0
Clinical Investigations: PULMONARY VASCULATURE |

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; Karlman Wasserman, MD, PhD, FCCP
Author and Funding Information

Affiliations: *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@ucla.edu



Chest. 2001;119(3):824-832. doi:10.1378/chest.119.3.824
Text Size: A A A
Published online

Study objectives: The ventilatory equivalent for CO2 (ie, the ratio of minute ventilation[ V̇e] to carbon dioxide output[ V̇co2]) 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 V̇e/V̇co2 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) V̇e/V̇co2 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 V̇e/V̇co2 ratio correlated with the physiologic dead space/tidal volume ratio (r = 0.78; p = 0.002). The V̇e/V̇co2 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 V̇e/V̇co2 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 V̇e/V̇co2 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 V̇e/V̇co2 ratio correlated significantly with TPVR but not with mPAP or cardiac index. The V̇e/V̇co2 ratio decreased systematically from baseline with the dose of Epo in some but not all patients. The V̇e/V̇co2 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.

Figures in this Article

Sign In to Access Full Content

MEMBER & INDIVIDUAL SUBSCRIBER

Want Access?

NEW TO CHEST?

Become a CHEST member and receive a FREE subscription as a benefit of membership.

Individuals can purchase this article on ScienceDirect.

Individuals can purchase a subscription to the journal.

Individuals can purchase a subscription to the journal or buy individual articles.

Learn more about membership or Purchase a Full Subscription.

INSTITUTIONAL ACCESS

Institutional access is now available through ScienceDirect and can be purchased at myelsevier.com.

Sign In to Access Full Content

MEMBER & INDIVIDUAL SUBSCRIBER

Want Access?

NEW TO CHEST?

Become a CHEST member and receive a FREE subscription as a benefit of membership.

Individuals can purchase this article on ScienceDirect.

Individuals can purchase a subscription to the journal.

Individuals can purchase a subscription to the journal or buy individual articles.

Learn more about membership or Purchase a Full Subscription.

INSTITUTIONAL ACCESS

Institutional access is now available through ScienceDirect and can be purchased at myelsevier.com.

Figures

Tables

References

NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Sign In to Access Full Content

MEMBER & INDIVIDUAL SUBSCRIBER

Want Access?

NEW TO CHEST?

Become a CHEST member and receive a FREE subscription as a benefit of membership.

Individuals can purchase this article on ScienceDirect.

Individuals can purchase a subscription to the journal.

Individuals can purchase a subscription to the journal or buy individual articles.

Learn more about membership or Purchase a Full Subscription.

INSTITUTIONAL ACCESS

Institutional access is now available through ScienceDirect and can be purchased at myelsevier.com.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Find Similar Articles
CHEST Journal Articles
PubMed Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543