Abnormal Arteriovenous Communications

Abstract

Clinical experiences and experimental studies provide evidence that an abnormal communication between the arterial and venous systems introduces into the circulation two circuits of flowing blood, one characterized by high arterial pressure and high peripheral resistance, and a second system bypassing part of the first, thus introducing a shorter circuit back to the heart, characterized by low pressure and low resistance, each supplied with flowing blood from the same central source, the heart. This shorter circuit acts solely as a parasitic circuit engrafted upon the normal circulation, serving no useful purpose, but capable of producing serious deleterious effects, depending upon the volume of blood diverted from the normal circulation into the shorter or parasitic circuit. Intimately dependent upon this diversion of differing volumes of blood into the shorter circuit is the great diversity in the effects of a peripheral fistula upon the heart: the complete absence of cardiac dilatation in some cases; the rapid development of cardiac dilatation and cardiac failure within 2½ months as exemplified in Mason's case; and the long delay of 57 years in the development of cardiac failure as observed by Dorney. Due to the high pressure in the normal circuit and the low resistance in the fistula circuit, there is a constant tendency for blood to be diverted or sequestered, as it were, in the fistulous or parasitic circuit, the factors determining the volume of blood so diverted being the size of the fistula and the distensibility of its rim or border, this, in turn, being dependent upon the character of the fibrous tissue deposited around the fistula in the course of healing. Firm, rigid, and excessive scarring permits only a small volume of blood to be sequestered in the fistula circuit, dilating only mildly the components of the parasitic circuit, whereas an elastic and distensible fistulous border permits progressive expansion of the fistulous opening with a progressive increase in the volume of blood sequestered in the fistula circuit, causing progressive dilatation of all components of this circuit including the four chambers of the heart, the aorta and artery proximal to the fistula, the fistula itself, the proximal vein, the vena cava, and the pulmonary vascular bed. All gradations in distensibility of the fistula may occur, and hence all gradations in cardiac dilatation will occur. Also, all gradations in the rapidity of fistulous expansion may occur and, therefore, all gradations in rapidity of cardiac dilatation will occur. This concept of a progressive expansion of a fistula of slow or rapid development permitting more and more blood to be shunted or sequestered in a shorter parasitic circuit at very rapid or very slow rates of increase provides the long-sought explanation of the rapid or long-delayed development of cardiac dilatation and failure in the presence of a peripheral fistula. It is suggested that the same explanation is applicable to the effects of all abnormal arteriovenous communications, including intracardiac shunts and even some hemangiomata, since all are subject to the same hydrodynamic law that flowing blood like flowing water seeks the path of least resistance.