Antiarrhythmic drugs arrhythmias caused

Explain how hyperkalemia hypokalemia or an antiarrhythmic drug can cause an arrhythmia. 

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. 

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. 

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. 

Proarrhythmic effects Antiarrhythmic agents may cause new or worsened arrhythmias. It is essential that each patient be evaluated electrocardiographically and clinically prior to and during therapy to determine whether the response to the drug supports continued treatment. ... 

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. 

As noted above, the antiarrhythmic drugs can modify impulse generation and conduction. More than a dozen such drugs that are potentially useful in treating arrhythmias are currently available. However, only a limited number of these agents are clinically beneficial in the treatment of selected arrhythmias. For example, the acute termination of ventricular tachycardia by lidocaine or supraventricular tachycardia by adenosine or verapamil are examples in which antiarrhythmic therapy results in decreased morbidity. In contrast, many of the antiarrhythmic agents are now known to have lethal proarrhythmic actions, that is, to cause arrhythmias. 

Correct answer = A. A bidirectional block can decrease arrhythmias caused by reentry. All antiarrhythmic drugs exert some negative inotropic effect and decrease cardiac output. The i side effects of this group of drugs are serious and include arrhythmias that can lead to sudden death. Some antiarrhythmic drugs affect K+ or Ca++ channels, or p adrenoreceptors. 

Arrhythmias are caused by abnormal pacemaker activity or abnormal impulse propagation. Antiarrhythmic drugs are often classified according to the Vaughan-William scheme, which organizes agents based on channel or receptor involved (Table 2-1). Class I agents block sodium channels and are sometimes referred to as "local anesthetics." The... 

This is a broad category of toxic action in which exaggeration of the therapeutic effects of many drugs in overdose can lead to poisoning. For example, general anesthetics are also respiratory depressants, and too high concentrations can cause fatalities. Many antihypertensives cause potentially fatal vascular collapse and shock when taken in overdose. Overdoses of certain antiarrhythmic drugs can themselves cause fatal arrhythmias, actions that are related to their action on ion channels. 

Answer D. The symptoms described are those of cinchonism, which usually include tinnitus and, when more severe, CNS effects including hallucinations. Cinchonism is characteristic of quinidine and its optical isomer, the antimalarial drug quinine. Like most antiarrhythmic drugs, quinidine can cause cardiac arrhythmias heralded by the ECG changes described. 

Antiarrhythmic drugs that block potassium channels, such as sotalol and quinidine, can cause the polymorphic ventricular tachycardia known as torsades de pointes (see Chapter 34). The abnormal repolarization that leads to polymorphic ventricular tachycardia is potentiated by hypokalemia, and diuretics that produce potassium loss increase the risk of this drug-induced arrhythmia. 

Since the achievement of steady-state mexiletine levels depends on the extent of absorption, not on its rate, it seems very unlikely that these drugs will affect the antiarrhythmic effects of mexiletine during chronic dosing. However, these drugs may cause variations in the antiarrhythmic effects of initial oral mexiletine doses, which may be a problem if rapid control ofthe arrhythmia is essential. In general, no special precautions would appear necessary. 

In approximately 50% of cases, antiarrhythmic drugs are required in patients with ICDs to reduce the frequency of recurrent ventricular arrhythmias (199). Antiarrhythmic drugs may also be necessary to suppress atrial arrhythmias, which may interfere with proper detection and lead to inappropriate shocks (200,201). In both situations, drugs must be used judiciously because of potential drug-device interactions. Drugs can (a) slow ventricular tachycardia below the programmed rate cutoff, (b) increase energy threshold to defibril-late, (c) have an effect on pace termination of ventricular tachycardia, (d) be proarrhythmic, and (e) cause bradycardia and AV block. The process of... 

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