Depression of the Heart by Quinidine and Its Treatment

Abstract

Sudden collapse, sometimes followed by death, still occurs during the administration of quinidine, in spite of selection of cases by criteria that are now widely accepted. Post-mortem examinations show in some cases an embolism in some vital organ, but in others no obvious cause of death can be found. The object of this investigation was to throw some light on the cause of death in these patients and to suggest possible remedies.Observations have been made on patients who collapsed while receiving quinidine and on the electrocardiogram of patients who, although receiving quinidine, showed no toxic effects from the drug: finally, a certain number of experiments were carried out on animals to supplement the observations on man. OBSERVATIONS ON MANAmong 115 patients treated with quinidine in the last six years at Guy's Hospital for cardiac arrhythmias there have been one fatal and two severe reactions.Case 1. Mrs. O., aged 28, had a successful mitral valvotomy and was left with minimal aortic stenosis. Two years later she developed auricular fibrillation and after preliminary control by digoxin, which was then omitted for two days, she was given quinidine, 0-2 g. stat. and 0-2 g. two-hourly. After a total of 1 2 g. she reverted to sinus rhythm and the quinidine was stopped when she had taken a total of 1-4 g. Half an hour later she became acutely distressed with signs of congestive cardiac failure. A cardiogram at this time ( Fig. 1) showed bradycardia, with a shifting pacemaker. She died suddenly a few minutes later. Necropsy revealed no cause of death.Case 2. Mrs. P., aged 55, developed auricular fibrillation without apparent cause. This was controlled by digoxin, which was then omitted for one day. She was then given quinidine, 0-3 g. on the first day, 0-6 g. on the second, 1 g. on the third and 1 3 g. on the fourth day. Immediately following the final dose on the fourth day the patient collapsed with dyspnoeic and generalized convulsions. Two hours later she again collapsed; the pulse disappeared and the heart sounds were inaudible for three minutes. She was then given I ml. of 1: 1000 adrenaline by intracardiac injection and the heart began to beat. A cardiogram taken a few minutes later showed sinus rhythm with prolongation of the P-R interval (0-22 sec.) and widening of the QRS complexes (0-12 sec.). Her blood pressure was 80/40. Following methyl amphetamine 10 mg. intramuscularly it rose to 90/66 and after a further 10 mg. of the same drug to 110/80. By next morning she had recovered. Case 3. Mrs. W., aged 25, had a successful mitral valvotomy. Following operation she was troubled by attacks of palpitation. She was admitted to Guy's Hospital a year later and was found to have auricular flutter with varying A-V block. This was converted to auricular fibrillation by digoxin and 24 hours after. stopping this drug she was given quinidine. She received 1 6 g. the first day and reverted to sinus rhythm. The following day, three hours after receiving a maintenance dose of 0-3 g. of quinidine, she developed a furthe...

The Prognosis of Atrial Fibrillation Following Mitral Valvotomy

“…There seems to be no way of predicting where this will occur, and it is doubtful whether the conventional test dose gives much help in this respect. Finnegan and Trounce (1954) have shown that the most valuable drug for reviving the animal heart depressed by quinidine is intracardiac adrenaline, but this was not effective in one of the patients reported here. Hay (1924) said that little or nothing is to be gained from the use of quinidine in badly damaged hearts with old-standing valvular disease.…”

“…in patients with mitral stenosis. Finnegan and Trounce (1954) reported one fatal and two severe reactions after moderate doses of quinidine (1I4 g., 1 -2 g.). In the present series, one fatality occurred after 0 9 g. and the other on a daily maintenance dose of 0-8 g. A similar fatality after mitral valvotomy has been reported by Fraser and Turner (1955).…”

Poisoning Due to Class IA Antiarrhythmic Drugs Quinidine, Procainamide and Disopyramide

“…Increase in the width ofthe QRS complex of more than 25% over baseline has been used as an indication of toxicity (Cheng et al 1956); more severe toxicity results in further widening with abnormal morphology of the QRS complex, bundle branch block and sinoatrial and/or atrioventricular block ( fig. Arrhythmias indicative of depressed automaticity and conduction include sinus bradycardia, sinus pause or arrest, junctional or ventricular escape rhythms, varying degrees of atrioventricular block and asystole (Finnegan & Trounce 1954). Arrhythmias indicative of depressed automaticity and conduction include sinus bradycardia, sinus pause or arrest, junctional or ventricular escape rhythms, varying degrees of atrioventricular block and asystole (Finnegan & Trounce 1954).…”

Cardiovascular Diseases (Medical)

“…How ever, it has been pointed out that were this the case the incidence of non fatal arterial embolism should be higher following conversion than it is in most series of cases (lOS, 106). It has been shown both experimentally and clinically that quinidine itself can produce ventricular arrhythmias, and it is now believed that at least certain of these fatalities are due to ventricular standstill or '\Tentricular fibrillation produced by the quinidine (107,108,109). If this is true, the use of procaine amide may prove to be no safer in this regard, because Grumbach (110) has shown in animal experiments that it [and potassium and most other agents which are used for their irri tability depressing properties (111)]' will also produce ventricular arrhy thmias under certain circumstances.…”