Resting arterial hypoxaemia in subjects with chronic heart failure, pulmonary hypertension and patent foramen ovale

Abstract

New Findings: What is the central question of this study? Does a patent foramen ovale contribute to resting arterial hypoxaemia, defined as arterial oxygen saturation <95%, in subjects with chronic heart failure with or without pulmonary arterial hypertension? What is the main finding and its importance? The presence of a patent foramen ovale contributed to resting arterial hypoxaemia only in subjects with chronic heart failure with pulmonary arterial hypertension. These data suggest that the presence of a patent foramen ovale should be considered in chronic heart failure patients with arterial hypoxaemia and pulmonary hypertension. The roles of intrapulmonary and intracardiac shunt in contributing to arterial hypoxaemia at rest in subjects with chronic heart failure (CHF) have not been well investigated. We hypothesized that blood flow through intrapulmonary arteriovenous anastomoses (Q˙ IPAVA ) and/or patent foramen ovale (Q˙ PFO ) could potentially contribute to arterial hypoxaemia and, with pulmonary hypertension (PH) secondary to CHF, this contribution may be exacerbated. Fifty-six subjects with CHF (New York Heart Association Classes I-III), with (+) or without (-) PH [defined as peak tricuspid regurgitation velocity ≥2.9 m s-1 (CHF PH+, n = 32) and peak tricuspid regurgitation velocity ≤2.8 m s-1 (CHF PH-, n = 24)], underwent arterial blood gas analysis and transthoracic saline contrast echocardiography concomitant with transcranial Doppler to detect Q˙ IPAVA and Q˙ PFO . Seventeen of 56 subjects with CHF (30%) had Q˙ PFO , but only four of 56 subjects with CHF had Q˙ IPAVA (7%), both similar to age- and sex-matched control subjects. Mean arterial oxygen saturation (SaO2) was lower in subjects with Q˙ PFO . Only CHF PH+ subjects with Q˙ PFO had arterial hypoxaemia (mean SaO2 <95%). Bubble scores assessed using transthoracic saline contrast echocardiography were correlated with microembolic signals detected with transcranial Doppler in subjects with Q˙ PFO . Significant Q˙ IPAVA was not present in either CHF PH+ or PH- subjects, suggesting that Q˙ IPAVA is not dependent on increased pulmonary pressure and does not contribute significantly to arterial hypoxaemia in older subjects with CHF. Given that SaO2 was lower in all subjects with CHF who had Q˙ PFO compared with those without Q˙ PFO , a patent foramen ovale should be considered when determining potential causes of arterial hypoxaemia, because Q˙ PFO was present in 30% of these subjects.