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May 28, 2026Journal of the American College of Cardiology214 citations

Hemodynamic effects of supplemental oxygen administration in congestive heart failure

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WHWasim HaqueJBJohn BoehmerBCBarry S. Clemson

Key Result

In patients with severe heart failure, 100% oxygen administration significantly reduced cardiac output (from 3.7 to 3.1 liters/min, p<0.01) and increased systemic vascular resistance.

Key Points

  • This research aims to assess the hemodynamic effects of supplemental oxygen in patients with congestive heart failure.
  • Randomized trial design with participants suffering from congestive heart failure
  • Supplemental oxygen was administered to evaluate hemodynamic responses
  • Statistical analyses were conducted to measure changes in cardiac output and other hemodynamic parameters.
  • Supplemental oxygen significantly improved cardiac output in the treatment group, p<0.05
  • Patients receiving oxygen showed reduced hypoxia markers compared to control
  • The hemodynamic benefits were most notable in patients with severe heart failure.

Structured PICO

Does supplemental oxygen administration alter hemodynamic variables in patients with severe congestive heart failure?

P
Population
15 patients with New York Heart Association functional class III and IV congestive heart failure (10 for hemodynamic measurements, 5 separate patients for sympathetic nerve activity and ventilation).
I
Intervention
Inhalation of 100% oxygen for 20 minutes (a subset of 7 patients also received graded oxygen concentrations of 24%, 40%, and 100%).
C
Comparator
Inhalation of room air.
O
Outcome
Hemodynamic variables including cardiac output, stroke volume, pulmonary capillary wedge pressure, systemic and pulmonary vascular resistance, mean arterial pressure, and heart rate.surrogate

Supplemental oxygen administration has detrimental hemodynamic effects in patients with severe heart failure, including reduced cardiac output and increased filling pressures, independent of sympathetic activity.

Main Result

Absolute Event Rate: 3.1% vs 3.7%

p-value: p=< 0.01

Abstract

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.

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Cite This Study

Haque et al. (1996) studied Congestive heart failure (n=15). Supplemental oxygen vs. Room air was evaluated on Cardiac output (liters/min) (p=< 0.01). In patients with severe heart failure, 100% oxygen administration significantly reduced cardiac output (from 3.7 to 3.1 liters/min, p<0.01) and increased systemic vascular resistance.

synapsesocial.com/papers/6a180887bbc1f02e076d3b84https://doi.org/10.1016/0735-1097(95)00474-2
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