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Effect of pulmonary flow heterogeneity and impaired diffusing capacity on oxygen uptake
Author(s) -
Roy Tuhin K,
Secomb Timothy W
Publication year - 2016
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.30.1_supplement.946.4
Subject(s) - diffusing capacity , pulmonary diffusing capacity , oxygenation , context (archaeology) , cardiology , medicine , oxygen , chemistry , lung , ventilation (architecture) , oxygen saturation , biology , lung function , thermodynamics , paleontology , physics , organic chemistry
Severe impairment of oxygenation in critically ill patients is a major cause of morbidity and mortality, and can occur even with normal alveolar ventilation and cardiac output under conditions of decreased diffusing capacity or increased flow heterogeneity. A theoretical model of pulmonary oxygen uptake under resting conditions is used to simulate decreased diffusing capacity (DL) as well as increased heterogeneity (characterized by an increase in the coefficient of variation [CV] of pulmonary capillary blood flow), with the assumed normal value of CV based on observations of microvascular networks. Under resting conditions with nominal values of DL and CV, the model predicts an oxygen saturation (SO 2 ) of 97% (PO 2 = 94 mmHg). Simulating a 10‐fold reduction in DL leads to an SO 2 of 85% (PO 2 = 51 mmHg), whereas doubling the CV from its normal value leads to an SO 2 of 95% (PO 2 = 78 mmHg); both of these predictions suggest a high degree of reserve in the healthy resting lung. However, simulating these conditions simultaneously leads to a large reduction in SO 2 to 71% (PO 2 = 37 mmHg), exhausting the reserve capacity of the lung and demonstrating the detrimental synergistic effect of heterogeneity in the context of an attenuated diffusing capacity. These results imply that a combination of increased heterogeneity and decreased diffusing capacity can explain the severe impairment in pulmonary oxygen uptake and decreased saturations seen in critical illness. Support or Funding Information Supported by NIH grant HL070657.