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Cardiovascular determinants of the hemodynamic response to acute endotoxemia in the dog

Pinsky, MR and Matuschak, GM (1986) Cardiovascular determinants of the hemodynamic response to acute endotoxemia in the dog. Journal of Critical Care, 1 (1). 18 - 31. ISSN 0883-9441

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The cardiovascular changes that occur early in hyperdynamic, hypotensive septic shock are poorly understood. In a splenectomized but otherwise intact pentobarbital-anesthetized canine model (n = 11), we simultaneously characterized the determinants of ventricular and peripheral vascular function in response to a bolus infusion of E. coli endotoxin (1.0 mg/kg). Right-ventricular (RV) and left-ventricular (LV) stroke volumes were measured by electromagnetic flow probes. Instantaneous RV function and venous return curves1,2 and steady state arterial pressure-flow (P/Q) and LV function curves were generated by incremental volume loading both before (control) and 30 minutes after (endo) endotoxin infusion. Blood volume (BV) was determined by indicator dilution. Within five minutes of endotoxin infusion, hypotension and hypoperfusion developed because of a decrease in mean systemic pressure (Pma) with no change in ventricular function of the arterial P/Q relation. However, after 30 minutes endo, compared with control, cardiac output increased (2.4 ± .3 to 3.2 ± .3 L/min, x̄ ± XE. P < .05); arterial pressure fell (132 ± 10 to 87 ± 10 mm Hg, P < .01), while the arterial P/Q slope was unchanged. BV remained constant (2,051 ± 149 to 1,942 ± 194 mL, NS), but Pma decreased further (11.3 ± 0.9 to 9.5 ± 0.9 mm Hg, P < .01). For the same BV, peripheral vascular compliance (ΔBV/ΔPma) was unchanged. Ventricular stroke volumes at similar filling pressures were increased (P < .05), while calculated stroke work was unchanged. The arterial P/Q relation and peripheral vascular compliance were unaffected by subsequent beta-adrenergic blockade, though ventricular function was depressed. We conclude that acute endotoxemia causes a biphasic hemodynamic response comprising an early, disproportionate reduction in venous return and a later, progressive peripheral vasomotor paralysis. © 1986, Grune & Stratton, Inc.. All rights reserved.


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Item Type: Article
Status: Published
CreatorsEmailPitt UsernameORCID
Pinsky, MRpinsky@pitt.eduPINSKY0000-0001-6166-700X
Matuschak, GM
Date: 1 January 1986
Date Type: Publication
Journal or Publication Title: Journal of Critical Care
Volume: 1
Number: 1
Page Range: 18 - 31
DOI or Unique Handle: 10.1016/s0883-9441(86)80113-7
Schools and Programs: School of Medicine > Critical Care Medicine
Refereed: Yes
ISSN: 0883-9441
Date Deposited: 25 Aug 2012 17:25
Last Modified: 22 Jun 2021 10:55


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