Redistribution of Pulmonary Blood Flow Impacts Thermodilution-based Extravascular Lung Water Measurements in a Model of Acute Lung Injury

Author:

Easley R Blaine1,Mulreany Daniel G.2,Lancaster Christopher T.3,Custer Jason W.4,Fernandez-Bustamante Ana5,Colantuoni Elizabeth6,Simon Brett A.7

Affiliation:

1. Assistant Professor.

2. Research Scientist.

3. Pediatric Critical Care Fellow.

4. Pediatric Critical Care Fellow, Departments of Anesthesiology/Critical Care Medicine and Pediatrics.

5. Research Fellow, Department of Anesthesiology/Critical Care Medicine.

6. Assistant Professor and Biostatistician, Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Medical Institutes, Baltimore, Maryland. Department of Biostatistics, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland.

7. Professor, Departments of Anesthesiology/Critical Care Medicine and Medicine, Johns Hopkins Medical Institutes, Baltimore, Maryland.

Abstract

Background Studies using transthoracic thermodilution have demonstrated increased extravascular lung water (EVLW) measurements attributed to progression of edema and flooding during sepsis and acute lung injury. The authors hypothesized that redistribution of pulmonary blood flow can cause increased apparent EVLW secondary to increased perfusion of thermally silent tissue, not increased lung edema. Methods Anesthetized, mechanically ventilated canines were instrumented with PiCCO (Pulsion Medical, Munich, Germany) catheters and underwent lung injury by repetitive saline lavage. Hemodynamic and respiratory physiologic data were recorded. After stabilized lung injury, endotoxin was administered to inactivate hypoxic pulmonary vasoconstriction. Computed tomographic imaging was performed to quantify in vivo lung volume, total tissue (fluid) and air content, and regional distribution of blood flow. Results Lavage injury caused an increase in airway pressures and decreased arterial oxygen content with minimal hemodynamic effects. EVLW and shunt fraction increased after injury and then markedly after endotoxin administration. Computed tomographic measurements quantified an endotoxin-induced increase in pulmonary blood flow to poorly aerated regions with no change in total lung tissue volume. Conclusions The abrupt increase in EVLW and shunt fraction after endotoxin administration is consistent with inactivation of hypoxic pulmonary vasoconstriction and increased perfusion to already flooded lung regions that were previously thermally silent. Computed tomographic studies further demonstrate in vivo alterations in regional blood flow (but not lung water) and account for these alterations in shunt fraction and EVLW.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Anesthesiology and Pain Medicine

Reference73 articles.

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