Can you take Isosorbide mononitrate with Lidocaine?

Isosorbide mononitrate has a major potential interaction with Anemia.

Some manufacturers and medical references consider the use of nitrates and nitrites to be contraindicated in patients with severe anemia. Nitrates and nitrites can cause methemoglobinemia, primarily in high-dose intravenous therapy or acute poisoning and in patients with NADH reductase deficiency. However, elevations of methemoglobin may also occur with commonly used dosages. While probably not of routine clinical significance, the increases may be important in certain patient populations such as those with coronary insufficiency or anemia.

Isosorbide mononitrate has a major potential interaction with Aortic Stenosis.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.

Isosorbide mononitrate has a major potential interaction with Brain Tumor.

Organic nitrates and nitrites can increase cerebrospinal fluid pressure. Therapy with these agents should be administered cautiously, if at all, in patients with or at risk for intracranial hypertension, including those with cerebral hemorrhage, intracranial lesions, or recent head trauma.

Isosorbide mononitrate has a major potential interaction with Cerebrovascular Insufficiency.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.

Isosorbide mononitrate has a major potential interaction with Constrictive Pericarditis.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.

Isosorbide mononitrate has a major potential interaction with Dehydration.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.

Isosorbide mononitrate has a minor potential interaction with Glaucoma/Intraocular Hypertension.

Some medical references state that organic nitrates and nitrites may increase intraocular pressure and should be used with caution in patients with glaucoma. However, the effect on intraocular pressure is variable and brief, and there is no evidence that these drugs precipitate narrow-angle glaucoma. Amyl nitrate typically may cause a slight rise of 3+ mm for several seconds followed by a fall in intraocular pressure for 10 to 20 minutes, the latter secondary to a fall in blood pressure. Nitroglycerin rarely produces ocular side effects, and oral nitroglycerin appears to have few to no significant ocular side effects.

Isosorbide mononitrate has a major potential interaction with Head Injury.

Organic nitrates and nitrites can increase cerebrospinal fluid pressure. Therapy with these agents should be administered cautiously, if at all, in patients with or at risk for intracranial hypertension, including those with cerebral hemorrhage, intracranial lesions, or recent head trauma.

Isosorbide mononitrate has a major potential interaction with Heart Attack.

The benefits of organic nitrates and nitrites in patients with acute myocardial infarction (AMI) or congestive heart failure have not been established and its use is not recommended in these settings. If used, it should be accompanied by careful clinical and hemodynamic monitoring to avoid the hazards of systemic hypotension and tachycardia, which in AMI can exacerbate myocardial ischemia. In general, oral or long-acting formulations of these drugs should not be used in the early management of AMI because of the difficulty in precisely controlling and rapidly terminating their hemodynamic effects should adverse reactions occur. Sublingual and other immediate- onset nitrates or nitrites should typically be avoided in suspected AMI with marked bradycardia or tachycardia, and should be used with extreme caution, if at all, in patients with right ventricular or inferior wall infarction. Rarely, sublingual nitroglycerin has produced hypotension accompanied by paradoxical bradycardia in patients with AMI and especially right ventricular infarction. The latter group of patients are also particularly dependent on adequate right ventricular preload to maintain cardiac output and can experience profound hypotension with nitrate or nitrite administration due to reduction of right ventricular preload.

Lidocaine 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.

Isosorbide mononitrate has a major potential interaction with Heart Failure.

The benefits of organic nitrates and nitrites in patients with acute myocardial infarction (AMI) or congestive heart failure have not been established and its use is not recommended in these settings. If used, it should be accompanied by careful clinical and hemodynamic monitoring to avoid the hazards of systemic hypotension and tachycardia, which in AMI can exacerbate myocardial ischemia. In general, oral or long-acting formulations of these drugs should not be used in the early management of AMI because of the difficulty in precisely controlling and rapidly terminating their hemodynamic effects should adverse reactions occur. Sublingual and other immediate- onset nitrates or nitrites should typically be avoided in suspected AMI with marked bradycardia or tachycardia, and should be used with extreme caution, if at all, in patients with right ventricular or inferior wall infarction. Rarely, sublingual nitroglycerin has produced hypotension accompanied by paradoxical bradycardia in patients with AMI and especially right ventricular infarction. The latter group of patients are also particularly dependent on adequate right ventricular preload to maintain cardiac output and can experience profound hypotension with nitrate or nitrite administration due to reduction of right ventricular preload.

Lidocaine 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.

Isosorbide mononitrate has a major potential interaction with Hemodialysis.

The combined effect of organic nitrates or nitrites with hemodialysis, which often lowers blood pressure, can cause life-threatening hypotension. Therapy with these agents should be administered cautiously in patients requiring hemodialysis. The medication should be withheld before undergoing dialysis, and hemodynamic stability should be established prior to resumption of medication following dialysis. Nitroglycerin and isosorbide dinitrate are moderately dialyzed.

Isosorbide mononitrate has a major potential interaction with Hemorrhagic Stroke.

Organic nitrates and nitrites can increase cerebrospinal fluid pressure. Therapy with these agents should be administered cautiously, if at all, in patients with or at risk for intracranial hypertension, including those with cerebral hemorrhage, intracranial lesions, or recent head trauma.

Lidocaine 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.

Isosorbide mononitrate has a moderate potential interaction with Hypertrophic Cardiomyopathy.

Organic nitrates and nitrites may aggravate the angina associated with hypertrophic cardiomyopathy and should be administered cautiously in patients with this condition.

Lidocaine 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.

Isosorbide mononitrate has a major potential interaction with Hypotension.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.

Lidocaine 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.

Lidocaine 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.

Lidocaine 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.

Isosorbide mononitrate has a major potential interaction with Pseudotumor Cerebri.

Organic nitrates and nitrites can increase cerebrospinal fluid pressure. Therapy with these agents should be administered cautiously, if at all, in patients with or at risk for intracranial hypertension, including those with cerebral hemorrhage, intracranial lesions, or recent head trauma.

Lidocaine 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.

Lidocaine 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.

Isosorbide mononitrate has a major potential interaction with Shock.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.