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Twenty-three moribund asthmatic patients admitted to the intensive care unit for resuscitation by bronchial lavage, intravenous fluid infusion and intermittent positive pressure ventilation were found to have severe derangements of the circulation. A tachycardia of 120-1 80/min was associated with marked pulsus paradoxus, visible and palpable epigastric thrust during systole and triple cardiac rhythm. Eleven patients had normal blood pressures, six had systemic hypotension and six hypertension (blood pressure more than 160/90). Electrocardiograms showed sinus tachycardia with a variation in amplitude of the waves during the respiratory cycle, P-pulmonale, extreme clockwise rotation of the P wave axis in the frontal plane and of the mean QRS axis; in some patients there was additional evidence of right heart strain. These changes resembled findings described by others during acute asthma 192. X-rays of the chest demonstrated narrowing of the cardiac silhouette which was only as wide as the vertebral column in some patients. The superior vena caval shadow could not be seen in six patients. These signs of cardiovascular derangement decreased during treatment with Intermittent Positive Pressure Ventilation (IPPV) and were absent when the patient recovered. It has been shown that, in prolonged asthmatic attacks, increased secretions and shed mucosa form bronchial plugs3 leading to a process of gradual suffocation, but when death occurred it was a sudden, sometimes unexpected event as other workers have described previously J, 5.Factors that may lead to cardiac death in asthma have not been adequately studied and cardiac catheterisation was therefore carried 134 Vol22ANBSTHESIA 135 out in order to obtain additional information about the circulatory changes. Only one patient has been studied because patients were admitted in a serious clinical condition as medical emergencies requiring immediate resuscitation. The results of the investigation focused attention on the effects of abnormal intrapleural pressure fluctuations during spontaneous respiration on the circulation, and the cardiovascular effects of IPPV in asthma. METHODSThe patient, a fifty-five year old man, was admitted to the intensive care unit for resuscitation because conventional medical care had failed. Catheters were placed in the right ventricle and aorta and respiratory pressure-volume loops were obtained with a method described elsewhere6. These observations were made with the trunk inclined at 45" to the horizontal. Arterial blood samples were analysed for gas tensions with the patient breathing a humidified, oxygenenriched mixture and saline was infused intravenously. The patient was then anasthetised with a halothane and oxygen mixture, intubated after intravenous injection of 40mg of suxamethonium and topical analgesia of the larynx with lignocaine and ventilated with a volumecycled Cape ventilator using airway pressures of +60cm/H 2 0 during inspiration and -20cm/H 2 0 during expiration ; high peak inspiratory flow-rates and a fixed inspiratory ...

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