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| __NOTOC__
| | #REDIRECT [[Digoxin#Warnings]] |
| {{Digoxin}}
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| {{CMG}}; {{AE}} {{AK}}
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| '''''For patient information, click <u>[[Digoxin (patient information)|here]]'''''</u>.
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| ==5 WARNINGS AND PRECAUTIONS==
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| ===5.1 Ventricular Fibrillation in Patients With Accessory AV Pathway (Wolff-Parkinson-White Syndrome)===
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| Patients with [[Wolff-Parkinson-White syndrome]] who develop[[ atrial fibrillation]] are at high risk of [[ventricular fibrillation]]. Treatment of these patients with digoxin leads to greater slowing of conduction in the [[atrioventricular node]] than in [[accessory pathways]], and the risks of rapid ventricular response leading to ventricular fibrillation are thereby increased.
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| ===5.2 Sinus Bradycardia and Sino-atrial Block===
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| Digoxin injection may cause severe [[sinus bradycardia]] or [[sinoatrial block ]]particularly in patients with pre-existing sinus node disease and may cause advanced or complete heart block in patients with pre-existing incomplete [[AV block]]. Consider insertion of a [[pacemaker]] before treatment with digoxin.
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| ===5.3 Digoxin Toxicity===
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| Signs and symptoms of digoxin toxicity include [[anorexia]], [[nausea]], [[vomiting]], visual changes and [[cardiac arrhythmias]] [first-degree heart block|first-degree]], [[second-degree heart block|second-degree]] ([[Wenckebach]]), or [[third-degree heart block]] (including [[asystole]]); [[atrial tachycardia ]]with block; [[AV dissociation]]; [[accelerated junctional (nodal) rhythm|accelerated junctional rhythm]]; unifocal or multiform [[ventricular premature contractions]] (especially [[bigeminy ]]or [[trigeminy]]); [[ventricular tachycardia]]; and ventricular fibrillation]. Toxicity is usually associated with digoxin levels greater than 2 ng/ml although symptoms may also occur at lower levels. Low body weight, advanced age or impaired renal function, [[hypokalemia]], [[hypercalcemia]], or [[hypomagnesemia ]]may predispose to digoxin toxicity. Obtain serum digoxin levels in patients with signs or symptoms of digoxin therapy and interrupt or adjust dose if necessary [see [[Adverse Reactions|DIGOXIN injection adverse reactions]] (6) and [[Overdosage|DIGOXIN injection overdosage ]](10)]. Assess serum electrolytes and renal function periodically.
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| The earliest and most frequent manifestation of digoxin toxicity in infants and children is the appearance of cardiac arrhythmias, including [[sinus bradycardia]]. In children, the use of digoxin may produce any arrhythmia. The most common are conduction disturbances or [[supraventricular]]tachyarrhythmias, such as[[ atrial tachycardia]] (with or without block) and[[ junctional (nodal) tachycardia| junctiona tachycardia]]. Ventricular arrhythmias are less common. [[Sinus bradycardia]] may be a sign of impending digoxin intoxication, especially in infants, even in the absence of first-degree heart block. Any arrhythmias or alteration in cardiac conduction that develops in a child taking digoxin should initially be assumed to be a consequence of digoxin intoxication.
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| Given that adult patients with heart failure have some symptoms in common with digoxin toxicity, it may be difficult to distinguish digoxin toxicity from heart failure. Misidentification of their etiology might lead the clinician to continue or increase digoxin dosing, when dosing should actually be suspended. When the etiology of these signs and symptoms is not clear, measure serum digoxin levels.
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| ===5.4 Risk of Ventricular Arrhythmias During Electrical Cardioversion===
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| It may be desirable to reduce the dose of or discontinue digoxin for 1 to 2 days prior to electrical [[cardioversion ]]of [[atrial fibrillation]] to avoid the induction of ventricular arrhythmias, but physicians must consider the consequences of increasing the ventricular response if digoxin is decreased or withdrawn. If digitalis toxicity is suspected, elective [[cardioversion ]]should be delayed. If it is not prudent to delay cardioversion, the lowest possible energy level should be selected to avoid provoking ventricular arrhythmias.
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| ===5.5 Risk of Ischemia in Patients With Acute Myocardial Infarction===
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| Digoxin is not recommended in patients with acute myocardial infarction because digoxin may increase myocardial oxygen demand and lead to [[ischemia]].
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| ===5.6 Vasoconstriction In Patients With Myocarditis===
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| Digoxin can precipitate vasoconstriction and may promote production of pro-inflammatory [[cytokines]]; therefore, avoid use in patients with [[myocarditis]]. | |
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| ===5.7 Decreased Cardiac Output in Patients With Preserved Left Ventricular Systolic Function===
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| Patients with heart failure associated with preserved left ventricular ejection fraction may experience decreased cardiac output with use of digoxin. Such disorders include[[ restrictive cardiomyopathy]], [[constrictive pericarditis]], [[amyloid ]]heart disease, and acute [[cor pulmonale]]. Patients with [[idiopathic hypertrophic subaortic stenosis]] may have worsening of the outflow obstruction due to the inotropic effects of digoxin. Patients with amyloid heart disease may be more susceptible to digoxin toxicity at therapeutic levels because of an increased binding of digoxin to extracellular amyloid fibrils.
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| Digoxin should generally be avoided in these patients, although it has been used for ventricular rate control in the subgroup of patients with [[atrial fibrillation]].
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| ===5.8 Reduced Efficacy In Patients With [[Hypocalcemia]]===
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| [[Hypocalcemia ]]can nullify the effects of digoxin in humans; thus, digoxin may be ineffective until serum calcium is restored to normal. These interactions are related to the fact that digoxin affects contractility and excitability of the heart in a manner similar to that of calcium.
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| ===5.9 Altered Response in Thyroid Disorders and Hypermetabolic States===
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| [[Hypothyroidism ]]may reduce the requirements for digoxin.
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| Heart failure and/or atrial arrhythmias resulting from hypermetabolic or hyperdynamic states (e.g., [[hyperthyroidism]], hypoxia, or arteriovenous shunt) are best treated by addressing the underlying condition. Atrial arrhythmias associated with hypermetabolic states are particularly resistant to digoxin treatment. Patients with [[beri beri heart disease]] may fail to respond adequately to digoxin if the underlying thiamine deficiency is not treated concomitantly.
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| ==References==
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| {{Reflist|2}}
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| http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=58f45aba-ff6f-43cc-bb88-be40a9f7beda
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| [[Category:Cardiovascular Drugs]]
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| [[Category:Drugs]]
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