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Myocardial dysfunction in sepsis.

J J Spitzer, L W Smith, E C Burke

    Progress in Clinical and Biological Research
    |January 1, 1987
    PubMed
    Summary
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    Sepsis can impair heart function by releasing mediators that affect myocardial contractility and calcium flux. Compensatory mechanisms, including elevated catecholamines and heart rate, aim to maintain cardiac output during sepsis.

    Area of Science:

    • Cardiovascular Physiology
    • Sepsis Pathophysiology
    • Myocardial Contractility

    Background:

    • Sepsis triggers immune responses involving macrophages and endotoxins.
    • These factors can negatively impact myocardial contractile function.
    • Early sepsis stages may present with impaired stroke volume.

    Purpose of the Study:

    • To elucidate the sequence of events leading to myocardial dysfunction in sepsis.
    • To understand the compensatory mechanisms that increase cardiac index during sepsis.
    • To investigate the role of mediators and endotoxins in sepsis-induced cardiac changes.

    Main Methods:

    • Schematic representation of postulated events (Fig. 10).
    • Analysis of mediator and endotoxin effects on myocardial function.

    Related Experiment Videos

  • Examination of cellular calcium flux alterations.
  • Assessment of catecholamine and heart rate responses.
  • Evaluation of myocardial substrate utilization in sepsis models.

    • Main Results:

    • Mediators and endotoxins can directly impair myocardial contractility and alter calcium flux, reducing stroke volume.
    • Circulating catecholamines and mediators elevate heart rate, restoring cardiac index.
    • The SA node's sensitivity to beta-adrenergic stimulation increases.
    • Myocardial substrate utilization (fatty acids, lactate, glucose) remains unaffected.
    • The hyperdynamic phase of sepsis is characterized by increased cardiac index via tachycardia.

    Conclusions:

    • The proposed sequence explains the hyperdynamic cardiac response in sepsis.
    • Tachycardia maintains cardiac index but is energy inefficient.
    • The myocardium can sustain high energy phosphate concentrations despite sepsis.
    • Further research is needed to confirm these findings in human sepsis.