A noninvasive assessment of pulmonary perfusion abnormality in patients with primary pulmonary hypertension

Study objectives: The ventilatory equivalent for CO, tie, the ratio of minu te ventilation [V/E] to carbon dioxide output [VCO2]) is increased in patie nts with primary pulmonary hypertension (PPH) consequent to an increase in physiologic dead space and alveolar ventilation. We wished to see whether t he VE/VCO2, ratio correlated with the abnormality in pulmonary hemodynamics in PPH patients and whether it changed in response to prostacylin infusion . Methods: Following light-sided heart catheterization, 10 patients with seve re PPH were studied in the coronary-care unit while hemodynamic and gas exc hange measurements were measured simultaneously before and after infusion w ith epoprostenol (Epo), a prostacyclin analog. Studies were performed at ba seline and during IV infusion of two to three increasing dosages of Epo in 10 PPN patients (NYHA class III-IV). Four patients had radial artery cathet ers for simultaneous blood gas measurements. Nine health, subjects who were matched by sex, height, and weight under ent gas exchange anal, ses only. Results: The mean (+/- SD) < (V)over dot >E/< (V)over dot > CO2 ratio was h igher 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 < (V)over dot >E/< (V)over dot > CO2 ratio correlated with the physiologic dead space/tidal volume ratio (r = 0.78; p = 0.002). The < (V)over dot >E/< (V)over dot > CO2 ratio measurement lit baseline correlated significantly with total pulmonary vascular resistance (TPVR) (r = 0.70; p = 0.02) but no t with mean pulmonary artery pressure (mPAP) ol cardiac index. During Epo i nfusion, the < (V)over dot >E/< (V)over dot > CO2 ratio decreased with incr easing dosage in 6 of 10 patients, with no change or slight increases in th e 4 remaining patients. Considering all doses, the < (V)over dot >E/< (V)ov er dot > CO2 ratio decreased significantly in response to the short-term ad ministration of Epo. The decrease tended to parallel the pattern of decreas e in TPVR, but the changes in both variables were too small to provide a st atistically 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 < (V)over dot >E/< (V)over do t>CO2, ratio correlated significantly with TPVR but not with mPAP or cardia c index. The < (V)over dot >E/<V()over dot > CO2 ratio decreased systematic ally from baseline with the dose of Epo in some but not all patients. The < (V)over dot >E/<V)over dot > CO2, ratio and TPVR decreased significantly i n response to Epo when all doses were considered. Further studies are neede d to elucidate whether noninvasive gas exchange measurements may be clinica lly useful in the evaluation of the severity of pulmonary vascular disease and the effectiveness of pulmonary vasodilator therapy.