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Myocardial dysfunction in sepsis.

R E Cunnion1, J E Parrillo

  • 1Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland.

Critical Care Clinics
|January 1, 1989
PubMed
Summary
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Septic shock causes heart dysfunction due to circulating factors, not ischemia. A canine model mimics human septic shock hemodynamics, aiding research into myocardial depressant substances.

Area of Science:

  • Cardiology
  • Critical Care Medicine
  • Pathophysiology

Background:

  • Septic shock presents a distinct hemodynamic profile: normal/elevated cardiac index (CI) and decreased systemic vascular resistance index (SVRI).
  • Low CI in septic shock often indicates concurrent hypovolemia.
  • Myocardial dysfunction, including ventricular dilatation and reduced ejection fraction, develops within 48 hours in most septic shock patients.

Purpose of the Study:

  • To characterize the hemodynamic profile and myocardial dysfunction in human septic shock.
  • To investigate a canine model for its utility in studying septic myocardial dysfunction.
  • To explore the underlying mechanisms of myocardial depression in sepsis.

Main Methods:

  • Hemodynamic monitoring in human septic shock patients.

Related Experiment Videos

  • Development and utilization of an experimental canine model of sepsis using infected fibrin clots.
  • Assessment of cardiac function, including ventricular dimensions and ejection fractions.
  • Exclusion of global myocardial ischemia as a cause of dysfunction.

    • Main Results:

    • Human septic shock exhibits a characteristic pattern of CI, SVRI, and ventricular function changes.
    • A canine model replicates the hemodynamic and myocardial abnormalities observed in human septic shock.
    • Myocardial dysfunction in sepsis is not attributed to global ischemia but likely involves circulating factors.
    • Cardiac function recovery observed in surviving patients within 10 days.

    Conclusions:

    • Septic shock induces a specific pattern of myocardial dysfunction.
    • The canine model effectively replicates human septic shock hemodynamics and cardiac dysfunction.
    • Circulating myocardial depressant substances are implicated in sepsis-induced cardiac dysfunction.
    • Further research is needed to identify these mediators.