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Biomedical subjects

M B Waxman

Publications and source records attributed to M B Waxman.

At least 19 recordsLinked to original sources
PubMed1992

Vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol.

UNLABELLED: Testing for the susceptibility for vasodepressor reaction in humans involves the combination of restriction of venous return by passive upright tilting and the administration of isoproterenol. To explore the basis of the vasodepressor test in humans, the present experiment examined whether a reduced cardiac volume coupled with adrenergic stimulation causes a vasodepressor reaction in rats. Vasodepressor reaction was defined as paradoxical heart rate slowing in conjunction with hypotension during inferior vena caval occlusion. Inferior vena caval occlusion was performed for 60 s and the maximum changes in R-R were measured during seven states as follows. (A) Under control conditions inferior vena caval occlusion alone accelerated the rate in 32 of 32 rats (delta R-R, -13.9 +/- 1.7 ms, p less than 0.001). (B) When inferior vena caval occlusion was performed during an infusion of isoproterenol (0.5-1.0 micrograms.min-1), a vasodepressor reaction was observed in all rats as the heart rate slowed (delta R-R, +138.1 +/- 14.8 ms, p less than 0.001). The vasodepressor reaction was further examined during isoproterenol and inferior vena caval occlusion under five additional states. (C) After atropine the vasodepressor reaction was unchanged (delta R-R, +132.7 +/- 24.8 ms, p less than 0.001). (D) After bilateral vagotomy the paradoxical slowing was eliminated. (E) After intrapericardial lidocaine the paradoxic slowing was eliminated. (F) After bilateral stellectomy nonsignificant slowing was still present, but this was markedly reduced when compared with B (p less than 0.001). (G) Following chronic chemical sympathetic denervation with 6-hydroxydopamine the paradoxic bradycardia was eliminated. CONCLUSIONS: (1) Reduced cardiac volume combined with adrenergic stimulation can stimulate a vasodepressor reaction; (2) the vasodepressor reaction requires signalling by the afferent but not efferent vagal fibers; (3) the bradycardia is mainly due to withdrawal of sympathetic efferent tone.

Animals↗
PubMed1992

Localization of the reflex pathway responsible for the vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol.

Vasodepressor reactions were induced in 27 rats by a combination of inferior vena caval occlusion and an infusion of isoproterenol. A vasodepressor reaction was defined as paradoxical heart rate slowing during inferior vena caval occlusion. The R-R intervals were measured at 5-s intervals before, during, and after 60 s of inferior vena caval occlusion. The purpose of this study was to examine the role of the right and left vagus nerve and the right and left stellate ganglia in this reflex. Under control conditions inferior vena caval occlusion accelerated the rate (R-R, -15.9 +/- 0.9 ms). During an infusion of isoproterenol (0.5-1.0 micrograms.min-1), inferior vena caval occlusion produced paradoxical rate slowing, i.e., a vasodepressor reaction (R-R, +75.0 +/- 2.2 ms). The vasodepressor reaction was examined during inferior vena caval occlusion and isoproterenol under the following additional states: atropine methyl bromide or right vagotomy did not alter the reaction; left vagotomy eliminated the reaction; and right or left stellectomy greatly reduced the vasodepressor reaction. We conclude the following: (1) left vagal afferents mediate the vasodepressor reaction; (2) cardiac sympathetic fibers participate in the vasodepressor reaction by withdrawing efferent tone through the right stellate ganglion, and by generating the afferent signal, which triggers the vasodepressor reaction through the left stellate ganglion.

Animals↗
PubMed1992

The effects of sympathetic denervation on spontaneous ventricular defibrillation in the rat.

Ventricular tachycardia or ventricular fibrillation was electrically induced in 38 normal rats (group 1) and 24 sympathetically denervated rats (6-hydroxydopamine) (group 2). The time for spontaneous reversion to sinus rhythm was measured during (1) control, (2) isoproterenol, and (3) the combination of isoproterenol and phenylephrine. The time for spontaneous reversion was the same in both groups in the three states. The reversion time was prolonged threefold by isoproterenol, and restored to control values when phenylephrine was added to the infusion of isoproterenol. The tachycardia duration and the refractory period were inversely related: log10 (tachycardia duration) = 3.466-0.091 (refractory period). Ventricular tachycardia/fibrillation induction was examined as follows: (i) Ventricular tachycardia/fibrillation was induced in 100% of normal rats (group 1), but only 42% of the denervated rats (group 2, p less than 0.001); (ii) during isoproterenol, ventricular tachycardia/fibrillation was induced in 100% of rats of both groups; and (iii) when phenylephrine was added to isoproterenol, ventricular tachycardia/fibrillation was induced in 100% of group 1 rats versus 82% of group 2 rats, (p = NS). These observations suggest (1) the induction of ventricular tachycardia/fibrillation is highly dependent on intact sympathetic innervation, and (2) exogenous adrenergic agonists modulate the duration of ventricular fibrillation through their effects on ventricular refractory period, independent of sympathetic innervation.

Animals↗
PubMed1991

Effects of posture, Valsalva maneuver and respiration on atrial flutter rate: an effect mediated through cardiac volume.

The effects of passive upright tilting from 0 degrees to +60 degrees (n = 27), Valsalva maneuver (n = 16) and respiration (n = 10) on the rate of atrial flutter were studied in 27 patients. After tilting to +60 degrees, the atrial flutter cycle length shortened in all patients from 247.5 +/- 7 to 236.7 +/- 6.9 ms (range of shortening 1 to 21 ms, p less than 0.001). The Valsalva maneuver (strain of 40 mm Hg) shortened the flutter cycle length during the strain (phase 2) from 242.2 +/- 4.6 to 230.5 +/- 5 ms (range of shortening 2 to 19 ms, p less than 0.001). In 10 patients whose respiration was monitored, the flutter cycle length consistently prolonged during inspiration and shortened during expiration. Combined beta-adrenergic and muscarinic receptor blockade in six patients did not significantly alter the flutter cycle length at rest or the effects of the various maneuvers on the changes in flutter cycle length. This study revealed that the atrial flutter cycle length can be shortened by passive upright tilting, the strain phase of the Valsalva maneuver and expiration. Changes in flutter cycle length were independent of autonomic tone, implying that by decreasing cardiac volume, these maneuvers affect characteristics of the atrial flutter circuit, thereby producing dynamic changes in the rate of atrial flutter.

Atrial Flutter↗
PubMed1990

The mechanism of flutter interval alternans.

The mechanism of atrial flutter alternans was investigated by observing the effects of ventricular systole on flutter intervals in a patient with atrioventricular dissociation. Interval measurements were made both from atrial electrograms recorded from an esophageal electrode, and from surface ECG recordings. Flutter cycle intervals that occurred during a well-defined period subsequent to ventricular systole were consistently prolonged by up to 30 msec relative to the baseline flutter cycle interval. This prolongation was observed in two vastly different electrode configurations, implying that motion artifact was not predominantly responsible. We concluded that, by altering the characteristics of the flutter reentry circuit, transient increases in atrial volume and/or pressure arising during ventricular systole were responsible for the lengthening of the flutter cycle intervals.

Adult↗
PubMed1979

Management of intractable ventricular tachyarrhythmias after myocardial infarction.

Twenty-five patients with recent or old myocardial infarction were studied because they had life-threatening ventricular arrhythmias that required repeated cardioversions and were intractable to medical management. All patients had had a large anterior infarction a mean of 4.6 weeks before the emergence of the arrhythmias and all had severe left ventricular dysfunction. Cardiac catheterization or autopsy revealed a left ventricular aneurysm in 18 of 18 patients and obstruction of the left anterior descending coronary artery in 20 of 20 patients. Of 16 patients treated surgically with aneurysm resection or coronary bypass grafting, or both, 10 (62 percent) were alive after 3 to 39 (mean 26) months of follow-up. The perioperative mortality rate was 31 percent and only one patient died during the postoperative follow-up period 4 months after discharge from the hospital. By contrast, all nine medically treated patients died either in the hospital (four patients) or suddenly within 2 months of discharge (five patients). Ventricular fibrillation was documented as the cause of death in five of these patients. Surgical intervention was found to improve significantly the survival of these patients (P less than 0.02). The perioperative mortality rate was lower when at least 4 weeks had elapsed from acute infarction to surgery (10 versus 67 percent) and when the procedure included coronary bypass grafting (13 versus 50 percent), although these differences were not statistically significant (P greater than 0.05).

Adult↗
PubMed1979

Carotid sinus massage induced elimination of rate related bundle branch block during paroxysmal atrial tachycardia: a simple method of proving bypass tract participation in the tachycardia.

Four cases of paroxysmal atrial tachycardia are described in whom rate related left bundle branch block (LBBB) was often present which persisted indefintely and showed no signs of spontaneous disappearance. Transient slowing of the tachycardia by carotid sinus massage in each case eliminated LBBB and this led to tachycardia acceleration. The tachycardia acceleration was traceable to a shortening in ventriculoatrial conduction. These observations proved the participation of a left sided bypass tract in the tachycardia circuit in each of these cases.

Bundle-Branch Block↗
PubMed1979

Autonomic pathways responsible for bradycardia on facial immersion.

The autonomic pathways mediating the bradycardia response to facial immersion (FI) have not been fully elaborated in man. By means of parasympathetic and sympathetic blockade we studied the heart rate response to FI in nine highly trained young swimmers, at rest and during dynamic cycle exercise. With no blockade, heart rate at rest declined with FI 36 +/- 18%. Under beta-blockade with propranolol or alpha-blockade with phentolamine FI produced a similar decrement. Atropine reduced the response. During exercise FI produced 48 +/- 9% decline without blockade. The response was similar with beta-blockade, but was completely abolished with atropine. Systolic blood pressure responses to FI measured by cuff in three subjects were small and bore no relation to the heart rate response. The results are compatible with parasympathetic efferent mediation of the heart rate response to FI. They are incompatible with a role for sympathetic mediation except as a complex interaction between parasympathetic and sympathetic influences. Hypertension and other sympathetic responses to FI do not play a role in production of bradycardia, but are apparently incidental effects. The heart rate decrement produced by FI increases with greater steady-state heart rate.

Adolescent↗
PubMed1978

Demand pacemaker slowing: a simple bedside technique.

We present a simple noninvasive bedside technique to slow gradually any R-wave inhibited ventricular demand pacemaker up to one-half its original rate for indefinite periods of time. Gradual pacemaker slowing allows accurate diagnostic observations and therapeutic interventions in pacemaker-induced arrhythmias and may possibly be used in the management of unstable angina in patients with ventricular demand pacemakers.

Aged↗
PubMed1978

Self-conversion of supraventricular tachycardia by rapid atrial pacing.

The use of pacemakers in the treatment of tachycardias is one of the most exciting and rapidly expanding applications of cardiac pacing. One of the more recent developments in this field has been the use of patient-activated radio frequency transmitted rapid atrial stimulation (RAS) in the treatment of paroxysmal supraventricular tachycardia (PSVT). Based on the previously established ability of asynchronous atrial pacing to interrupt a variety of re-entrant supraventricular rhythm disturbances, this modality of treatment is gaining increasing applicability in patients with PSVT associated with debilitating symptoms or other severe cardiovascular consequences in whom standard pharmacological regimens have either failed or are impossible to maintain for indefinite periods. This report describes our experience with five patients who underwent implantation of RAS units. The detailed electrophysiological studies required to ensure success and avoid any possible future complications are described. Over a follow-up period of four months to four years (mean 16 months) very few problems arose in the use of these units which have immeasurably improved the quality of life of the recipients. Our experience with RAS units has led to a few suggestions for future improvement and these are outlined in this report. The excellent patient acceptance and the reliability of this technique in terminating episodes of PSVT should, in the future, render RAS the treatment of choice in certain selected patients suffering from this common disorder.

Adult↗
PubMed1978

Cardiac manifestations of malignant hyperthermia susceptibility.

Malignant hyperthermia is a disease resulting from defective cellular membranes, usually presenting as drug-induced pyrexic crises. We describe four patients with life threatening ventricular arrhythmias or chest pain in the absence of pyrexic crises. Three presented with life threatening arrhythmias and the fourth with severe atypical chest pain. Two patients had a family history of multiple sudden deaths. Resting CKs were elevated in three patients while CK-MB was elevated in one. Resting ECGs were abnormal in three. Three patients had recurrent ventricular tachycardia, two had recurrent ventricular fibrillation and multiple cardiac arrests. Cardiac catheterization showed abnormal left ventricular wall motion in two and minimal mitral valve prolapse in one while all had normal coronary arteries. Thallium-201 myocardial imaging demonstrated large perfusion defects in the patient with electrocardiographic Q waves and normal coronary arteries. Myocardial involvement has been demonstrated by clinical, electrocardiographic, hemodynamic, angiographic and myocardial imaging abnormalities. Malignant arrhythmias occurred in these patients in the absence of pyrexic crises or drug admininstration. Abnormal calcium release in the myocardium, as documented in skeletal muscle membranes, may be a unifying concept for the various manifestations described.

Adult↗
PubMed1977

Recurrent paroxysmal supraventricular tachycardia: a complication of ventricular pacing in a patient with occult Wolff-Parkinson-White syndrome.

A 60 year old man suffering from syncope believed to be due to the sick sinus syndrome was treated with a permanent demand ventricular pacemaker. This led to almost continous bouts of paroxysmal supraventricular tachycardia (SVT) over the ensuing two years, mistakenly believed to be part of the sick sinus syndrome. Careful study showed that this man had a type A Wolff-Parkinson-White accessory atrioventricular connection which consistently conducted retrogradely, but only rarely antegradely, during applications of carotid sinus massage. Episodes of SVT were repeatedly induced whenever ventricular-paced impulses captured the atria retrogradely. All episodes of SVT stopped when the ventricular pacemaker was removed. Following insertion of an atrial pacemaker, the patient had no episodes of SVT or syncope over a nineteen month follow-up period. This case illustrates the care required in selecting a proper site for protective pacing in patients who suffer from paroxysmal SVT.

Heart Conduction System↗
PubMed1977

Termination of ventricular tachycardia by an increase in cardiac vagal drive.

Out of 12 patients in whom phenylephrine terminated ventricular tachycardia, four were selected for detailed studies of its mechanism of action. Pretreatment with edrophonium (15-20 mg, i.v.) decreased, while atropine (2.4 mg, i.v.) increased by at least a factor of two, the dose of phenylephrine required to break ventricular tachycardia. Carotid sinus massage following pretreatment with edrophonium in unusually high (15-20 mg, i.v.) doses broke ventricular tachycardia in all four patients. The evidence presented supports the assumption that a vagal mechanism caused both instances of termination. These findings significantly alter our interpretation of vagal interventions in the bedside clinical diagnosis of wide QRS complex tachycardias.

Atropine↗
PubMed1976

Cannon waves with A-V association.

Under appropriate circumstances, cannon waves can occur in the presence of A-V associated rhythms. Presented here is a case of first degree A-V block with cannon waves. Recognition of these waves and their behavior aided in diagnosing the patient's rhythm. The cannon waves were documented by jugular venous pulse recordings.

Electrocardiography↗
PubMed1975

Antazoline therapy of recurrent refractory supraventricular arrhythmias--a preliminary report.

Seven patients with chronic or recurrent supraventricular tachyarrhythmias were selected for a trial of antazoline therapy because sinus rhythm or a controlled ventricular response could not be achieved with quinidine, procainamide, digitalis or propranolol. Sinus rhythm was established by either intravenous administration of antazoline or direct-current countershock, and has been maintained in all for 4 to 16 months by oral administration of antazoline. Side effects were minor. Antazoline is a sufficiently promising antiarrhythmic agent to warrant large-scale controlled studies.

Adolescent↗