* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Levosimendan - Wellington ICU
Survey
Document related concepts
Remote ischemic conditioning wikipedia , lookup
History of invasive and interventional cardiology wikipedia , lookup
Heart failure wikipedia , lookup
Cardiac contractility modulation wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Antihypertensive drug wikipedia , lookup
Cardiac surgery wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
Coronary artery disease wikipedia , lookup
Transcript
Levosimendan 23/3/09 Sylvia Archan and Wolfgang Toller, (2008) “Levosimendan: current status and future prospects” Current Opinion in Anaesthesiology, 21:78–84 PY Mindmaps Class – Ca2+ sensitizer (novel inotrope) Mechanism of Action - sensitises cardiac muscle to Ca2+ - stabilises troponin C in a conformation that triggers and maintain contraction. - doesn’t impair diastolic relaxation - also produces vasodilation by opening ATP-sensitive K+ channels in vascular smooth muscle -> reduces preload, afterload, improves O2 supply to myocardium, increases coronary blood flow and renal blood flow. - increases: Q, SV, HR and increases coronary blood flow. - decreases: SVR, SBP, PCWP, PAP, coronary vascular resistance, myocardial oxygen consumption. - shown to improve symptoms, and BNP in cardiac failure (but, unfortunately not survival) - can be used with beta-blockers (doesn’t compete with levo) - also has anti-inflammatory and anti-apoptotic effects Pharmaceutics Dose - loading dose: 6-24mcg/kg over 10 min - infusion for 24 hours of 0.05-0.2mcg/kg/min Indications - heart failure (acute and chronic) sepsis post resuscitation myocardial dysfunction perioperative optimization of cardiac patients with cardiomyopathy Adverse Effects - hypotension headache N+V dysrrhythmias PK Jeremy Fernando (2011) Absorption – IV or PO Distribution – highly protein bound, peak concentrations reached after 2 days of treatment Metabolism – hepatic, active metabolite with t1/2 of 70 hours Elimination - dose adjust in renal insufficiency, eliminated in urine and faeces. Evidence Mebazza, (2007) SURVIVE – Levosimendan vs Dobutamine in patients with acute decompensated heart failure, JAMA - n = 1320 - seeked to prove an mortality reduction of 25%! -> no difference in 180 day mortality SUMMARY De Keulenaer, B. L. (2008) – “The case for Levosimendan” Critical Care and Resuscitation, Volume 10 (3) page 180 - decreased arrhythmias decreased myocardial oxygen consumption inodilator ?prevention of apoptosis and preservation of mitochondrial function improved right ventricular function in ARDS and in acute PE Jeremy Fernando (2011)