Eric Wise, MD, MA
Assistant Professor of Surgery
University of Minnesota Medical School
Minneapolis, Minnesota
Disclosure information not submitted.
Zachary Bergman, MD
Resident in Surgery
University of Minnesota, United States
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Roy Kiberenge, MD
Assistant Professor of Anesthesiology
University of Minnesota, Minnesota, United States
Disclosure information not submitted.
Gregory Beilman, MD, FCCM
Senior Vice President Acute Operations
University of Minnesota
Richfield
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Richard Bianco, PhD
Professor
University of Minnesota, United States
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Kyle Hocking, PhD
Assistant Professor
Vanderbilt University, United States
Disclosure information not submitted.
Colleen Brophy, MD
Professor
Vanderbilt University Medical Center, United States
Disclosure information not submitted.
Bret Alvis, MD
Vanderbilt University Medical Center
Nashville, Tennessee
Disclosure information not submitted.
Title: Hemodynamic parameters and systemic vascular resistance in a pig model of distributive hypotension
Introduction: To maintain perfusion, restoration of systemic vascular resistance (SVR) in distributive hypotension and shock is essential. Sepsis, a common etiology, is initially treated with intravenous (IV) fluid administration followed by vasoactive medications, titrating to maintain an adequate mean arterial pressure (MAP). In this investigation, a porcine model of lipopolysaccharide (LPS)-induced distributive hypotension and resuscitation is used to characterize hemodynamic parameters, and assess the influence of IV fluids and vasoactive medication on SVR.
Methods: Ten pigs were anesthetized, fully cannulated and equilibrated to a pulmonary capillary wedge pressure (PCWP) of ~10 mmHg. Pigs were infused with an escalating dose of intravenous LPS until a 25% decrement in systolic blood pressure was observed. Four subsequent 10 mg/kg crystalloid boluses were given, followed by a 30 minute uptitration of norepinephrine (NE) to 0.25 ug/kg/min. Hemodynamic parameters were transduced at baseline, critical hypotension, after each bolus, and after NE administration, followed by subsequent calculation of SVR in dynes/sec/cm-5. Medians and interquartile ranges (IQR) of all parameters were calculated at each milestone; comparisons among milestone timepoints were made using the Wilcoxon test or Friedman test with Tukey’s post-hoc analysis, as appropriate.
Results: At each milestone, PCWP, MAP, central venous pressure (CVP), cardiac output (CO) and heart rate (HR) were measured. From baseline to induction of LPS-induced hypotension, SVR decreased (924 [723-982] vs. 677 [521-852]; P=0.03). Relative to untreated LPS-induced hypotension, SVR was found to be further decreased at each post-bolus timepoint (P=0.002), though no differences in SVR among post-bolus timepoints were observed (P >0.05). Moreover, MAP was not restored by fluid bolus. Conversely, SVR increased from its value post-boluses after norepinephrine treatment (420 [348-548] vs. 590 [461-701]; P=0.02), but remained significantly below baseline (P=0.02).
Conclusions: In contrast to PCWP, MAP, CVP, CO or HR alone, SVR was most useful to detect physiologic response to resuscitation in distributive hypotension. Fluid administration further impaired SVR while norepinephrine increased it, an important consideration for preservation of critical organ perfusion.