title: Transient analysis of cardiopulmonary interactions. I. Diastolic events.
abstract: The etiology of the fall in left ventricular stroke volume (LVSV) with negative intrathoracic pressure (NITP) during inspiration has been ascribed to a reduction in LV preload. This study evaluated the effects of NITP with and without airway obstruction confined to early (ED), mid- (MD), or late diastole (LD) on the subsequent LVSV, anteroposterior (AP), and right-to-left (RL) aortic diameters (DAO) (series I, n = 6) as well as on phasic arterial blood flow out of the thorax (series II, n = 6) in anesthetized dogs. Transient NITP was obtained by electrocardiogram-triggered phrenic nerve stimulation. In series I, NITP applied for 60% of diastole with the airway obstructed caused decreases of LVSV during ED [-7.7 +/- 3.2% (SE) NS], MD (-11.7 +/- 3.9%, P less than 0.05), and LD (-14.6 +/- 1.5%, P less than 0.01) associated with significant increases of left ventricular end-diastolic pressures relative to both atmospheric and esophageal pressures during MD and LD. NITP increased DAO(AP) and DAO(RL), resulting in increases in diastolic aortic cross-sectional area by an average of 6.1-8.3% (P less than 0.01). Similar changes were seen with the airway unobstructed during NITP. In series II, NITP caused diminished diastolic antegrade carotid artery and/or descending aortic flow run off in all dogs. Transient retrograde arterial flows with NITP were observed in more than half of the animals consistent with increases in aortic diameters. We conclude that a decrease of intrathoracic pressure confined to diastole can 1) diminish the ensuing LVSV, presumptively reducing preload by ventricular interdependence; 2) distend the intrathoracic aorta; 3) diminish antegrade flow out of the thorax independent of effects on cardiac performance; and 4) cause transient retrograde carotid and aortic blood flow. The intrathoracic aorta and, presumably, the arterial intrathoracic vascular compartment can be viewed as an elastic container driven by changes in intrathoracic pressure.
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: D000818:Animals; D001794:Blood Pressure; D003971:Diastole; D004285:Dogs; D004558:Electric Stimulation; D004947:Esophagus / Q000294:innervation / Q000502:physiology; D006321:Heart / Q000502:physiology*; D006439:Hemodynamics; D008168:Lung / Q000502:physiology*; D009200:Myocardial Contraction; D010791:Phrenic Nerve / Q000502:physiology; D011312:Pressure; D012039:Regional Blood Flow; D012119:Respiration