Quinine may trigger torsades de pointes during astemizole therapy.

Because of serious cardiovascular events, warnings against concomitant use of certain medications with the use of antihistamine (HismanalR have been published and added to product labeling. Quinine, the optical isomer to quinidine, is included in these warnings. We present the case of a patient with only mild electrolyte disturbances who experienced an episode of torsades de pointes after a single dose of quinine while taking astemizole.

Evaluation of antiarrhythmic drugs on defibrillation energy requirements in dogs. Sodium channel block and action potential prolongation.

Antiarrhythmic drugs have been reported to produce variable effects on defibrillation energy requirements. However, the relation between the in vitro electrophysiologic effects of these agents and the changes in defibrillation energy requirements have not been systematically examined. Therefore, we evaluated the effects of the sodium channel blocking drugs lidocaine and procainamide, the action potential prolonging drugs N-acetyl procainamide and clofilium, and the potassium current blocker cesium in acute canine models with the same internal spring and epicardial patch electrodes used in humans for ventricular defibrillation testing. Ten series of experiments were performed in 78 dogs. Nonlinear regression was used to derive curves of energy dose versus percent successful defibrillation attempts and the 50% and 90% effective energy dose for each experimental condition. Saline control experiments indicated that the preparation was stable throughout the 6-hour duration of the experiments. Lidocaine doubled the defibrillation energy requirement (p less than 0.001) at a mean plasma concentration of 8.2 micrograms/ml. The effect of lidocaine on defibrillation energy was reversible, present at therapeutic plasma concentrations, linearly related to plasma concentration (r = 0.69, p less than 0.002), and present even after only 5-second episodes of ventricular fibrillation. In contrast, procainamide had no effect on defibrillation energy at mean plasma concentrations of 8.5 and 13 micrograms/ml, even after prolonged (30-second) episodes of ventricular fibrillation, whereas N-acetyl procainamide, clofilium, and cesium all decreased the energy requirement for defibrillation by 13-27%. Moreover, with the addition of N-acetyl procainamide, there was a trend toward diminishing the increase in defibrillation energy requirement caused by lidocaine. All agents prolonged the mean ventricular fibrillation cycle length. Lidocaine shortened the QT interval, whereas all other agents increased the QT (p less than 0.05). The major electrophysiologic effect of lidocaine is of sodium channel blockade, whereas, N-acetyl procainamide, clofilium, and cesium predominantly increase the action potential duration, and procainamide exerts both effects. Thus, these data indicate that sodium channel block and action potential prolongation exert significant and antagonistic modulating effects on defibrillation energy requirements.

Influence of ventricular fibrillation duration on defibrillation energy in dogs using bidirectional pulse discharges.

The automatic implantable defibrillator device typically discharges 5-30 seconds after detection of ventricular fibrillation. To investigate the importance of the duration of ventricular fibrillation on defibrillation, the effects of ventricular fibrillation durations of 5, 15, and 30 seconds on the energy requirements for successful internal defibrillation were compared in 15 closed chest dogs with internal electrodes. The electrode configuration utilized a transvenous right heart catheter with two electrodes and a precordial subcutaneous patch electrode, with a single bidirectional pulse discharged between the distal catheter electrode and the proximal catheter and patch electrodes. Curves of energy vs. percentage of successful defibrillation were constructed and logistic regression was used to derive 90% and 50% successful energy doses (ED90 and ED50). The mean ventricular fibrillation activation interval just prior to defibrillation was determined from discrete RV endocardial electrograms. Four dogs died during testing, all because of inability to defibrillate after 30 s of ventricular fibrillation. In the remaining 11 dogs, the ED90 increased from (mean +/- SD) 27 +/- 13J at 5 s to 41 +/- 14J at 30 s (p less than .01). The mean ventricular fibrillation activation interval decreased from 107 +/- 21 ms at 5 s to 95 +/- 18 ms at 30 s (p less than .01). In conclusion, the energy required for internal defibrillation in dogs using this electrode configuration increases with longer durations of ventricular fibrillation, and is associated with more rapid ventricular fibrillation activation intervals.

Extramedullary hematopoiesis within the hypotympanicum presenting as a glomus tympanicum.

We discuss the case of a 22-year-old black woman who presented with a mass in the left hypotympanicum. Both the pre- and postoperative diagnosis of the lesion was a glomus tympanicum. Histopathologic examination revealed the "tumor" to be a nodule of extramedullary hematopoiesis. Many sickled erythrocytes were also noted within the lesion. A multilingual literature search (English, French, German, Spanish, Portuguese, Italian, and Russian) failed to reveal a documented case of extramedullary hematopoiesis in the hypotympanicum. We assume that the patient's hemoglobinopathy was the cause of her unusual focus of extramedullary hematopoiesis.

Medical and surgical management of Meniere's disease.

Meniere's disease has been the focus of much controversy concerning its etiology and pathophysiology, not to mention treatment. A brief review is presented of the major proposed causative factors and therapy, both medical and surgical, founded upon these theories. We also present the diagnostic evaluation and therapeutic modalities employed by The Otology Group, P.C., as well as long-term, follow-up data on our patients.

Clinical chemistry of staphylococcal enterotoxin poisoning in monkeys.

Clinical chemistry values were examined in 90 monkeys administered a purified preparation of staphylococcal enterotoxin, type B, intravenously. These studies showed an early release of epinephrine accompanied by a mild increase in blood glucose. This was followed by progressively developing prolonged hypoglycemia. An early increase in bloodurea nitrogen occurred, presumably as a result of both prerenal azotemia and functional renal failure seen in association with the observed hypotension. Serum protein, Ca, and Cl concentrations decreased with time. Pi levels increased, whereas Na and K concentrations in serum remained unchanged. Serum enzyme concentrations were unchanged, with the exception of serum glutamic oxaloacetic transaminase, which rose rapidly when compared with prechallenge control observations or with values from sham-challenged monkeys. These changes were statistically significant. These results suggested that enterotoxin administered intravenously produced early change in glucose metabolism, possibly related initially to catecholamine release and later to increased utilization of glucose and metabolic acidosis. Other findings were compatible with tissue breakdown at as yet undetermined locations and with loss of endothelial membrane integrity, as evidenced by loss of protein from the vascular space.