Can you take Digoxin with Duradryl?

The methscopolamine in Duradryl has a moderate potential interaction with Arrhythmia.

Antimuscarinic agents block vagal inhibition of the SA nodal pacemaker. These agents should be administered cautiously in patients with tachycardia, congestive heart failure, or coronary artery disease. Premature ventricular depolarization or ventricular tachycardia or fibrillation associated with antimuscarinic drugs is rare.

The methscopolamine in Duradryl has a moderate potential interaction with Arrhythmia.

Anticholinergics block vagal inhibition of the SA nodal pacemaker. Therapy with anticholinergics should be administered cautiously in patients with tachycardia, congestive heart failure, or coronary artery disease. Premature ventricular depolarization or ventricular tachycardia or fibrillation associated with anticholinergics is rare.

The methscopolamine in Duradryl has a major potential interaction with Asthma.

The use of systemic anticholinergics is contraindicated in the treatment of lower respiratory tract symptoms including asthma. Muscarinic receptor antagonists reduce bronchial secretions, which can result in decreased fluidity and increased thickening of secretions. However, ipratropium does not produce these effects and can be used safely in treating asthma.

The chlorpheniramine in Duradryl has a moderate potential interaction with Asthma.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

The methscopolamine in Duradryl has a major potential interaction with Autonomic Neuropathy.

Agents with anticholinergic activity can exacerbate many of the manifestations of autonomic neuropathy, including tachycardia, anhidrosis, bladder atony, obstipation, dry mouth and eyes, cycloplegia and blurring of vision, and sexual impotence in males. Therapy with antimuscarinic agents and higher dosages of antispasmodic agents (e.g., dicyclomine or oxybutynin) should be administered cautiously in patients with autonomic neuropathy.

The phenylephrine in Duradryl has a moderate potential interaction with Benign Prostatic Hyperplasia.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

The methscopolamine in Duradryl has a moderate potential interaction with Bleeding Disorder.

Antimuscarinic agents may cause a delay in gastric emptying and possibly antral stasis in patients with gastric ulcer. Therapy with antimuscarinic agents should be administered cautiously to patients with gastric ulcer.

Digoxin has a major potential interaction with Cardiomyopathy.

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 experience decrease cardiac output. Therapy with digoxin should be administered cautiously in such patients. Patients with idiopathic hypertrophic subaortic stenosis may have worsening of the outflow obstruction due to the inotropic effects of digoxin.

Digoxin has a major potential interaction with Cardiomyopathy.

Digoxin can rarely precipitate vasoconstriction and may promote the development of cytokines; therefore, should be avoided in patients with myocarditis.

The phenylephrine in Duradryl has a major potential interaction with Cardiovascular Conditions and Disorders.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

The chlorpheniramine in Duradryl has a moderate potential interaction with Cardiovascular Conditions and Disorders.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

The methscopolamine in Duradryl has a moderate potential interaction with Cardiovascular Conditions and Disorders.

Anticholinergics block vagal inhibition of the SA nodal pacemaker. Therapy with anticholinergics should be administered cautiously to patients with tachycardia, congestive heart failure, or coronary artery disease. Premature ventricular depolarization, ventricular tachycardia, and fibrillation associated with anticholinergics are rare.

The phenylephrine in Duradryl has a major potential interaction with Cerebrovascular Insufficiency.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

Digoxin has a major potential interaction with Constrictive Pericarditis.

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 experience decrease cardiac output. Therapy with digoxin should be administered cautiously in such patients. Patients with idiopathic hypertrophic subaortic stenosis may have worsening of the outflow obstruction due to the inotropic effects of digoxin.

The chlorpheniramine in Duradryl has a moderate potential interaction with COPD.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

Digoxin has a major potential interaction with Cor Pulmonale.

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 experience decrease cardiac output. Therapy with digoxin should be administered cautiously in such patients. Patients with idiopathic hypertrophic subaortic stenosis may have worsening of the outflow obstruction due to the inotropic effects of digoxin.

The phenylephrine in Duradryl has a moderate potential interaction with Diabetes Mellitus.

Sympathomimetic agents may cause increases in blood glucose concentrations. These effects are usually transient and slight but may be significant with dosages higher than those normally recommended. Therapy with sympathomimetic agents should be administered cautiously in patients with diabetes mellitus. Closer monitoring of blood glucose concentrations may be appropriate.

Digoxin has a major potential interaction with Diarrhea.

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.

The methscopolamine in Duradryl has a minor potential interaction with Diarrhea.

Diarrhea may be a symptom of incomplete intestinal obstruction, especially in patients with ileostomy or colostomy. Antimuscarinic agents may further aggravate the diarrhea. Therefore, these drugs should be administered cautiously in patients with diarrhea.

Digoxin has a major potential interaction with Electrolyte Abnormalities.

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.

The methscopolamine in Duradryl has a major potential interaction with Esophageal Obstruction.

Anticholinergics are contraindicated in patients with obstructive diseases such as achalasia, esophageal stricture or stenosis, pyloroduodenal stenosis, stenosing peptic ulcer, pyloric obstruction, and paralytic ileus. Anticholinergics may further suppress intestinal motility with resultant precipitation or aggravation of toxic megacolon.

The methscopolamine in Duradryl has a minor potential interaction with Fever.

Atropine-like agents may increase the risk of hyperthermia in patients with fever by producing anhidrosis. Therapy with atropine-like agents should be administered cautiously in febrile patients.

The methscopolamine in Duradryl has a major potential interaction with Gastrointestinal Obstruction.

Anticholinergics are contraindicated in patients with obstructive diseases such as achalasia, esophageal stricture or stenosis, pyloroduodenal stenosis, stenosing peptic ulcer, pyloric obstruction, and paralytic ileus. Anticholinergics may further suppress intestinal motility with resultant precipitation or aggravation of toxic megacolon.

The chlorpheniramine in Duradryl has a moderate potential interaction with Gastrointestinal Obstruction.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

The methscopolamine in Duradryl has a moderate potential interaction with GERD.

Antimuscarinic agents decrease gastric motility and relax the lower esophageal sphincter which promotes gastric retention and can aggravate reflux. These drugs should be administered cautiously in patients with gastroesophageal reflux or hiatal hernia associated with reflux esophagitis.

The methscopolamine in Duradryl has a major potential interaction with Glaucoma/Intraocular Hypertension.

Anticholinergic agents are contraindicated in patients with primary glaucoma, a tendency toward glaucoma (narrow anterior chamber angle), or adhesions (synechiae) between the iris and lens, as well as for the elderly and others in whom undiagnosed glaucoma or excessive pressure in the eye may be present. Because anticholinergics cause mydriasis, they may exacerbate these conditions.

The chlorpheniramine in Duradryl has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

The phenylephrine in Duradryl has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

Sympathomimetic agents can induce transient mydriasis via stimulation of alpha-1 adrenergic receptors. In patients with anatomically narrow angles or narrow-angle glaucoma, pupillary dilation can provoke an acute attack. In patients with other forms of glaucoma, mydriasis may occasionally increase intraocular pressure. Therapy with sympathomimetic agents should be administered cautiously in patients with or predisposed to glaucoma, particularly narrow-angle glaucoma.

Digoxin has a moderate potential interaction with Heart Attack.

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

Digoxin has a major potential interaction with Heart Block.

Digoxin slows sinoatrial and AV conduction, 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.

Digoxin has a major potential interaction with Hemodialysis.

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.

The methscopolamine in Duradryl has a minor potential interaction with High Blood Pressure.

Cardiovascular effects of anticholinergics may exacerbate hypertension. Therapy with anticholinergic agents should be administered cautiously in patients with hypertension.

Digoxin has a major potential interaction with Hyperaldosteronism.

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.

Digoxin has a major potential interaction with Hypercalcemia.

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.

The phenylephrine in Duradryl has a major potential interaction with Hyperthyroidism.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

Digoxin has a moderate potential interaction with Hyperthyroidism.

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.

The chlorpheniramine in Duradryl has a moderate potential interaction with Hyperthyroidism.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

The methscopolamine in Duradryl has a minor potential interaction with Hyperthyroidism.

In general, agents with anticholinergic activity may exacerbate hyperthyroidism. Therapy with anticholinergics should be administered cautiously in patients with hyperthyroidism. Thyroid levels should be monitored if usage is prolonged.

Digoxin has a major potential interaction with Hypocalcemia.

Hypocalcemia can nullify the effects of digoxin. The drug may be ineffective in hypocalcemic patients until serum calcium levels are restored to normal. Restore serum calcium levels prior to initiating therapy with digoxin to obtain maximum results when using digoxin.

Digoxin has a major potential interaction with Hypokalemia.

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.

The chlorpheniramine in Duradryl has a moderate potential interaction with Hypotension.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

The methscopolamine in Duradryl has a major potential interaction with Infectious Gastroenteritis.

The use of drugs with antiperistaltic activity (primarily antidiarrheal and antimuscarinic agents, but also antispasmodic agents such as dicyclomine or oxybutynin at high dosages) is contraindicated in patients with diarrhea due to pseudomembranous enterocolitis or enterotoxin-producing bacteria. These drugs may prolong and/or worsen diarrhea associated with organisms that invade the intestinal mucosa, such as toxigenic E. coli, Salmonella and Shigella, and pseudomembranous colitis due to broad-spectrum antibiotics. Other symptoms and complications such as fever, shedding of organisms and extraintestinal illness may also be increased or prolonged. In general, because antiperistaltic agents decrease gastrointestinal motility, they may delay the excretion of infective gastroenteric organisms or toxins and should be used cautiously in patients with any infectious diarrhea, particularly if accompanied by high fever or pus or blood in the stool. Some cough and cold and other combination products may occasionally include antimuscarinic agents for their drying effects and may, therefore, require careful selection when necessary.

The methscopolamine in Duradryl has a moderate potential interaction with Ischemic Heart Disease.

Antimuscarinic agents block vagal inhibition of the SA nodal pacemaker. These agents should be administered cautiously in patients with tachycardia, congestive heart failure, or coronary artery disease. Premature ventricular depolarization or ventricular tachycardia or fibrillation associated with antimuscarinic drugs is rare.

The chlorpheniramine in Duradryl has a moderate potential interaction with Liver Disease.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

Digoxin has a major potential interaction with Magnesium Imbalance.

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.

Digoxin has a major potential interaction with Malnourishment.

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.

The methscopolamine in Duradryl has a major potential interaction with Myasthenia Gravis.

Because antimuscarinic agents have anticholinergic effects, they are contraindicated in patients with myasthenia gravis. Their use may be appropriate to reduce adverse muscarinic effects caused by an anticholinesterase agent.

The phenylephrine in Duradryl has a major potential interaction with Pheochromocytoma.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

Digoxin has a major potential interaction with Preexcitation Syndrome.

Digoxin may enhance accessory pathway conduction in conditions such as the Wolff-Parkinson-White syndrome. Patients with Wolf-Parkinson-White syndrome that presents atrial fibrillation are at higher risk for ventricular fibrillation. Treatment with digoxin should be used with caution in these patients.

The phenylephrine in Duradryl has a moderate potential interaction with Prostate Tumor, Benign.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

Digoxin has a major potential interaction with Renal Dysfunction.

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 chlorpheniramine in Duradryl has a moderate potential interaction with Renal Dysfunction.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

Digoxin has a major potential interaction with Sinus Node Dysfunction.

Digoxin slows sinoatrial and AV conduction, 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.

The methscopolamine in Duradryl has a moderate potential interaction with Ulcerative Colitis.

Antimuscarinic agents may suppress intestinal motility and produce paralytic ileus with resultant precipitation of toxic megacolon. These drugs should be administered cautiously to patients with ulcerative colitis.

Digoxin has a moderate potential interaction with Underactive Thyroid.

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 thyroid condition.

The methscopolamine in Duradryl has a major potential interaction with Urinary Retention.

In general, the use of anticholinergic agents is contraindicated in patients with urinary retention and bladder neck obstruction caused by prostatic hypertrophy. Dysuria may occur and may require catheterization. Also, anticholinergic drugs may aggravate partial obstructive uropathy. Caution is advised even when using agents with mild to moderate anticholinergic activity, particularly in elderly patients.

The chlorpheniramine in Duradryl has a moderate potential interaction with Urinary Retention.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

Digoxin has a major potential interaction with Ventricular Arrhythmia.

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 administered cautiously in patients with frequent ventricular premature contractions or ventricular tachycardia, especially if these arrhythmias are not caused by heart failure.

Digoxin has a moderate potential interaction with Vitamin B1 Deficiency.

Patients with beri beri heart disease may fail to respond adequately to digoxin if the underlying thiamine deficiency is not treated concomitantly.

Digoxin has a major potential interaction with Vomiting.

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.