tachycardias associated with accessory av pathways

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Tachycardias Associated with Accessory AV Pathways

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Page 1: Tachycardias associated with accessory av pathways

Tachycardias Associated with Accessory AV Pathways

Page 2: Tachycardias associated with accessory av pathways

Tachycardias Associated with Accessory AV Pathways

• normal QRS complex with a short or long RP interval.

• involve a large macroreentrant circuit that includes the ventricles

In the absence of an AP, the sinus impulse normally activates the ventricles via the AV node and His-Purkinje system, resulting in a PR interval of 120–200 ms.

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Tachycardias Associated with Accessory AV Pathways

When conducting AP is present, the sinus impulse bypasses the AV node and can rapidly activate the ventricles, resulting in ventricular preexcitation. The resulting PR interval is shorter than anticipated.

In addition, because the initial ventricular activation is due to muscle-to-muscle conduction, as opposed to rapid spread of activation via the His-Purkinje system, the initial portion of the QRS complex is slurred, creating the characteristic "delta wave."

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Tachycardias Associated with Accessory AV Pathways

• Atriofascicular accessory pathways - from RA > ventricle distant to AV groove - these pathways tend to be long, conduct more slowly• Mahaim fibers - typically manifest a normal PR interval with a delta wave.

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• MACROREENTERANT TACHYCARDIA assctd w/ WPW Syndrome:

A) orthodromicAV reentry, common ventricular activation occurs via the AV node and the His-Purkinje system. Conduction then returns or reenters the atria via retrograde conduction.

B) rapidly conducting AF, rapid antegrade conduction from the atria to the ventricles over the AP, the AP can conduct rapidly in response to AF, resulting in a faster ventricular rate than would occur normally via the AV node.

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C) antidromic AV reentry and/or preexcitated macroreentry, uncommon. The reentrant circuit can be reversed so that the impulse reaches the ventricle via the AP and conducts retrogradely through to the atria via the His-Purkinje system and the AV node

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Tachycardias Associated with Accessory AV Pathways

• Concealed APs, -it has no antegrade conduction over the AP; however, retrograde conduction is preserved. As a result, the AP is not manifest in sinus rhythm and is only manifest during the sustained tachycardia.-is suggested by the timing and pattern of atrial activation during the tachycardia: the P wave typically follows ventricular activation with a short RP wave interval.

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• TREATMENT:orthodromic tachycard-Vagal stimulation with the Valsalva maneuver and carotid sinus pressure may create sufficient AV nodal slowing to terminate the AVRT-adenosine, 6–12 mg, IV calcium channel blockers, verapamil or diltiazem, or beta blockers preexcitation and AF-preventing a rapid ventricular response: DC cardioversion, procainamide, Ibutilide

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Ventricular Premature Complexes (VPCs)

• from the Purkinje network produces slow ventricular activation and a wide QRS complex that is typically >140 ms in duration.

• Increase with age, structural heart dse• PATTERNs : bigeminy, trigeminy • multiformed, pairs or coupletsVPCs are termed VT when the rate is >100 beats/min. If the repetitive VPCs terminate spontaneously and are more than three beats in duration, the arrhythmia is referred to as nonsustained VT

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Ventricular Premature Complexes

Treatment: -primarily directed at eliminating severe symptoms associated with palpitations

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Accelerated Idioventricular Rhythm (AIVR)

• refers to a ventricular rhythm that is characterized by three or more complexes at a rate >40 beats/min and <120 beats/min.

• Arrhythmia is due to abnormal automaticity• present in the setting of acute myocardial

infarction, cocaine intoxication, acute myocarditis, digoxin intoxication, and postoperative cardiac surgery.

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Ventricular Tachycardia

• originates below the bundle of His at a rate >100 beats per minute; most VT patients have rates >120 beats per minute

• QRS complex during VT may be uniform (monomorphic) or may vary from beat to beat (polymorphic)

• Polymorphic VT in patients who demonstrate a long QT interval during their baseline rhythm typically is referred to as torsades des pointes.

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Ventricular Tachycardia

• Polymorphic ventricular tachycardia, a pause, and a sinus beat with along deformed QT interval followed by polymorphic ventricular tachycardia.

• The ventricular tachycardia with beat to beat change in the QRS axis often referred to as “twisting of the points” hence the name - torsade de pointes.

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Ventricular Tachycardia

• Monomorphic VT -a stable tachycardia focus in the absence of structural heart disease or a fixed anatomic substrate that can create the substrate for a stable reentrant VT circuit when structural disease is present -tends to be a reproducible and recurrent phenomenon and may be initiated with pacing and programmed ventricular stimulation

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Ventricular Tachycardia

• Polymorphic VT -a more dynamic and/or unstable process and, by its very nature, is less reproducible -produced by acute ischemia, myocarditis, or dynamic changes in the QT interval and enhanced dispersion of ventricular refractoriness -not reliably initiated with pacing or programmed stimulation

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Ventricular Tachycardia• ECG during the tachycardia that suggest VT

include:(1) the presence of a QRS duration >140 ms in the

absence of drug therapy(2) a superior and rightward QRS frontal plane axis(3) a bizarre QRS complex that does not mimic the characteristic QRS pattern associated with left or right bundle branch block(4) slurring of the initial portion of the QRS

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ECG showing AV dissociation (arrows mark P waves), wide QRS > 200 ms, superior frontal plane axis, slurring of the initial portion of the QRS, and large S wave in V6—all clues to the diagnosis of ventricular tachycardia.

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• Diagnosis: Refers to TABLE 233-6• TREATMENT:Sustained polymorphic VT, ventricular flutter, and VF all lead to immediate hemodynamic collapse -emergency asynchronous defibrillation with at least 200-J monophasic or 100-J biphasic shock

Monomorphic wide complex rhythm- R wave synchronous shock is required and conscious sedation should be provided

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Ventricular Tachycardia• Pharmacologic treatment -Intravenous procainamide -lidocaine -amiodarone