Lidocaine Propranolol

Cimetidine Lidocaine, propranolol, verapamil, imipramine Increased absorption... 

The cardiac arrhythmias are life-threatening, so the patient must be closely monitored, with facilities available for possible resuscitation. Drugs such as quinidine and procainamide are contraindicated, but lidocaine, propranolol, or phenytoin has been used safely and effectively. The arterial blood gas levels, pH, and electrolyte concentrations should be monitored so that metabolic acidosis or hypokalemia can be identified that would further aggravate the arrhythmias. Electrical pacing may be required if the antiarrhythmic drugs fail. Hyperpyrexia is treated by cooling. Seizures may be managed by intravenous doses of diazepam. 

A study in 6 healthy subjects receiving 30-hour infusions of lidocaine at a rate of 2 mg/minute found that pretreatment with propranolol 80 mg every 8 hours for 3 days raised the steady-state plasma lidocaine levels by 19% (from 2.1 to 2.5 micrograms/mL) and reduced the plasma clearance by 16%. Other similar studies have found a 22.5 to 30% increase in steady-state serum lidocaine levels and a 14.7 to 46% fall in plasma clearance due to the concurrent use of propranolol. Two cases of lidocaine toxicity attributed to a lidocaine-propranolol interaction were revealed by a search of the FDA adverse drug reaction file in 1981. A further case of lidocaine toxicity (seizures) has been described in a man on propranolol after accidental oral ingestion of lidocaine for oesophageal anaesthesia. High serum levels of lidocaine were detected. ... 

The lidocaine/propranolol interaction is established and of clinical importance. Monitor the effects of concurrent use and reduce the intravenous lidocaine dosage if necessary to avoid toxicity. The situation with other... 

Graham CF, Turner WM, Jones JK. Lidocaine-propranolol interactions. NEnglJMed(1981) 304,1301. 

The agent of choice for the treatment of ventricular arrhythmias and those associated with myocardial infarctions is lidocaine. Propranolol is also effective in some similar cases despite the potential hazards associated with e-blockade ... 

Propranolol may increase procainamide plasma levels. Additive cholinergic effects may occur when procainamide is administered with other drugp with anticholinergic effects. There is the potential of additive cardiodepressant effects when procainamide is administered with lidocaine. When a beta blocker, such as Inderal, is administered with lidocaine, there is an increased risk of lidocaine toxicity. 

The BBB also has sodium- and pH-independent transporters of organic cations. They are important for the homeostasis of choline and thiamine in the brain and for the permeation of cationic drugs like propranolol, lidocaine, fentanyl, Hl-an-... 

Smoking cessation, with or without nicotine substitutes, may alter response to concomitant medication in ex-smokers. Smoking may affect alcohol, benzodiazepines, beta-adrenergic blockers, caffeine, clozapine, fluvoxamine, olanzapine, tacrine, theophylline, clorazepate, lidocaine (oral), estradiol, flecanide, imipramine, heparin, insulin, mexiletine, opioids, propranolol, catecholamines, and cortisol. 

Concurrent administration of propafenone with digoxin, warfarin, propranolol, or metoprolol increases the serum concentrations of the latter four drugs. Cimetidine slightly increases the propafenone serum concentrations. Additive pharmacological effects can occur when lidocaine, procainamide, and quinidine are combined with propafenone. 

Omeprazole can inhibit the metabolism of drugs metabolised mainly by the cytochrome P-450 enzyme subfamily 2C (diazepam, phenytoin), but not of those metabolished by subfamilies lA (caffeine, theophylline), 2D (metoprolol, propranolol), and 3A (ciclosporin, lidocaine (lignocaine), quinidine). Since relatively few drugs are metabolised mainly by 2C compared with 2D and 3A, the potential for omeprazole to interfere with the metabolism of other drugs appears to be limited, but the half lives of diazepam and phenytoin are prolonged as much as by cimetidine. 

In patients with heart failure, lidocaine s volume of distribution and total body clearance may both be decreased. Thus, both loading and maintenance doses should be decreased. Since these effects counterbalance each other, the half-life may not be increased as much as predicted from clearance changes alone. In patients with liver disease, plasma clearance is markedly reduced and the volume of distribution is often increased the elimination half-life in such cases may be increased threefold or more. In liver disease, the maintenance dose should be decreased, but usual loading doses can be given. Elimination half-life determines the time to steady state. Thus, although steady-state concentrations may be achieved in 8-10 hours in normal patients and patients with heart failure, 24-36 hours may be required in those with liver disease. Drugs that decrease liver blood flow (eg, propranolol, cimetidine) reduce lidocaine clearance and so increase the risk of toxicity unless infusion rates are decreased. With infusions lasting more than 24 hours, clearance falls and plasma concentrations rise. Renal disease has no major effect on lidocaine disposition. 

Alpharacid glycoprotein exists in concentrations that are 50 to 100 times lower than those of albumin. Basic drugs (quinidine, imipramine, propranolol, and lidocaine) bind to the single site present on alpharacid glycoprotein. 

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