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Ventilation/Perfusion Ratios in Pulmonary Arterial Hypertension*: Effects of IV and Inhaled Prostacyclin Derivatives FREE TO VIEW

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

Chest. 2005;128(6_suppl):615S-616S. doi:10.1378/chest.128.6_suppl.615S
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In nine patients with severe pulmonary arterial hypertension (one primary and the others secondary to systemic sclerosis or pulmonary embolism), ventilation/perfusion (V̇/Q̇) ratios were measured during right-heart catheterization using a multiple inert gas elimination technique. V̇/Q̇ 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), V̇/Q̇ 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 V̇/Q̇ ventilation of 8.1% of minute ventilation (range, 2.9 to 36.8%), and increased dispersion of perfusion and ventilation for the V̇/Q̇ 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 V̇/Q̇ 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.

Abbreviations: log SDQ = SD of the distribution of perfusion; PVR = pulmonary vascular resistance; Svo2 = venous oxygen saturation; V̇/Q̇ = ventilation/perfusion




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