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Arrhythmias antiarrhythmic drugs

Antiarrhythmic drugs are substances that affect cardiac ionic channels or receptors, thereby altering the cardiac action potential or its generation or propagation. This results in changes of the spread of activation or the pattern of repolarization. Thereby, these drugs suppress cardiac arrhythmia. [Pg.96]

An arrhythmia may occur as a result of heart disease or from a disorder that affects cardiovascular function. Conditions such as emotional stress, hypoxia, and electrolyte imbalance also may trigger an arrhythmia An electrocardiogram (ECG) provides a record of the electrical activity of the heart. Careful interpretation of the ECG along with a thorough physical assessment is necessary to determine the cause and type of arrhythmia The goal of antiarrhythmic drug therapy is to restore normal cardiac function and to prevent life-threatening arrhythmias. [Pg.367]

The uses of the antiarrhythmic drug are given in the Summaiy Drug Table Antiarrhythmic Drug3. In general these drugp are used to prevent and treat cardiac arrhythmias, such as premature ventricular contractions (PVCs), ventricular tachycardia (VT), premature atrial contractions (PACs), paroxysmal atrial tachycardia (PAT), atrial fibrillation, and atrial flutter. Some of the antiarrhythmic dru are used for other... [Pg.370]

Antiarrhythmic drugs are capable of causng new arrhythmias as well as an exacerbation of existing arrhythmias. The nurse must report any new arrhythmia or exacerbation of an existing arrhythmia to the primary health care provider immediatety. [Pg.376]

Andreoli TE Ion transport disorders introductory comments. Am J Med 1998 104 85. (First of a series of articles on ion transport disorders published between January and August, 1998. Topics covered were structure and function of ion channels, arrhythmias and antiarrhythmic drugs, Liddle syndrome, cholera, malignant hyperthermia, cystic fibrosis, the periodic paralyses and Bartter syndrome, and Gittelman syndrome.)... [Pg.578]

They are used for arrhythmias associated with nervous stress, myocardial infarction, and thyrotoxicosis accompanied by elevated adrenergic activity. Moreover, many antiarrhythmic drugs themselves can cause arrhythmia, especially in patients with ischemic heart disease. The examined 8-adrenergic receptor blockers are an exception. Having said that, practically all )3-adrenergic receptor blockers can be used as antiarrhythmics. [Pg.251]

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. [Pg.418]

The applicability of these results to other populations (eg, those without recent Mis) is uncertain. Considering the known proarrhythmic properties of procainamide and the lack of evidence of improved survival for any antiarrhythmic drug in patients without life-threatening arrhythmias, the use of procainamide and other antiarrhythmic agents should be reserved for patients with life-threatening ventricular arrhythmias. [Pg.427]

Survival Antiarrhythmic drugs have not been shown to enhance survival in patients with ventricular arrhythmias. [Pg.439]

When starting amiodarone therapy, attempt to gradually discontinue prior antiarrhythmic drugs. When adequate arrhythmia control is achieved, or if side... [Pg.465]

A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. The antiarrhythmics versus implantable defibrillators (AVID) investigators. NEnglJMed. Nov 27 1997 337(22) 1576-1583. [Pg.47]

Ideally, if symptomatic sinus node dysfunction occurs in the presence of drugs known to impair sinus node function, the first treatment is to discontinue the offending drug [29]. However, this is typically not feasible in patients with heart failure who are dependent on several medications to improve long-term outcomes, or may need antiarrhythmic drug therapy for symptomatic arrhythmias. Accordingly, the treatment usually becomes a question of whether to apply pacing to increase heart rate. This is further complicated by the appropriate pacemaker prescription once the decision to pace has been made. [Pg.51]

Antiarrhythmic drugs are used with the aim to prevent or suppress those conditions of cardiac arrhythmias which are considered harmful or dangerous. [Pg.339]

Task Force of the Working Group on Arrhythmias of the European Society of Cardiology. The Sicilian gambit. A new approach to the classification of antiarrhythmic drugs based on their actions on arrhythmogenic mechanisms. Circulation 1991 84 1831-51. [Pg.606]

It is estimated that 80 to 90% of clinical arrhythmias have a reentry mechanism. One explanation of how an antiarrhythmic agent may abolish reentry is by converting unidirectional block to bidirectional block. A second mechanism to explain the action of antiarrhythmic drugs is that they can prevent reentry by increasing the ERP of the cardiac hbers within or surrounding the region of the reentrant circuit. [Pg.169]

Procainamide (Pwnestyl, Procan SR) is a derivative of the local anesthetic agent procaine. Procainamide has a longer half-life, does not cause CNS toxicity at therapeutic plasma concentrations, and is effective orally. Procainamide is a particularly useful antiarrhythmic drug, effective in the treatment of supraventricular, ventricular, and digitalis-induced arrhythmias. [Pg.173]

As with other antiarrhythmic drugs, moricizine has proarrhythmic activity, which may manifest as new ventricular ectopic beats or a worsening of preexisting ventricular arrhythmias. These effects are most common in patients with depressed left ventricular function and a history of congestive heart failure. Cardiovascular ef-... [Pg.176]

Amiodarone may elicit life-threatening side effects in addition to presenting substantial management difh-culties associated with its use. The oral formulation of amiodarone is indicated only for the treatment of life-threatening recurrent ventricular arrhythmias (e.g., recurrent ventricular hbrillation and/or recurrent hemo-dynamicaUy unstable ventricular tachycardia) that have not responded to other potentially effective antiarrhythmic drugs or when alternative interventions could not be tolerated. Despite its efficacy as an antiarrhythmic agent, there is no evidence from clinical trials that the use of amiodarone favorably affects survival. [Pg.187]

I. ink MS et al. Antiarrhythmic drug therapy for ventricular arrhythmias Current perspectives. J Cardiovasc Electrophys 1996 7 653-670. [Pg.194]

Cardiac arrhythmias are a common problem in clinical practice, occurring in up to 25% of patients treated with digitalis, 50% of anesthetized patients, and over 80% of patients with acute myocardial infarction. Arrhythmias may require treatment because rhythms that are too rapid, too slow, or asynchronous can reduce cardiac output. Some arrhythmias can precipitate more serious or even lethal rhythm disturbances for example, early premature ventricular depolarizations can precipitate ventricular fibrillation. In such patients, antiarrhythmic drugs may be lifesaving. On the other hand, the hazards of antiarrhythmic drugs—and in particular the fact that they can precipitate lethal arrhythmias in some patients—has led to a reevaluation of their relative risks and benefits. In general, treatment of asymptomatic or minimally symptomatic arrhythmias should be avoided for this reason. [Pg.271]


See other pages where Arrhythmias antiarrhythmic drugs is mentioned: [Pg.578]    [Pg.578]    [Pg.163]    [Pg.102]    [Pg.996]    [Pg.367]    [Pg.370]    [Pg.370]    [Pg.375]    [Pg.376]    [Pg.125]    [Pg.495]    [Pg.745]    [Pg.55]    [Pg.245]    [Pg.245]    [Pg.246]    [Pg.252]    [Pg.433]    [Pg.443]    [Pg.447]    [Pg.128]    [Pg.341]    [Pg.599]    [Pg.600]    [Pg.605]    [Pg.160]   
See also in sourсe #XX -- [ Pg.325 , Pg.326 , Pg.327 , Pg.328 ]




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