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Ann Thorac Surg 1991;52:51-58
© 1991 The Society of Thoracic Surgeons
a Departments of Surgery and Intensive Care, Prince George's Hospital Center, Cheverly, Maryland USA
b Department of Thoracic Surgery, Walter Reed Army Medical Center, Washington, DC USA
c Department of Surgery, Uniformed Services University of Health Sciences, Bethesda, Maryland USA
* Address reprint requests to Dr Wagner, 50 West Edmonston Dr, Rockville, MD 20852.
Our purpose was to examine changes in pulmonary hemodynamics for patients with pulmonary contusion. Pulmonary vascular resistance index (PVRI) and shunt fraction were calculated from standard measurements in 25 traumatized patients. The percent of lung volume injured, measured as air-space filling disease (ASF), was quantitated from computed tomograms using a previously described technique. The amount of reactive pulmonary vasoconstriction per unit of injury (PVRI/ASF) identified 3 groups of patients: 5 were reactors (PVRI/ ASF > 15), 10 were weak-reactors (PVRI/ASF = 5 to 15), and 10 were nonreactors (PVRI/ASF < 5). In the reactor group PVRI increased as the size of contusion (ASF) increased (r = 0.99). In weak-reactors PVRI also increased with the size of contusion (r = 0.93), but the slope was less pronounced. In both groups shunt fraction did not rise above 0.31. In the nonreactors, PVRI remained normal while shunt fraction increased with the extent of injury (r = 0.95). These results indicate that pulmonary vasoconstriction often occurs after pulmonary contusion. The vasoconstriction most probably represents a compensatory mechanism to limit perfusion of traumatized parenchyma, thereby minimizing increases in shunt fraction. Some patients (nonreactors) not demonstrating this response have unchecked increases in shunt fraction. This insight into the hemodynamic sequelae of pulmonary contusions may enhance our ability to provide optimal care for patients suffering from this injury.
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