Ectopic beats

Otherwise known as extrasystoles or premature beats, ectopics are caused by an intracellular build-up of positive ions, (usually calcium) that can trigger an impulse causing depolarisation that does not originate from the SAN. The other principle mechanism is altered automaticity. This includes increased/enhanced automaticity, where another part of the conduction system below the SAN takes over as the dominant pacemaker temporarily (as discussed in Chap. 1). In contrast abnormal 

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Propafenone. Propafenone hydrochloride, an arylketone, is stmcturaHy similar to the P-adrenoceptor blocking agents. It has been in use in the former West Germany since 1977 and was introduced in the United States in 1990. Its effects may result from a combination of weak calcium channel blocking, weak nonselective -adrenoceptor blocking, and sodium channel blocking activity. Propafenone is effective in treating supraventricular tachyarrhythmias, ventricular ectopic beats, and ventricular arrhythmias. It is the most frequendy prescribed medication for ventricular arrhythmias in Europe (32). 

Headache, nausea, increased heart rate, increase in systolic blood pressure, palpitations, anginal and nonspecific chest pain Nausea, vomiting, ectopic beats, tachycardia, anginal pain, palpitations, hypotension, dyspnea Anxiety, insomnia, tenseness, restlessness, headache, light-headedness, dizziness, nausea, dysuria, pallor... 

Report 957-77, E.I. du Pont de Nemours and Co., Newark, DE. Test species/Strain/Sex/Number male beagle dogs (1-2 per exposure group) Exposure route/Concentrations/Durations Inhalation 2,600, 5,200, 10,000, and 21,600 ppm for 10 min (the cardiac sensitization test is a 10-min test) epinephrine dose at 8 g/kg. The cardiac sensitization test is based on the observation that some halocarbons make the mammalian heart abnormally sensitive to epinephrine, resulting in ectopic beats and/or ventricular fibrillation, which may result in death. 

In rats, 40% propene caused light anesthesia with no other toxic symptoms within 6 hours 55% propene for 3-6 minutes or 70% propene for 1-3 minutes produced deep anesthesia with no additional central nervous system disturbances. Animal experiments with cats have shown no toxic signs when anesthesia was induced at concentrations of 20-31% however, 70% propene resulted in a drop in blood pressure and an increased pulse rate, and an unusual ventricular ectopic beat occurred at concentrations ranging from 50% to 80%. 

QRS complex, ventricular tachyarrhythmias, frequent ventricular ectopic beats, or tachycardia) dictates immediate discontinuation of quinidine closely monitor the ECG. 

Blockers are antiarrhythmics of class II according to the Vaughan-Williams classification, effective in the treatment of both supraventricular and ventricular tachyarrhythmias. These drugs can also reduce ectopic beats, especially if they are a result of sympathetic activity. Sotalol is a racemic mixture of the -blocking L-isomer and the class III antiarrhythmic D-isomer. This racemic mixture as well as D-sotalol are used as class Ill-antiarrhythmic. 

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-... 

Headache, ectopic beats, tachycardia, anginal pain, palpitations, vasoconstriction,... 

Adverse effects of dopamine include nausea, vomiting, ectopic beats, anginal pain, tachycardia, palpitation and widened QRS. 

It is a anticonvulsant drug and depresses the ventricular automaticity and accelerates the AV conduction. It also reduces the duration of action potential like quinidine. It also shortens the QT interval. It mainly blocks inactivated Na+ channels. It is used for the suppression of ectopic beats and for prophylaxis of recurrent paroxysmal tachycardia and also for the treatment of rapid supraventricular or ventricular tachycardia. 

As with most data for reboxetine, this information primarily comes from summary papers rather than primary sources (473, 474). With this caveat, the adverse-effect profile of reboxetine is consistent with its pharmacology as an NSRI. Thus, it is similar to that of desipramine and maprotiline but without the risk of serious CNS (i.e., seizures, delirium) or cardiac (i.e., conduction disturbances) toxicity. The most common adverse effects of reboxetine are dry mouth, constipation, urinary hesitancy, increased sweating, insomnia, tachycardia, and vertigo. Whereas the first three adverse effects are commonly called anticholinergic, they are well known to occur with sympathomimetic drugs as well. In other words, these effects can be either the result of decreased cholinergic tone or increased sympathetic tone, although they tend to be more severe with the former than the latter. In contrast to TCAs, reboxetine does not directly interfere with intracardiac conduction. The tachycardia produced by reboxetine, however, can be associated with occasional atrial or ventricular ectopic beats in elderly patients. 

The acute phase of ischemia is followed by 3-6 h of predominantly sinus rhythm. Thereafter, the number of ventricular ectopic beats increases. In the subacute phase of infarction (12-24 h) ventricular arrhythmias often occur. One of the mechanisms involved is reinfarction. If there is no acute reinfarction involved, these arrhythmias have been suggested to originate from surviving strands of Purkinje fibers in the subendocardium. The predominant mechanism has been postulated to be abnormal automaticity in these fibers. These fibers exhibit an increased sensitivity for catecholamines. In some cases a combination of focal activity and reentry in these fibers may be possible. 

Treatment with potassium and magnesium may be indicated. Potassium is recommended for patients with digitalis-induced ectopic beat or tachycardia, provided the patient is not hyperkalemic, uremic, or oliguric. It is the preferred drug if the patient is hypokalemic. 

Haissaguerre M, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med 1998 339(I0) 659 666. 

Proarrhythmic effects of antiarrhythmic drugs In the Cardiac Arrhythmia Suppression Trial (CAST) treatment with encainide and flecainide, two class IC antiarrhythmic agents, successfully prevented ventricular ectopic beats in patients who had myocardial infarction. However, continued therapy with either drug was associated with a two- to three-fold increase in death due to cardiac arrhythmias. Similar results were reported for moricizine. Increased death was probably due to drug-induced fatal arrhythmias triggered by recurrent myocardial ischemia. 

Action potentials with upstrokes not within 80 ms of a given stimulus are considered to be ectopic. The number of such ectopic beats is assessed each minute during the last 3 minutes of drug exposure. 

The sodium pump normally creates a small potential across cardiac cell membranes when digoxin blocks this pump, there is some depolarization of the cell. The heart then becomes more excitable and abnormal rhythms or ectopic beats may occur. Some patients also experience gastrointestinal disturbances, such as anorexia, nausea or vomiting. When blood concentration of digoxin is high, there may also be CNS effects, which can include confusion and visual disturbances. 

Cardiovascular system. Both caffeine and theophylline directly stimulate the myocardium and cause increased cardiac output, tachycardia and sometimes ectopic beats and palpitations. This effect occurs almost at once after i.v. injection and lasts half an hour. Theophylline contributes usefuUy to the relief of acute left ventricular failure. There is peripheral (but not cerebral) vasodilatation due to a direct action of the drugs on the blood vessels, but stimulation of the vasomotor centre tends to counter this. Changes in the blood pressure are therefore somewhat unpredictable, but caffeine 250 mg (single dose) usually causes a transient rise of blood pressure of about 14/10 mmHg in occasional coffee drinkers (but has no additional effect in habitual drinkers) this effect can be used advantageously in patients with autonomic nervous system failure who experience postprandial hypotension (2 cups of coffee with breakfast may suffice for the day). In occasional coffee drinkers 2 cups of coffee (about 160 mg caffeine) per day raise blood pressure by 5/4 mmHg. Increased coronary artery blood flow may occur but increased cardiac work counterbalances this in angina pectoris. 

P-adrenoceptor antagonists are effective for a range of supraventricular arrhythmias, in particular those associated with exercise, emotion or hyperth5o oidism. Sotalol may be used to suppress ventricular ectopic beats and ventricular tachycardia possibly in conjimction with amiodarone. 

Reduction in the use of tea, coffee and other methylxanthine-containing drinks, and of tobacco, may suffice for ectopic beats not due to organic... 

This occurs in otherwise healthy individuals, who possess an anomalous (accessory) atrioventricular pathway they often experience attacks of paroxj mal AV re-entrant tachycardia or atrial fibrillation. Drugs that both suppress the initiating ectopic beats and delay conduction through the accessory pathway are used to prevent attacks e.g. flecainide, sotalol or amiodarone. Verapamil and digoxin may increase conduction through the anomalous pathway and should not be used. Electrical conversion may be needed to restore sinus rhythm when the ventricular rate is very rapid. Radiofrequency ablation of aberrant pathways will almost certainly provide a cure. 

These are common after myocardial infarction. Their particular significance is that the R-wave (ECG) of an ectopic beat, developing during the early or peak phases of the T-wave of a normal beat, may precipitate ventricular tachycardia or fibrillation (the R-on-T phenomenon). About 80% of patients with myocardial infarction who proceed to ventricular fibrillation have preceding ventricular premature beats. Lignocaine (lidocaine) is effective in suppression of ectopic ventricular beats but is not often used as its addition increases overall risk. 

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