POSITIVE PRESSURE RESPIRATION AND ITS APPLICATION TO THE TREATMENT OF ACUTE PULMONARY EDEMA

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Abstract
A physiologic basis is presented for the use of positive pressure respiration in treatment of pulmonary edema. Anesthetized rabbits were given adrenalin sufficient to stop breathing for 15 sec. to 2 minutes; pulmonary edema resulted with enlargement of right heart. Tidal air, pulmonary ventilation, arterial pressure, venous pressure, intrapleural and intratracheal pressure were measured, x-rays were taken at 15 sec. intervals. When positive pressure was applied by intermittent inflation of the lungs, pulmonary edema might be prevented. Respiratory measurements after intraven. injn. of adrenalin in the rabbit were found to have a very small range between inspiration and expiration with a marked increase in respiratory rate; but intermittent inflation of the lung restored these values to a more nearly normal figure. Positive pressure respiration did not consistently modify arterial or venous pressure after adrenalin was given. In pulmonary edema, there was an inequality in output of the 2 ventricles, the right discharging an increased vol. and the left smaller; therefore blood accumulated in the capillaries of the lung under increased pressure. The increased positive pressure within the chest (1) exerted an opposing force tending to hinder the outpouring of both red corpuscles and serum from the pulmonary capillaries; (2) diminished the vol. of blood entering the right heart; (3) relieved anoxemia. The physiological effects of positive pressure respiration of 3-8 cm of water in normal subjects were studied. The pulse rate was unchanged, the respiratory rate slightly increased, the blood pressure was unchanged, the venous pressure was elevated, circulation time prolonged, and the vital capacity decreased. In patients with congestive heart failure, the pulse rate increased, blood pressure remained unchanged, the respiratory rate decreased, and the venous pressure was elevated. There were inconsistent results in circulation time, and no consistent change in vital capacity under 8 cm but rise when under 6 cm. The authors used positive pressure continuously with a closed circuit apparatus with the motor blower unit and a hood modelled after Benedict helmet metabolism apparatus. 8 patients were relieved with positive pressure. There was evidence that sudden removal e.g., by tracheotomy of a previously existing backward pressure on pulmonary capillaries was followed by an increased permeability of capillary wall and that this might be prevented by positive pressure. The expiratory grunt of lobar pneumonia was described as an attempt to maintain increased positive pressure. When patients with emphysema and asthma partially closed their lips during expiration, breathing became easier. The author advised the cautious use of morphine. Positive pressure would probably be of great help in acute pulmonary edema caused by irritant gases.

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