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(Chest. 2005;128:615S-616S.)
© 2005 American College of Chest Physicians

Ventilation/Perfusion Ratios in Pulmonary Arterial Hypertension*

Effects of IV and Inhaled Prostacyclin Derivatives

Tomas Bratel, MD; Lars Lagerstrand, MD; Lars-Åke Brodin, MD; Jacek Nowak, MD and Ivar Randmaa, MD

* From the Department of Pulmonary Diseases (Dr. Bratel), Karolinska Hospital, Karolinska; and Department of Clinical Physiology (Drs. Lagerstrand, Brodin, Nowak, and Randmaa), Huddinge University Hospital, Stockholm, Sweden.

Correspondence to: Tomas Bratel, MD, Department of Pulmonary Diseases, Karolinska Hospital, Karolinska, Sweden

In nine patients with severe pulmonary arterial hypertension (one primary and the others secondary to systemic sclerosis or pulmonary embolism), ventilation/perfusion (V/Q) ratios were measured during right-heart catheterization using a multiple inert gas elimination technique. V/Q ratios were assessed before and after administration of IV epoprostanol, 8.5 ± 1.8 ng/kg/min. Following 5.1 ± 1.5 months of inhaled iloprost therapy (20 µg tid), V/Q ratios were again measured before and 15 min after inhalation of 20 µg of iloprost. Before treatment, mean (± SD) pulmonary artery pressure was 46.2 ± 13.5 mm Hg. Pulmonary vascular resistance (PVR) was 8.61 ± 4.52 mm Hg/L/min, and cardiac output was 4.22 ± 0.75 L/min. There was a moderately elevated shunt of 5.1% (range, 1.6 to 19.5%) of cardiac output and substantial high V/Q ventilation of 8.1% of minute ventilation (range, 2.9 to 36.8%), and increased dispersion of perfusion and ventilation for the V/Q ratios (SD of the distribution of perfusion [log SDQ], 0.93 ± 0.31; and SD of the distribution of ventilation, 08 ± 0.23). Epoprostanol infusion resulted in a 21 ± 18% reduction in PVR and a 36 ± 14% reduction in systemic vascular resistance. log SDQ was further increased by 30 ± 33%. The mean increase in shunt was approximately 60% higher during epoprostanol than after iloprost (p = 0.06). However, due to increased cardiac output and raised venous oxygen saturation (SvO2), PaO2 was not significantly altered.

PVR was not changed by long-term iloprost. Fifteen minutes after iloprost, PVR and systemic vascular resistance both decreased by approximately 15% and log SDQ increased by 13 ± 14%, SvO2 was not altered, but PaO2 was lowered from 9.2 ± 2.1 to 8.0 ± 1.5 kPa (p = 0.06). IV epoprostanol and inhaled iloprost reduce PVR to a similar degree, and both worsen V/Q mismatching. However, during epoprostanol, the increased log SDQ and the higher increase in shunt was compensated by increased SvO2, resulting in a PaO2 that was not significantly changed. After iloprost, the increased log SDQ was not compensated by increased SvO2, and thus PaO2 was more consistently decreased.


   Footnotes
 
Abbreviations: log SDQ = SD of the distribution of perfusion; PVR = pulmonary vascular resistance; SvO2 = venous oxygen saturation; V/Q = ventilation/perfusion





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