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The Effect of a Patent Foramen Ovale and Sex on the Hypercapnic Ventilatory Response
Author(s) -
Hardin Alyssa M.,
Boulet Lindsey M.,
Davis James T.,
Chang Alex J.,
Foster Glen E.,
Lovering Andrew T.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1072.11
Subject(s) - hypercapnia , medicine , patent foramen ovale , cardiology , anesthesia , foramen ovale (heart) , ventilation (architecture) , hypoxia (environmental) , shunt (medical) , population , respiratory system , oxygen , chemistry , mechanical engineering , organic chemistry , environmental health , migraine , engineering
A patent foramen ovale (PFO) is a right‐to‐left intracardiac shunt pathway present in approximately 35% of the general healthy population. Individuals with a PFO (PFO+) exhibit higher alveolar to arterial oxygen difference (AaDO 2 ) 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. Additionally, PFO+ subjects have blunted ventilatory acclimatization to hypoxia compared to PFO− subjects. While the presence of a PFO is known to influence hypoxic chemosensitivity, it has yet to be determined if the presence of a PFO has an effect on the hypercapnic ventilatory response (HCVR). Thirty subjects (15 female) matched for height, weight, sex and age participated in this study. Subjects completed two hypercapnic breathing trials in a randomized and balanced order, separated by ≥ 40 minutes of rest between trials. At the start of each trial, subjects began breathing room air until steady‐state values for end‐tidal oxygen and carbon dioxide (P ET O 2 and P ET CO 2 ) were established. P ET O 2 and P ET CO 2 were then controlled utilizing a dynamic end‐tidal forcing system (AirForce). During the hyperoxic hypercapnia (HH) trial, P ET O 2 was clamped at 250 mmHg and P ET CO 2 was increased in a stepwise fashion to target values of +3 mmHg, +6 mmHg and +9 mmHg of each subject's baseline P ET CO 2 . Each stage consisted of a 90 second steady‐state data collection period after each increase. The procedure for the normoxic hypercapnia (NH) trial was identical to the HH trial except that P ET O 2 was clamped at the resting baseline value for each subject and P ET CO 2 increased as above. Hypercapnic ventilatory response (HCVR) was calculated as the change in minute ventilation (V E ) divided by the change in P ET CO 2 (L/min/Torr CO 2 ). PFO+ subjects demonstrated a blunted, significantly lower HCVR than PFO− subjects during both the HH (PFO−: 1.80 L/min/Torr CO 2 ± 0.17, PFO+: 1.19 L/min/Torr CO 2 ± 0.14, p < 0.05) and NH (PFO−: 1.79 L/min/Torr CO 2 ± 0.23, PFO+: 1.24 L/min/Torr CO 2 ± 0.26, p < 0.05) trials. These data suggest that PFO+ subjects have a blunted ventilatory response to acute exposure to hypercapnia. Within the subset of female subjects, PFO+ females had a significantly lower HCVR than PFO− females in the HH trial (PFO−: 1.85 L/min/Torr CO 2 ± 0.27, PFO+: 1.06 L/min/Torr CO 2 ± 0.13, p < 0.05) and NH trial (PFO−: 1.81 L/min/Torr CO 2 ± 0.28, PFO+: 1.15 L/min/Torr CO 2 ± 0.11, p < 0.05). However, no differences were observed between the male PFO+ and PFO− subjects in the HH (PFO−: 1.77 L/min/Torr CO 2 ± 0.37, PFO+: 1.35 L/min/Torr CO 2 ± 0.24, p > 0.05) or NH (PFO−: 1.76 L/min/Torr CO 2 ± 0.24, PFO+: 1.33 L/min/Torr CO 2 ± 0.28, p > 0.05) trials. These results suggest that female PFO+ subjects have a blunted HCVR compared to female PFO− subjects.