THE HAEMODYNAMICS OF COMPLETE TRANSPOSITION OF THE GREAT VESSELS.

In the normal circulation blood goes around the body in one circuit. Two resistances are encountered by the blood in this circuit, the systemic and the pulmonary vascular resistances. In complete transposition of the great vessels, blood goes round in two separate circuits, namely the systemic and pulmonary circuits. Owing to the separate nature of the two circuits, any shunt that occurs between them has to be bidirectional and exactly equal in both directions. Theoretically if a large communication, such as a ventricular septal defect, exists between the two circuits, a shunt occurs from the circuit with the higher pressure to that with the lower pressure only until the pressures in the two ventricles equalize. The fact that the pulmonary and systemic resistances are often different in complete transposition of the great vessels will not result in itself in the exchange of blood between the two circuits, because even if it explains the direction of the shunt from the circuit with the higher resistance to that with the lower resistance, it will not explain the occurrence of an equal shunt in the reverse direction, that is from the circuit with the lower resistance to that with the higher. Several views have been expressed about the mechanism of blood shunting in transposition of the great vessels (Astley and Parsons, 1952; Wood, 1956; Kjellberg et al., 1959; Taussig, 1960). These authors thought that the volume and the direction of the shunt in transposition of the great vessels was probably determined by the total resistances in the two vascular systems. The reason why some of the deeply cyanosed patients have evidence of increased systemic blood flow (Campbell and Suzman, 1951; Astley and Parsons, 1952; Cleland et al., 1957; Kjellberg et al., 1959; Noonan et al., 1960; D. C. Deuchar, 1962, personal communication) has never been explained. The object of this paper is to discuss the hemodynamics of complete transposition of the great vessels. The belief that cardiac catheterization contributes little to the diagnosis of this condition (Campbell et al., 1949; Blalock and Hanlon, 1950; Lillehei and Varco, 1953; Keith, Rowe, and Vlad, 1958) has probably led to the scarcity of the data in any one hospital. For this reason the majority of the patients studied haemodynamically in this paper have been obtained from published reports, particularly from the excellent paper by Noonan et al. (1960).