Jack J. Kleid

Role of the nervous system in the genesis of cardiac rhythm disorders

The search for effective prophylaxis of sudden cardiac death has led to a consideration of the basic pathogenic mechanisms underlying disorders of cardiac rhythm. Although the myocardmm is undeniably important m the genesis of these disorders, the nervous system may be equally important. Several independent lines of evidence lead to this conclusion Experimental evidence: Experimental procedures that alter central nervous system function have repeatedly been demonstrated to result in cardiac arrhythmias or electrocardiographic changes, or both. Nearly every arrhythmia observed clinically can be reproduced by stimulation of the dlencephalon and mesencephalon l Evans and Gill& have demonstrated that rhythm disorders produced by hypothalamic stimulation can be blocked by the use of antladrenergic and anticholinergic drugs. Simultaneous stimulation of sympathetic and parasympathetic nerve trunks can also produce disorders of rhythm 3 Randall and coworkers4v5 observed that stimulation of the sympathetic nerves could induce both atria1 and ventricular ectopic rhythms Similarly, Alessl, Moe et a1.6 and Ninomaya7 have demonstrated that parasympathetic stlmulatlon

Familial atrial myxoma

This report of a 14 year old boy with a left atrial myxoma and his 16 year old brother with a right atrial myxoma documents the familial occurrence of cardiac myxoma. The noninvasive techniques utilized to help establish the diagnosis of intracardiac tumor are described.

Unusual echocardiographic manifestation of pericardial effusion

Echocardiographic and sector scanning examinations were performed in a patient with pericardial effusion. In addition to the demonstration of fluid posterior to the left ventricle and anterior to the right ventricle, as in most significant pericardial effusions, there was an echo-free space representing fluid recorded posterior to the left atrium. Several possible explanations of this finding are offered.

Neural basis for the genesis and control of digitalis arrhythmias.

The pharmacokinetics of ouabain associated with toxicity were studied in the cat and the guinea pig both in vivo and in vitro using ouabain-H3. After spinal cord transection a higher dose of ouabain was required to reach the lethal endpoint. This intervention also increased the myocardial and serum levels associated with toxicity were studied in the cat and the guinea pig both in vivo and in vitro using ouabain-H3. After spinal cord transection a higher dose of ouabain was required to reach the lethal endpoint. This intervention also increased the myocardial and serum levels associated with death. These findings were corroborated in experiments using digitoxin H3. In vitro, substantially higher ouabain tissue contents were associated with a lethal event. In addition, in cats and guinea pigs, the lethal myocardial ouabain content did not change when the infusion rate of ouabain was varied in vivo or the perfusate ouabain concentration was changed in vitro. In vivo, propranolol increases the myocardial ouabain content associated with death to in vitro levels. In vitro, the drugs prolongs the time to death by retarding the myocardial uptake of ouabain. These data suggest that the toxic effects of ouabain in the whole animal are largely neural and in the isolated heart, substantially myocardial.

Pseudofusion beats masquerading as pacemaker failure

Summary A 42-year old man with a permanent transvenous demand pacemaker demonstrated an extreme example of pseudofusion beats. Misinterpretation of these beats as representing failure of the sensing circuitry contributed to unnecessary replacement of the impulse generator. The mechanisms of pseudofusion beats are discussed and maneuvers to allow easy differentiation of pseudofusion beats from failure of demand function are described.

Pseudotachycardia during 24-hour electrocardiographic monitoring.

Twenty-four-hour electrocardiographic monitoring is widely accepted as a valuable tool in detecting arrhythmias and electrocardiographic changes in the ambulatory patient.1-4 The results of 24-hour monitoring should always be interpreted in conjunction with the patient’s diary of activities and symptoms during the taping. Dysfunction of the electrocardiocorder, faulty lead placement, and inadequate battery voltage may produce false and misleading electrocardiographic changes. A case is described below in which a tachycardia was spuriously recorded as a result of insufficient battery voltage.

Mechanical Conversion of Supraventricular Tachycardia (Atrial Tickle)

A 19-year-old female who presented with a history of trauma to the abdomen and palpitations, was found to have a supraventricular tachycardia. All pharmacologic interventions, and DC cardioversion were ineffective in terminating the arrhythmia. Manipulation of a pacing wire within the right atrium induced extrasystoles which abruptly abolished the arrhythmia.