Arterial hypoxaemia: a side-effect of intravenous isoprenaline used after cardiac surgery.

A side-effect of intravenous isoprenaline used after cardiac surgery Intravenous administration of isoprenaline following cardiac surgery has been shown to cause an increase in existing arterial hypoxaemia. This is considered to be due to an increase in venous admixture following interference with the normal compensatory mechanism which in the presence of alveolar hypoxia tends to maintain normal ventilation-perfusion relationships. The occurrence of arterial hypoxaemia following cardiopulmonary bypass has been demonstrated by many workers despite the fact that the post-operative course is uncomplicated An increase in pulmonary venous admixture secondary to alveolar collapse has been suggested as the mechanism, although the precise aetiology remains uncertain. The presence of non-ventilated alveoli is shown by a high venous admixture even when 100% oxygen is inhaled. Intravenous isopropylnoradrenaline sulphate (isoprenaline) is a drug commonly used after cardiac surgery in the treatment of low output states and heart-block. Whilst investigating the cardiovascular effects of isoprenaline after cardiac surgery it was noted that arterial oxygen saturation decreased during infusion of the drug. This paper describes the finding and attempts to explain its mechanism. METHODS Seven patients aged 39 to 56 years who had undergone homograft replacement of the aortic valve under total cardiopulmonary bypass were studied 16 to 20 hours post-operatively. Three patients had aortic valve disease with stenosis and regurgita-tion, one had aortic regurgitation, one had aortic stenosis, and one had mixed aortic valve disease with, in addition, mitral stenosis; one patient had aortic valve stenosis with mitral stenosis and regurgitation. Mitral valve disease was corrected surgically at the time of homograft replacement of the aortic valve in the two patients with associated mitral valve disease. The post-operative state of all the patients studied was satisfactory and no patient required therapy other than routine post-operative care. The position of the patients was constant during the study, with a head-up tilt of 150 to 30°, and all patients were breathing air spontaneously. Pulmonary arterial and left atrial pressures were measured through catheters inserted towards the end of the operation, using a pressure transducer (Statham P.23G) and an oscillographic recorder (Sanborn Model 296). Two-or three-minute expired air collections were made using a mouthpiece , noseclip, and one-way valve, the total dead space of the apparatus being 60 ml. During the collections of expired air mixed venous blood was drawn into siliconized, heparinized syringes via the pulmonary arterial catheter, and arterial blood through a catheter (T.F.10) inserted into …