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Arrhythmias and EKGs Amirhossein Azhari M.D Fellowship of electrophysiology Chamran heart center Mechanisms of Arrhythmogenesis Tachycardia Abnormally rapid heart rhythm May result from: Abnormal impulse formation – Automaticity – Triggered activity Abnormal impulse conduction – Reentry Tachycardia Enhanced Normal Automaticity Basal condition Increased slope of phase 4 depolarization Symptoms the following:Include •Your pulse rate becomes 150 – 200 beats per minute. •Palpitations (Feeling your heart beat) •Dizziness, or Feeling Light Headed •You may become breathless •If you have angina, then an angina pain may be • triggered by an episode of SVT •You may have no symptoms, • You may only be aware that your heart is beating fast. Sinus Tachycardia Sinus Tachycardia Is characterized by: SA node discharge rate of 100 to 180 x m. Normal P waves and QRS complexes Most often arises from increased sympathetic stimulation of the SA node. Physiologic response to exercise. Pathologic conditions including fever, hyperthyroidism and hypoxemia. Physiologic Sinus Tachycardia: Treatment Treatment of sinus tachycardia is directed at the underlying condition causing the tachycardia response. Uncommonly, beta blockers are used to minimize the tachycardia response if it is determined to be potentially harmful, as may occur in a patient with ischemic heart disease and rate-related anginal symptoms. Premature Atrial Complex (PAC) V5 Non-Compensatory Pause P P P P’ P Timing of Expected P Premature Atrial Complex (PAC): Alternative Terminology Premature atrial contraction Atrial extrasystole Atrial premature beat Atrial ectopic beat Atrial premature depolarization PACs: Bigeminal Pattern P P’ P P’ P P’ PAC with “Aberrant Conduction” (Physiologic Delay in the His Purkinje System) V1 P P P’ P RRbbBBB PACs with Aberrant Conduction (Physiologic RBBB and LBBB) V1 RBBB LBBB Normal conduction Treatment PACs uncommonly require intervention. For extremely symptomatic patients who do not respond to explanation and reassurance, an attempt can be made to suppress the PACs with pharmacologic agents. Beta blockers are typical first-line therapy. The repetitive focus can even be targeted for catheter ablation. Atrial Fibrillation Focal firing or multiple wavelets Chaotic, rapid atrial rate at 400-600 beats per min Atrial Fibrillation www.uptodate.com EKG Characteristics: Absent P waves Presence of fine “fibrillatory” waves which vary in amplitude and morphology Irregularly irregular ventricular response Atrial Fibrillation: Characteristic “Irregularly Irregular” Ventricular Response II Atrial Fibrillation with Rapid Ventricular Response II Irregularity may be subtle AF is the most common sustained arrhythmia. It is marked by disorganized, rapid, and irregular atrial activation. The ventricular response to the rapid atrial activation is also irregular. In the untreated patient, the ventricular rate also tends to be rapid and is entirely dependent on the conduction properties of the AV junction. Although typically the rate will vary between 120 and 160 beats/min. The mechanism multiple wavelets of (micro)reentry. The drivers appears to originate predominantly from the atrialized musculature that enters the pulmonary veins . Sustained forms of microreentry as drivers have also been documented around the orifice of pulmonary veins; nonpulmonary vein drivers have also been demonstrated. incidence The incidence of AF increases with age such that >5% of the adult population over 70 will experience the arrhythmia. Occasionally AF appears to have a welldefined etiology, such as acute hyperthyroidism, an acute vagotonic episode, or acute alcohol intoxication. Clinical symptoms clinical importance related to: (1) the loss of atrial contractility, (2) the inappropriate fast ventricular response (3) the loss of atrial appendage contractility and emptying leading to the risk of clot formation and subsequent thromboembolic events Acute Management of Atrial Fibrillation In emergency department because of AF generally have a rapid ventricular rate, and control of the ventricular rate is most rapidly achieved with intravenous diltiazem or esmolol. If the patient is hemodynamically unstable, immediate transthoracic cardioversion may be appropriate. If the AF has been present for more than 48 hours or if the duration is unclear and the patient is not already anticoagulated, cardioversion ideally should be preceded by transesophageal echocardiography to rule out a left atrial thrombus. However, a delay in cardioversion may not be appropriate in the setting of severe cardiovascular decompensation If the patient is hemodynamically stable, the decision to restore sinus rhythm by cardioversion is based on several factors, including symptoms, prior AF episodes, age, left atrial size, and current antiarrhythmic drug therapy. . For example, in an elderly patient whose symptoms resolve once the ventricular rate is controlled and who already has had early recurrences of AF despite rhythmcontrol drug therapy, further attempts at cardioversion usually are not appropriate. On the other hand, cardioversion usually is appropriate for patients with symptomatic AF who present with a first episode of AF or who have had long intervals of sinus rhythm between prior episodes. anticoagulation Regardless of whether cardioversion is performed pharmacologically or electrically, therapeutic anticoagulation is necessary for 3 weeks or more before cardioversion to prevent thromboembolic complications if the AF has been ongoing for more than 48 hours. If the time of onset of AF is unclear, for the sake of safety, the AF duration should be assumed to be more than 48 hours Atrial Flutter (“Typical,”Counterclockw ise) Reentrant mechanism Atrial flutter (SVT) Re-entrant loop just above AVN in right atrium Atrial rate 240-360 without medications 2:1 block, vent rate 150 most common Regular, fixed; or regularly irregular Narrow if no aberrancy Flutter waves, sawtooth pattern--Always visible in lead II Adenosine can help to diagnose, not treat Conversion vs. Ventricular slowing – 50 Joules, Ibutilide/Amiodarone Atrial Flutter II 4:1 2:1 Classic inverted “sawtooth” flutter waves at 300 min-1 (best seen in II, III and AVF) V1 Note variable ventricular response Atrial Flutter 2:1 Conduction (common) 2:1 & 3:2 Conduction 1:1 Conduction (rare but dangerous) V. rate 140-160 beats/min Multifocal Atrial Tachycardia EKG Characteristics: Discrete P waves with at least 3 different morphologies. Atrial rate > 100 bpm. The PP, PR, and RR intervals all vary. Paroxysmal Supraventricular Tachycardia Refers to supraventricular tachycardia other than afib, aflutter and MAT Occurs in 35 per 100,000 person-years Usually due to reentry—AVNRT or AVRT AV Nodal Reentrant Tachycardia Circuit F = fast AV nodal pathway S = slow AV nodal pathway (His Bundle) During sinus rhythm, impulses conduct preferentially via the fast pathway Initiation of AV Nodal Reentrant Tachycardia PAC PAC PAC = premature atrial complex (beat) Sustainment of AV Nodal Reentrant Tachycardia Rate 150-250 beats per min P waves generated retrogradely (AV node atria) and fall within or at tail of QRS Sustained AV Nodal Reentrant Tachycardia V1 P P P P Note fixed, short RP interval mimicking r’ deflection of QRS AVNRT (60% of SVT) Typical AVNRT: (90% AVNRT) 1. A and V Simultaneously 2.Pseudo “r” in V1/AVR AVNRT Therapy Acute therapy: Please record ECG at the same time. 1.) Vagal maneuver 2.) Adenosine 3.) Verapamil Chronic therapy: 1.) RFA (cure >95%, complication rate of <1%, Mortality < 1/10,000, heart block 0.5%) 2.) Medications beta-blocker, calcium channel blocker Flecainide, propafenone Accessory Pathway with Ventricular Preexcitation (Wolff-Parkinson-White Syndrome) Sinus beat Hybrid QRS shape “Delta” Wave AP PR < .12 s QRS .12 s Fusion activation of the ventricles Preexcitation Preexcitation is a condition characterized by an accessory pathway of conduction, which allows the heart to depolarize in an atypical sequence. The most common form of preexcitation is called Wolfe-ParkinsonWhite (WPW) syndrome, in which a direct atrioventricular connection allows the ventricles to begin depolarization while the standard action potential is still traveling through the AV node. ECG Characteristics of WPW: 1. Short PR interval 2. QRS prolongation 3. Delta wave Varying Degrees of Ventricular Preexcitation Intermittent Accessory Pathway Conduction V Preex V Preex Normal Conduction Note “all-or-none” nature of AP conduction AV Reentrant Tachycardia (AVRT) In patients with WPW, a reentrant rhythm can be generated where the AV node serves as one arm of the reentrant circuit, and the accessory pathway as the other. Types of AVRT Orthodromic AVRT (More common) – Narrow complex tachycardia in which the wave of depolarization travels down the AV node and retrograde up the accessory pathway. Antidromic AVRT (Less common) – Wide complex tachycardia in which the wave of depolarization travels down the accessory pathway and retrograde up the AV node. Mechanism of orthodromic AVRT Mechanism of antidromic AVRT Orthodromic AV Reentrant Tachycardia Retrograde conduction via ac pathway (AP) AP Anterogade conduction via normal pathway Initiation of Orthodromic AV Reentrant Tachycardia PAC Atria AP AVN Ventricles PAC = premature atrial complex (beat) Sustainment of Orthodromic AV Reciprocating Tachycardia Atria Rate 150-250 beats per min AP AVN Ventricles Retrograde P’s fall in the ST segment with fixed, short RP Orthodromic AV Reentrant Tachycardia NSR with V Preex SVT: V Preex gone Note retrograde P waves in the ST segment AVRT (30% of SVT) Wolff-Parkinson-White (WPW) pattern: “death pattern” 1. The initial delta wave 2. PR < 120ms 3. The QRS > 100ms AVRT: orthodromic (95%) and antidromic tachycardia Normal PR (short RP SVT) A fib. in a patient with WPW 1.) can degenerate into V fib (death) 2.) No beta-blocker, calcium channel blocker, digoxin. 3.) drug blocks AP: procainamide, amiodarone, ibutilide, Ic drug AVRT Therapy 1.) No beta-blocker, calcium channel blocker, digoxin in WPW. 2.) drug blocks AP: procainmide, amiodarone, ibutilide, Ic But do not reduce SCD risk. 3.) Asymptomatic WPW, EP study if in high risk profession 4.) AVRT in WPW patients needs ESP and likely RFA. AT 10% (now more) Normal PR Can have AVN block Long RP (most) Adenosine for SVT Terminate all AVNRT or AVRT Terminate 30 AT only ECG at the same time please! AT Therapy 1.) More likely to be treated with medications traditionally. (success rate: 20-50%). 2.) Now more and more ATs are treated with RFA, (success rate: 70-95%). PSVT Initial eval: Is the patient stable? Determine quickly if sinus rhythm If not sinus and unstable, cardioversion Unstable sinus tachycardia---treat cause Sxs of instability would include: chest pain, decreased consciousness, short of breath, shock, hypotension—unstable sxs require shock SVT If stable, determine whether regular rhythm (sinus or PSVT) vs irregular (afib/flutter, MAT)? p waves (MAT vs. AF)? If regular, determine whether p waves are present, if can’t see---At first CSM or other vagal maneuvers then administer adenosine (6mg, can give 2 doses) SVT CSM or adenosine commonly terminate the arrhythmia, esp, AVRT or AVNRT Can also use CCB or beta blockers to terminate, if available Counsel to avoid triggers, caffeine, Etoh, pseudoephedrine, stress Adenosine Adenosine interacts with A1 receptors present on the extracellular surface of cardiac cells, activating K+ channels (IK.Ach, IK.Ade) in a fashion similar to that produced by acetylcholine. Transient prolongation of the A-H interval results, often with transient first-, second-, or third-degree AV node block. Pharmacokinetics washout, enzymatically by degradation to inosine, by phosphorylation to adenosine monophosphate. The vascular endothelium and the formed blood elements contain these elimination systems, which result in very rapid clearance of adenosine from the circulation. Elimination half-life is 1 to 6 seconds. Dosage and Administration To terminate tachycardia, a bolus of adenosine is rapidly injected intravenously at doses of 6 to 12 mg, followed by a flush. Pediatric dosing should be 0.1 to 0.3 mg/kg. When it is given into a central vein and in patients after heart transplantation or those receiving dipyridamole, the initial dose should be reduced to 3 mg. Transient sinus slowing or AV node block results, lasting less than 5 seconds. Doses of more than 18 mg are unlikely to revert a tachycardia and should not be used. Indications Adenosine has become the drug of first choice to terminate an SVT acutely, such as AV node or AV reentry . It is useful in pediatric patients and to judge the effectiveness of ablation of accessory pathways. It results in only transient AV block during atrial flutter or fibrillation and is thus useful only for diagnosis, not therapy. Adenosine terminates a group of VTs most often located in the right ventricular outflow tract. Calcium Channel Antagonists Verapamil Verapamil, a synthetic papaverine derivative, is the prototype of a class of drugs that block the slow calcium channel and reduce ICa.L in cardiac muscle In humans, verapamil prolongs conduction time through the AV node (the A-H interval) without affecting the P wave or QRS duration or H-V interval and lengthens AV nodal anterograde and retrograde refractory periods. More commonly, the sinus rate does not change significantly because verapamil causes peripheral vasodilation, transient hypotension, and reflex sympathetic stimulation. After intravenous administration, AV nodal conduction delay occurs within 1 to 2 minutes and A-H interval prolongation is still detectable after 6 hours. The elimination half-life of verapamil is 3 to 7 hours, with up to 70% of the drug excreted by the kidneys. For acute termination of SVT or rapid achievement of ventricular rate control during atrial fibrillation, the most commonly used intravenous dose of verapamil is 10 mg infused during 1 to 2 minutes while cardiac rhythm and blood pressure are monitored. A second injection of an equal dose may be given 30 minutes later. Adverse Effects Verapamil must be used cautiously in patients with significant hemodynamic impairment or in those receiving beta blockers, as noted earlier. Hypotension, bradycardia, AV block, and asystole are more likely to occur when the drug is given to patients who are already receiving betablocking agents Hemodynamic collapse has been noted in infants, and verapamil should be used cautiously in patients younger than 1 year. Contraindications 1) advanced heart failure 2) second- or third-degree AV block without a pacemaker in place 3) atrial fibrillation and anterograde conduction over an accessory pathway 4) hypotensive states 5) significant sinus node dysfunction 6) Iv B-blocker Diagnosis ? Diagnosis ? What is this arrhythmia? Antidromic AVRT Classification Scheme for Arrhythmias Abnormalities in Conduction Bradyarrhythmias Conduction Block SA node – SA block Atria - NA AV node – AV block Ventricles – NA Reentry Tachyarrhythmias SA node – SA nodal reentry Atria – Intraatrial reentrant tachycardia, a-flutter, a-fib AV node – AVNRT Ventricles – Ventricular tachycardia (common) Accessory pathways – AVRT Abnormalities in Automaticity Decreased Automaticity SA node – Sinus bradycardia Atria – NA AV node – NA Ventricles - NA Increased/Abnormal Automaticity SA node – Sinus tachycardia Atria – Ectopic atrial tachycardia AV – Junctional tachycardia Ventricles – Ventricular tachycardia (rare) Additional important arrhythmias: Multifocal atrial tachycardia, torsade de pointes The end