Cardiac dysfunction in severe sepsis and septic shock.
OBJECTIVE
Severe sepsis and septic shock are among the most important causes of morbidity and mortality in patients admitted to the intensive care unit. The purpose of this review is to review current understanding of sepsis-induced cardiac dysfunction and discuss pertinent findings regarding its clinical presentation, underlying mechanisms of disease, and therapy.


RESULTS
Cardiac dysfunction in sepsis is characterized by decreased contractility, impaired ventricular response to fluid therapy, and in some patients ventricular dilatation. Current data support a complex underlying physiopathology with a host of potential pathways leading to myocardial depression. Circulating factors such as cytokines (TNF-alpha, IL-1beta), lysozyme c, endothelin-1 have direct inhibitory actions on myocyte contractility. Nitric oxide has a complex role in sepsis-induced cardiac dysfunction. Current data suggest a combination of deleterious and positive effects on the myocardium determined by the specific type of nitric oxide expressed. Recent studies have shown that mitochondrial dysfunction and apoptosis also play a role in the development of sepsis-induced cardiac dysfunction. Current treatment for sepsis-induced cardiac dysfunction is based on appropriate treatment for the infectious focus (antibiotics and source control) and hemodynamic support (fluids, vasopressors, and inotropes).


CONCLUSIONS
Cardiac dysfunction is common in patients with severe sepsis and septic shock. Current understanding of the underlying mechanisms responsible is rapidly evolving and future novel therapeutic targets may be soon available. Present therapy for sepsis-induced cardiac dysfunction is based on treatment of underlying sepsis with antibiotics and hemodynamic support.
Zanotti-Cavazzoni
Sergio L
SL
Division of Critical Care Medicine, Cooper University Hospital, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Camden, New Jersey 08103, USA. zanotti-sergio@cooperhealth.edu
Hollenberg
Steven M
SM
D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D016207:Cytokines / Q000378:metabolism; D004452:Echocardiography; D006331:Heart Diseases / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D006439:Hemodynamics; D006801:Humans; D007362:Intensive Care Units; D009569:Nitric Oxide / Q000378:metabolism; D011379:Prognosis; D018805:Sepsis / Q000150:complications*; D012772:Shock, Septic / Q000150:complications; D020107:Troponin T / Q000097:blood
D000900:Anti-Bacterial Agents; D015415:Biomarkers; D016207:Cytokines; D020107:Troponin T; D009569:Nitric Oxide