Septic shock is a major health problem, with several million cases annually worldwide and a
mortality approaching 45%. Tachycardia is associated with excess mortality during septic
shock. This pejorative effect could be related to the increase in cardiac metabolic demand,
impaired cardiac diastolic function, and/or poorer tolerance of administered exogenous
catecholamines. Recent studies suggest that controlling the heart rate with the use of beta
blockers has beneficial effects on the morbidity and mortality of septic shock. However, the
negative effects of beta-blockers on cardiac contractility and blood pressure complicate
their use during septic shock, particularly because about one-half of patients exhibit a
septic-associated systolic dysfunction, which often requires the use of inotropes.
Ivabradine is a selective inhibitor of If channels in the sinoatrial node. It is a pure
bradycardic agent with no deleterious effect on other aspects of cardiac function
(contractility, conduction and repolarization) nor on blood pressure. Ivabradine can
therefore alleviate sinus tachycardia without negative inotropic effects nor hypotension.
Moreover, the improvement in diastolic function (ventricular filling) with ivabradine may
increase stroke volume, even in case of severe impairment of systolic function. Controlling
sinus tachycardia with ivabradine during septic shock would allow reducing cardiac metabolic
demand (and potentially associated ischemic events) and improving the chronotropic tolerance
of exogenous catecholamines. The effectiveness of ivabradine in controlling the heart rate
was demonstrated in various clinical settings such as coronary artery disease, chronic heart
failure and cardiogenic shock. Encouraging preliminary data are reported in critically ill
patients.