Can you take Bitolterol with Disopyramide?

Disopyramide has a major potential interaction with Cardiogenic Shock.

The use of disopyramide is contraindicated in patients with cardiogenic shock, second- or third-degree AV block in the absence of a functional artificial pacemaker, or congenital QT prolongation. Therapy with disopyramide should be administered with extreme caution in patients with sick sinus syndrome (bradycardia-tachycardia), Wolff-Parkinson White syndrome, or bundle-branch block. The effect of disopyramide in these conditions has not been determined.

Bitolterol has a moderate potential interaction with Diabetes Mellitus.

Adrenergic bronchodilators 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. Large doses of IV albuterol (not commercially available in the U.S.) and terbutaline sulfate have been reported to cause exacerbation of preexisting diabetes mellitus and ketoacidosis. Therapy with adrenergic bronchodilators should be administered cautiously in patients with diabetes mellitus. Closer monitoring of blood glucose concentrations may be appropriate. Systemic adverse effects are minimized, but not abolished, by administration of these agents via oral inhalation.

Disopyramide has a moderate potential interaction with Diabetes Mellitus.

Rare cases of hypoglycemia have been reported during administration of disopyramide. Therapy with disopyramide should be administered cautiously in patients with diabetes mellitus or other conditions that alter normal glucoregulatory mechanisms such as chronic malnutrition, congestive heart failure, renal or hepatic dysfunction, or drugs (beta blockers).

Disopyramide has a major potential interaction with Glaucoma/Intraocular Hypertension.

Disopyramide has anticholinergic activity, and therapy with disopyramide should be administered with extreme caution in patients who may be adversely affected by this. Disopyramide should not be used in patients with glaucoma, myasthenia gravis, or urinary retention unless adequate overriding measures are taken.

Disopyramide has a major potential interaction with Heart Block.

The use of disopyramide is contraindicated in patients with cardiogenic shock, second- or third-degree AV block in the absence of a functional artificial pacemaker, or congenital QT prolongation. Therapy with disopyramide should be administered with extreme caution in patients with sick sinus syndrome (bradycardia-tachycardia), Wolff-Parkinson White syndrome, or bundle-branch block. The effect of disopyramide in these conditions has not been determined.

Bitolterol has a moderate potential interaction with Heart Disease.

Adrenergic bronchodilators can stimulate cardiovascular beta- 1 and beta- 2 receptors, resulting in adverse effects such as tachycardia, palpitation, peripheral vasodilation, blood pressure changes, and ECG changes (e.g., flattening of the T wave; prolongation of the QT interval; ST segment depression). Direct stimulation of cardiac tissues is mediated by beta- 1 receptors and thus less likely to occur with beta-2-selective agents such as albuterol. However, beta-2-selectivity is not absolute and can be lost with larger doses. High dosages of these agents have been associated with precipitation or aggravation of angina, myocardial ischemia, and cardiac arrhythmias. Therapy with adrenergic bronchodilators should be administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, and/or underlying cardiovascular disorders such as coronary insufficiency, cardiac arrhythmias, or hypertension. The recommended dosages should not be exceeded.

Disopyramide 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.

Bitolterol has a moderate potential interaction with High Blood Pressure.

Adrenergic bronchodilators can stimulate cardiovascular beta- 1 and beta- 2 receptors, resulting in adverse effects such as tachycardia, palpitation, peripheral vasodilation, blood pressure changes, and ECG changes (e.g., flattening of the T wave; prolongation of the QT interval; ST segment depression). Direct stimulation of cardiac tissues is mediated by beta- 1 receptors and thus less likely to occur with beta-2-selective agents such as albuterol. However, beta-2-selectivity is not absolute and can be lost with larger doses. High dosages of these agents have been associated with precipitation or aggravation of angina, myocardial ischemia, and cardiac arrhythmias. Therapy with adrenergic bronchodilators should be administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, and/or underlying cardiovascular disorders such as coronary insufficiency, cardiac arrhythmias, or hypertension. The recommended dosages should not be exceeded.

Disopyramide 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.

Bitolterol has a moderate potential interaction with Hyperthyroidism.

Adrenergic bronchodilators can stimulate cardiovascular beta- 1 and beta- 2 receptors, resulting in adverse effects such as tachycardia, palpitation, peripheral vasodilation, blood pressure changes, and ECG changes (e.g., flattening of the T wave; prolongation of the QT interval; ST segment depression). Direct stimulation of cardiac tissues is mediated by beta- 1 receptors and thus less likely to occur with beta-2-selective agents such as albuterol. However, beta-2-selectivity is not absolute and can be lost with larger doses. High dosages of these agents have been associated with precipitation or aggravation of angina, myocardial ischemia, and cardiac arrhythmias. Therapy with adrenergic bronchodilators should be administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, and/or underlying cardiovascular disorders such as coronary insufficiency, cardiac arrhythmias, or hypertension. The recommended dosages should not be exceeded.

Bitolterol has a moderate potential interaction with Hypokalemia.

Adrenergic bronchodilators may cause decreases in serum potassium concentrations, primarily when given by nebulization or intravenous administration. Although this effect is usually transient and does not require supplementation, clinically significant hypokalemia may occur in some patients, with the potential to induce cardiovascular adverse effects. The relevance of these observations to oral or oral aerosol/powder for inhalation therapy is unknown. Therapy with adrenergic bronchodilators should be administered cautiously in patients with or predisposed to hypokalemia.

Disopyramide 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.

Disopyramide 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.

Disopyramide has a moderate potential interaction with Liver Disease.

Disopyramide is partially metabolized by the liver. The plasma half-life of disopyramide is prolonged in patients with hepatic dysfunction. Therapy with disopyramide should be administered cautiously and dosages reduced in patients with compromised hepatic function. Clinical monitoring of cardiac function (ECG) and hepatic function is recommended.

Disopyramide has a major potential interaction with Long QT Syndrome.

The use of disopyramide is contraindicated in patients with cardiogenic shock, second- or third-degree AV block in the absence of a functional artificial pacemaker, or congenital QT prolongation. Therapy with disopyramide should be administered with extreme caution in patients with sick sinus syndrome (bradycardia-tachycardia), Wolff-Parkinson White syndrome, or bundle-branch block. The effect of disopyramide in these conditions has not been determined.

Disopyramide 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.

Disopyramide has a major potential interaction with Myasthenia Gravis.

Disopyramide has anticholinergic activity, and therapy with disopyramide should be administered with extreme caution in patients who may be adversely affected by this. Disopyramide should not be used in patients with glaucoma, myasthenia gravis, or urinary retention unless adequate overriding measures are taken.

Disopyramide has a moderate potential interaction with Renal Dysfunction.

Disopyramide is primarily eliminated by the kidney. Approximately 50% of disopyramide is excreted in the urine as unchanged drug. The serum concentration of disopyramide is increased and the elimination half-life is prolonged in patients with renal impairment. Patients with renal impairment may be at increased risk of disopyramide-associated toxicity such as hypotension, conduction disturbances, or worsening of congestive heart failure. Therapy with disopyramide should be administered cautiously and dosage and/or frequency of administration modified in patients with compromised renal function. Clinical monitoring of cardiac function (ECG) and renal function is recommended.

Bitolterol has a moderate potential interaction with Seizures.

Adrenergic bronchodilators may cause CNS stimulation. Therapy with adrenergic bronchodilators should be administered cautiously in patients with seizure disorders. Systemic adverse effects are minimized, but not abolished, by administration of these agents via oral inhalation.

Disopyramide has a major potential interaction with Urinary Retention.

Disopyramide has anticholinergic activity, and therapy with disopyramide should be administered with extreme caution in patients who may be adversely affected by this. Disopyramide should not be used in patients with glaucoma, myasthenia gravis, or urinary retention unless adequate overriding measures are taken.