BACKGROUND: Although the haemodynamic effects of oxygen in healthy subjects are well documented, there have been no well-controlled studies of the effects of oxygen in patients with heart failure (HF). AIMS: To non-invasively evaluate haemodynamic and neurohumoral effects of oxygen in patients with HF at rest. METHODS AND RESULTS:13 men with heart failure and left ventricular systolic dysfunction (LVSD) were randomised in a double-blind, placebo-controlled, crossover trial to receive medical air or oxygen (40% and high concentration via Hudson non-rebreathing mask). Haemodynamic measurements were made with applanation tonometry, impedance cardiography and venous occlusion plethysmography. Plasma C-terminal B-type natriuretic peptide and A-type natriuretic peptide were measured. Data were analysed with paired t tests. Cardiac output fell by -0.58 (0.62) l/min on high-flow oxygen compared with -0.02 (0.58) l/min on air, p=0.031. Oxygen caused a reduction in heart rate (-4.02 (4.21) vs 0.41 (5.35) beats/min, respectively, p=0.021) and a trend towards increased systemic vascular resistance (875 (1174) vs 235 (321) dyne/s/m(5), p=0.050). Oxygen led to a paradoxical increase in forearm blood flow (0.513 (0.391) vs 0.024 (0.246) ml/min/100 ml forearm volume on air, p=0.01). Natriuretic peptides were unchanged with oxygen. CONCLUSIONS: High-concentration inhaled oxygen has significant haemodynamic effects in patients with LVSD and mild HF. Such effects may be detrimental in patients with decompensated HF.
RCT Entities:
BACKGROUND: Although the haemodynamic effects of oxygen in healthy subjects are well documented, there have been no well-controlled studies of the effects of oxygen in patients with heart failure (HF). AIMS: To non-invasively evaluate haemodynamic and neurohumoral effects of oxygen in patients with HF at rest. METHODS AND RESULTS: 13 men with heart failure and left ventricular systolic dysfunction (LVSD) were randomised in a double-blind, placebo-controlled, crossover trial to receive medical air or oxygen (40% and high concentration via Hudson non-rebreathing mask). Haemodynamic measurements were made with applanation tonometry, impedance cardiography and venous occlusion plethysmography. Plasma C-terminal B-type natriuretic peptide and A-type natriuretic peptide were measured. Data were analysed with paired t tests. Cardiac output fell by -0.58 (0.62) l/min on high-flow oxygen compared with -0.02 (0.58) l/min on air, p=0.031. Oxygen caused a reduction in heart rate (-4.02 (4.21) vs 0.41 (5.35) beats/min, respectively, p=0.021) and a trend towards increased systemic vascular resistance (875 (1174) vs 235 (321) dyne/s/m(5), p=0.050). Oxygen led to a paradoxical increase in forearm blood flow (0.513 (0.391) vs 0.024 (0.246) ml/min/100 ml forearm volume on air, p=0.01). Natriuretic peptides were unchanged with oxygen. CONCLUSIONS: High-concentration inhaled oxygen has significant haemodynamic effects in patients with LVSD and mild HF. Such effects may be detrimental in patients with decompensated HF.
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