It has been assumed by many workers [Inman, 1969] that cardiac arrhythmia and ventricular fibrillation may follow excessive bronchodilator therapy in asthma. This assumption has been mainly based on the experimental work of Lockett [1965] on the isolated cat heart-lung preparation exposed to artificial strain. It does not appear to have been appreciated that this situation is not confirmed in the reports on human asthmatic subjects who have been monitored during status asthmaticus. Such patients have been observed to have progressive bradycardia followed by cardiac arrest in asystole [Grant, 1968; Miller and Semple, 1967]. Recent experiments by Collins [1969] have now shown that under hypoxic conditions the heart of dogs arrests in asystole preceded by bradycardia when exposed to moderately large amounts of isoprenaline; the usual effect of isoprenaline being reversed. It is known that sudden death may occur when patients are apparently recovering from status asthmaticus, and those who have been severely hypoxic may take up to 14 days to recover a normal oxygen tension. It has also been observed that many patients who are suffering from apparently moderate asthma may be walking about with a PaO2 well below normal. Bronchodilator drugs can be tolerated by the human asthmatic in very high dosage under conditions of normal PaO2 The danger lies when hypoxia is present both during and after status asthmaticus. These facts are consistent with the rise in asthma mortality from 1960–1966 and the fall since this time which has paralleled the free prescription of pressurised isoprenaline.

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