Venous blood pressure in broilers during acute inhalation of five percent carbon dioxide or unilateral pulmonary artery occlusion

We evaluated the hypothesis that venous congestion (increased venous volume ), as reflected by venous hypertension (increased venous pressure), can ari se when the right ventricle is unable to elevate the pulmonary arterial pre ssure sufficiently to propel the cardiac output through an anatomically ina dequate or inappropriately constricted pulmonary vasculature. Changes in ve nous pressure were evaluated in clinically healthy broilers during modest i ncreases in pulmonary vascular resistance induced by inhalation of 5% CO2 a nd during large increases in pulmonary vascular resistance accomplished by acutely tightening a snare around one pulmonary artery. Inhalation of 5% CO 2 induced a pronounced respiratory acidosis, as reflected by increases the partial pressure of CO2 and the hydrogen ion concentration in arterial bloo d. Inhalation of 5% CO2 also increased pulmonary arterial pressure by appro ximately 3 mm Hg and increased venous pressure by approximately 1 mm Hg whe n compared with the pre-inhalation venous pressure. Tightening the pulmonar y artery snare increased the pulmonary arterial pressure by approximately 1 0 mm Hg, and this degree of pulmonary hypertension was sustained until the snare was released. When compared with the pre- and post-snare intervals, t ightening of the pulmonary artery snare induced a sustained increase in ven ous pressure of 11 mm Hg. Veins have highly compliant walls that permit an approximate doubling in volume with only small (4 to 6 mm Hg) increases in central venous pressure. Presumably the apparently modest 1 mm Hg increase in venous pressure measured after CO2 inhalation or unilateral pulmonary ar tery occlusion reflects a large increase in venous volume and, thus, substa ntial venous congestion. These observations support the hypothesis that inc reases in pulmonary vascular resistance can initiate increases in venous pr essure by challenging the capacity of the right ventricle to propel all of the returning venous blood through the lungs. Central venous congestion pre disposes broilers to the onset of cirrhosis and ascites by impeding the out flow of hepatic venous blood and increasing the hydrostatic pressure within hepatic sinusoids.