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(Circulation. 1969;39:I-193.)
© 1969 American Heart Association, Inc.

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Changes in Pulmonary Vascular Resistance Following Closure of Ventricular Septal Defects

C. D. PARK M.D.¹; H. NICODEMUS M.D.¹; J. J. DOWNES M.D.¹; WILLIAM W. MILLER M.D.¹; JOHN A. WALDHAUSEN M.D.¹

¹ From the Departments of Surgery, Anesthesia, and Pediatrics (Division of Cardiology), University of Pennsylvania School of Medicine and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.

In five patients with pulmonary arterial hypertension (PAH) associated with ventricular septal or endocardial cushion defects, measurements of pulmonary vascular resistance (PVR) were made up to seven days after surgical closure. Before operation, the ratio of mean pulmonary arterial pressure [See Equation in PDF File] to mean systemic arterial pressure [See Equation in PDF File] averaged 0.77. Catheters placed at operation were used to measure pressure in the pulmonary artery, a systemic artery, and right and left atria. Cardiac output was determined by dye dilution. Controlled mechanical ventilation maintained a normal alveolar ventilation and arterial PO₂.

Postoperative [See Equation in PDF File], [See Equation in PDF File], and PVR were initially elevated, averaging 42 mm Hg, 0.57, and 1,132 dyne sec cm^-5, respectively. These values decreased to 29, 0.38, and 459 in three to seven days in the four survivors, but rose in the single death. With unassisted ventilation and 100% 0₂, or with acidosis (pH 7.21), [See Equation in PDF File] and PVR increased as much as +177% and 570%, respectively.

These studies show the relative pulmonary vasoconstricting effect of systemic acidosis and of spontaneous unassisted breathing with 100% O₂. In patients with markedly elevated, but reversible, hyperkinetic pulmonary vascular resistance, the beneficial effects of prolonged mechanical ventilation enabled the pulmonary circulation to return toward normal.