Intracavitary electrode catheter cardioversion of atrial tachyarrhythmias in the dog.

This study examined factors determining efficacy of intracavitary cardioversion of atrial tachyarrhythmias in closed chest, anesthetized dogs with talc pericarditis. Electrode catheters were positioned transvenously with the cathode in the right atrial appendage. In Group 1 dogs (n = 6), three anode sites (superior and inferior venae cavae ostia and mid-right atrium) were tested with graded energy shocks to determine the lowest effective cardioversion energy at each anode position. In Group 2 dogs (n = 9), multiple cardioversion attempts with energy levels of 0.01 to 5.0 J were used to evaluate reproducibility of energy thresholds. In Group 3 dogs (n = 6) without talc-induced pericarditis, atrial pathologic study was done after five intracavitary shocks (0.5 or 5.0 J). In Group 1, cardioversion was achieved with 0.75 J or less with no significant difference in minimal effective cardioversion energies among the three anode positions tested. In Group 2, 98 (26%) of 372 cardioversion attempts were successful. Intra-animal minimal effective cardioversion energies varied widely, and timing of shocks relative to atrial electrograms did not influence efficacy. Complications were infrequent and included delayed sinus rhythm recovery, transient atrioventricular block and ventricular fibrillation. Ventricular fibrillation occurred in 9 (2.4%) of 372 shocks, and was associated with higher delivered energies (6 of 9 with greater than or equal to 1.0 J) and with shocks delivered 116 to 180 ms after onset of the QRS complex. In Group 3, two dogs had no histologic damage, three dogs had multiple small foci of subendocardial necrosis and in one dog these foci coalesced to involve half the atrial wall thickness. Thus, low energy cardioversion of atrial tachyarrhythmias is feasible using intracavitary electrodes. Synchronization of energy delivery to the QRS complex is important to minimize risk of ventricular fibrillation.

Ventricular arrhythmias in elderly patients. Evaluation and management.

In evaluating and managing ventricular arrhythmias in elderly patients, the clinician must first decide which patients are appropriate candidates for therapy. Arrhythmias can be categorized as to their potential for causing sudden cardiac death as benign, potentially malignant, or malignant by considering their type and the underlying structural cardiac disease present. Factors that may aggravate the arrhythmias should be identified and corrected. The ventricular arrhythmias should be well characterized using ambulatory monitoring or electrophysiologic studies to gauge the efficacy of subsequent therapy. If pharmacologic therapy is to be initiated, the most appropriate antiarrhythmic drug should be chosen with consideration of potential efficacy, potential adverse cardiovascular and systemic side effects, pharmacokinetics, and drug interactions. In selected patients with malignant ventricular arrhythmias, the failure of antiarrhythmic medication may lead the clinician to consider nonpharmacologic therapy such as surgical endocardial resection or the automatic implantable cardioverter-defibrillator.

Serum electrolytes and catecholamines after cardioversion from ventricular tachycardia and atrial fibrillation.

We have observed hypokalemia after cardioversion from spontaneous out-of-hospital ventricular fibrillation and induced ventricular tachycardia. To test the hypothesis that the hormone response to the hemodynamic stress of the arrhythmia initiated the change in potassium, we compared the electrolytes and hormones in three groups of patients. We observed a decrease in serum potassium and magnesium after cardioversion from ventricular tachycardia induced by programmed stimulation, but not after normal programmed stimulation of the ventricle or after cardioversion from stable atrial fibrillation. These changes were preceded first by a rise in norepinephrine and epinephrine, then a rise in glucose, followed by a rise in insulin. The stimulus for these changes was probably the hypotension associated with ventricular tachycardia. The sequence of changes suggests that the decrease of potassium and magnesium after ventricular tachycardia was due to a shift of the electrolytes into cells, related to the insulin-mediated movement of glucose from the blood into cells.

Cocaine and chest pain: clinical features and outcome of patients hospitalized to rule out myocardial infarction.

OBJECTIVE: To investigate the clinical features, electrocardiographic findings, and hospital course in patients admitted with acute chest pain temporally related to cocaine use. DESIGN: Retrospective data analysis. SETTING: A 485-bed county hospital. PATIENTS: One hundred and one consecutive patients with cocaine-related chest pain admitted to the hospital to rule out myocardial infarction. MEASUREMENTS AND MAIN RESULTS: The quality of the chest pain frequently suggested myocardial ischemia. Dyspnea was common (56%). The onset of chest pain occurred during cocaine use in 21% of patients, within 1 hour of use in 37%, and after 1 hour of use in 42%. Admission electrocardiographic findings were interpreted as normal in 32% of patients; as acute myocardial injury in 8%; as early repolarization variant in 32%; as left ventricular hypertrophy in 16%; and as "other" in 12%. Forty-three percent of patients had ST-segment elevation meeting the electrocardiographic criteria for use of thrombolytic therapy, but such elevation was usually due to the early repolarization variant. The initial total creatine kinase was elevated more than 3.3 mu kat/L (200 U/L) in 43% of patients, and an elevated total creatine kinase was recorded at some time during the hospital course in 47% of patients. The creatine kinase MB fraction was less than 0.02 in all patients. Myocardial infarction was ruled out in all patients. No patient experienced in-hospital cardiovascular complications. CONCLUSION: The quality of acute chest pain related to cocaine use is indistinguishable from that experienced in acute myocardial ischemia. Abnormal or normal variant electrocardiographic findings are common in patients with chest pain related to cocaine use, but nevertheless the incidence of acute myocardial infarction is low. The ST-segment and T-wave changes can mimic acute myocardial injury and are most likely normal findings in young black men that can be readily recognized in the emergency department. Most of these patients do not require admission to an intensive care unit.