Arrhythmias and EKGsArrhythmias and EKGs

Amirhossein Azhari M.DAmirhossein Azhari M.D

Fellowship of electrophysiologyFellowship of electrophysiology

Chamran heart centerChamran heart center

Mechanisms of ArrhythmogenesisMechanisms of Arrhythmogenesis

TachycardiaTachycardia

Abnormally rapid heart rhythmAbnormally rapid heart rhythm

May result from:May result from:

Abnormal impulse formation Abnormal impulse formation

– AutomaticityAutomaticity

– Triggered activityTriggered activity

Abnormal impulse conductionAbnormal impulse conduction

– ReentryReentry

TachycardiaTachycardiaEnhanced Normal AutomaticityEnhanced Normal Automaticity

Basal condition

Increased slope of phase 4 depolarization

•Your pulse rate becomes 150 – 200 beats per minute.Your pulse rate becomes 150 – 200 beats per minute.•Palpitations (Feeling your heart beat)Palpitations (Feeling your heart beat)•Dizziness, or Feeling Light HeadedDizziness, or Feeling Light Headed•You may become breathlessYou may become breathless•If you have angina, then an angina pain may beIf you have angina, then an angina pain may be• triggered by an episode of SVTtriggered by an episode of SVT•You may have no symptomsYou may have no symptoms,,• You may only be aware that yourYou may only be aware that your heart is beating fastheart is beating fast. .

Symptoms the following:Include Symptoms the following:Include

Sinus TachycardiaSinus Tachycardia

Sinus TachycardiaSinus TachycardiaIs characterized by:Is characterized by:

SA node discharge rate of 100 to 180 x m.SA node discharge rate of 100 to 180 x m.

Normal P waves and QRS complexesNormal P waves and QRS complexes

Most often arises from increased sympathetic Most often arises from increased sympathetic stimulation of the SA node.stimulation of the SA node.

Physiologic response to exercise.Physiologic response to exercise.

Pathologic conditions including fever, Pathologic conditions including fever, hyperthyroidism and hypoxemia.hyperthyroidism and hypoxemia.

Physiologic Sinus Tachycardia: Physiologic Sinus Tachycardia: TreatmentTreatment

Treatment of sinus tachycardia is directed Treatment of sinus tachycardia is directed at the underlying condition causing the at the underlying condition causing the tachycardia response. tachycardia response.

Uncommonly, beta blockers are used to Uncommonly, beta blockers are used to minimize the tachycardia response if it is minimize the tachycardia response if it is determined to be potentially harmful, as determined to be potentially harmful, as may occur in a patient with ischemic heart may occur in a patient with ischemic heart disease and rate-related anginal disease and rate-related anginal symptoms.symptoms.

V5

P P P P’ P

Timing of Expected P

Premature Atrial Complex (PAC)

Non-Compensatory Pause

Premature Atrial Complex (PAC):Premature Atrial Complex (PAC): Alternative Terminology Alternative Terminology

Premature atrial Premature atrial contractioncontraction

Atrial Atrial extrasystoleextrasystole

Atrial Atrial premature beatpremature beat

Atrial Atrial ectopic beatectopic beat

Atrial Atrial prematurepremature depolarizationdepolarization

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

V1

PACs with Aberrant Conduction(Physiologic RBBB and LBBB)

RBBB LBBB Normalconduction

TreatmentTreatment

PACs uncommonly require intervention. PACs uncommonly require intervention. For extremely symptomatic patients who For extremely symptomatic patients who do not respond to explanation and do not respond to explanation and reassurance, an attempt can be made to reassurance, an attempt can be made to suppress the PACs with pharmacologic suppress the PACs with pharmacologic agents. agents.

Beta blockers are typical first-line therapy.Beta blockers are typical first-line therapy.

The repetitive focus can even be targeted The repetitive focus can even be targeted for catheter ablation. for catheter ablation.

Atrial Fibrillation

Focal firingormultiplewavelets

Chaotic, rapidatrial rate at400-600beats per min

Atrial FibrillationAtrial Fibrillation

EKG Characteristics: Absent P waves

Presence of fine “fibrillatory” waves which vary in amplitude and morphology

Irregularly irregular ventricular response

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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 AF is the most common sustained arrhythmia. It is marked by disorganized, arrhythmia. It is marked by disorganized, rapid, and irregular atrial activation. The rapid, and irregular atrial activation. The ventricular response to the rapid atrial ventricular response to the rapid atrial activation is also irregular. activation is also irregular.

In the untreated patient, the ventricular In the untreated patient, the ventricular rate also tends to be rapid and is entirely rate also tends to be rapid and is entirely dependent on the conduction properties of dependent on the conduction properties of the AV junction. Although typically the rate the AV junction. Although typically the rate will vary between 120 and 160 beats/min.will vary between 120 and 160 beats/min.

The mechanismThe mechanism

multiple wavelets of (micro)reentry.multiple wavelets of (micro)reentry.

The drivers appears to originate The drivers appears to originate predominantly from the atrialized musculature predominantly from the atrialized musculature that enters the pulmonary veins .that enters the pulmonary veins .

Sustained forms of microreentry as drivers Sustained forms of microreentry as drivers have also been documented around the have also been documented around the orifice of pulmonary veins; nonpulmonary vein orifice of pulmonary veins; nonpulmonary vein drivers have also been demonstrated. drivers have also been demonstrated.

incidenceincidence

The incidence of AF increases with age The incidence of AF increases with age such that >5% of the adult population over such that >5% of the adult population over 70 will experience the arrhythmia.70 will experience the arrhythmia.

Occasionally AF appears to have a well-Occasionally AF appears to have a well-defined etiology, such as acute defined etiology, such as acute hyperthyroidism, an acute vagotonic hyperthyroidism, an acute vagotonic episode, or acute alcohol intoxication.episode, or acute alcohol intoxication.

Clinical symptomsClinical symptoms

clinical importance related to:clinical importance related to:

(1) the loss of atrial contractility, (1) the loss of atrial contractility,

(2) the inappropriate fast ventricular (2) the inappropriate fast ventricular responseresponse

(3) the loss of atrial appendage (3) the loss of atrial appendage contractility and emptying leading to the contractility and emptying leading to the risk of clot formation and subsequent risk of clot formation and subsequent thromboembolic eventsthromboembolic events

Acute Management of Atrial Acute Management of Atrial FibrillationFibrillation

In emergency department because of AF In emergency department because of AF generally have a rapid ventricular rate, and generally have a rapid ventricular rate, and control of the ventricular rate is most control of the ventricular rate is most rapidly achieved with intravenous diltiazem rapidly achieved with intravenous diltiazem or esmolol.or esmolol.

If the patient is hemodynamically unstable, If the patient is hemodynamically unstable, immediate transthoracic cardioversion immediate transthoracic cardioversion may be appropriate.may be appropriate.

If the AF has been present for more than If the AF has been present for more than 48 hours or if the duration is unclear and 48 hours or if the duration is unclear and the patient is not already anticoagulated, the patient is not already anticoagulated, cardioversion ideally should be preceded cardioversion ideally should be preceded by transesophageal echocardiography to by transesophageal echocardiography to rule out a left atrial thrombus.rule out a left atrial thrombus.

However, a delay in cardioversion may However, a delay in cardioversion may not be appropriate in the setting of severe not be appropriate in the setting of severe cardiovascular decompensationcardiovascular decompensation

If the patient is hemodynamically stable, If the patient is hemodynamically stable, the decision to restore sinus rhythm by the decision to restore sinus rhythm by cardioversion is based on several factors, cardioversion is based on several factors, including symptoms, prior AF episodes, including symptoms, prior AF episodes, age, left atrial size, and current age, left atrial size, and current antiarrhythmic drug therapy. .antiarrhythmic drug therapy. .

For example, in an elderly patient whose symptoms For example, in an elderly patient whose symptoms resolve once the ventricular rate is controlled and resolve once the ventricular rate is controlled and who already has had early recurrences of AF who already has had early recurrences of AF despite rhythm-control drug therapy, further despite rhythm-control drug therapy, further attempts at cardioversion usually are not attempts at cardioversion usually are not appropriate. appropriate.

On the other hand, cardioversion usually is On the other hand, cardioversion usually is appropriate for patients with symptomatic AF who appropriate for patients with symptomatic AF who present with a first episode of AF or who have had present with a first episode of AF or who have had long intervals of sinus rhythm between prior long intervals of sinus rhythm between prior episodes.episodes.

anticoagulationanticoagulation

Regardless of whether cardioversion is Regardless of whether cardioversion is performed pharmacologically or electrically, performed pharmacologically or electrically, therapeutic anticoagulation is necessary for 3 therapeutic anticoagulation is necessary for 3 weeks or more before cardioversion to weeks or more before cardioversion to prevent thromboembolic complications if the prevent thromboembolic complications if the AF has been ongoing for more than 48 AF has been ongoing for more than 48 hours. If the time of onset of AF is unclear, hours. If the time of onset of AF is unclear, for the sake of safety, the AF duration should for the sake of safety, the AF duration should be assumed to be more than 48 hoursbe assumed to be more than 48 hours

Atrial Flutter (“Typical,”Counterclockwise)

Reentrant mechanism

Atrial flutter (SVT)Atrial flutter (SVT)Re-entrant loop just above AVN in right atriumRe-entrant loop just above AVN in right atriumAtrial rate 240-360 without medicationsAtrial rate 240-360 without medications2:1 block, vent rate 150 most common2:1 block, vent rate 150 most commonRegular, fixed; or Regular, fixed; or regularlyregularly irregular irregularNarrow if no aberrancyNarrow if no aberrancyFlutter waves, sawtooth pattern--Always visible in lead IIFlutter waves, sawtooth pattern--Always visible in lead IIAdenosine can help to diagnose, not treatAdenosine can help to diagnose, not treatConversion vs. Ventricular slowing Conversion vs. Ventricular slowing – 50 Joules, Ibutilide/Amiodarone50 Joules, Ibutilide/Amiodarone

II

V1

Atrial Flutter

4:1 2:1

Classicinverted “sawtooth”flutter wavesat 300 min-1 (best seen inII, III and AVF)

Note variableventricularresponse

Atrial Flutter

2:1Conduction(common)

2:1 & 3:2Conduction

1:1Conduction(rare but dangerous)

V. rate 140-160beats/min

Multifocal Atrial TachycardiaMultifocal 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 Paroxysmal Supraventricular TachycardiaTachycardia

Refers to supraventricular tachycardia other Refers to supraventricular tachycardia other than afib, aflutter and MATthan afib, aflutter and MAT

Occurs in 35 per 100,000 person-yearsOccurs in 35 per 100,000 person-years

Usually due to reentry—AVNRT or AVRTUsually 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 preferentiallyvia the fast pathway

Initiation of AV Nodal Reentrant Tachycardia

PAC = premature atrial complex (beat)

PAC

PAC

Sustainment of AV Nodal Reentrant Tachycardia

Rate 150-250beats per min

P waves generatedretrogradely(AV node atria) andfall within orat tail of QRS

P P P P

Sustained AV Nodal Reentrant Tachycardia

Note fixed, short RP interval mimicking r’ deflection of QRS

V1

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 blockerFlecainide, propafenone

Accessory Pathway with Ventricular Preexcitation(Wolff-Parkinson-White Syndrome)

Fusion activation of the ventricles

“Delta” Wave

APPR < .12 s

QRS .12 s

Sinusbeat

Hybrid QRS shape

PreexcitationPreexcitation

ECG Characteristics of WPW:

1. Short PR interval

2. QRS prolongation

3. Delta wave

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-Parkinson-White (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.

Varying Degrees of Ventricular Preexcitation

Intermittent Accessory Pathway Conduction

NormalConduction

V Preex V Preex

Note “all-or-none” nature of AP conduction

AV Reentrant Tachycardia (AVRT)AV Reentrant Tachycardia (AVRT)

In patients with WPW, a reentrant rhythm can be In patients with WPW, a reentrant rhythm can be generated where the AV node serves as one arm generated where the AV node serves as one arm of the reentrant circuit, and the accessory pathway of the reentrant circuit, and the accessory pathway as the other.as the other.

Types of AVRTTypes of AVRT

Orthodromic AVRT (More common) – Narrow Orthodromic AVRT (More common) – Narrow complex tachycardia in which the wave of complex tachycardia in which the wave of depolarization travels down the AV node and depolarization travels down the AV node and retrograde up the accessory pathway. retrograde up the accessory pathway.

Antidromic AVRT (Less common) – Wide Antidromic AVRT (Less common) – Wide complex tachycardia in which the wave of complex tachycardia in which the wave of depolarization travels down the accessory depolarization travels down the accessory pathway and retrograde up the AV node. pathway and retrograde up the AV node.

Mechanism of orthodromic AVRTMechanism of orthodromic AVRT

Mechanism of antidromic AVRTMechanism of antidromic AVRT

Orthodromic AV Reentrant Tachycardia

APAnterogadeconduction via normal pathway

Retrograde conductionvia acpathway (AP)

Initiation of Orthodromic AV Reentrant Tachycardia

AVN

Ventricles

Atria

AP

PAC = premature atrial complex (beat)

PAC

Sustainment of Orthodromic AV Reciprocating Tachycardia

Atria

AP

AVN

Ventricles

Retrograde P’s fall in the ST segmentwith fixed, short RP

Rate 150-250beats per min

Orthodromic AV Reentrant Tachycardia

NSR with V Preex

SVT:V Preex gone

Note retrograde P wavesin 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)

1.) can degenerate into V fib (death)2.) No beta-blocker, calcium channel blocker, digoxin.3.) drug blocks AP: procainamide, amiodarone, ibutilide, Ic drug

A fib. in a patient with WPW

AVRT Therapy

1.) No beta-blocker, calcium channel blocker, digoxin in WPW.2.) drug blocks AP: procainmide, amiodarone, ibutilide, IcBut do not reduce SCD risk.3.) Asymptomatic WPW, EP study if in high risk profession4.) AVRT in WPW patients needs ESP and likely RFA.

AT 10% (now more)

Normal PRCan have AVN blockLong RP (most)

Adenosine for SVT

Terminate all AVNRT or AVRTTerminate 30 AT onlyECG 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%).

PSVTPSVT

Initial eval: Is the patient stable?Initial eval: Is the patient stable?Determine quickly if sinus rhythmDetermine quickly if sinus rhythmIf not sinus and unstable, cardioversionIf not sinus and unstable, cardioversionUnstable sinus tachycardia---treat cause Unstable sinus tachycardia---treat cause

Sxs of instability would include: chest pain, Sxs of instability would include: chest pain, decreased consciousness, short of breath, decreased consciousness, short of breath, shock, hypotension—unstable sxs shock, hypotension—unstable sxs require shockrequire shock

SVTSVT

If stable, determine whether If stable, determine whether regularregular rhythm (sinus or PSVT) vs rhythm (sinus or PSVT) vs irregularirregular (afib/flutter, MAT)? p waves (MAT vs. AF)?(afib/flutter, MAT)? p waves (MAT vs. AF)?

If If regularregular, determine whether p waves are , determine whether p waves are present, if can’t see---At first CSM or other present, if can’t see---At first CSM or other vagal maneuvers then administer vagal maneuvers then administer adenosine (6mg, can give 2 doses)adenosine (6mg, can give 2 doses)

SVTSVT

CSM or adenosine commonly terminate CSM or adenosine commonly terminate the arrhythmia, esp, AVRT or AVNRTthe arrhythmia, esp, AVRT or AVNRT

Can also use CCB or beta blockers to Can also use CCB or beta blockers to terminate, if availableterminate, if available

Counsel to avoid triggers, caffeine, Etoh, Counsel to avoid triggers, caffeine, Etoh, pseudoephedrine, stresspseudoephedrine, stress

Adenosine

Adenosine interacts with AAdenosine interacts with A11 receptors receptors

present on the extracellular surface of present on the extracellular surface of cardiac cells, activating Kcardiac cells, activating K++ channels (I channels (IK.AchK.Ach, ,

IIK.AdeK.Ade) in a fashion similar to that produced ) in a fashion similar to that produced

by acetylcholine.by acetylcholine.

Transient prolongation of the A-H interval Transient prolongation of the A-H interval results, often with transient first-, second-, results, often with transient first-, second-, or third-degree AV node block.or third-degree AV node block.

PharmacokineticsPharmacokinetics

washout, enzymatically by degradation to washout, enzymatically by degradation to inosine, by phosphorylation to adenosine inosine, by phosphorylation to adenosine monophosphate.monophosphate.

The vascular endothelium and the formed The vascular endothelium and the formed blood elements contain these elimination blood elements contain these elimination systems, which result in very rapid systems, which result in very rapid clearance of adenosine from the clearance of adenosine from the circulation. Elimination half-life is 1 to 6 circulation. Elimination half-life is 1 to 6 seconds.seconds.

Dosage and Administration Dosage and Administration To terminate tachycardia, a bolus of To terminate tachycardia, a bolus of adenosine is rapidly injected intravenously adenosine is rapidly injected intravenously at doses of 6 to 12 mg, followed by a flush.at doses of 6 to 12 mg, followed by a flush.

Pediatric dosing should be 0.1 to Pediatric dosing should be 0.1 to 0.3 mg/kg. 0.3 mg/kg.

When it is given into a central vein and in When it is given into a central vein and in patients after heart transplantation or patients after heart transplantation or those receiving dipyridamole, the initial those receiving dipyridamole, the initial dose should be reduced to 3 mg. dose should be reduced to 3 mg.

Transient sinus slowing or AV node block Transient sinus slowing or AV node block results, lasting less than 5 seconds. Doses results, lasting less than 5 seconds. Doses of more than 18 mg are unlikely to revert a of more than 18 mg are unlikely to revert a tachycardia and should not be used.tachycardia and should not be used.

IndicationsIndications

Adenosine has become the drug of first choice Adenosine has become the drug of first choice to terminate an SVT acutely, such as AV node or to terminate an SVT acutely, such as AV node or AV reentry .AV reentry .

It is useful in pediatric patients and to judge the It is useful in pediatric patients and to judge the effectiveness of ablation of accessory pathways.effectiveness of ablation of accessory pathways.

It results in only transient AV block during atrial It results in only transient AV block during atrial flutter or fibrillation and is thus useful only for flutter or fibrillation and is thus useful only for diagnosis, not therapy.diagnosis, not therapy.

Adenosine terminates a group of VTs most Adenosine terminates a group of VTs most often located in the right ventricular outflow tract.often located in the right ventricular outflow tract.

Calcium Calcium Channel AntagonistsChannel Antagonists

VerapamilVerapamil

Verapamil, a synthetic papaverine Verapamil, a synthetic papaverine derivative, is the prototype of a class of derivative, is the prototype of a class of drugs that block the slow calcium channel drugs that block the slow calcium channel and reduce Iand reduce ICa.LCa.L in cardiac muscle in cardiac muscle

In humans, verapamil prolongs conduction time In humans, verapamil prolongs conduction time through the AV node (the A-H interval) without through the AV node (the A-H interval) without affecting the P wave or QRS duration or H-V affecting the P wave or QRS duration or H-V interval and lengthens AV nodal anterograde interval and lengthens AV nodal anterograde and retrograde refractory periods.and retrograde refractory periods.

More commonly, the sinus rate does not More commonly, the sinus rate does not change significantly because verapamil causes change significantly because verapamil causes peripheral vasodilation, transient hypotension, peripheral vasodilation, transient hypotension, and reflex sympathetic stimulation.and reflex sympathetic stimulation.

After intravenous administration, AV nodal After intravenous administration, AV nodal conduction delay occurs within 1 to 2 conduction delay occurs within 1 to 2 minutes and A-H interval prolongation is minutes and A-H interval prolongation is still detectable after 6 hours.still detectable after 6 hours.

The elimination half-life of verapamil is 3 to The elimination half-life of verapamil is 3 to 7 hours, with up to 70% of the drug 7 hours, with up to 70% of the drug excreted by the kidneys.excreted by the kidneys.

For acute termination of SVT or rapid For acute termination of SVT or rapid achievement of ventricular rate control achievement of ventricular rate control during atrial fibrillation, the most commonly during atrial fibrillation, the most commonly used intravenous dose of verapamil is used intravenous dose of verapamil is 10 mg infused during 1 to 2 minutes while 10 mg infused during 1 to 2 minutes while cardiac rhythm and blood pressure are cardiac rhythm and blood pressure are monitored.monitored.

A second injection of an equal dose may A second injection of an equal dose may be given 30 minutes later.be given 30 minutes later.

Adverse EffectsAdverse EffectsVerapamil must be used cautiously in patients Verapamil must be used cautiously in patients with significant hemodynamic impairment or in with significant hemodynamic impairment or in those receiving beta blockers, as noted earlier. those receiving beta blockers, as noted earlier. Hypotension, bradycardia, AV block, and Hypotension, bradycardia, AV block, and asystole are more likely to occur when the drug asystole are more likely to occur when the drug is given to patients who are already receiving is given to patients who are already receiving beta-blocking agentsbeta-blocking agents

Hemodynamic collapse has been noted in Hemodynamic collapse has been noted in infants, and verapamil should be used infants, and verapamil should be used cautiously in patients younger than 1 year.cautiously in patients younger than 1 year.

ContraindicationsContraindications

1) advanced heart failure1) advanced heart failure

2) second- or third-degree AV block 2) second- or third-degree AV block without a pacemaker in place without a pacemaker in place

3) atrial fibrillation and anterograde 3) atrial fibrillation and anterograde conduction over an accessory pathwayconduction over an accessory pathway

4) hypotensive states4) hypotensive states

5) significant sinus node dysfunction5) significant sinus node dysfunction

6) Iv B-blocker6) Iv B-blocker

Diagnosis ?

Diagnosis ?

What is this arrhythmia?What is this arrhythmia?

Antidromic AVRT

Classification Scheme for ArrhythmiasClassification Scheme for ArrhythmiasAbnormalities in Abnormalities in

ConductionConductionAbnormalities in Abnormalities in

AutomaticityAutomaticity

BradyarrhythmiasBradyarrhythmias

Conduction BlockConduction Block

SA node – SA blockSA node – SA block

Atria - NAAtria - NA

AV node – AV blockAV node – AV block

Ventricles – NA Ventricles – NA

Decreased AutomaticityDecreased Automaticity

SA node – Sinus bradycardiaSA node – Sinus bradycardia

Atria – NAAtria – NA

AV node – NAAV node – NA

Ventricles - NA Ventricles - NA

TachyarrhythmiasTachyarrhythmias

ReentryReentry

SA node – SA nodal reentrySA node – SA nodal reentry

Atria – Intraatrial reentrant Atria – Intraatrial reentrant

tachycardia, a-flutter, a-fibtachycardia, a-flutter, a-fib

AV node – AVNRTAV node – AVNRT

Ventricles – Ventricular Ventricles – Ventricular tachycardia (common)tachycardia (common)

Accessory pathways – AVRT Accessory pathways – AVRT

Increased/Abnormal Increased/Abnormal

AutomaticityAutomaticity

SA node – Sinus tachycardiaSA node – Sinus tachycardia

Atria – Ectopic atrial Atria – Ectopic atrial

tachycardiatachycardia

AV – Junctional tachycardiaAV – Junctional tachycardia

Ventricles – Ventricular Ventricles – Ventricular tachycardia (rare) tachycardia (rare)

Additional important arrhythmias: Multifocal atrial tachycardia, torsade de pointes

The endThe end