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

Abstract

New Findings r 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? r 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 detectQ IPAVA andQ PFO . Seventeen of 56 subjects with CHF (30%) hadQ PFO , but only four of 56 subjects with CHF hadQ IPAVA (7%), both similar to age-and sex-matched control subjects. Mean arterial oxygen saturation (S aO 2 ) was lower in subjects withQ PFO . Only CHF PH+ subjects withQ PFO had arterial hypoxaemia (mean S aO 2 <95%). Bubble scores assessed using transthoracic saline contrast echocardiography were correlated with microembolic signals detected with transcranial Doppler in subjects withQ PFO . SignificantQ IPAVA was not present in either CHF PH+ or PH− subjects, suggesting thatQ IPAVA is not dependent on increased A. T. Lovering and others pulmonary pressure and does not contribute significantly to arterial hypoxaemia in older subjects with CHF. Given that S aO 2 was lower in all subjects with CHF who hadQ PFO compared with those withoutQ PFO , a patent foramen ovale should be considered when determining potential causes of arterial hypoxaemia, becauseQ PFO was present in 30% of these subjects.

Patent foramen ovale in idiopathic pulmonary arterial hypertension: Long-term risk and morbidity

“…This finding of higher pulmonary pressures in the PFO group was not expected. As the presence of PFO has been associated with worse resting hypoxia [27], which was also supported by our study, a theoretical explanation for higher PA pressures in our study may be reflexive vasoconstriction in response to hypoxemia, though this is currently unconfirmed. A prior study suggested patients with concomitant IPAH and PFO awaiting transplantation had better survival [28].…”

Characterization of blood flow through intrapulmonary arteriovenous anastomoses and patent foramen ovale at rest and during exercise in stroke and transient ischemic attack patients

“…The absolute number of microembolic signals in the MCA and PCA was noted each time after agitated saline was injected. We have previously shown strong agreement between TCD and TTSCE …”

Physiological impact of patent foramen ovale on pulmonary gas exchange, ventilatory acclimatization, and thermoregulation

“…11 and 37. There are several reports in the literature suggesting that the presence of a PFO does have a negative impact on pulmonary gas exchange efficiency and/or arterial hypoxemia in patient populations (13,24,27,35,36,38). Additionally, surgical closure of a PFO has been shown to improve arterial oxygenation at rest and during exercise, demonstrating that blood flow through a PFO can have a measurable impact on pulmonary gas exchange efficiency (12,19).…”