title: Beta-block the septic heart.
abstract: OBJECTIVE
  Cardiac depression is a well-described manifestation of the sepsis syndrome. An important underlying mechanism is the attenuation of the adrenergic response at the cardiomyocyte level. By reducing their cell-specific function (contractility), the cardiomyocytes reduce their energy expenditure. Consequently, the cardiac myocytes survive in a hibernation-like state as long as intracellular energy generation is limited. The objective of this study was to review β-blocker therapy for the treatment of septic patients.
  
  
  METHODS
  MEDLINE database.
  
  
  RESULTS
  During established sepsis with organ failure, external adrenergic stimulation of the heart must be kept at a minimum. To blunt the adrenergic response, β-blockers have been used in several preclinical and clinical studies. In septic animals, β-blockers reduced heart rate, whereas stroke volume was maintained. Esmolol in vivo prevented the downregulation of adrenergic pathways, preserving full cardiac function ex vivo. In addition, β-blockers reduced the inflammatory response and the degree of lung injury. Some animal studies documented survival benefits, particularly when β-blockers were administered before the septic insult. In patients with septic shock, blood pressure increased and cardiac indices remained stable with metoprolol administration.
  
  
  CONCLUSIONS
  Preclinical and clinical studies with β-1 receptor blockers during sepsis show promising results. Future studies are needed to establish the optimal dose and timing of its administration.
authors.affiliation: Intensive Care Unit, University Hospital Zurich, Zurich, Switzerland. alain.rudiger@usz.ch
authors.forename: Alain
authors.initials: A
authors.lastname: Rudiger
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000818:Animals; D002316:Cardiotonic Agents / Q000627:therapeutic use; D004195:Disease Models, Animal; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006801:Humans; D011412:Propanolamines / Q000627:therapeutic use; D011433:Propranolol / Q000627:therapeutic use; D051381:Rats; D018805:Sepsis / Q000150:complications / Q000188:drug therapy*; D018746:Systemic Inflammatory Response Syndrome / Q000188:drug therapy / Q000503:physiopathology
chemical_list: D000319:Adrenergic beta-Antagonists; D002316:Cardiotonic Agents; D011412:Propanolamines; D011433:Propranolol; C036604:esmolol