Mechanisms determining the behaviour of the left atrial pressure during cardioplegia.

Abstract

The technique of inducing profound hypothermia by peripheral cannulation in man without opening the chest and using a heart-lung machine does not permit the surgeon to vent the left side of the heart (Woodhall, Sealy, Hall, and Floyd, 1960;Patterson and Ray, 1962). In open-heart surgery this is considered to be a vital step in preventing dilatation of the left heart and the pulmonary vasculature from continuing bronchial venous return. Indeed, if this is not done, in particular in the repair of defects with a large bronchial circulation, e.g., tetralogy of Fallot, the left heart may be irreversibly damaged by distension and the pulmonary vasculature may likewise be damaged beyond repair. This latter state was considered to be one of the most potent causes of the perfusion lung syndrome in the early days of bypass. Nevertheless when this method is used to produce profound hypothermia when operating on intracranial aneurysms little difficulty is experienced in reversing ventricular fibrillation to sinus rhythm, and post-operatively cardiopulmonary difficulties are minimal (Patterson and Ray, 1962;Michenfelder, Kirklin, Uihlein, Svien, and MacCarty, 1964;Gonski, Johnston, Hercus, Rollison, and Nield, 1964;Gonski and Johnston, 1966).Earlier studies which we performed (Johnston, Nield, Pritchard, and Hercus, 1965), when direct measurement of the left atrial pressure was made using a modification of the Ross (1959) technique, showed that at normal flow rates of 60 ml./kg./ min., although the left atrial pressure rose, it did not reach dangerous levels. When the flow was artificially increased to 120 ml. /kg. /min. by transfusion, the left atrial pressure rose still further, but again the level was tolerable. It was of interest that the highest left atrial pressures were attained during the period before fibrillation, due presumably to the failing left ventricle being unable to eject its contents against the perfusion pressure. For this reason it is now our practice 'Supported by a grant from the National Heart Foundation, Australia in operations on patients to fibrillate the heart deliberately at 28 to 300 C. The left atrial pressure then falls and the venous return is augmented, allowing more rapid cooling to take place. In a further group of animals when the period of cardioplegia with a circulation was greatly prolonged, the animals all regained consciousness, and, although several died in the early postoperative period, the deaths were not attributable to cardiopulmonary failure.The mechanism determining the behaviour of the left atrial pressure during cardioplegia when bronchial return is continuing was hinted at by Ross, Gilbert, Sharp, and Morrow (1958). They suggested that the left heart might be being decompressed through the lungs and then, by means of the incompetent pulmonary and tricuspid valves, into the systemic venous reservoir. The following group of experiments was undertaken to determine whether this indeed was the mechanism involved. MATERIAL AND METHODSHealthy mongrel dogs, weighing between 20 and...