Extravascular lung water as an indicator of pulmonary dysfunction in acute hemorrhagic pancreatitis.

This study quantifies lung water in acute hemorrhagic pancreatitis to determine the degree to which pulmonary dysfunction occurs subclinically, before alterations in the arterial blood gases can be measured. Pancreatitis was induced in ten dogs by injecting 0.5 ml/kg of bile into the pancreatic ducts, which had been surgically cannulated. Pulmonary and systemic blood gases and blood pressures, heart rate, extravascular lung water, and lung blood flows were studied over 5 hours while cardiac output and mean arterial pressure were maintained at control values by Ringer's lactate infusion. The percentage of water in lung tissue was determined at the time of sacrifice using gravimetric measurements. Mean arterial pressure, cardiac output, and pulmonary capillary wedge pressure, reflecting intravascular volume status, did not change through at the experiment. By contrast, major disturbances were measured in the pulmonary bed with pulmonary artery pressures rising from 15.6 +/- 1.8/8.1 +/- 1.3 mmHg to 22.0 +/- 1.2/15.6 +/- 1.7 mmHg over 5 hours (p less than 0.01). Peripheral vascular resistance rose from 3.6 +/- 0.6 units to 6.6 +/- 0.4 units (p less than 0.05), whereas bronchial blood flow to the lung fell significantly. These changes in pulmonary hemodynamics were not reflected by changes in the arterial blood gases. Arterial oxygenation was maintained during 5 hours of pancreatitis. The partial pressure of carbon dioxide and the serum pH did not change significantly. There was, however, a progressive rise in extravascular lung water measured by the double-dilution technique from 10.2 +/- 0.8 ml/kg at control to 18.1 +/- 2.8 ml/kg (p less than 0.01) at 5 hours. This was confirmed by direct gravimetric measurements, which revealed an increase in the water content of the lung from 78.1 +/- 0.3% to 86.4 +/- 2.4% over the course of the experiment. Arterial blood gases, therefore, do not necessarily reflect the pulmonary deterioration in acute pancreatitis. These data supported a mechanism of lung dysfunction independent of the circulatory compromise, which often accompanies the disease in the clinical setting.