title: Cardiovascular effects of airways obstruction.
abstract: Airways obstruction is usually associated with substantial decreases in inspiratory and mean intrathoracic pressure (ITP). The change in ITP is correlated with the degree of inspiratory fall in arterial pressure, pulsus paradoxus. The factors influencing the degree of pulsus include venous return, afterload effects on the left ventricle (LV), diastolic ventricular interdependence, lung volume, and circulatory reflexes. I have reviewed these factors and attempted to demonstrate that their relative importance changes under different circumstances. I have discussed the importance of measuring transmural pressures to assess ventricular performance, and pointed out some possible pitfalls in the use of esophageal or pleural pressure to estimate LV surface pressure. During normal and loaded inspiration, decreased LV preload, probably related to right ventricle (RV)-LV diastolic interdependence, appears to be the primary mechanism responsible for decreased stroke volume during inspiration. During Mueller maneuvers, and possibly with severe decreases in ITP. LV afterload may be more important. When lung volume increases, as with asthma, venous return from the lower body may be a more important determinant of pulsus paradoxus. Although previous predictions that decreased ITP would lead to increased myocardial O2 consumption were not borne out, coronary blood flow did increase with inspiratory loading. This appears to be due to a nonvagally mediated change in autonomic tone with loaded breathing. This and other reflex-mediated effects deserve more attention in future studies of stressed or abnormal inspiration. As a final point, pericardial tamponade probably leads to pulsus paradoxus by exaggerating normal diastolic right-left interactions.
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Long Island Jewish Medical Center, New Hyde Park, New York 11042.
authors.forename: S M
authors.initials: SM
authors.lastname: Scharf
mesh_terms: D001794:Blood Pressure / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008173:Lung Diseases, Obstructive / Q000503:physiopathology*; D008176:Lung Volume Measurements; D011674:Pulse / Q000502:physiology; D012119:Respiration / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology