Robert W. Wald

Isoproterenol induction of vasodepressor-type reaction in vasodepressor-prone persons

The ability of isoproterenol to induce symptoms and laboratory findings of a vasodepressor reaction was tested in 48 patients, ages 17 to 74, divided into 4 groups according to the reason for their referral. Group 1 comprised 12 patients with vasodepressor syncope, group 2 had 8 patients with syncope of unknown origin, group 3 included 11 patients with syncope due to seizures in 2 and ventricular tachycardia in 9, group 4 had 17 patients with various arrhythmias not associated with syncope. Isoproterenol boluses were administered starting at 2 micrograms and increased in 2-micrograms steps to a maximum of 8 micrograms at 0 degree and +60 degrees. The responses at 0 degrees were all normal. At +60 degrees a vasodepressor reaction consisting of syncope or near syncope, hypotension and bradycardia was produced by isoproterenol (mean dose 6.0 +/- 0.26 micrograms) in 8 patients from group 1 (66.6%), 4 from group 2 (50%), 0 from group 3 and 4 from group 4 (23.5%). Three of the 4 patients in group 4 had a remote history of classic vasodepressor syncope. The overall sensitivity and specificity of the test were 73 and 85%, respectively, while the predictive accuracy of a test with positive or negative outcome were 69 and 89%, respectively. Muscarinic receptor blockade with atropine in 4 patients prevented isoproterenol-induced bradycardia but not hypotension or symptoms of fainting. Beta-adrenergic receptor blockade with propranolol inhibited all aspects of the isoproterenol-induced faint. Thus, the administration of isoproterenol during a passive upright tilt may identify persons who suffer from or are prone to a vasodepressor reaction.

Vagal techniques for termination of paroxysmal supraventricular tachycardia

Maneuvers that reflexly increase vagal tone were deployed to terminate the tachycardia in 68 consecutive patients with paroxysmal supraventricular tachycardia. The order and success rate of the protocol was as follows: 57 episodes were terminated with carotid sinus pressure alone or after pretreatment with edrophonium, 5 were terminated with the Valsalva maneuvers and 6 were terminated with phenylephrine. Potency testing showed that phenylephrine evoked the greatest increase in vagal tone. All cases demonstrated slowing of tachycardia ranging from 40 to 220 ms +/- standard error of the mean (mean 79.0 +/- 3.8 ms) followed by abrupt termination. Pauses after termination ranged from 900 to 3,300 ms (mean 1,683.8 +/- 66.6) with 54 patients showing pauses of 2,000 ms or less. Termination was highly reproducible showing an overall success of 148 (92 percent) of 160 trials among 22 selected cases. The extent of increased vagal tone needed to terminate paroxysmal supraventricular tachycardia was raised by augmented sympathetic tone (infusion of isoproterenol) and decreased by reduced sympathetic tone (pretreatment with propranolol). Thus, paroxysmal supraventricular tachycardia can be rapidly, safety and consistently terminated by maneuvers that reflexly increase vagal tone.

Reflex mechanisms responsible for early spontaneous termination of paroxysmal supraventricular tachycardia

The incidence and possible mechanism of early spontaneous termination of paroxysmal supraventricular tachycardia was studied in 20 consecutive patients. Episodes of induced tachycardia that terminated spontaneously within the 1st minute after initiation were included. Tachycardias ending spontaneously were associated with a reproducible course of hypotension at the onset followed by blood pressure recovery above control levels and termination. Spontaneous termination of tachycardias occurred within the A-V node 18 to 45 seconds (mean +/- standard error of the mean 27.9 +/- 5.3) after their onset. In the supine position (0 degrees) 9 (45 percent) of 20 patients showed spontaneous termination in 36 (16 percent) of 219 episodes of tachycardia. In the head-dependent position (-20 degrees) only 1 (8 percent) of 13 patients manifested spontaneous termination in 2 (4 percent) of 54 episodes. In the head up position (+60 degrees) only 1 (6 percent) of 18 patients exhibited termination in 2 (2 percent) of 102 episodes. After partial cholinergic blockade with intravenous hyoscine butylbromide, 20 mg, or atropine, 0.6 mg, none of five patients showed spontaneous termination in 25 episodes. After beta adrenergic blockade with 10 mg of propranolol intravenously, none of 16 patients showed spontaneous termination in 87 episodes of tachycardia. We conclude that the initial hypotension during tachycardia evokes a sympathetic response that increases blood pressure and this increase in turn causes a rise in vagal tone that breaks the tachycardia.

Torsade de pointes ventricular tachycardia a complication of disopyramide shared with quinidine

Two cases of documented torsade de pointes ventricular tachycardia in association with the use of disopyramide are described. One patient had previously experienced an episode suggestive of quinidine induced ventricular tachycardia while the other developed ventricular tachycardia during quinidine treatment which was later exacerbated and sustained by the administration of disopyramide. Both patients exhibited a prolonged QTc or QUc interval at the time of the arrhythmia. These cases suggest that a propensity of ventricular arrhythmias induced by quinidine may identify individuals who are likely to develop similar arrhythmias disopyramide treatment as well.

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).

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 supra‐ventricular 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.

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.

Effects of Autonomic Tone on Tachycardias

The pioneering work of Bernard [70B], Gaskell [40G], Langley [12L], Cannon [12C], Herring [76H], and Heymans and Neil [84H, 85H] established that the autonomic nervous system plays a major role in regulating cardiac function, arterial and venous tone, blood pressure, and heart rate [127S]. In the last 30 years, beginning with a classification of adrenergic receptors by Alquist in 1948 [38A], there has been intense research into every facet of autonomic control of cardiovascular function [1A, 118B, 89K, 44V]. This has included exacting anatomic descriptions of afferent and efferent pathways [4A, 91H], central interconnections [87K], cardiac localization of receptors and nerves [3J, 39K], physiologic description and measurement of diverse reflexes [99C, 106D, 47F, 88K, 58L, 92L], measurement of neurotransmitters [30], the development of selective alpha- and beta-receptor agonists and antagonists [22D, 182W], characterization of the mechanisms of modulation of the release and reuptake of neurotransmitters [241, 10L, 12V, 5Y), and elucidation of the mechanisms of binding and action of agonists and antagonists on cell receptors [33L, 34L, 35R, 172S, 228S, 36W, 37W].

Continuous On‐Line Beat‐to‐Beat Analysis of AV Conduction Time

A simple analog circuit is described which is capable of measuring on a beat‐to‐beat basis P‐R, R‐P, P‐P, and R‐R intervals during sinus rhythm and paroxysmal supra ventricular tachycardia. In addition the circuit will emit a pulse when the consecutively alternating P and R wave sequence is interrupted thereby signalling a trigger problem or a change in rhythm. The operation of the device requires proper P and R wave sensing and provides outputs which are linear over a range of rates which are applicable to the human heart.

Respiratory and vagal modulation of ventricular tachycardia

This is a report of a case of stable uninterrupted spontaneous ventricular tachycardia which could be temporarily terminated by a strong increase in vagal tone reflexly induced by phenylephrine, 0.2 mg I.V. Following its abolition with procaine amide, 100 mg I.V., ventricular tachycardia was found to be reinducible by deep inspiration for limited periods of time which varied directly with the magnitude of the inspiratory volume. This effect was enhanced by vagal inhibition (atropine, 0.6 mg I.V.) and attenuated or prevented by vagal stimulation (carotid sinus massage or edrophonium 10 mg I.V.). It was concluded that a deep inspiration can, under some circumstances, induce ventricular tachycardia by a mechanism of vagal withdrawal.