Quantification of Systemic-to-Pulmonary Artery Collateral Flow

Abstract

Abnormal vascular connections between systemic arteries and the pulmonary vascular bed—systemic-to-pulmonary collateral (SPC) vessels—manifest in patients with a variety of congenital and acquired heart disease. These vessels, which originate from branches off the brachiocephalic arteries, chest wall arteries, and the descending aorta, vary markedly in size, number, course, and distribution. Although the precise mechanisms that lead to development of SPCs are incompletely understood, hypoxemia, diminished global or regional pulmonary blood flow, and nonpulsatile flow in the pulmonary arteries are some of the commonly cited contributors.1 Indeed, SPCs are frequently encountered in patients with cardiac anomalies that include ≥1 of these abnormalities such as severe forms of tetralogy of Fallot and functional single ventricle (FSV). In the latter group, the clinical importance of SPCs and their optimal management have been topics of intense debate for >2 decades.2–6 Article see p 218 The physiology of SPC flow involves both beneficial and deleterious effects.1,2 SPCs can augment blood flow to hypoperfused lung segments, improve gas exchange, and potentially inhibit the development of pulmonary arteriovenous malformations in patients in whom hepatic venous flow does not reach the pulmonary circulation. In contrast, like other shunts, SPC flow is inherently inefficient because relatively highly oxygenated blood returns to the pulmonary circulation and potentially competes with the more efficient antegrade flow to the lungs through the native pulmonary arteries. Consequently, SPC flow results in volume load on the FSV, which can lead to ventricular dilatation and dysfunction, atrioventricular valve regurgitation, and heart failure symptoms. Other deleterious effects of excessive SPCs include flow energy loss,7 exuberant blood flow returning through the pulmonary veins to the surgical field during cardiopulmonary bypass, respiratory distress, pulmonary hypertension, and hemoptysis.8 In patients with FSV, the hemodynamic burden from SPCs has been the topic …