| Sepsis-associated cardiac complications contribute to a major increase in mortality and morbidity of critically ill patients (1). Sepsis is often characterized by increased catecholamine levels and associated with increased cardiac contractility and heart rate. Throughout the disease procedure, mitochondrial dysfunction leads to supply/demand imbalance increasing the risk of cardiac myocytes death. However, reducing cell-specific functions enables cells to balance energy production and demand. Through this down-regulation, cardiomyocytes survive in a hibernation-like state and when the septic insult is overcome and cellular energy supply reestablished, the contraction is restarted (2). Decatecholaminization, the reduction of endogenous and exogenous adrenergic stimulation, has been accepted to be important in the management of critically ill patients particularly in the transition between acute and chronic critical illness; beta-blockers are considered as a choice option in this respect. Therefore, beta blockers should be titrated in septic patients and close hemodynamic monitoring is warranted for early detection of potential negative effects (3). For instance, administration of esmolol has been shown to be associated with reduction in heart rate without increasing the adverse events (4). |