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Intrapulmonary Shunting is an Important Contributor to Exercise‐Induced Arterial Hypoxemia
Author(s) -
Bates Melissa L.,
Pegelow David F.,
Farrell Emily T.,
Baker Kim,
Brodell Elizabeth,
Eldridge Marlowe W.
Publication year - 2012
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.26.1_supplement.1146.2
Subject(s) - hypoxia (environmental) , medicine , hypoxemia , shunting , cardiology , cardiac output , oxygenation , hemodynamics , anesthesia , oxygen , chemistry , organic chemistry
Large diameter, intrapulmonary arteriovenous anastomoses (IPAV) are recruited by exercise in normoxia and hypoxia. We tested the hypothesis that IPAVs are important contributors to exercise‐induced arterial hypoxemia (EIAH) in both conditions by directly quantifying IPAV recruitment and gas exchange dysfunction. Human subjects (n=7) were studied while quietly breathing 21% or 10% O 2 and at 85% of maximal exercise while breathing 21% or 10% O 2 . In each condition, we quantified the percentage of Tc99m ‐labelled albumin microspheres traversing the pulmonary circulation and the alveolar‐arterial oxygen difference (A‐aDO 2 ). Exercise increased microsphere passage in both normoxic (5/7 subjects, 2.5±3.5%) and hypoxic (4/7 subjects, 1.3±2.9%) exercise and in hypoxia alone (7/7subjects, 4.9±2.7%). Normoxic and hypoxic exercise increased the A‐aDO 2 (7.6±13.4 and 17.7±5.2 mmHg, p<0.05) but not hypoxia alone. Microsphere passage was correlated with the A‐aDO 2 in exercise (R 2 =0.61, p=0.001), suggesting that IPAVs contribute to EIAH by functioning as shunts. Interestingly, shunting through IPAVs was not observed in the absence of exercise (R 2 <0.01, p=0.93). We conclude that IPAVs are not true anatomic shunts, but function as diffusion‐limiting pathways when the cardiac output is elevated.