Abstract

In healthy individuals, reducing inspired oxygen concentrations to 15% (equivalent to an altitude of ∼2500 metres or usual aircraft cabin pressure) causes an increase in heart rate (HR), left ventricular ejection fraction (LVEF) and pulmonary arterial pressure (PAP). The clinical and haemodynamic responses to hypoxia (15% oxygen) have not been reported in patients with chronic heart failure (CHF). Patients with CHF were enrolled who met at least one of the following criteria: NYHA≥III, LVEF <40%, or diuretic dose equivalent to furosemide ≥ 80mg. Patients inspired 15% oxygen from a Douglas bag through a mouthpiece whilst lying supine. Clinical and echocardiographic measurements were performed at baseline and after one hour of hypoxia. Thirty two CHF patients (mean age and LVEF were 63±13yrs and 33±9% respectively) were recruited. 70% had ischemic heart disease and 22% had permanent atrial fibrillation. Hypoxia was well tolerated and was not associated with worsening HF-symptoms. Arterial oxygen saturation (SpO2) decreased from 97.2±1.2 to 85.7±5.0%, p<0.0001. Mean systemic blood pressure (MSBP) increased from 84±11mmHg to 92±11mmHg, p<0.0001, whilst HR remained unchanged at 69±14bpm. LVEF and E/A ratio were unchanged. Diastolic LV function tended to improved (E/Ea from 13.6±7.2 to 12.3±7.7 p=0.09). Systolic PAP increased (from 34±9mmHg to 38±9mmHg, p<0.05 in n=16 patients with tricuspid regurgitation) and the right ventricular systolic function assessed by the tricuspid annular systolic excursion was unchanged. Hypoxia caused no symptoms in any patients despite a significant increase in MSBP and a decrease in arterial SpO2. Further investigations in a larger patient group and with longer periods of hypoxia are being conducted.

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