The effect of acutely induced hypervolemia on resistance to pulmonary blood flow and pulmonary arterial compliance in patients with chronic obstructive lung disease

Abstract

The presence of alveolar hypoxia and respiratory acidemia in patients with chronic obstructive lung disease alters the normal relation between pulmonary arterial and left heart pressures at the end of diastole; usually these pressures are the same. With vasoconstriction of the small pulmonary arteries the pulmonary arterial diastolic pressure rises, whereas the mean wedge pressure remains unchanged. Thus, a pressure gradient across the pulmonary circulation appears at the end of diastole representing an increased resistance to pulmonary blood flow. The magnitude of this gradient is closely related to the systemic arterial blood oxyhemoglobin saturation, which is used as an index of alveolar oxygen tension, and to the blood hydrogen ion concentration. In the present study acutely induced hypervolemia caused striking alterations in mean wedge pressure and blood flow. However, the diastolic gradient did not change. The pulmonary diastolic pressure gradient reflects the degree of resistance to pulmonary blood flow regardless of the level of the left heart pressure or the cardiac output. On the other hand, left heart pressure does contribute to the level of the pulmonary arterial diastolic pressure. The pulse pressures recorded in the elastic pulmonary arteries reflect their compliance characteristics and the effect of stroke volume imposed upon them. We have assessed compliance indirectly by examining the relationships between pulmonary arterial systolic pressure, diastolic pressure and stroke volume. The compliance characteristics of the elastic arteries in patients with chronic obstructive lung disease do not differ from normal before or during acutely induced hypervolemia.