Arrhythmias In Man Research Articles

Time course of vagal effects studied in clinical electrocardiograms

We consider the transient effects of brief bursts of vagal stimulation on cardiac excitation and conduction as manifested in the clinical electrocardiogram. We hypothesize that such vagal effects may be more frequent than commonly recognized and that they may account for some types of arrhythmias that are commonly ascribed to other mechanisms. We first briefly review the direct chronotropic and dromotropic effects of brief vagal stimulus bursts in animals and man. We next consider the effects of brief vagal bursts on heart period in various arrhythmias in man, particularly ventriculophasic sinus arrhythmia with various degrees of A-V block, and various patterns of A-V dissociation. We illustrate these points with numerous clinical ECGs from our patient population, and with other cases from the literature. We next consider the effects of brief vagal bursts on A-V conduction time, and illustrate this with clinical cases of: (a) prolongation of A-V conduction after premature beats, (b) 'supernormal' A-V conduction, (c) Wenckebach periodicities, and (d) alternation of A-V conduction times. We review the evidence that brief vagal bursts are generated in vivo, and are a naturally occurring reflex phenomenon. We therefore suggest that such brief vagal effects should perhaps be considered more commonly when ascribing mechanisms to some complex and often difficult to interpret arrhythmias.

Effects of intravenous sotalol, aprindine and the combination of sotalol and aprindine on chronic high frequency ventricular arrhythmias in man

The comparative antiarrhythmic efficacy of three different intravenous drug regimens was evaluated in 12 symptomatic patients (mean age: 72 years) with chronic high frequency ventricular arrhythmias (mean: 834 PVCs h-1). In a cross-over study with latin square distribution the following drug regimens were administered intravenously to all patients aprindine 2 mg kg-1, sotalol 1.5 mg kg-1, aprindine 1 mg kg-1 & sotalol 0.75 mg kg-1. The mean percentage of PVC reduction was 41% (P less than 0.05) for aprindine 2 mg kg-1; 51% (P less than 0.05) for sotalol 1.5 mg kg-1 and 72% (P less than 0.01) for the combined drug therapy (aprindine 1 mg kg-1 and sotalol 0.75 mg kg-1). The mean plasma concentration was 1371 ng ml-1 after administration of aprindine 2 mg kg-1 and 1730 ng ml-1 after infusion of sotalol 1.5 mg kg-1. After combined drug therapy, mean plasma levels were 942 ng ml-1 for aprindine and 992 ng ml-1 for sotalol. The different drug regimens were well tolerated in all patients and no side-effects occurred. Combination therapy consisting of a drug that prolongs action potential duration with an antiarrhythmic agent that has a high affinity for the inactivated channels may thus achieve an antiarrhythmic efficacy comparable to single agent therapy, permitting the use of lower dosages.

Does the sympathetic nervous system influence sinus arrhythmia in man? Evidence from combined autonomic blockade.

The influences of vagal and sympathetic efferent activity on sinus arrhythmia in man have been studied in healthy subjects by administration of hyoscine butylbromide and atenolol alone and combined using a microcomputer-linked electrocardiogram (e.c.g.) system. Sinus arrhythmia was quantitated as the S.D. of the R-R interval. Sinus arrhythmia was reduced by hyoscine butylbromide, in some subjects to near abolition, but this end-point was unchanged by pre-treatment with atenolol. Atenolol alone prolonged the mean R-R interval and increased sinus arrhythmia. It is suggested that sinus arrhythmia in man is mediated through vagal efferents alone but that atenolol increases the arrhythmia through a central vagotonic effect.

Application of statistical methods for the analysis or interval related cardiac performance variations during cardiac arrhythmia in man.

To study the influence of the sequence of stimulation intervals on cardiac performance indices the relationship between properties of succeeding arrhythmic aortic pressure pulses of patients with atrial fibrillation has been analysed by methods of correlation and regression analysis. There are high correlations between properties of succeeding pulses and it can be shown that the pressure amplitude of one pulse correlates to the properties (diastole, diastolic pressure, pressure amplitude) of up to five preceding pulses. Furthermore, the diastolic pressure is also highly correlated with properties of more than one preceding pulse whereas the duration of the diastole and the RR-interval is independent of preceding pulse properties. We, therefore, conclude that there is no beat to beat regulation of intervals during atrial fibrillation. The relations between properties of succeeding pressure pulses have been summarised in a transfer function model, which allows the description of pulse properties from preceding pulse properties without lack of it. The parameters of the transfer function models are estimated from a sequence of arrhythmic pressure pulses and a parameter selection procedure was developed which identifies the optimal number of input variables (= properties of preceding pulses) required to describe the time course of one pulse property. In order to obtain informations about the presence of possible interval dependent potentiation effects, the transfer function model was used to stimulate the behaviour of the aortic pressure for different stimulation sequences, which have been used in the literature to study potentiation effect experimentally. From typical sequences of potentiation phenomena in the stimulated pulse sequence we conclude that frequency potentiation effects exist in the human myocardium.

Effect of intravenous flecainide on atrial vulnerability in man.

Sixteen patients were investigated by means of programmed atrial stimulation at two different driving rates: 100 and 120/min. All patients had an increased atrial vulnerability at both driving rates. After intravenous flecainide application (1 mg/kg body weight as a bolus followed by the same amount given by infusion over a period of 20 min) the increased vulnerability was abolished in 11 and 9 patients respectively. In the remaining patients the rate of induced atrial tachyarrhythmia decreased. These findings correlate with a significant prolongation of the effective refractory period of the right atrium and a significant shortening of the relative refractory period of the right atrium. It is concluded that flecainide may be effective in the treatment of atrial arrhythmias in man.

Longterm effects of cryosurgery in the sheep heart.

This study concerns the longterm effects of both epicardial and endocardial cryosurgery with particular reference to the coronary arteries. Sheep were subjected to epicardial cryosurgery without cardiopulmonary bypass, and to endocardial application with bypass. In both groups the heart was kept beating throughout the operation. Neither cardioplegia nor aortic cross-clamping was used. In the first group applications were made for 5 min directly over or adjacent to a major branch of the left coronary artery. In the second, the cryoprobe was applied for 5 min or until atrioventricular dissociation occurred. No sheep developed late arrhythmias or evidence of myocardial ischaemia. Only minimal arterial changes were observed and all the major coronary arteries remained widely patent. Cryothermia to the heart produced a small discrete lesion without complication. Bright fluorescence of necrotic myocytes was observed in all the immature lesions when sections stained with haematoxylin and eosin were examined under ultraviolet light. This vivid fluorescence clearly delineated the extent of the lesions and persisted while cytoplasmic elements remained. Our results indicate that cryosurgery provides a safe and permanent technique for the surgical treatment of arrhythmias in man, and may safely be used even in proximity to the coronary arteries. Cardioplegia is contraindicated.

Role of Mahaim fibers in cardiac arrhythmias in man.

Twelve patients with evidence of Mahaim fibers are reported, six with nodoventricular (NV) fibers and six with fasciculoventricular (FV) fibers. All patients with NV fibers had left bundle branch block morphology, and a sustained reentrant tachycardia with this morphology was proved in each case. In three of the six, ventriculoatrial dissociation occurred during tachycardia. We postulate that the mechanism of this tachycardia is a macroreentry circuit using the NV fiber for the antegrade limb and the His-Purkinje system with a portion of the atrioventricular node for the retrograde limb. ECGs of patients with FV fibers were varied, suggesting a functional relation to the right or left side of the septum. No direct relationship of FV fibers to observed arrhythmias could be found.

Treatment of malignant ventricular arrhythmias in man with an implanted automatic defibrillator.

From the Department of Medicine, Sinai Hospital of Baltimore, MD, and the Cardiovascular Division of the Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, MD.

Arrhythmias of cultured heart cells and their reversal by antiarrhythmic and antimalarial drugs

Summary The antiarrhythmic drugs: quinidine, procainamide. lidocaine, diphenylhydantoin and propranolol; and the antimalarial agents: chloroquine and pyrimethamine were tested for 8 to 16 h for their effectiveness in reversing arrhythmias of cultured neonatal rat heart myocytes. Arrhythmias induced by changing to hypoxic and normexic serumless medium were completely reversed for >15 h by quinidine (10 −6 M). Lidocaine (10 −7 M) produced partial reversal for 2 h, while procainamide (10 −5 M) was nearly completely effective for 2 h with partial protection for >15 h. Effective concentrations were from 1/100 to 1/10 of plasma concentrations required to suppress arrhythmias in man. The antimalarial chloroquine was effective at 10 −6 M while pyrimethamine was only moderately active at 10 −6 –10 −3 M. The dose-time-effect relationships of the antimalarials were erratic with both the highest (10 −5 M) and lowest (10 −9 M) concentrations being arrhythmogenic. Diphenylhydantoin and propranolol were arrhythmogenic rather than antiarrhythmic at concentrations of from 10 −7 to 10 −10 M. These observations suggest that monolayer cultures of neonatal rat heart myocytes, when properly prepared and rendered arrhythmic, can effectively detect antiarrhythmic activity of drugs thought to act on cell membranes.

The electrocardiogram in the assessment of the effect of drugs on cardiac arrhythmias.

The search for the ideal antiarrhythmic drug continues since none of the available agents offers optimum antiarrhythmic therapy. The continuing search coupled with the interest in the mechanisms of cardiac arrhythmias has led to the development of new techniques for the study of arrhythmias and antiarrhythmic drugs. In this article it is proposed to discuss the electrocardiographic methods used in the assessment of antiarrhythmic drugs. Firstly, to discuss the electrocardiogram in the assessment of the clinical electrophysiological properties of a drug and secondly, the electrocardiogram in the assessment of the value of the drug in the management of cardiac arrhythmias in man.

Phasic aortocoronary bypass graft blood velocity during ventricular arrhythmias in man

With use of the Doppler ultrasonic flowmeter catheter, phasic aortocoronary bypass graft blood velocity was measured in 16 conscious subjects during ventricular arrhythmias. Ventricular extrasystoles reduced peak systolic and diastolic graft blood velocities by 20 to 80 percent, generally in relation to their respective coupling intervals. When extrasystoles appeared in closely coupled salvos diastolic bypass blood velocity virtually ceased. Nineteen episodes of ventricular tachycardia produced an average 50 percent decrease in peak graft blood velocity (control mean ±1 standard deviation blood velocity 28 ± 11 cm/sec; value during ventricular tachycardia 14 ± 8 cm/sec, P < 0.001). An “overshoot” of peak blood velocity was observed after ventricular extrasystoles and tachycardia. All such changes in aortocoronary bypass blood velocity related to tachyarrhythmia were more prominent during the systolic fraction of flow. It is concluded that (1) ventricular arrhythmias adversely influence aortocoronary bypass graft function, and (2) this finding supports an aggressive approach to the treatment of these arrhythmias in subjects with bypass grafts.

Sinus Arrhythmia in Man: Influence of Tidal Volume and Oesophageal Pressure

The effect of tidal volume (VT) and of the intrathoracic pressure (Poes) on the respiratory sinus arrhythmia (RSA) was studied in healthy subjects. They breathed into a spirometer with a VT of 1, 1.5, and 2 1, at a standardized, slow respiratory rate, 6-min-1 (A). Poes was varied by (B) adding a negative inspiratory pressure (NIP) of 5 cm of water and by (C) intermittent positive pressure ventilation (IPPV) at identical VT and respiratory frequency. In separate study (D), intermittent negative pressure ventilation (INPV) was induced by applying negative pressure on the thorax. In A, increasing VT provoked an augmented RSA by a more marked tachycardia as well as bradycardia. On increasing the amplitude of Poes in B, RSA was somewhat more marked due to a lower minimum heart rate. Whem comparing respiratory cycles that had similar Poes but a different VT, the larger VT caused a slight increase in the RSA amplitude due to a more marked deceleration of the heart rate. IPPV almost abolished RSA, whereas INPV did not reduce the arrhythmia. It is concluded that pulmonary stretch reflexes to a minor extent contribute to RSA, whereas the hypothesis of a central nervous origin does not gain support. Cardiovascular reflexes remain the main possible cause of RSA.

Potassium canrenoate in the treatment of long-term digoxin-induced arrhythmias in conscious dogs

The effects of potassium canrenoate on arrhythmias induced by longterm progressive digoxin toxicity were studied in eight conscious beagle dogs. Sinus bradycardia and sinoatrial block, as well as atrioventricular (A-V) conduction disturbances, were consistently alleviated by administration of potassium canrenoate. Premature supraventricular (including junctional) and ventricular depolarizations as well as ventricular tachycardias were also suppressed. Although potassium canrenoate always terminated the digitalis-induced arrhythmias, it usually converted the rhythm to sinus arrhythmia rather than to normal sinus rhythm. Equimolar sodium canrenoate, but not potassium chloride, had similar reversal effects on arrhythmias induced by long-term digoxin intoxication. These data indicate that canrenoate, a diuretic agent with reported positive inotropic effects, may be useful in the treatment of digitalis-induced arrhythmias in man.

Blood velocity at mitral valve during atrial arrhythmias in man

By means of the Doppler ultrasonic flowmeter catheter, phasic instantaneous left ventricular blood velocity was measured at the mitral valves of 184 conscious human subjects during atrial arrhythmias. Atrial extrasystoles and pacemaker-induced atrial tachycardias reduced peak mitral valve blood velocities in direct relation to shortened diastolic cycle length. Atrial fibrillation with irregular ventricular responses produced beat-to-beat alternations of peak mitral velocity, with smaller peak mitral blood velocities usually associated with shortened R-R intervals on the electrocardiogram. This report represents the first comprehensive description of instantaneous and continous phasic blood velocity at the mitral valve during atrial arrhythmias in man. It is concluded that atrial tachyarrhythmias exert an adverse influence on left ventricular filling velocities.

The triple pulse generator: Clinical evaluation of a new multipurpose external pulse generator

This report describes our experience with a new, versatile battery operated, multi-purpose pulse generator especially designed for the electrophysiological investigation and treatment of cardiac arrhythmias in man. The unit was constructed according to our specifications and has been clinically in 75 patients over a period of 18 months. We have found the triple pulse pacemaker safe, reliable and functioning precisely according to specifications both clinically and when repeatedly checked with a storage oscilloscope.

Left ventricular blood flow velocity during atrial arrhythmias in man

With use of the Doppler ultrasonic flowmeter catheter telemetry system, blood flow velocity was recorded from various left ventricular cavity sites in 57 conscious subjects with atrial arrhythmias. Premature atrial depolarizations reduced peak left ventricular blood flow velocity in direct relation to their respective coupling intervals. Paroxysmal supraventricular and multifocal atrial tachycardias produced a decrease in peak left ventricular blood velocity, with the most marked reductions measured at the onset of the tachyarrhythmias. Atrial flutter and fibrillation resulted in midcavity and inflow tract diastolic blood velocity waves that were inscribed in conjunction with atrial depolarizations seen on the simultaneously recorded electrocardiogram. Irregular ventricular responses and changing atrioventricular conduction ratios produced marked irregularity of peak flow velocity. These findings provide the first comprehensive description of left ventricular blood flow velocity during atrial arrhythmias in man.

Pulmonary capillary blood flow during normal spontaneous breathing in man.

ArticlePulmonary capillary blood flow during normal spontaneous breathing in man.H R Astrom, K H Lin, and M B McIlroyH R Astrom, K H Lin, and M B McIlroyPublished Online:01 Dec 1973https://doi.org/10.1152/jappl.1973.35.6.823MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByA model of the pulmonary arterial bed in adults and infantsComputers and Biomedical Research, Vol. 23, No. 2Measurement of Cardiac Output by Alveolar Gas Exchange1 January 2011Does Abdominal Breathing Affect Regional Gas Exchange?Chest, Vol. 76, No. 3Respiratory Sinus Arrhythmia in Man: Relation to Right Ventricular Output8 July 2009 | Scandinavian Journal of Clinical and Laboratory Investigation, Vol. 36, No. 5 More from this issue > Volume 35Issue 6December 1973Pages 823-9 https://doi.org/10.1152/jappl.1973.35.6.823PubMed4765818History Published online 1 December 1973 Published in print 1 December 1973 Metrics

Cardiac dysrhythmias induced by autonomic nerve stimulation

Cardiac tachydysrhythmias were induced in anesthetized dogs by electrical stimulation of the ventral lateral cardiac nerve at the level of the left pulmonary veins. Electrical activity was recorded from seven myocardial segments including the areas near the sinoatrial node, anterior, middle and posterior internodal pathways, the atrioventricular (A-V) nodal region (His bundle electrogram), the right bundle branch and the left ventricular epicardium. Electrical stimulation of the ventral lateral cardiac nerve induced a variety of supraventricular and ventricular tachydysrhythmias. Various degrees of heart block were induced, second degree block rostral to the His bundle, and total A-V dissociation. A-V junctional rhythms, bundle of His pacemakers, ventricular pacemakers and Wenckebach arrhythmias were also observed. Atrial rates during the tachydysrhythmias frequently exceeded 500/min; ventricular rates sometimes approached 350/min. The tachydysrhythmias are interpreted as arising from ectopic foci located in the lower right atrium-upper ventricular septal areas. Use of standard pharmacologic blocking agents such as intravenously administered atropine, propranolol and phentolamine did not abolish the induced tachydysrhythmias, but administration of lidocaine or procaine was effective in the termination and prevention of the dysrhythmias. The tachydysrhythmias were also induced in partially sympathectomized dogs, but higher voltages were required. Neurally induced tachydysrhythmias resemble spontaneous arrhythmias in man, thus suggesting the possibility that arrhythmias in the human subject may be of autonomic nervous origin.

Phasic coronary arterial flow velocity during arrhythmias in man

The influence of cardiac arrhythmias on coronary arterial flow velocity studied by means of a Doppler catheter flowmeter system is described in 47 patients. The arrhythmias examined included atrial and ventricular extrasystoles, atrial fibrillation, pacemaker-induced atrial tachycardia, paroxysmal atrial tachycardia, ventricular tachycardia, Wenckebach second degree atrioventricular block and complete heart block. In atrial and, less frequently, in ventricular extrasystolic beats, peak coronary arterial flow velocity did not change significantly when the preceding R-R interval was greater than 0.50 second. However, when this interval was shorter than 0.50 second, a proportional decrease in peak coronary arterial flow velocity occurred. Variations in beat to beat coronary arterial flow velocity were seen uniformly in patients with atrial fibrillation. However, there was no correlation between peak coronary arterial flow velocity and the preceding R-R interval; in addition, no correlation was found between peak coronary arterial flow velocity and the same cycle length. In pacemaker-induced atrial tachycardia, decreased peaked coronary arterial flow velocity was observed at pacing rates greater than 140/min. In 1 patient with paroxysmal atrial tachycardia with an atrial rate of 200/min, there was a marked decrease and irregularity in coronary arterial flow velocity. The more abrupt decrease in flow velocity occurred in ventricular tachycardia. In Wenckebach second degree atrioventricular block, no measurable coronary arterial flow velocity was observed in the cycle encompassed by the dropped beat. However, the total area under the velocity curve was greater in the pre-dropped atrial beat than in other beats. In patients with complete heart block, the systolic component of flow velocity was greater than in patients in sinus rhythm.

Control mechanisms of whole number ratios of heart rate and breathing frequency.

ArticleControl mechanisms of whole number ratios of heart rate and breathing frequency.H R Weiss, and J SalzanoH R Weiss, and J SalzanoPublished Online:01 Sep 1971https://doi.org/10.1152/jappl.1971.31.3.466MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByFrom physics to social interactions: Scientific unification via dynamicsCognitive Systems Research, Vol. 52Chaotic dynamics of cardioventilatory coupling in humans: effects of ventilatory modesLaurence Mangin, Christine Clerici, Thomas Similowski, and Chi-Sang Poon1 April 2009 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 296, No. 4Better quantification of neonatal respiratory sinus arrhythmia—progress by modelling and model-related physiological examinationsMedical & Biological Engineering & Computing, Vol. 27, No. 3The Hierarchical Order of Cardiovascular-Respiratory CouplingRESPIRATORY SINUS ARRHYTHMIA (RSA) IN MAN: ALTERED INSPIRED O2 AND CO2 More from this issue > Volume 31Issue 3September 1971Pages 466-71 https://doi.org/10.1152/jappl.1971.31.3.466PubMed4398760History Published online 1 September 1971 Published in print 1 September 1971 Metrics