Cardiovascular performance during bronchospasm in dogs.

Abstract

In 8 anesthetized mongrel dogs, we studied the effects of carbachol-induced bronchoconstriction (BC) on the cardiovascular system. Inhalation of carbachol in an amount sufficient to produce at least a 50% decrease in lung conductance (GL) did not lead to significant changes in cardiac output, mean transmural left atrial (Pla) or right atrial pressure, end-diastolic left ventricular septal-lateral dimension, left ventricular apex to base dimension, or in end-diastolic right ventricular septal to lateral dimension during expiration. Mean transmural pulmonary arterial pressure rose and mean transmural aortic pressure (Pao) fell during BC. During inspiration, there were significant increases in transmural left atrial pressure, Pla, associated with decreases in end-diastolic left ventricular septal-lateral and apex-base dimensions. End-diastolic right ventricular septal-lateral dimension increased during inspiration. Beat-to-beat aortic flow (Qao) decreased during inspiration, while pulmonary arterial flow increased. There were no changes in transmural Pao during inspiration measured at the nadir of aortic flow. During BC, these changes were exaggerated, but remained qualitatively the same. The magnitude of the inspiratory decrease in pleural pressure (Ppl) was shown to be linearly related to the magnitude of the change in GL, and the magnitude of the inspiratory decrease in Pao and Qao (pulsus paradoxus) was shown to be linearly related to the magnitude of the inspiratory swing in Ppl. Although vagotomy significantly altered the pattern of respiration such that tidal volume increased and respiratory rate decreased, it did not substantially alter the responses of the cardiovascular system to breathing during BC. We conclude: the inspiratory decrease in Pao and Qao (pulsus paradoxus) is associated with a decrease in left ventricular end-diastolic filling, and a stiffening of the left ventricle; these changes are exaggerated during BC as a result of the exaggerated inspiratory swings in Ppl; the effects on left ventricular dynamics are mediated only in part through increases in right ventricular end-diastolic filling operating through the mechanism of ventricular interdependence; changes in left ventricular afterload appear to play little role in determining the responses seen.