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A Noninvasive Assessment of Pulmonary Perfusion Abnormality in Patients With Primary Pulmonary Hypertension^*

Hua Ting, MD; Xing-Guo Sun, MD; Ming-Lung Chuang, MD; David A. Lewis, MD, FCCP; James E. Hansen, MD, FCCP and Karlman Wasserman, MD, PhD, FCCP

^* From the Division of Respiratory and Critical Care Physiology and Medicine, Department of Medicine, Harbor-UCLA Medical Center, Torrance, CA. Visiting scientist from Chung Shan Medical and Dental College, Taichung, Taiwan. Visiting scientist from Chang Gung Memorial Hospital, Taipei, Taiwan.

Correspondence to: Karlman Wasserman, MD, PhD, FCCP, St. John’s Cardiovascular Research Center, Harbor-UCLA Medical Center, RB-2, Box 405, Torrance, CA 90509; e-mail: kwasserm{at}ucla.edu

Study objectives: The ventilatory equivalent for CO₂ (ie, the ratio of minute ventilation [E] to carbon dioxide output [CO₂]) is increased in patients with primary pulmonary hypertension (PPH) consequent to an increase in physiologic dead space and alveolar ventilation. We wished to see whether the E/CO₂ ratio correlated with the abnormality in pulmonary hemodynamics in PPH patients and whether it changed in response to prostacyclin infusion.

Methods: Following right-sided heart catheterization, 10 patients with severe PPH were studied in the coronary-care unit while hemodynamic and gas exchange measurements were measured simultaneously before and after infusion with epoprostenol (Epo), a prostacyclin analog. Studies were performed at baseline and during IV infusion of two to three increasing dosages of Epo in 10 PPH patients (NYHA class III-IV). Four patients had radial artery catheters for simultaneous blood gas measurements. Nine healthy subjects who were matched by sex, height, and weight underwent gas exchange analyses only.

Results: The mean (± SD) E/CO₂ ratio was higher in PPH patients than in control subjects (50.7 ± 9.7 vs 30.6 ± 3.8; p < 0.001). Thirteen measurements made in four patients showed that the E/CO₂ ratio correlated with the physiologic dead space/tidal volume ratio (r = 0.78; p = 0.002). The E/CO₂ ratio measurement at baseline correlated significantly with total pulmonary vascular resistance (TPVR) (r = 0.70; p = 0.02) but not with mean pulmonary artery pressure (mPAP) or cardiac index. During Epo infusion, the E/CO₂ ratio decreased with increasing dosage in 6 of 10 patients, with no change or slight increases in the 4 remaining patients. Considering all doses, the E/CO₂ ratio decreased significantly in response to the short-term administration of Epo. The decrease tended to parallel the pattern of decrease in TPVR, but the changes in both variables were too small to provide a statistically significant correlation. The mPAP did not change significantly in response to Epo infusion, although TPVR did change at the highest dosage.

Conclusions: In patients with severe PPH, the E/CO₂ ratio correlated significantly with TPVR but not with mPAP or cardiac index. The E/CO₂ ratio decreased systematically from baseline with the dose of Epo in some but not all patients. The E/CO₂ ratio and TPVR decreased significantly in response to Epo when all doses were considered. Further studies are needed to elucidate whether noninvasive gas exchange measurements may be clinically useful in the evaluation of the severity of pulmonary vascular disease and the effectiveness of pulmonary vasodilator therapy.

Key Words: cardiac output • physiologic dead space/tidal volume ratio • pulmonary vascular resistance • ventilation-perfusion mismatching • ventilatory equivalent for CO₂

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