The obscure physiology of poststenotic dilatation; its relation to the development of aneurysms.

SUMMARY A mass of fluid ejected through a narrow and limited constriction under high velocity strikes against a more slowly moving mass of fluid distal to the stenosis resulting, first, in the conversion of high kinetic energy into high potential energy or lateral pressure and, second, in the lateral deflection of the rapid stream and even in a complete reversal in its direction of flow, thus resulting in a clash of opposing streams that produces eddies of alternating high and low pressures whose repeated impacts over a prolonged period against an elastic wall are capable of inducing structural fatigue and distention of that wall. Accentuating the play of these forces is a third factor: the hydraulic principle that a widening stream causes decreasing velocity which in turn produces increasing lateral pressure. The resulting interplay of these three factors recurring repetitively with each systole in a pulsating stream, and operating in a limited segment of an elastic vessel, produces eventually and inevitably the phenomenon of poststenotic dilatation. It is a highly intriguing thought that this sequence of events may be the initiating and possibly the most important factor in the development of the fusiform dilatations, the saccular aneurysms, or even of the dissecting aneurysms commonly observed in the arteriosclerotic aorta in which segmental atherosclerosis or fibrosis may produce a localized or relative stenosis. The recognition of the potential power of the hydraulic forces liberated beyond a real or relative stenosis may assist in the explanation of the destruction of bone and surrounding structures that occasionally accompanies the development of a thoracic aneurysm. They explain also the aneurysmal dilatation of the vein usually seen at the site of an arteriovenous fistula where the arterial stream under high pressure and high velocity is ejected through an abnormal communication into the widened bed of the accompanying vein. The occasional aneurysmal dilatation of the pulmonary artery in the presence of a patent ductus may also be ascribed to the hydraulic forces liberated when the arterial stream of high pressure and high velocity is ejected from the narrow ductus into the wider and less rapidly flowing stream of the pulmonary artery with its lower pressure. It is highly probable, also, that the sudden cerebral hemorrhage attributed to the rupture of a small aneurysmal dilatation has its inception in the precipitate unleashing of hydraulic forces suddenly augmented by the heightened pressure and increased velocity of flow incident to emotional stress or physical exertion. Similarly, sudden death from rupture of a larger thoracic or abdominal aneurysm may follow the sudden increase in blood pressure and pulse rate that accompanies emotional stress or physical exertion and produce an increase in neocity of flow which greatly augments the play of hydraulic forces, with resulting sudden increase in lateral pressure just distal to the junction of the narrow arterial lumen with the greatly widened bed of the aneurysmal dilatation. These and other similar vascular phenomena may find their proper explanation in the application of the hydraulic laws that govern the pulsatile flow of fluid through a system of elastic vessels subjected to real or relative narrowing by congenital abnormalities, by degenerative processes, or by accidental injuries. They give stern warning also of the need to employ, in vascular surgery, methods of end-to-end anastomosis that permit growth at the site of union as the child grows, thus avoiding future stenosis, and methods that prevent or minimize the development of constriction at the site of anastomosis, either by puckering at the time of operation, or by cicatricial contracture as healing progresses. Grateful acknowledgment is hereby accorded to Professor J. K. Vennard of the Department of Civil Engineering at Stanford University for his helpful advice and criticism, and to Drs. Ernest Schnoor, Eldon Ellis, and Iseu da Costa, fellows in surgery, for their invaluable help in executing the experimental studies presented in this paper.