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(Chest. 2006;130:85-92.)
© 2006 American College of Chest Physicians

Therapeutic Hypercapnia and Ventilation-Perfusion Matching in Acute Lung Injury*

Low Minute Ventilation vs Inspired CO2

Scott E. Sinclair, MD{dagger}; David A. Kregenow, MD{dagger}; Ian Starr, BS; Carmel Schimmel, BS; Wayne J.E. Lamm, MA; Michael P. Hlastala, PhD and Erik R. Swenson, MD

* From the Department of Medicine (Dr. Sinclair), University of Tennessee, Memphis, TN; Virginia Mason Medical Center (Dr. Kregenow), Seattle, WA; and the Department of Medicine (Mr. Starr, Mr. Schimmel, Mr. Lamm, and Drs. Hlastala and Swenson), University of Washington, Seattle, WA. {dagger} These authors contributed equally to the manuscript

Correspondence to: Scott E. Sinclair, MD, University of Tennessee, 956 Court Ave, Room H314, Memphis, TN 38163; e-mail: ssincla1{at}utmem.edu

Abstract

Study objectives: Hypercapnic acidosis has antiinflammatory effects in animal models of acute lung injury (ALI) and improves ventilation-perfusion (V/Q) matching in normal lungs. The effect of hypercapnia on V/Q matching in ALI is conflicting. Hypercapnic acidosis produced by reduced tidal volumes (VTs) was associated with an increased shunt fraction (QS/QT) in patients with ALI compared with control subjects. VT differences between groups make the assessment of hypercapnic acidosis on V/Q matching difficult. Adding CO2 to the inhaled gas allows the comparison of gas exchange under identical VT conditions. We hypothesized the presence of hypercapnic acidosis from inspired carbon dioxide (ICD) would improve gas exchange in ALI and would be superior to that of low minute ventilation (LVE) produced by reduced respiratory rate, rather than VT.

Design: University laboratory study of anesthetized New Zealand White rabbits.

Interventions: Assessment of V/Q relationships using the multiple inert gas elimination technique was performed in 10 saline solution-lavaged animals, which were ventilated with 6 mL/kg VTs and a positive end-expiratory pressure of 8 cm H2O. Each rabbit was studied while it was in eucapnia, followed by hypercapnia (PaCO2, 95 to 100 mm Hg) induced by LVE from decreased respiratory rate and by 10% ICD, in random order.

Measurements and results: The PaO2 was greater in ICD and LVE compared to eucapnia, but no significant differences in alveolar-arterial oxygen pressure difference or Pao2/fraction of inspired oxygen ratio occurred. LVE statistically reduced the mean V/Q distributions compared with ICD and eucapnia. Log SDs of ventilation and combined retention and excretion curves of the dispersion index were both increased during LVE, indicating the presence of unfavorable changes in ventilation distribution. Neither LVE nor ICD altered the QS/QT.

Conclusions: LVE slightly impairs overall gas exchange and ventilation distribution, but does not increase QS/QT compared with eucapnia and ICD. While ICD does not significantly improve gas exchange, it may be superior to LVE in achieving the antiinflammatory effects of "therapeutic" hypercapnia, since it does not adversely alter gas exchange and has the potential to make the lung more uniformly acidotic.

Key Words: acute lung injury • gas exchange • hypercapnia • hypercapnic acidosis • mechanical ventilation • permissive hypercapnia • therapeutic hypercapnia • saline lavage






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