Tachycardia intravenous drug dose

A man with sustained ventricular tachycardia taking high-dose intravenous procainamide 2 g every 8 hours had a 70% increase in his steady-state plasma procainamide levels, from 9.1 to 15.4 nanograms/mL, when he also took quinidine gluconate 324 mg every 8 hours. The procainamide half-life increased from 3.7 to 7.2 hours and its clearance fell from 27 to 16 L/hour. His QTc interval increased from 648 to 678 milliseconds. In another study in patients with ventricular arrhythmias, quinidine was combined with procainamide. The doses were adjusted based in part on the QT interval. The QTc interval was longer with the combination (499 milliseconds) than each drug alone (quinidine 470 milliseconds, procainamide 460 milliseconds) despite using reduced doses in the combination (mean quinidine dose reduced by 28% mean procainamide dose reduced by 32%) ... 

Salbutamol may be administered parenterally as an intravenous infusion at 3-20 pg min-1 with the dose being titrated to therapeutic effect. Side effects notably tachycardia are more common with parenteral or nebulised formulations. The drug may also be administered by the subcutaneous or intramuscular routes. Salbutamol is conjugated in the liver and excreted both in the urine as unchanged drug and metabolites, and also in the faeces. 

Cyclizine has antimuscarinic properties and is a potent anti-emetic, effective for the control of postoperative and drug-induced nausea and vomiting. It has been used to prevent motion sickness, although diphenhydramine and promethazine are more effective. It is available in oral and parenteral formulations. In contrast to many other first-generation antihistamines sedation is not marked. It is available in tablet form as the hydrochloride and in injectable form as the lactate. Because of its anticholinergic action, blurred vision and dry mouth are associated with clinical doses. When given by rapid intravenous injection tachycardia may be a problem. Meclozine is a related drug which, like cyclizine, is used primarily for motion sickness. 

Adenosine is a naturally occurring nucleoside, but at high doses the drug decreases conduction velocity, prolongs the refractory period, and decreases automaticity in the AV node. Intravenous adenosine is the drug of choice for abolishing acute supraventricular tachycardia. It has low toxicity, but causes flushing, chest pain and hypotension. Adenosine has an extremely short duration of action (about 15 seconds). 

IL-2 usually is administered intravenously, although the subcutaneous and intramuscular routes are used. The infusion can produce. severe hypotension and life-threatening cardiovascular toxicity when given at the maximally tolerated dose. Patients receiving such a do.se must be monitored closely, and facilities mu.st be available to treat them for hypotension, tachycardia, pulmonary edema, and (occasionally) delirium. The drug is rapidly cleared from the bloodstream following parenteral administration. The elimination is biphasic for an Intravenous bolus injection. The pritnary route of elimination is renal, with catabolism occurring in the renal tubules. 

A man with paroxysmal tachycardia, treated with oral procainamide 1 g every 5 hours and increasing doses of lidocaine by intravenous infusion (550 mg within 3.5 hours), became restless, noisy and delirious when given a further 250 mg intravenous dose of procainamide. The symptoms disappeared within 20 minutes of discontinuing the lidocaine. The reason is not understood but the symptoms suggest that the neurotoxic effects of the two drugs might be additive. Other studies in patients have shown that lidocaine plasma levels are unaffected by intravenous or oral procainamide. ... 

---