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Tachycardia/tachyarrhythmias

Reentry mechanism Intranodal (AV node) reentry Extranodal reentry Reentrant tachyarrhythmia Atrial flutter Atrial fibrillation Ventricular tachycardia Ventricular fibrillation Conduction B/ocks ... [Pg.112]

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). [Pg.119]

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). [Pg.96]

Supraventricular bradycardia is treated by implantation of a pacemaker device or has been treated pharmacologically with atropine. Supraventricular paroxysmal tachycardia is treated with aj marine or praj marine. Supraventricular tachyarrhythmias or AV reentrant arrhythmia typically can be terminated using adenosine. [Pg.101]

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. [Pg.110]

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,... [Pg.124]

Adverse effects include nausea, vomiting, tachycardia, jitteriness, and difficulty sleeping more severe toxicities include cardiac tachyarrhythmias and seizures. [Pg.930]

Presynaptic a2-adrenoceptors function like sensors that enable norepinephrine concentration outside the axolemma to be monitored, thus regulating its release via a local feedback mechanism. When presynaptic a2-re-ceptors are stimulated, further release of norepinephrine is inhibited. Conversely, their blockade leads to uncontrolled release of norepinephrine with an overt enhancement of sympathetic effects at Pi-adrenoceptor-mediated myocardial neuroeffector junctions, resulting in tachycardia and tachyarrhythmia. [Pg.90]

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. [Pg.122]

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. [Pg.253]

QRS complex, ventricular tachyarrhythmias, frequent ventricular ectopic beats, or tachycardia) dictates immediate discontinuation of quinidine closely monitor the ECG. [Pg.425]

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. [Pg.38]

Inappropriate sinus bradycardia, sinoatrial block, and bradycardia-tachycardia syndrome (bradycardia followed by supraventricular tachyarrhythmias such as atrial fibrillation) are included in this syndrome. Treatment of sick sinus syndrome is generally based upon the patients symptoms. In general, bradycardia... [Pg.600]

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. [Pg.183]

Amiodarone is effective in maintaining sinus rhythm in most patients with paroxysmal atrial hbrillation and in many patients with persistent atrial hbrillation. It is also effective in preventing recurrences of A-V nodal reentry and atrial tachyarrhythmias and in the prevention of reentrant rhythms and atrial hbrillation in patients with Wohf-Parkinson-White syndrome. Also, it is the most efficacious therapy for postoperative junctional ectopic tachycardia. [Pg.187]

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. [Pg.191]

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. [Pg.192]

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,... [Pg.193]

The prominent depressant action of verapamil and diltiazem at the SA and A-V nodes finds use in specific arrhythmias. They are of proven efficacy in acute control and long-term management of paroxysmal supraventricular tachycardia (see Chapter 16).Their ability to inhibit conduction at the A-V node is employed in protecting ventricles from atrial tachyarrhythmias, often in combination with digitalis or propranolol. [Pg.221]

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. [Pg.191]

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. [Pg.193]

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. [Pg.160]

The short-acting cholinesterase inhibitor edrophonium was used to treat supraventricular tachyarrhythmias, particularly paroxysmal supraventricular tachycardia. In this application, edrophonium has been replaced by newer drugs (adenosine and the calcium channel blockers verapamil and diltiazem). [Pg.145]

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. [Pg.179]


See other pages where Tachycardia/tachyarrhythmias is mentioned: [Pg.463]    [Pg.463]    [Pg.204]    [Pg.75]    [Pg.918]    [Pg.165]    [Pg.40]    [Pg.154]    [Pg.165]    [Pg.166]    [Pg.184]    [Pg.234]    [Pg.294]    [Pg.261]    [Pg.62]    [Pg.504]    [Pg.505]    [Pg.202]   
See also in sourсe #XX -- [ Pg.508 ]




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Tachycardia

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Tachycardia/ tachyarrhythmias ventricular

Tachycardia/tachyarrhythmias treatment

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