Abstract. Electrocardiographic abnormalities in various cerebrovascular accidents are described, based on a clinical material. The incidence of the ECG changes was 71.5% in the group with subarachnoid haemorrhage. The figures for the groups with intracerebral haemorrhage and unclassified cerebrovascular accidents were 57.1 and 41.1%, respectively. Attention has been focused on positive, abnormal T waves, and on S‐T segment elevations in connection with an acute increase of blood pressure in the early phase after cerebrovascular accident. These changes were often shown to precede the T wave inversions which followed later. Subendocardial haemorrhages and in one case distinct myocardial infarction were observed. The authors believe that the prime factor responsible for ECG changes is an acute increase in left ventricular pressure following elevation of intracranial pressure. A short review of the literature is also given.
Sympathetic beta-blocking agents such as alprenolol are not for routine use in resuscitation, but they may be life saving in certain cases. We report three cases of myocardial infarction in which alprenolol was successfully used with direct-current shock when other measures had failed to terminate recurring ventricular fibrillation. Case 1A 44-year-old man who had two myocardial infarctions and who was taking thyroid 100 mg daily for hypothyroidism after thyroidectomy had a cardiac arrest. Ventricular fibrillation was successfully defibrillated. Thirteen days later, as he was about to leave hospital, he had another attack of ventricular fibrillation. Sinus rhythm was restored but not maintained for longer than 15 to 30 seconds after each defibrillation, despite the fact that acidosis was corrected, the patient well oxygenated, and given adequate doses of lignocaine. After one hour alprenolol 10 mg was given intravenously. The first 200 W/s direct-current shock three minutes later terminated the fibrillation. The patient recovered without any signs of brain damage. Lignocaine and procainamide (500 mg six hourly) were not enough to control tachyarrhythmias, and alprenolol 100 mg daily was added to the treatment. Sinus rhythm was then maintained. Thyroid had been discontinued in view of the tachyarrhythmias. The patient was discharged after six weeks, but anginal attacks increased and after four days he was readmitted because of intractable chest pain. Five days later he had another cardiac arrest. Once again resuscitation was prolonged and defibrillation had to be repeated eight times. Recovery was uneventful. For the past 18 months the patient has been maintained on thyroid 50 mg and alprenolol 300-400 mg daily. Anginal attacks have been rare and less severe. Case 2A 52-year-old man with a long history of anginal attacks was admitted to hospital with a transmural anteroseptal infarction. A fortnight later he had an attack of ventricular fibrillation. Resuscitation lasted over four hours, and the patient had to be defibrillated 20 times despite the administration of lignocaine 800 mg and the correction of acidosis. Glucagon 6 mg and hydrocortisone 1,000 mg were also given. After intravenous alprenolol 9 mg and atropine 1 5 mg had been given defibrillation terminated the attacks and the patient recovered. Eight days later, on two occasions he again had to be resuscitated. On the first occasion alprenolol 4 mg was given intravenously before successful defibrillation. Alprenolol had already been given by mouth for two days previously but in a dose of only 50 mg three times a day. This was increased to 100 mg four
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