Ventricular tachycardia and

The amide local anaesthetic lidocaine may also be used as an antianhythmic for ventricular tachycardia and exra-systoles after injection into the blood circulation. Drugs with high lipid solubility such as bupivacaine cannot be used for these purposes because their prolonged binding to the channel may induce dysrhythmias or asystolic heart failure [3]. Systemically applied lidocaine has also been used successfully in some cases of neuropathic pain syndromes [4]. Here, electrical activity in the peripheral nervous system is reduced by used-dependent but incomplete sodium channel blockade. 

TABLE 6-10. Etiologies of Ventricular Tachycardia and Ventricular Fibrillation... 

Mexiletine is used for ventricular extrasystole and ventricular tachycardia, and ventricular fibrillation (including during the severe period of myocardial infarction). A synonym of this drug is mexitil. 

Clinical use of amiodarone is limited because of its high toxicity, which consists of cardiac block, bradycardia, cardiac insufficiency, damaged thyroid gland function, neuropathology, and increased sensitivity to light, all of which significantly limit use of amiodarona, and it is only used in therapy for extremely serious tachyarrhythmias such as reoccurring ventricular fibrillation and hemodynamic unstable ventricular tachycardia, and only under supervision of a physician in a clinical situation. Synonyms of amiodarone are cordarone, rythmarone, and others. 

Cardiovascular effects Several instances of hypotension, hypertension, pulmonary edema, and ventricular tachycardia and fibrillation have been reported in postoperative patients. 

Pharmacology Bretylium tosylate inhibits norepinephrine release by depressing adrenergic nerve terminal excitability, inducing a chemical sympathectomy-like state. Bretylium blocks the release of norepinephrine in response to neuron stimulation. Peripheral adrenergic blockade causes orthostatic hypotension but has less effect on supine blood pressure. It has a positive inotropic effect on the myocardium. Pharmacokinetics Peak plasma concentration and peak hypotensive effects are seen within 1 hour of IM administration. However, suppression of premature ventricular beats is not maximal until 6 to 9 hours after dosing, when mean plasma concentration declines to less than 50% of peak level. Antifibrillatory effects occur within minutes of an IV injection. Suppression of ventricular tachycardia and other ventricular arrhythmias develops more slowly, usually 20 minutes to 2 hours after parenteral administration. 

Gomes JA, Winters SL, Stewart D, Horowitz S, Milner M, Barreca P. A new noninvasive index to predict sustained ventricular tachycardia and sudden death in the first year after myocardial infarction based on signal-averaged electrocardiogram, radionuclide ejection fraction and Holter monitoring. J. Am. Coll. Cardiol. 1987 10 349-57. 

Ventricular tachycardia and high risk bi-ventiicular pacing... 

A patient with heart failure developed a serious abnormal heart rhythm, ventricular tachycardia, and it was decided to treat this with lig-nocaine (also known as lidocaine) by the intravenous route. He was given a loading dose designed to raise the plasma concentration to an effective 2 mg/1, and then given a constant-rate intravenous infusion aimed at maintaining that concentration. In about an hour he was observed to be tremulous and then had a brief generalized convulsion (a fit). The plasma lig-nocaine concentration was found to be 8 mg/1 (desired therapeutic range 1 - no more than 5 mg/1). 

Primary indications for the use of quinidine include (1) abolition of premature complexes that have an atrial, A-V junctional, or ventricular origin (2) restoration of normal sinus rhythm in atrial flutter and atrial fibrillation after controlling the ventricular rate with digitahs (3) maintenance of normal sinus rhythm after electrical conversion of atrial arrhythmias (4) prophylaxis against arrhythmias associated with electrical countershock (5) termination of ventricular tachycardia and (6) suppression of repetitive tachycardia associated with Wolff-Parkinson-White (WPW) syndrome. 

Ventricular tachycardia and atrial fibrillation occur occasionally. 

Cardiotoxicity may occur if ipecac syrup is not vomited (noted as hypotension, tachycardia, precordial chest pain, pulmonary congestion, dyspnea, ventricular tachycardia and fibrillation, cardiacarrest). 

Pat ients with cardiovascular disease may experience hypotension or hypertension, ventricular tachycardia and fibrillation, and pulmonary edema. 

Cardiotoxic effects occur most commonly with IV administration and appear as conduction changes (50% widening of QRS complex, frequent ventricular premature contractions, ventricular tachycardia, and complete AV block). 

Bradycardia, CHF, hypotension, bronchospasm, hypoglycemia, prolonged QT interval, torsades de pointes, ventricular tachycardia, and premature ventricular complexes may occur... 

Overdose with TCAs causes tachycardia, hypotension, prolonged EKG intervals, and fatal arrhythmias, including ventricular tachycardias and bundle branch blocks (lack of conduction of the cardiac impulse). Conduction deficits alone and in combination with hypotension account for most of the morbidity and mortality associated with TCA overdose (Baldessarini, 1996). 

It is indicated in ventricular arrhythmia, ventricular premature depolarization and paroxysmal ventricular tachycardia, supra-ventricular tachycardia and atrial arrhythmia. 

It is indicated in tachyarrhythmias associated with WPW syndrome, atrial flutter and fibrillation, paroxysmal tachyarrhythmias not responding to other agents. Ventricular tachycardia and ventricular arrhythmia refractory to other treatment. 

It is used in the treatment of ventricular tachycardia and ventricular fibrillation. 

Lidocaine is the agent of choice for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia. However, routine prophylactic use of lidocaine in this setting may actually increase total mortality, possibly by increasing the incidence of asystole, and is not the standard of care. Most physicians administer IV lidocaine only to patients with arrhythmias. 

Lidocaine Sodium channel (INa) blockade Blocks activated and inactivated channels with fast kinetics does not prolong and may shorten action potential Terminate ventricular tachycardias and prevent ventricular fibrillation after cardioversion IV first-pass hepatic metabolism reduce dose in patients with heart failure or liver disease Toxicity Neurologic symptoms... 

Vomiting is common in patients with digitalis overdose. Hyperkalemia may be caused by acute digitalis overdose or severe poisoning, whereas hypokalemia may be present in patients as a result of long-term diuretic treatment. (Digitalis does not cause hypokalemia.) A variety of cardiac rhythm disturbances may occur, including sinus bradycardia, AV block, atrial tachycardia with block, accelerated junctional rhythm, premature ventricular beats, bidirectional ventricular tachycardia, and other ventricular arrhythmias. 

Raitt, M. H., Connor, W. E., Morris, C., Kron, J., Halperin, B., Chugh, S. S., McClelland, J., Cook, J., and MacMurdy, K. (2005). Fish oil supplementation and risk of ventricular tachycardia and ventricular fibrillation in patients with implantable defibrillators A randomized controlled trial. JAMA 293, 2884-2891. 

Cerrone, M., Colombi, B., Santoro, M., di Barletta, M. R., Scelsi, M., Villani, L., Napolitano, C., and Priori, S. G. (2005). Bidirectional Ventricular Tachycardia and Fibrillation Elicited in a Knock-in Mouse Model Carrier of a Mutation in the Cardiac Ryanodine Receptor. Circ Res 96(10) e77-82. 

Jiang, D., Wang, R., Xiao, B., Kong, H., Hunt, D. J., Choi, P., Zhang, L., and Chen, S. R. (2005). Enhanced Store Overload-Induced Ca2+ Release and Channel Sensitivity to Luminal Ca2+ Activation are Common Defects of RyR2 Mutations Linked to Ventricular Tachycardia and Sudden Death. Circ Res 97(11) 1173-81. 

Exhibit Catecholamine-Induced Ventricular Tachycardia and Mild Cardiomyopathy. Proc Natl Acad Sci USA 103(32) 12179-12184. 

Class 1C. These drugs produce both a marked decrease in the rate of phase 0 depolarization and a marked slowing of cardiac conduction. They have little effect on repolarization. Class IC drugs include fle-cainide and propafenone (see Table 23-2), and appear to be best suited to treat ventricular arrhythmias such as ventricular tachycardia and PVCs. 

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