The Effect of a Patent Foramen Ovale on the Hypercapnic Ventilatory Response
Hardin, Alyssa Marie
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Hardin, Alyssa Marie
A patent foramen ovale (PFO) is an intracardiac shunt pathway present in approximately one-third of the general, healthy population that allows varying degrees of blood flow to pass directly from the right to the left heart, bypassing pulmonary circulation and gas exchange at the lungs. Subjects with a PFO (PFO+) exhibit higher alveolar to arterial oxygen difference (AaDO2) values at rest than subjects without a PFO (PFO–), indicating that PFO+ subjects have a source of right-to-left shunt significant enough to decrease gas exchange efficiency at rest (Lovering et al., 2011). Additionally, PFO+ subjects have blunted ventilatory acclimatization to hypoxia compared to PFO– subjects (Elliott et al., 2015). Therefore, the aim of this research was to determine if the presence of a PFO affects an individual’s response to acute hypercapnic conditions, as quantified by calculating each individual’s hypercapnic ventilatory response (HCVR). It was hypothesized that, when compared to PFO- subjects, PFO+ subjects would exhibit a blunted HCVR during exposure to normoxic hypercapnia and hyperoxic hypercapnia when compared to PFO- subjects. Accordingly, 31 healthy, non-smoking subjects – 16 PFO+ (9 female) and 15 PFO- (8 female) – participated in this study. Subjects completed both a normoxic hypercapnia (NH) and hyperoxic hypercapnia (HH) breathing trial, in a randomized and balanced order, separated by ≥ 40 minutes. End-tidal oxygen and carbon dioxide (PETO2 and PETCO2) were controlled utilizing a dynamic end-tidal forcing system (AirForce). During the HH trial, PETO2 was clamped at 250 mmHg and PETCO2 was increased in a stepwise fashion to target values of +3 mmHg, +6 mmHg and +9 mmHg of each subject’s baseline PETCO2. Each stage consisted of a 90 second steady-state data collection period after each increase. The procedure for the NH was identical to the HH trial except that PETO2 was clamped at the resting baseline value for each subject and PETCO2 increased as above. Hypercapnic ventilatory response (HCVR) was calculated as slope of the ventilation (VE) versus end-tidal carbon dioxide (PETCO2) regression line for each subject (L/min/mmHg CO2). PFO+ subjects demonstrated a blunted HCVR in both the NH and HH trials compared to PFO- subjects (p < .05). Overall, these results indicate that PFO+ subject have a blunted response to acute hypercapnic challenges in both normoxic and hyperoxic conditions suggesting a difference in central but not peripheral chemosensitivity to increased CO2. Therefore, PFO+ subjects may be more susceptible to developing sleep apnea and subsequent comorbidities as a result of differences in central CO2 chemosensitivity.