Can you take Digoxin with Flavalta?

The EPINEPHrine in Flavalta has a moderate potential interaction with Acidosis.

Acidosis, hypoxia, and hypercapnia may reduce the effectiveness of sympathomimetic amines in raising blood pressure. These conditions should be corrected before initiating therapy with sympathomimetic amines, if possible. Monitoring the patients acid-base balance, carbon dioxide levels, and oxygen saturation is recommended.

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 EPINEPHrine in Flavalta 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.

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.

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 EPINEPHrine in Flavalta has a major potential interaction with Dehydration.

The use of sympathomimetic amines has been infrequently associated with significant hypotension especially in dehydrated patients secondary to the drug's beta-2 mediated vasodilation. Hypovolemia should be corrected, if possible, before administering sympathomimetic amines. Blood pressure and ECG should be monitored at regular intervals. Monitoring of cardiac output and pulmonary wedge pressure may also be desired.

The EPINEPHrine in Flavalta 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.

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.

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.

The lidocaine in Flavalta has a major potential interaction with Heart Block.

The use of lidocaine is contraindicated in patients with Stokes-Adam syndrome, Wolff-Parkinson White syndrome, or second- or third-degree AV block in the absence of a functional artificial pacemaker, or congenital QT prolongation.

The lidocaine in Flavalta has a major potential interaction with Heart Failure.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

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.

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 lidocaine in Flavalta has a moderate potential interaction with Hyperkalemia.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

The EPINEPHrine in Flavalta 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.

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 lidocaine in Flavalta has a moderate potential interaction with Hypokalemia.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

The lidocaine in Flavalta has a major potential interaction with Hypotension.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

The lidocaine in Flavalta has a major potential interaction with Liver Disease.

Lidocaine is rapidly and extensively metabolized by the liver. Less than 10% is eliminated unchanged in the urine. Several inactive and two active forms (MEGX and GX) have been identified. MEGX and GX exhibit antiarrhythmic and convulsant properties. GX accumulates during prolonged intravenous lidocaine infusion. The pharmacokinetic disposition of lidocaine is altered by changes in hepatic function, including hepatic blood flow. Therapy with lidocaine should be administered cautiously and dosing modifications for repeated or loading and maintenance doses may be necessary. Clinical monitoring of cardiac (continuous ECG) is required and serum metabolite concentrations and monitoring hepatic function are recommended.

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.

The lidocaine in Flavalta has a moderate potential interaction with Magnesium Imbalance.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

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 EPINEPHrine in Flavalta has a moderate potential interaction with Neurological Disorders.

Epinephrine should be administered with caution to patients with Parkinson's disease as these patients may experience psychomotor agitation or notice a temporary worsening of symptoms.

The EPINEPHrine in Flavalta has a moderate potential interaction with Parkinsonism.

Epinephrine should be administered with caution to patients with Parkinson's disease as these patients may experience psychomotor agitation or notice a temporary worsening of symptoms.

The EPINEPHrine in Flavalta 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.

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 lidocaine in Flavalta has a major potential interaction with Renal Dysfunction.

Lidocaine is primarily eliminated by the kidney. Less than 10% is eliminated unchanged in the urine. Two active metabolites (MEGX and GX) have been identified that exhibit antiarrhythmic and convulsant properties. GX accumulates during prolonged intravenous lidocaine infusion. Serum concentrations of lidocaine and the active metabolites are increased and the half-life prolonged in patients with renal impairment. Therapy with lidocaine should be administered cautiously and dosing modified for repeated or maintenance doses in patients with compromised renal function. Clinical monitoring of cardiac function (continual ECG) is required and serum metabolite concentrations and monitoring renal function are recommended.

The lidocaine in Flavalta has a major potential interaction with Seizures.

Seizures have occurred during lidocaine therapy and have been associated with the rapid administration of a large intravenous doses or accumulation of active metabolites with maintenance therapy. Therapy with lidocaine should be administered cautiously to patients with or predisposed to seizure disorders. Clinical monitoring of cardiac (continuous ECG) is required, and serum metabolite concentrations are recommended.

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.

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.

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.