Myocardial depression in sepsis: From pathogenesis to clinical manifestations and treatment

Article Outline

• Abstract
• 1. Introduction
• 2. Pathogenesis
  • 2.1. Genetic factors
  • 2.2. Molecular alterations
    • 2.2.1. Calcium channels
    • 2.2.2. Nitric oxide
    • 2.2.3. Endothelin-1
    • 2.2.4. Cytokines
    • 2.2.5. Toll-like receptors
  • 2.3. Metabolic alterations
    • 2.3.1. Ischemia
    • 2.3.2. Mitochondrial dysfunction and oxidative stress
    • 2.3.3. Autonomic dysregulation
  • 2.4. Structural modifications
  • 2.5. Hemodynamic alterations: from sepsis to myocardial dysfunction
    • 2.5.1. Decreased intravascular volume (reduced preload)
    • 2.5.2. Decreased vascular tone (reduced afterload)
    • 2.5.3. Microcirculatory alterations
    • 2.5.4. VO2/DO2 dependency
    • 2.5.5. Lactate
    • 2.5.6. Mechanical ventilation and septic cardiomyopathy
• 3. Left and right ventricular dysfunction: double trouble
  • 3.1. Septic cardiomyopathy
  • 3.2. Diagnostic tools
    • 3.2.1. Pulmonary artery catheter
    • 3.2.2. Tissue Doppler imaging
    • 3.2.3. Myocardial perfusion echocardiography
• 4. Treatment
  • 4.1. Hemodynamic stabilization
    • 4.1.1. Fluid therapy
    • 4.1.2. Inotropic agents
    • 4.1.3. Vasopressors
  • 4.2. Other treatments
• 5. Conclusions
• References
• Copyright

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