Pulmonary Venous Wedge Pressures Accurately Predict Pulmonary Arterial Pressures in Children with Single Ventricle Physiology J. Thompson, P. Moore, D.F. Teitel Department of Pediatrics, University of California at San Francisco, 505 Parnassus Avenue, San Francisco, CA 94143-0130, USA Abstract. We investigated the relationship between pulmonary venous wedge and pulmonary arterial pressures in patients with single ventricle physiology. This relationship has been studied in other cardiac conditions but not in this unique group of patients. We made 60 paired measurements from one or both lungs in 40 patients, and divided the patients into three groups. Group 1 consisted of patients whose pulmonary blood supply was via an aortopulmonary shunt (n = 14), group 2 included patients with a bi- directional Glenn anastomosis (n = 20), and group 3 included patients with a pulmonary arterial band (n = 6). Venous wedge pressure estimated arterial pressure within 3 mmHg in 59 of 60 paired meas- urements. Plots of the difference between pulmonary artery and pulmonary venous wedge pressures versus the mean showed excellent correlation, with a mean difference of approximately 1 for group 1 (mean difference, )0.15 ± 1.3 mmHg) and group 2 (mean difference, 0.52 ± 1.12 mmHg). The relationship was poor in group 3 (mean difference, )2.00 ± 4.80 mmHg) but was much better with the exclusion of the one outlying patient in whom pulmonary venous wedge pressure significantly overestimated pulmo- nary arterial pressure (mean difference, )0.33 ± 2.07 mmHg). We conclude that pulmonary venous wedge pressure accurately estimates pulmonary arterial pressure in patients palliated for single ventricle physiology, but care must be taken in patients with a pulmonary arterial band. Keywords: Pulmonary venous wedge pressure — Single ventricle — Cardiac catheterization Accurate assessment of pulmonary arterial pressures and blood flow is essential for clinical decision mak- ing in infants and children with complex congenital heart disease who have single ventricle physiology. Such patients must have normal pulmonary vascular resistance and low transpulmonary mean pressure gradients in order to undergo the preferred staged surgical approaches, which include a bidirectional Glenn anastomosis followed by a modified Fontan procedure. If pulmonary hemodynamics are not suitable, less desirable palliations or heart transplant must be considered. In some of these patients, it is difficult to measure pulmonary arteria pressures di- rectly because of their complex anatomy. (e.g., transposed great arteries and severe subpulmonic obstruction) or because of previous surgery (e.g., a proximally placed modified Blalock–Taussig shunt). In others, direct measurement of pulmonary arterial pressures may carry a significant risk (e.g., a patient with a stenotic aortopulmonary shunt that is the sole source of pulmonary blood flow). An accurate esti- mate of pulmonary arterial mean pressure that is easily obtainable and carries minimal risk is desirable in such patients. Pulmonary venous wedge pressures are usually easy to obtain in children with single ventricle phys- iology because venous access to the left atrium is al- most invariably possible via a native or surgically created atrial communication. Studies in adults with acquired heart disease have shown good correlation between pulmonary venous wedge and pulmonary arterial pressures in patients without pulmonary hy- pertension [6, 14]. Studies comparing venous wedge and arterial pressures in patients with pulmonary hypertension or in children with complex congenital heart disease have shown conflicting results [8, 15]. No study has specifically determined this relationship in children with single ventricle physiology. In order to use venous wedge pressures as an estimate of ar- terial pressures in patients with single ventricle physiology, it is essential to undertake such a study because pulmonary arterial flow patterns and wave- forms in such patients are rarely normal. At various Correspondence to: D.F. Teitel, email: dfteitel@pedcard.ucsf.edu Pediatr Cardiol 24:531–537, 2003 DOI: 10.1007/s00246-003-0428-0 Original Articles