Tachycardia/tachyarrhythmias ventricular

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. 

In addition to its prominent P-adrenergic blocking effect, it does possess independent quinidine-like anti-arrhythmic actions. Hence, it finds its utility to minimise ventricular and atrial extrasystoles, digitalis-induced tachyarrhythmias, ventricular tachycardia and above all paroxysmal atrial tachycardia. 

B. With chronic intoxication, visual disturbances, weakness, sinus bradycardia, atrial fibrillation with slowed ventricular response rate or junctional escape rhythm, and ventricular arrhythmias (ventricular bigeminy or trigeminy, ventricular tachycardia, bidirectional tachycardia, and ventricular fibrillation) are common. Accelerated junctional tachycardia and paroxysmal atrial tachycardia with block are frequently seen. Hypokalemia and hypomagnesemia from chronic diuretic use may be evident and appear to worsen the tachyarrhythmias. 

Reentry mechanism Intranodal (AV node) reentry Extranodal reentry Reentrant tachyarrhythmia Atrial flutter Atrial fibrillation Ventricular tachycardia Ventricular fibrillation Conduction B/ocks ... 

Propranolol. Propranolol hydrochloride, considered the prototype of the P-adrenoceptor blocking agents, has been in use since 1964. It is a nonselective, highly Hpid-soluble P-adrenoceptor blocker having no ISA. It is a mixture of (+) and (—) enantiomers, and the (—) enantiomer is the active moiety. The local anesthetic effects of propranolol are equipotent to those of Hdocaine [137-58-6] C 4H22N20, (see Anesthetics). Therapeutic effects include termination of catecholamine-induced arrhythmias, conversion of SA nodal tachycardias (including flutter and fibrillation) and AV nodal tachyarrhythmias to normal sinus rhythm, digitahs-induced arrhythmias, and ventricular arrhythmias (1,2). The dmg also has cardioprotective properties (37,39). 

Normal rhythmic activity is the result of the activity of the sinus node generating action potentials that are conducted via the atria to the atrioventricular node, which delays further conduction to the His-Tawara-Purkinje system. From the Purkinje fibres, action potentials propagate to the ventricular myocardium. Arrhythmia means a disturbance of the normal rhythm either resulting in a faster rhythm (tachycardia, still rhythmic) or faster arrhythmia (tachyarrhythmia) or slowed rhythm (bradycardia, bradyarrhythmia). 

Abnormal initiation of electrical impulses occurs as a result of abnormal automaticity. If the automaticity of the SA node increases, this results in an increased rate of generation of impulses and a rapid heart rate (sinus tachycardia). If other cardiac fibers become abnormally automatic, such that the rate of initiation of spontaneous impulses exceeds that of the SA node, other types of tachyarrhythmias may occur. Many cardiac fibers possess the capability for automaticity, including the atrial tissue, the AV node, the Purkinje fibers, and the ventricular tissue. In addition, fibers with the capability of initiating and conducting electrical impulses are present in the pulmonary veins. Abnormal atrial automaticity may result in premature atrial contractions or may precipitate atrial tachycardia or atrial fibrillation (AF) abnormal AV nodal automaticity may result in junctional tachycardia (the AV node is also sometimes referred to as the AV junction). Abnormal automaticity in the ventricles may result in ventricular premature depolarizations (VPDs) or may precipitate ventricular tachycardia (VT) or ventricular fibrillation (VF). In addition, abnormal automaticity originating from the pulmonary veins is a precipitant of AF. 

FIGURE 6-10. Decision algorithm for termination of paroxysmal supraventricular tachycardia. HF, heart failure LVEF, left ventricular ejection fraction PSVT, paroxysmal supraventricular tachycardia. (Algorithm adapted with permission from Tisdale JE, Moser LR. Tachyarrhythmias. In Mueller BA, Bertch KE,... 

Indications. Verapamil is used as an antiarrhythmic drug in supraventricular tachyarrhythmias. In atrial flutter or fibrillation, it is effective in reducing ventricular rate by virtue of inhibiting AV-conduction. Verapamil is also employed in the prophylaxis of angina pectoris attacks (p. 308) and the treatment of hypertension (p. 312). Adverse effects Because of verapamil s effects on the sinus node, a drop in blood pressure fails to evoke a reflex tachycardia Heart rate hardly changes bradycardia may even develop. AV-block and myocardial insufficiency can occur. Patients frequently complain of constipation. 

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. 

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

Abstract Two thirds of the nearly half a million deaths per year in the United States due to sudden cardiac death (SCD) is attributed to coronary artery disease (CAD) and most commonly results from untreated ventricular tachyarrhythmias. Patients with ischemic cardiomyopathy and left ventricular dysfunction are at highest risk for SCD, but this still defines only a small subset of patients who will suffer SCD. Multiple lines of evidence now support the superiority of implantable cardioverter defibrillator (ICD) therapy over antiarrhythmic therapy for both primary and secondary prevention of SCD in advanced ischemic heart disease. Optimization of ICD therapy in advanced ischemic cardiomyopathy includes preventing right ventricular pacing as well as the use of highly effective anti-tachycardia pacing to reduce the number of shocks. While expensive, ICD therapy has been shown to compare favorably to the accepted standard of hemodialysis in cost effectiveness analyses. 

Clinically, tachyarrhythmias associated with digitalis excess (including supraventricular and ventricular extrasystoles) and ventricular tachycardia have been suppressed by propranolol. Although propranolol is highly effective in the treatment of digitalis-induced arrhythmias, phenytoin and Udocaine are preferred. 

Verapamil is useful for slowing the ventricular response to atrial tachyarrhythmias, such as atrial flutter and fibrillation. Verapamil is also effective in arrhythmias supported by enhanced automaticity, such as ectopic atrial tachycardia and idiopathic left ventricular tachycardia. 

The most profound effect of adenosine is the induction of an A-V block within 10 to 20 seconds of administration. Mild sinus slowing may be observed initially followed by sinus tachycardia. There is no effect on the QRS duration or QT interval. Rarely, an adenosine bolus injection is accompanied by atrial fibrillation or ventricular tachyarrhythmias. 

Magnesium sulfate may be effective in terminating refractory ventricular tachyarrhythmias, particularly polymorphic ventricular tachycardia. DigitaUs-induced arrhythmias are more likely in the presence of magnesium deficiency. Magnesium sulfate can be administered orally, intramuscularly, or, preferably, intravenously,... 

Adverse effects include SA block or arrest, high grade AV block, ventricular tachycardia, arrhythmia or ventricular asystole, polymorphic ventricular tachyarrhythmia, hypotension (particularly when given IV), cinchonism, tinnitus, loss of hearing, gastrointestinal upset, severe headache, diplopia, photophobia, etc. 

These are class IC drugs with similar pharmacological profiles and with the same indication range and adverse effects. They are mainly used for the treatment of severe, lifethreatening ventricular tachyarrhythmias, and non-sustained ventricular tachycardia or high-frequency premature ventricular beats. The main adverse effects are cardiovascular, including proarrhythmic actions and severe negative inotropic effects, especially in patients with impaired cardiac function. Both flecainide and encainide increase the risk of sudden death in patients with myocardial infarction and asymptomatic unsustained ventricular arrhythmias. 

Therapeutic uses Quinidine is used in the treatment of a wide variety of arrhythmias, including atrial, AV junctional, and ventricular tachyarrhythmias. Quinidine is used to maintain sinus rhythm after direct current cardioversion of atrial flutter or fibrillation and to prevent frequent ventricular tachycardia. 

Amiodarone is indicated for the suppression and prevention of documented life-threatening, recurrent, ventricular tachycardia or fibrillation when other agents have failed. Amiodarone is also used in the management of supraventricular tachyarrhythmias including paroxysmal atrial fibrillation and atrial flutter, ectopic or multifocal atrial tachycardia, junctional tachycardia, and paroxysmal reentrant supraventricular tachycardia when other agents have failed to suppress or prevent their recurrence. Amiodarone has also been used to treat wide-complex tachycardia of uncertain mechanism. 

Quinidine, available as either quinidine sulfate or quinidine gluconate, is used in the treatment of atrial premature contraction, paroxysmal supraventricular tachycardia, supraventricular tachyarrhythmia, PVCs, and ventricular tachycardia and in prophylactic treatment after myocardial infarction. It is also used with care in the treatment of atrial... 

Arterial pulses are an accurate measure of the ventricular rate in healthy persons with good ventricular function. In patients with a rapid ventricular rate—because of supraventricular tachyarrhythmias such as atrial flutter or fibrillation or rapid ventricular rates (e.g., ventricular tachycardia or premature ventricular beats)—extremity pulses (e.g., radial pulse) may be considerably slower than the true ventricular rate. A more accurate ventricular rate is determined by listening to the ventricles with the stethoscope (usually at the apex) or counting from an ECG. In patients with atrial fibrillation and a fast ventricular rate, a pulse deficit (measure of the difference in true ventricular rate and peripheral pulse rate) may exist. This may be as much as 10 to 20 beats per minute. Thus the location of the pulse (radial or apical) should be recorded. The pulse deficit will be reduced as the ventricular rate is controlled with drug therapy or normal sinus rhythm is restored. 

Verapamil (80 mg p.o. q. 6 to 8 hours) is indicated in the management of Prinzmetal s or variant angina or unstable or chronic, stable angina pectoris verapamil (0.075 to 0.15 mg/kg rv pnsh over a 2-minnte period) is indicated in the treatment of supraventricnlar tachyarrhythmias verapamil (240 to 480 mg p.o. daily) is indicated in the prevention of recurrent paroxysmal supraventricular tachycardia verapamil (240 to 320 mg p.o. daily) is indicated in the control of the ventricular rate in digitalized patients with chronic atrial flatter and/or fibrillation and verapamil (80 mg p.o. t.i.d.) is indicated in the management of hypertension. 

Propranolol has been reported to exhibit quinidine-like antiarrhythmic actions which are quiet independent of beta-adrenergic blockade. Hence, these pharmacological properties are usually employed to suppress ventricular tachycardia, digitalis-induced tachyarrhythmias, paroxysml atrial tachycardia, and lastly ventricular and atrial extra-systoles. It is also currently receiving a lot of attention in the treatment and management of essential hypertension. 

Quinidine (e.g., Cin-Quin) Depresses automaticity of ectopic foci. Siows conduction veiocity in atria His-Purkinje ceils. Prolongs refractory period throughout heart (except nodes) and accessory pathways. Has anticholinergic effects which may actuaiiy enhance A-V conduction in patients with rapid atrial depolarization. Multifocal atrial tachycardia, premature atrial depolarization, premature ventricular depolarization, atrial fibrillation (these result from increased automaticity of ectopic foci), and ventricular tachycardia. Torsades de pointes (recurrent, temporary arrhythmia), increases ventricle response to atrial tachyarrhythmia, nausea, vomiting, diarrhea, hypersensitivity, cinchonism, thrombocytopenic purpura. 

Adverse reactions Tachycardia, palpitations and other arrhythmias, premature and ventricular contractions, tachyarrhythmias and myocardial necrosis... 

A. The earliest symptoms of acute caffeine poisoning are usually anorexia, tremor, and restlessness. These are followed by nausea, vomiting, tachycardia, and confusion. With serious intoxication, delirium, seizures, supraventricular and ventricular tachyarrhythmias, hypokalemia, and hyperglycemia may occur. Hypotension is caused by excessive beta-2-mediated vasodilation and is characterized by a low diastolic pressure and a wide pulse pressure. 

The introduction and manipulation of pacing leads are frequently associated with both tachyarrhythmias and bradyarrhythmias as a lead negotiates the chambers of the right heart. Ventricular tachycardia is extremely common as the pacing electrode or guidewire contacts the right ventricular myocardium. Simple withdrawal of these objects usually terminates the arrhythmia. In extreme cases, sustained monomorphic ventricular tachycardia and even ventricular fibrillation may occur. Some institutions have instituted a policy of placing external defibrillation pads prophylactically in anticipation of required cardioversion. 

Undersensing. Inappropriate delivery of pacing stimuli when the pacemaker system fails to sense P-waves or QRS complexes defines undersensing. Delivery of stimuli can be harmful if they occur during the atrial and ventricular relative refractory periods that are predisposed to tachyarrhythmia induction. Of particular concern is the induction of ventricular tachycardia or fibrillation when ventricular pacing occurs on the terminal portion of the T-wave ( R-on-T ), especially in the critical care setting where concomitant ischemia, metabolic and electrolyte abnormalities are frequently present. 

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