Ventricular fibrillation outside hospital.
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Biomedical subjects
Publications and source records attributed to J F Pantridge.
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The mean current required for ventricular defibrillation was measured and found to be 0.35 +/- SE 0.03 A/kg body weight, which is about one-third of that predicted from animal experiments. There was no apparent correlation between the current required and body weight (r = -0.007 +/- SE 0.213). There is no evidence of need for defibrillators storing more than 400 J.
The haemodynamic effects of intravenous mexiletine have been studied in 16 patients with valvular heart disease without clinical evidence of heart failure. A bolus injection of 150 mg administered to 6 of the 16 patients resulted in a mean plasma concentration above the therapeutic range for at least 5 minutes after the drug was given. A small but significant rise in the mean pulmonary artery pressure occurred. In 10 patients, the effects of intravenous mexiletine were compared with those of intravenous saline in a double blind trial. No significant difference was found in the haemodynamic effects, though both saline and mexiletine produced a small rise in the mean pulmonary artery pressure. Mexiletine when administered to patients without heart failure in doses known to be clinically effective did not have important adverse haemodynamic effects.
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Lignocaine was administered intravenously to 36 patients with acute myocardial infarction. A bolus of 100 mg followed by an infusion of 2 mg/minute failed to maintain plasma levels above 2 microgram/ml. A bolus of 100 mg followed by 4 mg/minute also failed to maintain satisfactory plasma concentrations during the first hour of therapy. A bolus of 75 mg was combined with an infusion of 10 mg/minute for 20 minutes followed by 1.5 mg/minute. Satisfactory plasma concentrations during the first hour were observed in 94 per cent of the estimations. No important adverse side effects occurred during the infusion of 10 mg/minute.
Forty-eight patients with ischaemic heart disease received oral mexiletine for the control or prevention of ventricular arrhythmias. The most frequently used doses were 200, 250, and 300 mg 8-hourly. The treatment period varied from 2 days to more than 1 year (median 3 months). No ventricular arrhythmias were detected in more than one-half of the patients. Severe side effects occurred in 15 (31%) of the 48 patients. Major ventricular arrhythmias were observed in 14 (29%) of the 48 patients at a time when the majority had plasma concentrations within the therapeutic range. The value of mexiletine in the management of patients at risk of sudden death is likely to be limited.
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A prospective study of the energy required for transthoracic ventricular defibrillation in adults showed that in 42 (81%) out of 52 episodes of ventricular fibrillation shocks of 100 watt-seconds (Ws) of stored energy were successful. Out of 233 episodes, 222 (95%) were converted by 200 W s shocks. Among patients in whom primary ventricular fibrillation occurred within one hour of the onset of acute myocardial infarction, 200 W s shocks were successful in 40 (98%) out of 41 episodes. When low-energy shocks failed, a stored energy of 400 W s invariably succeeded. The need for large and expensive defibrillators that store more than 400 W s and are less readily available is therefore questioned.
The minimum current required to cause ventricular fibrillation was determined by electrical stimulation of the normal or ischemic canine left ventricle. The threshold for ventricular fibrillation in the normal heart decreased when the heart rate was rapid. Strong vagal stimulation did not affect the ventricular fibrillation threshold when the heart rate was fixed. The fall in the ventricular fibrillation threshold in the presence of acute myocardial ischemia was greater and more prolonged when the heart rate was rapid. These findings indicate the importance of the immediate correction of tachycardia in patients suffering from acute myocardial infarction.
Mexiletine administered either intravenously or orally was found to be an effective antiarrhythmic agent. Unfortunately, important adverse effects occurred in approximately half of the patients. Adverse effects which appeared during oral therapy were dose related. Mexiletine controlled lignocaine-resistant ventricular dysrhythmias in more than half of the patients treated. Ventricular tachycardia and ventricular fibrillation occurred at plasma concentrations which were not significantly different from those associated with severe side-effects, suggesting that when mexiletine is used to control these major dysrhythmias the incidence of important side effects will be high.
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Most deaths from ischaemic heart disease are sudden, occur outside hospital, and result from ventricular fibrillation. But defibrillators have only limited availability because of their size and weight. A miniature defibrillator has been developed. A singe low-energy shock succeeded in removing ventricular fibrillation in 73 out of 82 episodes, and a further shock was successful in seven more episodes. Primary ventricular fibrillation probably always responds to low-energy electrical shocks, which challenges the conventional view that correction of ventricular fibrillation requires high-energy direct-current shock. Thus even smaller and lighter defibrillators are possible. Furthermore low-energy shocks cause less myocardial damage.
The cardioselective beta-adrenoceptor blocking agent practolol was used in the management of ventricular and supraventricular dysrhythmias associated with acute myocardial infarction in 134 patients, and in the management of these dysrhythmias in 19 atients with acute myocardial ischemia. Practolol was frequently effective in controlling ventricular dysrhythmias which occurred within the first 24 hours after the onset of symptoms of acute myocardial infarction. It was also effective in controlling the ventricular dysrhythmias which occurred after resuscitation from ventricular fibrillation. It was of particular value when therapeutic doses of lidocaine had been ineffective. Practolol was much less effective in controlling ventricular dysrhythmias which occurred more than 24 hours after acute infarction. Atrial fibrillation and atrial flutter were infrequently abolished by practolol in undigitalized patients after acute myocardial infarction. There was no correlation between the effectiveness of practolol and the blood concentration of the drug. One adverse effect of practolol was the occurence of sinus bradycardia with or without an increase in the frequency of ventricular ectopic beats. Bradycardia was sometimes accompanied by hypotension. Severe hypotension occasionally occurred in the absence of bradycardia.
Since the lower the energy used, the less the possible myocardial damage, two studies of 214 patients in ventricular fibrillation (VF) were conducted, using two types of defibrillators each charged to 200 Wsec and 100Wsec. In the first study, each defibrillator was charged to 200 Wsec (150-165 Wsec delivered). Up to three 200-Wsec shocks successfully converted 222 of 233 VF episodes. In 199 episodes, a single shock successfully removed the fibrillation. In 48 episodes in patients weighing more than 80 kg, VF was removed in 43 (90 percent). In the second study, from a stored energy of 100 Wsec, 74 to 82 Wsec of energy were delivered in the initial shock to treat 161 VF episodes in 94 patients. The first shock was successful in 101 (63 percent) of the 161 episodes. Up to three 100-Wsec shocks achieved 81 percent conversion in 52 episodes. A third 100-Wsec shock seldom succeeded. Using a sequence of 100 - 200 - 400 Wsec shocks, 93 (91 percent) of 102 episodes were successfully converted. There was not a single instance of failure to remove VF among the 214 patients with a maximal delivered energy of 330 Wsec. Thus, the direction towards the production of larger instruments storing more than 400 Wsec energy seems unwarranted.