Beta-block the septic heart.

Abstract

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. MEDLINE database. 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. 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.