title: Myocardial dysfunction in sepsis: clinical and experimental investigations.
abstract: OBJECTIVE
  To review the clinical manifestations and mechanisms of cardiac dysfunction in septic shock.
  
  
  METHODS
  Literature review of selected clinical studies and animal models.
  
  
  RESULTS
  Depressed myocardial contractile function is a common consequence of severe infections. Bacterial factors, in conjunction with host inflammatory mediators, produce a profile of reversible cardiac dysfunction manifested by a decrease in ventricular ejection fraction, ventricular dilatation, and increased cardiac output. Global ischemia is not the major mechanism that mediates cardiac dysfunction during sepsis. Inflammatory mediators contribute to myocardial dysfunction by damaging the coronary microcirculation and contributing to myocardial edema and cardiocyte damage. However, trials of anti-inflammatory agents have not prevented or increased the rate of reversal of septic shock or improved survival. The link between nitric oxide and clinical myocardial depression remains unclear, as nonselective nitric oxide synthase inhibition does not block the development of ventricular dysfunction.
  
  
  CONCLUSIONS
  Serious bacterial infections result in inflammatory injury to the heart manifested by a common profile of cardiac dysfunction. Therapy remains limited to treatment of the infection with antibiotics and supportive care, with fluid resuscitation and selective use of inotropes and vasopressors. Experimental models suggest that new anti-inflammatory strategies (e.g. tyrosine kinase inhibitors) may offer some advantages over those that target a single mediator; these agents remain to be clinically evaluated.
authors.affiliation: Critical Care Medicine Department, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, MD 20892-1662, USA. anthony_suffredini@nih.gov
authors.forename: A F
authors.initials: AF
authors.lastname: Suffredini
mesh_terms: D000818:Animals; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology; D012772:Shock, Septic / Q000503:physiopathology* / Q000628:therapy; D018754:Ventricular Dysfunction / Q000503:physiopathology / Q000628:therapy
chemical_list: D018836:Inflammation Mediators; D009569:Nitric Oxide