Interactions between Midodrine and Quin-G

Midodrine has a major potential interaction with Diabetes Mellitus.

Midodrine can cause marked elevation of supine blood pressure (BP>200 mmHg systolic) and should not be used in patients with persistent and excessive supine hypertension. Systolic elevations of this degree are most likely to be observed in patients with relatively elevated pre-treatment systolic blood pressures (mean 170 mmHg). There is no experience in patients with initial supine systolic pressure above 180 mmHg, as those patients were excluded from the clinical trials. Use of midodrine in such patients is not recommended. Additionally, care should be taken when using this agent in orthostatic hypotensive patients who are also diabetic. Supine and sitting hypertension should be evaluated at the beginning of therapy, and blood pressure (supine, sitting, and orthostatic) should be monitored regularly.

The quiNIDine in Quin-G has a major potential interaction with Glaucoma/Intraocular Hypertension.

The use of quinidine is contraindicated in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as myasthenia gravis, glaucoma, and urinary retention or obstruction.

The quiNIDine in Quin-G has a major potential interaction with Heart Block.

The use of quinidine is contraindicated for use in patients without a functioning artificial pacemaker whose cardiac rhythm is dependent upon a junctional or idioventricular pacemaker, including patients with complete AV block. Therapy with quinidine should be administered with caution in patients with severe sinus-node dysfunction such as sick sinus syndrome, bradycardia-tachycardia syndrome, or second- or third-degree heart block.

Midodrine has a major potential interaction with Heart Disease.

The use of midodrine is contraindicated in patients with severe organic heart disease, pheochromocytoma, or thyrotoxicosis.

The quiNIDine in Quin-G 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.

Midodrine has a major potential interaction with High Blood Pressure.

Midodrine can cause marked elevation of supine blood pressure (BP>200 mmHg systolic) and should not be used in patients with persistent and excessive supine hypertension. Systolic elevations of this degree are most likely to be observed in patients with relatively elevated pre-treatment systolic blood pressures (mean 170 mmHg). There is no experience in patients with initial supine systolic pressure above 180 mmHg, as those patients were excluded from the clinical trials. Use of midodrine in such patients is not recommended. Additionally, care should be taken when using this agent in orthostatic hypotensive patients who are also diabetic. Supine and sitting hypertension should be evaluated at the beginning of therapy, and blood pressure (supine, sitting, and orthostatic) should be monitored regularly.

The quiNIDine in Quin-G 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 quiNIDine in Quin-G 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 quiNIDine in Quin-G 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.

Midodrine has a moderate potential interaction with Liver Disease.

Midodrine, a prodrug, undergoes bioactivation in a variety of tissues to desglymidodrine, an alpha-1 agonist. The liver functions in the metabolism of midodrine and desglymidodrine. The pharmacokinetic disposition of midodrine has not been studied in patients with hepatic impairment. Therapy with midodrine should be administered cautiously in patients with compromised hepatic function. Clinical monitoring of hepatic function prior to initiation of therapy.

The quiNIDine in Quin-G has a moderate potential interaction with Liver Disease.

Quinidine is primarily metabolized by the liver to active and inactive forms. Hepatic dysfunction causes a slowed metabolism and elimination of the drug which can lead to quinidine toxicity if dosage is not appropriately reduced. Clinical monitoring of hepatic function is recommended.

The quiNIDine in Quin-G 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.

The quiNIDine in Quin-G has a major potential interaction with Myasthenia Gravis.

The use of quinidine is contraindicated in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as myasthenia gravis, glaucoma, and urinary retention or obstruction.

Midodrine has a major potential interaction with Pheochromocytoma.

The use of midodrine is contraindicated in patients with severe organic heart disease, pheochromocytoma, or thyrotoxicosis.

Midodrine has a major potential interaction with Renal Dysfunction.

The use of midodrine is contraindicated in patients with acute renal disease or urinary retention/obstruction disorder. Midodrine is primarily eliminated by the kidney as desglymidodrine (active metabolite). The serum concentration of midodrine is expected to be increased in patients with renal impairment. Desglymidodrine induces urinary retention by increasing bladder neck tone. Therapy with midodrine should be administered cautiously and initiated at 2.5 mg doses in patients with compromised renal function. Clinical monitoring of renal function prior to initiation of therapy and subsequently as appropriate and blood pressure (supine, sitting, and orthostatic) is recommended. Midodrine is removed by dialysis.

The quiNIDine in Quin-G has a moderate potential interaction with Renal Dysfunction.

Renal dysfunction causes a slowed elimination of quinidine which can lead to quinidine toxicity if dosage is not appropriately reduced. Therapy with quinidine should be administered cautiously and dosages reduced in patients with compromised renal function. Quinidine is not appreciably removed by hemodialysis.

Midodrine has a major potential interaction with Thyrotoxicosis.

The use of midodrine is contraindicated in patients with severe organic heart disease, pheochromocytoma, or thyrotoxicosis.

Midodrine has a major potential interaction with Urinary Retention.

The use of midodrine is contraindicated in patients with acute renal disease or urinary retention/obstruction disorder. Midodrine is primarily eliminated by the kidney as desglymidodrine (active metabolite). The serum concentration of midodrine is expected to be increased in patients with renal impairment. Desglymidodrine induces urinary retention by increasing bladder neck tone. Therapy with midodrine should be administered cautiously and initiated at 2.5 mg doses in patients with compromised renal function. Clinical monitoring of renal function prior to initiation of therapy and subsequently as appropriate and blood pressure (supine, sitting, and orthostatic) is recommended. Midodrine is removed by dialysis.

The quiNIDine in Quin-G has a major potential interaction with Urinary Retention.

The use of quinidine is contraindicated in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as myasthenia gravis, glaucoma, and urinary retention or obstruction.