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

The roles of intrapulmonary and intracardiac shunt in contributing to arterial hypoxemia at rest in chronic heart failure (CHF) subjects 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 hypoxemia and, with pulmonary hypertension (PH) secondary to CHF, this contribution may be exacerbated. Fifty-six CHF subjects (New York Heart Association Classes I-III), with (+) and without (−) PH defined as peak tricuspid regurgitation velocity (TRV) ≥2.9 m/s (CHF PH+, n = 32), and peak TRV ≤2.8 m/s (CHF PH–, n = 24), underwent arterial blood gas analysis and transthoracic saline contrast echocardiography (TTSCE) concomitant with transcranial Doppler (TCD) to detect Q_IPAVA and Q_PFO. Seventeen/56 CHF subjects (30%) had Q_PFO but only 4/56 CHF subjects had Q_IPAVA (7%), both similar to age and gender matched controls. Mean oxygen saturation (SaO₂) was lower in subjects with Q_PFO. Only CHF PH+ subjects with Q_PFO had arterial hypoxemia (mean SaO₂ < 95%). Bubbles scores assessed using TTSCE were correlated with microembolic signals detected with TCD in subjects with Q_PFO. Significant Q_IPAVA was not present in either CHF PH+ or PH-subjects suggesting Q_IPAVA is not dependent on increased pulmonary pressure and does not contribute significantly to arterial hypoxemia in older CHF subjects. Because SaO₂ was lower in all CHF subjects with Q_PFO compared to CHF subjects without Q_PFO, a PFO should be considered when determining potential causes of arterial hypoxemia since Q_PFO was present in 30% of these subjects.

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