Is Hypoxic Pulmonary Vasoconstriction Exaggerated During One-Lung Ventilation in Patients With Patent Ductus Arteriosus?

Abstract

We read with interest the recently published clinical report by Baraka et al. (1). Although we were fascinated by their observation, we are disturbed by a potentially serious flaw in the deduction of their final conclusion. Without properly addressing certain physiologic variables (as discussed in the following paragraphs), the conclusion that "(less pulmonary shunt is) . . . attributed to an exaggerated HPV response in these patients" is simply inadequate.When a patient is placed in the lateral decubitus position, the three zones of pulmonary blood flow distribution, as dictated by gravity, are determined by pulmonary arterial pressure (2). In zone 3, with both transmural pulmonary arterial pressure and transmural pulmonary venous pressure higher than the alveolar pressure, the lung units receive the most pulmonary blood flow. On the other hand, in zone 1, where alveolar pressure is higher than both transmural pulmonary arterial pressure and transmural pulmonary venous pressure, the lung units receive the least blood flow (3). The dependent lung, with most of its units situated in zone 3, will receive more pulmonary blood flow than the nondependent lung, which has most of the units situated in zone 1. Decreasing the pulmonary arterial pressure will cause expansion of zone 1 and contraction of zone 3. Pulmonary arterial pressure must be controlled when evaluating hypoxic pulmonary vasoconstriction.The cardiac catheterization measurement of patient 1 revealed a right ventricular pressure of 3 5 D 1 mm Hg with a pulmonary artery pressure of 21/4 mm Hg. Similarly, in patient 2, the catheterization measurement revealed a right ventricular pressure of 50/20 mm Hg and pulmonary arterial pressure of 36/12 mm Hg. In both cases, there existed a 14-mm Hg systolic pressure gradient across the pulmonic valve. Without aortic blood flow through a patent ductus arteriosus, the pressure gradient across the pulmonary valve can only be higher. The existence of this gradient indicated that both patients have subclinical pulmonary valvular stenosis. In otherwise normal patients, the closure of patent ductus arteriosus will cause a decrease in pulmonary arterial pressure. In patients with pulmonary stenosis, the closure of a patent ductus arteriosus could cause an even more significant decrease in pulmonary arterial pressure. In the face of a changing pulmonary arterial pressure, it is unreasonable to assume that the amount of hypoxic pulmonary vasoconstriction can be quantitated with any degree of certainty.In conclusion, as a result of surgical closure of the patent ductus arteriosus, we would expect to see an increased proportion of pulmonary blood flow to the dependent lung. This redistribution of pulmonary blood flow will be even more pronounced in patients with concomitant pulmonary stenosis. The quantitation of hypoxic pulmonary vasoconstriction in this situation is not possible without quantitating the exact change in pulmonary arterial pressure.