tricles, and so increase in excitability. It also decreases the conduction of electrical impulses through the AV node by vagal stimulation leading to negative chrono- tropic effect.6 Digoxin decreases the function of α-subunit of the Na+/K+ ATPase pump in the membranes of heart my- ocytes by binding to it. So the level of the sodium ions in the myocytes increases, and as a consequence of sodium/calcium exchanger function intracellular calcium ions rise. Increased amount of Ca2+ storing in the sarcoplasmic reticulum leads to increased con- tractility of the heart.7 Digoxin is used in congestive heart failure, especially in patients with refractory symptoms along with diuretic and ACE inhibitor treatment, but it is ineffective at decreasing morbidity and mortality while improving the quality of life.2 Safe therapeutic plasma level is 1-2.6 nmol/l. Di- goxin plasma level should be checked in the setting of questioned toxicity or ineffectiveness. Plasma potas- sium levels should be monitored frequently.2 Due to narrow therapeutic index, the dose-dependent adverse effects (rare if plasma digoxin concentration is <0.8 μg/l) are common.8 Hypokalemia increases the risk because digoxin competes with K+ for binding to the Na+/K+ ATPase pump.9 In overdose, supportive care should be undertaken. Digoxin antidote is digibind and digifab which is given in life threatening ar- rhythmias or malignant hyperkalemia which defines as unavoidably increasing potassium level owing to paralysis of the cell membrane bound ATPase- dependent Na/K pumps.10 EKG findings are increased PR interval, decreased QT interval, inverted T wave and ST depression. Other changes are AV junctional Digoxin toxicity rhythm and ectopic beats (bigemminy) leading to ventricular tachycardia and fibrillation.2 Digoxin toxicity should be considered when de- ciding to start any new medication in a patient on di- goxin therapy especially in ICU settings where poly pharmacy is not uncommon. Patients with acute car- diac glycoside toxicity and hyperkalemia especially those with serum potassium level above 5.5 meq/lit have a grave prognosis, but early and aggressive sup- portive therapy my significantly improve the outcome despite unavailability of digifab. Acknowledgements The authors would like to thank Dr. Nasrin Shokrpour at Center for Development of Clinical Research of Nemazee Hospital for editorial assistance. Keywords: Digoxin toxicity; Serum potassium level Conflict of interest: None declared. F Zand 1 , S Asadi1*, P Katibeh 2 1 Department of Anesthesiology, Shiraz University of Medical Sciences, Shiraz, Iran 2Department of Pediatrics, Shiraz University of Medical Sciences, Shiraz, Iran *Correspondence: Saman Asadi, MD, Department of Anesthesiol- ogy, Anesthesiology and Critical Care Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Tel: +98-711- 2318072, Fax: +98-711-2307072, e-mail: Asadisa@sums.ac.ir Received: January 30, 2011 Accepted: April 25, 2011 References 1 2 3 4 5 Hollman A. Digoxin comes from Digitalis lanata. BMJ 1996;312:912. [8611904] Digoxin. [cited]; Available from: http://en.wikipedia.org/wiki. Lexi-Comp Online™ Interaction Lookup. 2010. Available in: http:// www.uptodate.com/crlsql/interact/fra meset.jsp. Doering W, Konig E, Sturm W. Digi- talis intoxication: specifity and signif- icance of cardiac and extracardiac symptoms. Part I: Patients with digi- talis-induced arrhythmias. Z Kardiol 1977;66:121-8. [857452] Levine M, O'Conor A. Digitalis (car- diac glycoside) poisoning. 2010. Available in: http://www.uptodate. com/online/content/topic. 6 7 8 Eddleston M, Ariaratnam CA, Sjöström L, Jayalath S, Rajakanthan K, Rajapakse S, Colbert D, Meyer WP, Perera G, Attapattu S, Kularat- ne SA, Sheriff MR, Warrell DA. Acute yellow oleander (Thevetia pe- ruviana) poisoning: cardiac arrhyth- mias, electrolyte disturbances, and serum cardiac glycoside concentra- tions on presentation to hospital. Heart 2000;83:301-6. [10677410] Smith TW. Digitalis. Mechanisms of action and clinical use. N Engl J Med 1988;318:358-65. [3277052] [http://dx.doi.org/10.1056/NEJM198 802113180606] Williamson KM, Thrasher KA, Ful- ton KB, Allen LaPointe NM, Dunham GD, Cooper AA, Barrett PS, Patter- son JH. Digoxin toxicity: An evalua- tion in current clinical practice. Arch Intern Med 1998;158:2444-9. [985 5382] [http://dx.doi.org/10.1001/archinte.1 58.22.2444] 9 Smith TW, Antman EM, Friedman PL, Blatt CM, Marsh JD. Digitalis glycosides: Mechanisms and mani- festations of toxicity. Part III. Prog Cardiovasc Dis 1984;27:21-56. [614 6162] [http://dx.doi.org/10.1016/00 33-0620(84)90018-5] 10 Flanagan RJ, Jones AL. Fab Anti- body Fragments: some applications in clinical toxicology. Drug Saf 2004;27:1115-33. [15554746] [http:// dx.doi.org/10.2165/00002018- 200427140-00004] WWW.ircmj.com Vol 13 September 2011 681