Author + information
- Received June 9, 1995
- Revision received September 6, 1995
- Accepted September 15, 1995
- Published online February 1, 1996.
- Wasim A. Haque, MDa,b,
- John Boehmer, MDa,b,
- Barry S. Clemson, MD,FACCa,b,
- Urs A. Leuenberger, MDa,b,3,
- David H. Silber, MDa,b,2 and
- Lawrence I. Sinoway, MD,FACC*,a,b,1
- ↵*Address for correspondence: Dr. Lawrence I. Sinoway, Division of Cardiology, The Milton S. Hershey Medical Center, P.O. Box 850, Hershey, Pennsylvania 17033.
Objectives. This study sought to determine the hemodynamic effects of oxygen therapy in heart failure.
Background. High dose oxygen has detrimental hemodynamic effects in normal subjects, yet oxygen is a common therapy for heart failure. Whether oxygen alters hemodynamic variables in heart failure is unknown.
Methods. We studied 10 patients with New York Heart Association functional class III and IV congestive heart failure who inhaled room air and 100% oxygen for 20 min. Variables measured included cardiac output, stroke volume, pulmonary capillary wedge pressure, systemic and pulmonary vascular resistance, mean arterial pressure and heart rate. Graded oxygen concentrations were also studied (room air, 24%, 40% and 100% oxygen, respectively; n = 7). In five separate patients, muscle sympathetic nerve activity and ventilation were measured during 100% oxygen.
Results. The 100% oxygen reduced cardiac output (from 3.7 ± 0.3 to 3.1 ± 0.4 liters/min [mean ± SE], p < 0.01) and stroke volume (from 46 ± 4 to 38 ± 5 ml/beat per min, p < 0.01) and increased pulmonary capillary wedge pressure (from 25 ± 2 to 29 ± 3 mm Hg, p < 0.05) and systemic vascular resistance (from 1,628 ± 154 to 2,203 ± 199 dynes's/cm5, p < 0.01). Graded oxygen led to a progressive decline in cardiac output (one-way analysis of variance, p < 0.0001) and stroke volume (p < 0.017) and an increase in systemic vascular resistance (p < 0.005). The 100% oxygen did not alter sympathetic activity or ventilation.
Conclusions. In heart failure, oxygen has a detrimental effect on cardiac output, stroke volume, pulmonary capillary wedge pressure and systemic vascular resistance. These changes are independent of sympathetic activity and ventilation.
↵3 Dr. Leuenberger is the recipient of Clinical Investigator Development Award HL-02654 from the National Heart, Lung, and Blood Institute, National Institutes of Health.
↵2 Dr. Silber is the recipient of a National Research Service Award from the National Institutes of Health.
↵1 Dr. Sinoway is an Established Investigator of the American Heart Association, Dallas, Texas.
This study was supported by Grants HL44667 and AG12227 to Dr. Sinoway from the National Heart, Lung, and Blood Institute and National Institute of Aging, National Institutes of Health, Bethesda, Maryland.
- Received June 9, 1995.
- Revision received September 6, 1995.
- Accepted September 15, 1995.