Digoxin Disease Interactions

There are 11 disease interactions with digoxin:

Accessory Av Pathway Bradyarrhythmia/Av Block Hypercalcemia Hypocalcemia Hypokalemia/Hypomagnesemia Preserved Left Ventricular Ejection

Renal Dysfunction Ventricular Arrhythmia Acute Mi Hyperthyroidism Hypothyroidism

Digoxin may enhance accessory pathway conduction in conditions such as the Wolff-Parkinson-White syndrome. Following intravenous digoxin therapy, some patients with paroxysmal atrial fibrillation or flutter and a coexisting accessory AV pathway have developed increased antegrade conduction across the accessory pathway bypassing the AV node, leading to a very rapid ventricular response or ventricular fibrillation. Unless conduction down the accessory pathway has been blocked, either pharmacologically or by surgery, digoxin should not be used in such patients. The treatment of paroxysmal supraventricular tachycardia in such patients is usually direct-current cardioversion.

Digoxin slows sinoatrial and AV conduction, commonly prolonging the PR interval. When treated with digoxin, patients with preexisting sinus node disease may develop severe sinus bradycardia or sinoatrial block, and patients with incomplete AV block may progress to advanced or complete heart block. In such patients, consideration should be given to the insertion of a pacemaker prior to initiating treatment with digoxin. Digoxin may be administered to patients with complete, stable AV block who have congestive heart failure, provided the block was not induced by cardiac glycosides.

Calcium and digoxin have additive inotropic effects. Therefore, hypercalcemia from any cause will predispose patients to digoxin toxicity and serious arrhythmias. Hypercalcemia should be corrected prior to initiating treatment with digoxin, and serum calcium levels should be monitored during therapy.

Hypocalcemia can nullify the effects of digoxin. The drug may be ineffective in hypocalcemic patients until serum calcium levels are restored to normal.

Potassium and/or magnesium depletion sensitizes the myocardium to digoxin. In patients with hypokalemia or hypomagnesemia, digoxin toxicity may occur despite serum drug concentrations below 2.0 ng/ml. Therapy with digoxin should be administered cautiously in patients with or predisposed to potassium and/or magnesium deficiency, including patients on diuretic therapy; those with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; those with malnutrition; and renal dialysis patients. Electrolyte imbalances should be corrected prior to initiation of treatment. Serum potassium and magnesium concentrations should be monitored during therapy.

Patients with heart failure associated with preserved left ventricular systolic function, such as in restrictive cardiomyopathy, constrictive pericarditis, amyloid heart disease and acute cor pulmonale, may be particularly susceptible to the toxicity of digoxin. Therapy with digoxin should be considered and administered cautiously in such patients. In hypertrophic cardiomyopathy (idiopathic hypertrophic subaortic stenosis), the inotropic effects of digoxin may worsen the outflow obstruction.

Digoxin is primarily eliminated by the kidney. Patients with renal impairment may be at increased risk for digoxin toxicity, including ventricular arrhythmias and AV conduction disturbances, due to decreased drug clearance. Therapy with digoxin should be administered cautiously in patients with impaired renal function. Dosage adjustments should be made according to product package labeling and patient attributes such as age, ideal body weight and other concomitant disease states and medication usage. Dosage increments should be made very gradually, since the elimination half-life may be prolonged in these patients and a longer period of time is required to establish steady-state serum concentrations than normal. These patients should be monitored closely for manifestations of toxicity, and dosages further adjusted as necessary. If toxicity occurs, clinicians should be aware that the adverse effects may also be prolonged.

The use of digoxin is contraindicated in patients with ventricular fibrillation. Digoxin toxicity is associated with adverse cardiac effects, including ventricular arrhythmias, which are most commonly seen in chronic toxicity. Digoxin-induced ventricular tachycardia is associated with a high mortality rate, since ventricular fibrillation or asystole may result. Therapy with digoxin should be considered and administered cautiously in patients with frequent ventricular premature contractions or ventricular tachycardia, especially if these arrhythmias are not caused by heart failure.

The use of inotropic drugs in some patients with acute myocardial infarction may lead to increases in myocardial oxygen demand and ischemia. Therapy with digoxin should be administered cautiously in this setting.

Heart failure and/or atrial arrhythmias resulting from hypermetabolic or hyperdynamic states such as hyperthyroidism, hypoxia, or arteriovenous shunt are best managed by treating the underlying condition. Atrial arrhythmias associated with hypermetabolic states are particularly refractory to digoxin, possibly due to altered pharmacokinetics. Specifically, the apparent volume of distribution and renal elimination of the drug may be increased, resulting in lower serum concentrations. Therapy with digoxin should be administered cautiously in patients with hyperthyroidism. Serum digoxin levels should be monitored regularly and dosage adjustments may be required secondary to changes in their thyroid condition.

Hypothyroidism may reduce the requirements for digoxin due to decreased volume of distribution and plasma clearance of the drug. Therapy with digoxin should be initiated at lower dosages in patients with hypothyroidism to avoid toxicity. Serum digoxin levels should be monitored regularly and dosage adjustments may be required secondary to changes in their thyroid condition.

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