الفهرس | Only 14 pages are availabe for public view |
Abstract Septic shock is associated with excessive sympathetic outflow, high plasma catecholamine levels, myocardial depression, vascular hyporeactivity, and autonomic dysfunction. Typically, patients have a low resistance, high cardiac output circulation with tachycardia and arterial hypotension that may be poorly or even nonresponsive to exogenous catecholamine vasopressors. Although norepinephrine is the current recommended mainstay of treatment for sepsis-related hypotension, excessive adrenergic stress has multiple adverse effects including direct myocardial damage, cardiomyopathy and tachyarrhythmias. High plasma catecholamine levels, the extent and duration of catecholamine therapy, and tachycardia are all independently associated with poor outcomes in critically ill patients. Numerous evidences identify elevated heart rate as an independent isk factor for early death both in the general population and various groups of patients with cardiovascular conditions. There are many potential benefits of beta-blockers for acutely ill patients. This includes decreased oxygen demand related to decreased heart rate. Beta-blocker drugs are widely used as heart rate lowering drugs. However, these agents have negative inotropic activity, which is inappropriate in hemodynamic instability. A selective heart-rate-lowering agent could thus be of therapeutic value in this context. Ivabradine is a pure HR-lowering drug that acts specifically on the sinoatrial node by selectively inhibiting the If current of cardiac pacemaker cells by entering and binding to a site in the channel pore from the intracellular side without affecting the other cardiac ionic currents. |