anesthesia was maintained with 50% nitrous-oxide in oxygen with pancuronium 2 mg im. Dogs in groups I, III, and V were anesthetized with 0.8% halothane and 50% nitrous-oxide in oxygen. We observed interactions between halothane and intravenous administration of either verapamil 0.1 mg/kg, diltiazem 0.15 mg/kg, or nifedipine 0.01 mg/kg respectively. Dogs in groups II, IV, and VI were administered either verapamil, diltiazem, or nifedipine iv without halothane. There were prolongations of sinus cycle length (SCL) (414 +/- 10 to 542 +/- 19 msec.), atrium-His (AH) interval (73 +/- 3 to 97 +/- 5 msec.), and functional refractory period (FRP) of the AV-node (227 +/- 5 to 260 +/- 5 msec.) in halothane anesthesia in groups I, III, and V. There were more prolongations of these variables after iv administration of verapamil (SCL; 617 +/- 35, AH; 118 +/- 7, FRP of the AV node; 311 +/- 4) and diltiazem (SCL; 554 +/- 19, AH; 118 +/- 12, FRP of the AV node; 283 +/- 12) but no prolongations after nifedipine (SCL; 533 +/- 19, AH; 99 +/- 8, FRP of the AV node; 272 +/- 9). Comparing effects of calcium entry blockers with and without halothane in groups I and II, III and IV, or V and VI, there were additive depressing effects of halothane with either verapamil or diltiazem on AV nodal function. And there is a difference between the effects of nifedipine on SCL with and without halothane.

Electrophysiological effects of ethmozine in perfused rabbit hearts.

His-bundle electrocardiography was used to evaluate the effects of ethmozine on cardiac conduction in isolated perfused rabbit hearts electrically driven at cycle lengths of 320 and 250 ms. There was no significant change in conduction until high concentrations of ethmozine were reached. His-Purkinje and atrioventricular (AV) nodal conduction were slowed significantly at 0.1 microgram/mL and atrial conduction at 1.0 microgram/mL. Conduction block occurred at 10.0 micrograms/mL in all the hearts treated. Effects of the drug (0.1 and 0.01 microgram/mL) on conduction of extrasystoles were also studied in hearts driven at a basic cycle length of 270 ms. No significant change was observed in atrial conduction of extrasystoles throughout the coupling intervals tested at both concentrations. Ethmozine (0.01 and 0.1 microgram/mL) caused slowing of His-Purkinje conduction of extrasystoles but the effect of the drug did not change as a function of the coupling interval. An interval-dependent increase in AV-nodal conduction time was observed, with the maximum slowing of conduction occurring at coupling intervals close to the effective refractory period of the AV node. AV-nodal functional refractory period was increased significantly by ethmozine (0.01 and 0.1 microgram/mL). The effective refractory period was significantly increased only at the higher concentration.

Left Ventricular to Right Atrial Defect and Tricuspid Insufficiency Secondary to Nonpenetrating Cardiac Trauma

We present a report of a 28-year-old male patient who developed a left ventricular to right atrial communication associated with tricuspid insufficiency secondary to nonpenetrating cardiac trauma. The patient's heart block was clarified by serial observation of electrocardiograms and the use of HIS bundle electrocardiography. The patient's fistula was surgically repaired, and 20 months postinjury he is asymptomatic and pacemaker dependent. Echocardiography may aid in the early diagnosis of a left to right shunt and/or tricuspid insufficiency in the setting of possible cardiac trauma.

The clinical significance of an exercise test during His-bundle electrocardiography.

In 39 patients with an average age of 47±17 years (14 to 75 years) submaximal exercise was performed in addition to atrial pacing (AP) during necessaryHis-bundle Ecg (HBE) diagnostic procedure. AP induced a rate dependent AH prolongation without alterations of the HV time. During the exercise stress test (bicycle ergometer) the AH interval decreased from 113±32 msec to 87±23 msec significantly, whereas the HV time increased from 45±8 msec at rest to 51±9 msec significantly in 32 patients. In contrast, 5 patients revealed AH prolongation or decrease of the HV time during exercise. In 12 patients treated with an iv. injection of 0.8 mg prindolol the AH intervals were prolonged compared with the pre-medication phase, whereas the HV times remained unchanged. Again exercise induced a decrease of the AH intervals, but the exercise induced HV prolongation in the pre-medication phase could not be reproduced after administration of the betablocker. Therefore we suggest that alterations of the conduction velocities of the AV-node (AVN) as well as the His-Purkinje system are the result of the relative influences of the direct sympathetic effect mainly on the AVN and the indirect parasympathetic tonus as the result of the carotid sinus reflex mechanism with its negative dromotropic effect, predominantly on the His-Purkinje system (HPS). The stress HBE is discussed as an additional diagnostic provocative test for clarifying the indication of pacemaker implantation especially in patients with conduction disturbances.

An approach to direct detection of sinus nodal activity in man

We are reporting a series of 13 out of a total of 16 patients in whom sinus nodal activity was recorded with the use of intra-atrial electrodes, during diagnostic His-bundle electrocardiography investigations. The protocol consisted of the simultaneous monitoring of the following intra-atrial points: high right atrium, low lateral right atrium, left atrium and the His-bundle electrogram (HBE), which accompanied the detecting sonde placed as a loop in the superior vena cava, with the electrodes facing the sinus nodal area. This permitted an adequate assessment of the sequence of the depolarizing activity. All patients showed sinus nodal potentials preceding the initiation of the P-wave in the surface-EKG or the atrial potential in the high right atrial lead, respectively, in the range of 60 to 270 msec depending upon the functional status of the sinus node in each patient. Such waves were clearly separated from the initiation of the atrial potential by an isoelectric line and showed functional traits compatible with the S-A nodal functions, as many authors have previously reported in experimental animal models. The text contains a review of the relevant literature and discussion upon the diagnostic significance of this method in the assessment of sinus nodal disease.

Atrioventricular Conduction Times and Atrioventricular Nodal Conductivity during Enflurane Anesthesia in Dogs

Because alterations in conduction may be important as a cause of arrhythmias during anesthesia, the authors used His-bundle electrocardiography to evaluate the effects of enflurane on atrioventricular (AV) nodal, His–Purkinje, and ventricular conduction times in dogs. Evaluations were made in hearts beating spontaneously and during atrial pacing at rates between 120 and 200 beats/min. To test the effects of enflurane on the atrial effective refractory period, functional refractory period of the AV node, and AV nodal conductivity, atrial extrastimuli (test beats) were delivered at various cycle lengths (500 msec or less) after the last of a series of paced beats at 120 or 200 beats/min. AV nodal conductivity was evaluated by measurements of minimum conduction time, fatigue (the relation of minimum conduction time to change in heart rate), and interval-related conductivity (the prolongation of AV nodal conduction time beyond minimum conduction time related to prematurity of test response). Increasing concentrations of enflurane from 1.0 to 2.0 MAC prolonged AV nodal, but not His–Purkinje or ventricular, conduction times. AV nodal conduction time increased as heart rate was increased, and this rate-dependency was enhanced by enflurane. His–Purkinje and ventricular conduction times were not affected by rate or enflurane. The atrial effective refractory period, functional refractory period of the AV node, and AV nodal conductivity were depressed by enflurane. For the His–Purkinje and ventricular conduction system, the present results are in contrast to those previously reported for halothane. Conduction changes are necessary for ventricular arrhythmias caused by re-entry of excitation. These findings may in part explain the clinical impression that ventricular arrhythmias appear less likely to occur with enflurane than with halothane.

Halothane effects on conductivity of the AV node and His-Purkinje system in the dog.

His-bundle electrocardiography was used to evaluate the effect of halothane on AV nodal and His-Purkinje system conduction times in the spontaneously beating dog heart. During artrial pacing at basic heart rates of 120 or 200 beats per minute (bpm), an extrastimulus (cycle length longer or shorter than that of the basic rate) was delivered to test the effect of halothane on several parameters of AV nodal conductivity. Included were the functional refractory period, basal conduction time, and fatigue effect (prolongation of basal conduction time as heart rate was increased from 120 to 200 bpm). Increasing MAC level of halothane (1.25 to 2.75 MAC) prolonged both AV node and His-Purkinje conduction times, yet had little effect on the parameters of nodal conductivity tested for. These effects of halothane could be potentially dangerous in the clinical setting for patients with defective AV conduction. In addition, changes in conduction may be in part responsible for arrhythmias seen during halothane anesthesia.

Pancuronium bromide enhances atrioventricular conduction in halothane-anesthetized dogs.

The effect of pancuronium bromide on atrioventricular conduction was studied by His-bundle electrocardiography during atrial pacing at different heart rates in halothane-anesthetized dogs. Pancuronium bromide, 0.1 mg/kg, uniformly enhanced atrioventricular conduction, as evidenced by decreased A-H interval (the time from the onset of the first high-frequency component of atrial depolarization to His deflection). Wenckebach second-degree atrioventricular block appeared in five of 14 animals during atrial pacing with halothane anesthesia. This block was uniformly abolished by pancuronium. The enhancement of atrioventricular conduction may contribute to the development of tachyarrhythmias following administration of pancuronium in certain patients, particularly those who have atrial fibrillation or atrial flutter.