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Related Experiment Videos

Load-independent left ventricular function in a hemorrhagic shock model

A Chendrasekhar1, L S Barringer, J C Fagerli

  • 1Department of Surgery, West Virginia University, Morgantown, 26505, USA.

The Journal of Surgical Research
|April 1, 1996
PubMed
Summary

Hemorrhagic shock impairs left ventricular (LV) function, even after resuscitation. The peak systolic pressure to end systolic volume ratio (PSP/ESV) remained depressed, indicating persistent cardiac dysfunction in this swine model.

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Area of Science:

  • Cardiovascular Physiology
  • Hemorrhagic Shock Research
  • Septic Shock Pathophysiology

Background:

  • Load-independent left ventricular (LV) function can be depressed in septic shock.
  • The peak systolic pressure to end systolic volume ratio (PSP/ESV) is a validated measure of LV function, independent of loading conditions.

Purpose of the Study:

  • To evaluate the PSP/ESV ratio in a porcine model of hemorrhagic shock.
  • To determine if LV function, assessed by PSP/ESV, recovers after resuscitation from hemorrhagic shock.

Main Methods:

  • Hemorrhagic shock was induced in five swine by arterial bleeding to a mean arterial pressure of 45-65 mmHg for 30 minutes.
  • Resuscitation was performed using shed blood and crystalloid solution to restore baseline mean arterial pressure.

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  • Echocardiography-derived ejection fraction and oxygen transport parameters were measured at baseline, during hypotension, and postresuscitation.

    • Main Results:

    • Mean arterial pressure, cardiac index, and oxygen delivery/consumption returned to baseline levels postresuscitation.
    • Despite adequate resuscitation, the PSP/ESV ratio remained significantly lower than baseline levels.
    • This suggests a persistent, load-independent cardiac dysfunction following hemorrhagic shock.

    Conclusions:

    • Hemorrhagic shock induces a reproducible, hemodynamically stable cardiac dysfunction in swine.
    • The PSP/ESV ratio is a sensitive indicator of persistent LV dysfunction after hemorrhagic shock, even when other hemodynamic parameters normalize.
    • This model is valuable for studying the mechanisms and potential treatments for shock-induced cardiac dysfunction.