title: Transient analysis of cardiopulmonary interactions. II. Systolic events.
abstract: The etiology of the fall in left ventricular stroke volume (LVSV) and arterial pressure with a negative intrathoracic pressure (NITP) during inspiration is controversial. An increase in LV afterload produced by NITP has been proposed as one explanation but is difficult to evaluate if preload is also altered. To test the hypothesis that a systolic event alone, i.e., a change in LV afterload or contractility, can reduce LVSV during inspiration independent of changes in LV preload, a rapid transient NITP confined to systole was produced by electrocardiogram-triggered phrenic nerve stimulation in eight anesthetized dogs. Intrathoracic descending aortic diameters were measured by sonomicrometry to transduce qualitative changes in aortic transmural pressure. With the airway completely obstructed systolic NITP resulted in a decrease in LVSV (-8.1%, P less than 0.001) but an increase in the systolic anteroposterior (0.54 mm, P less than 0.01) and right-to-left (0.45 mm, P less than 0.01) aortic diameters compared with preceding beat. Similar significant changes were observed with the airway unobstructed. These observations are consistent with an increased afterload imposed on the LV reducing LVSV and egress of blood out of the thorax. Prolonging NITP to include both systole and diastole, a profound fall in LVSV is observed, consistent with the independent influences of systolic and diastolic events combining to diminish LVSV.(ABSTRACT TRUNCATED AT 250 WORDS)
authors: Department of Anesthesiology and Critical Care Medicine, Francis Scott Key Medical Center, Johns Hopkins University Medical Institutions, Baltimore, Maryland 21205.
authors: J
authors: J
authors: Peters
authors: M K
authors: MK
authors: Kindred
authors: J L
authors: JL
authors: Robotham
mesh_terms: D000402:Airway Obstruction / Q000503:physiopathology; D000818:Animals; D001011:Aorta / Q000502:physiology; D004285:Dogs; D004558:Electric Stimulation; D004947:Esophagus / Q000502:physiology; D006321:Heart / Q000502:physiology*; D006439:Hemodynamics; D008168:Lung / Q000502:physiology*; D009200:Myocardial Contraction; D010791:Phrenic Nerve / Q000502:physiology; D013599:Systole