Therapy of Cardiac Arrhythmias

Optimal therapy of cardiac arrhythmias requires documentation, accurate diagnosis, and modification of precipitating causes, and if indicated, proper selection and use of antiarrhythmic drugs. These drugs are classified according to their effects on the action potential of cardiac cells and their presumed mechanism of action. 

Arrhythmias can be treated with the drugs discussed in this chapter and with nonpharmacologic therapies such as pacemakers, cardioversion, catheter ablation, and surgery. This chapter describes the pharmacology of drugs that suppress arrhythmias by a direct action on the cardiac cell membrane. Other modes of therapy are discussed briefly (see The Nonpharmacologic Therapy of Cardiac Arrhythmias). 

A firm arrhythmia diagnosis should be established. For example, the misuse of verapamil in patients with ventricular tachycardia mistakenly diagnosed as supraventricular tachycardia can lead to catastrophic hypotension and cardiac arrest. As increasingly sophisticated methods to characterize underlying arrhythmia mechanisms become available and are validated, it may be possible to direct certain drugs (or other therapies—see The Nonpharmacologic Therapy of Cardiac Arrhythmias) toward specific arrhythmia mechanisms. 

Hypokalemia. Hypokalemia associated with thia2ide diuretic therapy has been knpHcated in the increased incidence of cardiac arrhythmias and sudden death (82). Several large clinical trials have been conducted in which the effects of antihypertensive dmg therapy on the incidence of cardiovascular complications were studied. The antihypertensive regimen included diuretic therapy as the first dmg in a stepped care (SC) approach to lowering the blood pressure of hypertensive patients. 

Antiarrhythmic dragp are used to treat various types of cardiac arrhythmias. There are initial preadministration assessments the nurse performs before starting therapy that are the same for all antiarrhythmic drags. These assessments include ... 

Contraindications to interferon alfa therapy include hepatic decompensation, autoimmune disease, and history of cardiac arrhythmia. Caution is advised in the setting of psychiatric disease, epilepsy, thyroid disease, ischemic cardiac disease, severe renal insufficiency, and cytopenia. Alfa interferons are abortifacient in primates and should not be administered in pregnancy. Potential drug-drug interactions include increased theophylline levels and increased methadone levels. Co-administration with didanosine is not recommended because of a risk of hepatic failure, and co-administration with zidovudine may exacerbate cytopenias. 

In most cases, the reversal of symptomatic myocardiopathy has been achieved without drug toxicity (19,43). Davis and Porter (19) and Tsironi et al. (44) confirmed clinically the laboratory data of Link et al. (45) that DFO therapy reverses cardiac arrhythmias in some patients previously unresponsive to medical treatment. This may be attributed to removal of a toxic labile iron pool. They also mentioned improvement of left ventricular ejection fraction in seven of nine patients. It is important to note that oral chelators are less effective than DFO and are unable to prevent cardiac mortality in patients with established heart disease (46). 

Currently available arrhythmic drugs were developed at a time when the molecular basis of cardiac arrhythmias was not understood. Thus, therapy has been largely empiric, efficacy has been unpredictable, and serious side effects have been common. Some of variability in clinical action of antiar-rhythmic drugs can be attributed directly to variable drug disposition, through specific pathways whose activity is now well recognized to be modulated by common DNA polymorphisms. 

Ravid S, Podrid PJ, Novrit B. Safety of long-term propafenone therapy for cardiac arrhythmia—experience with 774 patients. J Electrophysiol 1987 1 580-90. 

Isoproterenol, a sympathomimetic amine with bronchodi-lating and cardiac stimulant properties, is indicated in the treatment of complete heart block, after closnre of ventricular septal defect, to prevent heart block, as maintenance therapy in AV block, as treatment of bronchospasm dnring mild acute asthma attacks, bronchospasm in chronic obstructive pulmonary disease, bronchospasm dnring mild acute asthma attacks or in chronic obstrnctive pnhnonary disease, acute asthma attacks unresponsive to inhalation therapy or control of bronchospasm dnring anesthesia, for bronchodilation, emergency treatment of cardiac arrhythmias, immediate temporary control of atropine-resistant hemodynamically significant bradycardia, and as adjnnct therapy in the treatment of shock. 

Yes. The drug is effective in the therapy of both reentrant and nonreentrant forms of cardiac arrhythmia. 

Discuss the therapeutic use of cardiac glycosides in the therapy of atrial arrhythmias. 

Members of the Sicilian Gambit (Dec 4, 2001). New approaches to antiarrhythmic therapy, part I emerging therapeutic applications of the cell biology of cardiac arrhythmias. Circulation 104(23) 2865-2873. 

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). 

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