Adenosine/lidocaine/magnesium sulfate Disease Interactions

The use of adenosine is contraindicated in patients with second- or third-degree AV block, sick sinus syndrome, or symptomatic bradycardia in the absence of a functional artificial pacemaker.

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.

Antiepileptic drugs can increase depression and suicidal thoughts or behaviors in patients receiving these drugs for any indication. Patients should be monitored for the emergence or worsening of depression, suicidal thoughts and unusual changes in mood or behavior. Caregivers and family should be alert for the emergence or worsening of symptoms. Behaviors of concern should be reported immediately to the healthcare providers.

The use of laxatives is contraindicated in patients with inflammatory bowel disease. Patients with inflammatory bowel disease may experience colonic perforation with use of stimulant laxatives.

The use of laxatives is contraindicated in patients with intestinal obstruction disorders. Patients with intestinal obstruction disorders may need their underlying condition treated to correct the constipation. Some laxatives require reduction in the colon to their active form to be effective which may be a problem in patients with intestinal obstruction.

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 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.

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.

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 parenteral administration of magnesium is contraindicated in patients with heart block or heart damage from myocardial infarction. These conditions may be exacerbated during magnesium infusion. High serum levels of magnesium (> 4.5 mEq/L) can cause sinus bradycardia, AV block, nodal rhythms, and bundle branch block, which can progress to asystole and cardiac arrest at magnesium levels of approximately 14 mEq/L to 15 mEq/L. If parenteral magnesium is used in patients with preexisting conduction disturbances, it should be infused at a slower rate, and cardiac function and serum magnesium level should be closely monitored. The usual precautionary measures should be observed to prevent hypermagnesemia, and IV calcium salts (e.g., calcium gluconate), pressors, cardiac pacemakers, and equipment for supportive care should be immediately available in case of acute magnesium intoxication.

Magnesium is eliminated by the kidney. The serum concentration of magnesium is increased in patients with renal impairment. Magnesium toxicity includes CNS depression, muscular paralysis, respiratory depression, hypotension and prolonged cardiac conduction time. Disappearance of the patellar reflex is a useful clinical sign of magnesium intoxication. Therapy with magnesium should be administered cautiously and dosages should be modified in patients with compromised renal function. Clinical monitoring of serum magnesium levels is recommended.

The use of magnesium sulfate is contraindicated in patients with myasthenia gravis as it can precipitate a myasthenic crisis. Myasthenic crisis is a life-threatening condition characterized by neuromuscular respiratory failure. Symptoms of myasthenic crisis may include difficulty swallowing, ptosis, facial droop, weakness and/or difficulty breathing that may require intubation.

Adenosine induces mast cell degranulation and histamine release. Bronchoconstriction has been reported in patients with asthma during therapy with adenosine. Therapy with adenosine should be administered cautiously in patients with obstructive lung disease not associated with bronchoconstriction (emphysema or bronchitis) and should be avoided in patients with bronchoconstriction or bronchospasm (asthma).

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 use of osmotic laxatives preparations, containing sodium sulfate, potassium sulfate, and magnesium sulfate may cause cardiac arrhythmias. There have been rare reports of serious arrhythmias associated with the use of ionic osmotic laxative products for bowel preparation. Patients with electrolyte abnormalities should have them corrected before treatment is initiated. Use caution when prescribing preparations in patients at increased risk of arrhythmias or with a history of seizures. It is recommended to conduct a pre-dose and post-colonoscopy ECGs in patients at increased risk of serious cardiac arrhythmias.