0
Clinical Investigations: PULMONARY CIRCULATION |

Comparison of the Effects of Nitric Oxide, Nitroprusside, and Nifedipine on Hemodynamics and Right Ventricular Contractility in Patients With Chronic Pulmonary Hypertension*

Barbara A. Cockrill, MD; Robert M. Kacmarek, PhD, RRT, FCCP; Michael A. Fifer, MD; Luca M. Bigatello, MD; Leo C. Ginns, MD; Warren M. Zapol, MD, FCCP; Marc J. Semigran, MD
Author and Funding Information

Correspondence to: Barbara A. Cockrill, MD, Pulmonary and Critical Care Unit, Massachusetts General Hospital, 32 Fruit St, Boston, MA 02114; e-mail: bcockrill@partners.org



Chest. 2001;119(1):128-136. doi:10.1378/chest.119.1.128
Text Size: A A A
Published online

Study objectives: The effects of inhaled nitric oxide (NO) on hemodynamics and right ventricular (RV) contractility were compared with those of nitroprusside and nifedipine in 14 patients with severe chronic pulmonary hypertension.

Study design: Micromanometer and balloon-tipped right heart catheterization were performed. Inhaled NO, IV nitroprusside, and sublingual nifedipine were administered sequentially while patients breathed > 90% oxygen.

Setting: Cardiac catheterization laboratory in a tertiary care teaching hospital.

Patients: Fourteen patients with severe pulmonary hypertension unrelated to left ventricular dysfunction.

Measurements and results: During NO inhalation, mean systemic arterial pressure (MAP) was unchanged, but pulmonary artery (PA) pressure ([mean ± SEM] 49 ± 2 mm Hg vs 44 ± 2 mm Hg; p < 0.01), pulmonary vascular resistance (PVR; 829 ± 68 vs 669 ± 64 dyne · s · cm−5; p < 0.01) and RV end-diastolic pressure (RVEDP; 12 ± 1 vs 10 ± 1 mm Hg; p < 0.01) decreased. Stroke volume index (SVI; 31 ± 2 vs 35 ± 3 mL/m2; p < 0.05) increased, and the first derivative of RV pressure at 15 mm Hg developed pressure (RV +dP/dt at DP15) was unchanged. During nitroprusside administration, MAP decreased (105 ± 5 vs 76 ± 5 mm Hg; p < 0.01), PA was unchanged (48 ± 2 vs 45 ± 3 mm Hg; p = not significant), and PVR decreased (791 ± 53 vs 665 ± 53 dyne · s · cm−5; p < 0.01). RV +dP/dt at DP15 increased (425 ± 22 vs 465 ± 29 mm Hg/s; p < 0.05), but SVI was unchanged. Nifedipine decreased MAP (103 ± 5 vs 94 ± 5 mm Hg; p < 0.01), PA and PVR were unchanged, RVEDP increased (12 ± 1 vs 14 ± 2 mm Hg; p < 0.01), and RV +dP/dt at DP15 decreased (432 ± 90 vs 389 ± 21 mm Hg/s; p < 0.05).

Conclusions: Inhaled NO is a selective pulmonary vasodilator in patients with chronic pulmonary hypertension that improves cardiac performance without altering RV contractility. Nitroprusside caused a similar degree of pulmonary vasodilation. In contrast to inhaled NO, nitroprusside caused systemic hypotension associated with an increase in RV contractility. Acute administration of nifedipine did not cause pulmonary vasodilation, but RVEDP increased and RV contractility decreased.

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