electrocardiography & cardiac arrhythmias

Electrocardiography&

Cardiac Arrhythmias

Saeed Oraii MD, Cardiologist

Interventional Electrophysiologist

Tehran Arrhythmia Clinic

Tehran Arrhythmia Center

Some slides have accompanied notes. To view them you can right

click on the screen, choose ‘Screen’ and then ‘Speaker Notes’.


ECG

A graphic recording of electrical potentials generated by the heart

A noninvasive, inexpensive and highly versatile test


Normal Pathway of Electrical Conduction


Cardiac Action Potential


Cardiac action potentials from different locations have different shapes


Electrophysiology

• Electric currents that spread through the heart are produced by three components– Cardiac pacemaker cells– Specialized conduction tissue– The heart muscle

• ECG only records the depolarization and repolarization potentials generated by atrial and ventricular myocardium.


Electrocardiograph 1903


Normal Electrocardiogram

ECG WaveformsLabeled alphabetically beginning with the P wave



QRS-T Cycle Corresponds to Different Phases of Ventricular

Action Potential


Limb Leads


Precordial Leads


Position of Precordial Electrodes


Precordial Leads


3-D Representation of Cardiac Electrical Activity


Timing Intervals


Vector Concept

• Cardiac depolarization and repolarization waves have direction and magnitude.

• They can, therefore, be represented by vectors.

• ECG records the complex spatial and temporal summation of electrical potentials from multiple myocardial fibers conducted to the surface of the body.


Limb Leads Directions


Vector Concept


Ventricular Depolarization


QRS Axis


Determination of QRS Axis


Direction of Propagation


Determination of QRS Axis


Main Vector


Normal QRS Axis


Left Axis Deviation


Right Axis Deviation

Major ECG Abnormalities



Right Atrial Enlargement


Left Atrial Enlargement


Left Ventricular Hypertrophy


Right Ventricular Hypertrophy


RVH, RA enlargement


Left Bundle Branch Block


Right Bundle Branch Block


RBBB


RBBB, RAD (Bifascicular Block)


RBBB, LAD (Bifascicular Block)


Myocardial Ischemia

• ECG is the cornerstone in the diagnosis of myocardial ischemia

• Findings depend on several factors:– Nature of the process, reversible vs. irreversible– Duration, acute vs. chronic– Extent, transmural vs. subendocardial– Localization, anterior vs. inferoposterior– Other underlying abnormalities


Acute Ischemia


Myocardial Infarction


Acute Pericarditis


Metabolic Abnormalities


Hyper-kalemia K 6.9


Same patient

K 3.9


Hypothermia, Osborn Wave


Hypothermia, Corrected


Right Axis Deviation



Superior P Wave Axis



Normal Sinus Rhythm



Anterior MI



RBBB and Inferior MI



LA Enlargement and Prolonged PR Interval



LBBB



LA Enlargement and Prolonged PR Interval



Left Anterior Hemiblock



LVH and LA Enlargement



Anterior MI



Old Inferior MI



RA Enlargement



RBBB, LAH, Prolonged PR (Trifascicular Block)



RBBB and Inferior MI


Cardiac Arrhythmias



Normal Pathway of Electrical Conduction


Normal Sinus Rhythm

• Normal and constant P wave contours

• Normal P wave axis

• Rate between 60 and 100 bpm


Normal Sinus Rhythm



Anatomical Aspects of Normal Sinus Node

• Located at the superior anterolateral portion of right atrium near its border with the superior vena cava

• It is an epicardial structure near sulcus terminalis

• From endocardial approach the closest approach is near the superior end of crista terminalis


Sinus Node Function

• The dominant cardiac pacemaker

• Highly responsive to autonomic influences

• Decreasing rate with vagal stimulation

• Increasing rate with sympathetic activity

• Normal sinus rate under basal conditions is 60-100 bpm.


Sinus Tachycardia

• Sinus rhythm exceeding 100 bpm in adults

• Usually between 100 and 180 bpm but may be higher with extreme exertion

• Maximum heart arte decreases wit age from near 200 bpm to less than 140 bpm

• Gradual onset and termination


Sinus Tachycardia


Sinus TachycardiaCauses

• Common in infancy and childhood• Normal response to a variety of physiological and

pathological stresses– Exertion, anxiety

– Hypovolemia, anemia

– Fever

– Congestive heart failure

– Myocardial ischemia

– Thyrotoxicosis

• Drugs• Inflammation


Sinus Bradycardia

• Sinus rhythm at a rate less than 60 bpm

• Can result from excessive vagal or decreased sympathetic tone as well as anatomic changes in sinus node

• Frequently occurs in healthy young adults, particularly well-trained athletes

• Sinus arrhythmia often coexists


Sinus Bradycardia


Sinus Bradycardia Causes

• Hypothyroidism

• Drugs

• During vomiting or vasovagal syncope

• Increased intracranial pressure

• Hypoxia, hypothermia

• Infections

• Depression

• Jaundice


Sinus Arrhythmia

• Phasic variation in sinus cycle length

• Maximum minus minimum sinus cycle length exceeds 120 msec.

• May be considered the most common form of arrhythmia

• Respiratory form is a normal event

• Common in the young esp. with slower heart rates or enhanced vagal tone


Sinus Arrhythmia


Wandering Pacemaker

• Passive transfer of dominant pacemaker focus from sinus node to latent pacemakers in other atrial sites or AV junctional tissue

• Occurs in a gradual fashion over the duration of several beats


Wandering PacemakerECG

• A cyclical increase in RR interval

• A PR interval that gradually shortens to less than 120 msec

• A change in P wave contour that becomes negative in lead I or II or is lost within the QRS


Wandering Pacemaker


Inappropriate Sinus Tachycardia• Persistent sinus tachycardia at rest or with

minimal exertion• Usually occurs in otherwise healthy people• More common in health care personnel• May result from a defect in either

sympathetic or vagal nerve control of sinus node automaticity or an abnormality of intrinsic heart rate

• Some cases may need radiofrequency ablation of sinus node


Sinus Node Dysfunction Mechanisms

• A disease affecting a limited amount of tissue at or near the sinus node causing dysfunction of impulse formation or propagation or recovery from overdrive suppression

• A disease affecting the atria in general that consequently affects the sinus node function and also frequently generates atrial arrhythmias


Sinus Node DysfunctionECG Manifestations

• Sinus bradycardia

• Sinus pauses

• Sinus arrest

• Atrial asystole

• Sinus exit block


Sinus Pause


Sinoatrial Exit Block1st and 2nd degree


Sinus Node DysfunctionEtiology

• Most often in elderly as an isolated phenomenon

• Drugs

• Infiltration of atrial myocardium

• Interruption of blood supply

• Hypothyroidism, advanced liver disease, severe hypoxia, acidemia …


High Vagal Tone

• Usually in the young

• Normal heart rate response during exercise

• Normal intrinsic heart rate

• Bradycardia may be severe enough to cause syncope (especially in familial form)

Sick Sinus Syndrome•A combination of symptoms (dizziness,

fatigue, confusion, syncope and congestive heart failure) caused by sinus node dysfunction

•Atrial tachyarrhythmias may accompany sinus node dysfunction

<bradycardia-tachycardia syndrome>



Sick Sinus Syndrome Clinical Manifestations

• Predominantly seen in the elderly

• Most patients with sinus node dysfunction are asymptomatic

• Two types of presentations– Syncope or near-syncope– Fatigue or worsening heart failure


Sick Sinus SyndromeDiagnosis

• Holter monitor recordings

• Intrinsic heart rate by autonomic blockade

• Sinus node recovery time

• Sinoatrial conduction time

The most important step is to correlate symptoms with ECG findings.


Normal SNRT


Abnormal SNRT


SA Block during Overdrive Pacing


Sinus Arrest after Termination of AF


Loop Recorder Showed Junctional Rhythm during Syncope


Sinus arrest with syncope


Therapy for Sick Sinus Syndrome

• Based mostly on symptoms and any clinical documentation of cardiac arrhythmia associated with these symptoms

• Drug therapy is rather limited

• Most effective treatment is pacing therapy

• Anticoagulation in certain situation


Heart Block

• Disturbance of impulse conduction• Transient or permanent• Due to anatomical or functional impairment• Must be distinguished from interference, a

normal phenomenon that is a disturbance of impulse conduction caused by physiological refractoriness due to inexcitability from a preceding impulse


AV Conduction DisturbancesClinical Significance

• Heart block may be asymptomatic or lead to syncope or cardiac arrest

• Clinical significance of conduction abnormalities depend on:– The site of disturbance– The risk of progression to complete block– The probability that a subsidiary escape rhythm

distal to the site of block develops and is stable


AV BlockTypes

• First degree AV block

• Second degree AV block– Mobitz type I (Wenckebach)– Mobitz type II

• Third degree block (Complete heart block)

• High degree (advanced) AV block


First Degree AV Block

• Conduction time is prolonged but all impulses are conducted.

• PR interval exceeds 0.2 sec in adults

• Site of conduction delay may be in the AV node (most commonly), in the His-Purkinje system or both.


First Degree AV Block


Second Degree AV Block

• Block of some atrial impulses at a time when physiological interference is not involved

• Non-conducted P waves can be infrequent or frequent, at regular or irregular intervals, and can be preceded by fixed or lengthening PR intervals.

• The association of P with QRS is not random.


Mobitz Type I Second Degree AV Block

• Also called Wenckebach block

• Typical type characterized by progressive PR prolongation culminating in a non-conducted P wave

• Narrow QRS in most cases


WB


Wenckebach Block


Wenckebach Block

• Atypical pattern in over half the cases

• The site of block is almost always in the AV node.

• Generally benign and does not advance to more advanced AV block

• Can occur in normal children and well-trained athletes


Mobitz Type II Second Degree AV Block

• PR interval remains constant prior to the blocked P wave

• Commonly associated with bundle branch blocks



• Site of block His-Purkinje system in most case

• Often antedates the development of Adams-Stokes syncope and complete AV block

• Never observed in normal people

• An indication for implantation of permanent pacemaker even in asymptomatic cases


2:1 AV Block


2:1 AV block


Complete AV block

• No atrial activity conducts to the ventricles• AV dissociation is present. The atria and

ventricles are controlled by independent pacemakers.

• Ventricular focus is usually located just below the site of block.

• Higher sites are more stable with a more faster escape rate.


Complete AV block


Complete AV blockIsorhythmic AV Dissociation


Advanced AV block

Block in two or more consecutive P waves


AV Conduction DisturbancesEtiology

• Degenerative diseases are the most common causes

• A variety of other diseases may be responsible: myocardial infarction, drugs, acute infections, infiltrative diseases, neoplasms, etc.

• Hypervagotonia


Investigation of the Site of AV Conduction Disease by

Electrophysiologic Study (EPS)


Cardiac Pacemakers

• The treatment of symptomatic bradyarrhythmias is implantation of cardiac pacemakers.


Cardiac Pacing


First Implanted Pacemaker


Common Uses for Permanent Pacemaker Therapy


AV Block With Carotid Massage


Long Asystole


Sinus Pauseand

Junctional Escape Beats


Sinus Pauseand Junctional Escape Beats



Bradycardia- Tachycardia Syndrome


Mobitz Type I (Wenckebach)


2:1 AV block



Complete Heart Block



Sinus Pause



Sinus Arrhythmia



Sinus Tachycardia



Wandering Pacemaker



Sinus Tachycardia



Wandering Pacemaker



Asystole and Junctional Escape Rhythm


Tachyarrhythmias

TachyarrhythmiasMechanisms

Automaticity



Triggered activity



Reentry



Premature Complexes


Ventricular Premature Complexes

Compensatory Pause

Interpolated VPC


Premature Complexes

• The most common arrhythmias

• Detected during 24h Holter monitoring in over 60% of adults

• May cause palpitations or be asymptomatic

• May trigger more serious tachyarrhythmias

• May be associated with a normal heart or a variety of cardiac disturbances


Variability of Ventricular Ectopy with Age

• Effect of age on probability (%) ofhaving more than agiven number ofPVCs per 24 hoursin subjects withnormal hearts.

0%

10%

20%

30%

40%

50%

60% > 0 PVCs

> 50 PVCs

> 100 PVCs

10-29 30-39 40-49 50-59 60-69

Data from Kostis JB. Circulation. 1981;63(6):1353.

Age


Ventricular Premature Complexes

• Without heart disease, PVCs have not been shown to be associated with any increased incidence in morbidity or mortality

• In the presence of underlying disease (ischemia, heart failure …) they may add to the risk of the disease. No treatment is, however, shown to definitely decrease this increased risk.


Atrial Fibrillation

• The most common sustained arrhythmia

• Incidence increases progressively with age.

• Prevalence: 0.4% of overall population

• Mortality rate double that of control

• AF is characterized by disorganized atrial activity without discrete P waves


Atrial Fibrillation


Atrial Fibrillation

• Undulating baseline or atrial deflections of varying amplitude and frequency ranging from 350 to 600 bpm.

• Irregularly irregular ventricular response.


Atrial Fibrillation

• Morbidity related to:– Excessive ventricular rate– Pause following cessation of AF– Systemic embolization– Loss of atrial kick– Anxiety secondary to palpitations– Irregular ventricular rate


Atrial Fibrillation• Persistent AF usually in patients with

cardiovascular disease– Valvular heart disease

– Hypertensive heart disease

– Congenital heart disease

• Paroxysmal AF may occur with acute hypoxia, hypercapnia or metabolic or hemodynamic derangements

• Normal people with emotional stress or surgery or acute alcoholic intoxication

• Lone AF


Atrial Fibrillation

• Therapeutic Goals:– Control of ventricular rate– Restoration and maintenance of sinus rhythm– Prevention of thromboembolism


Atrial Flutter

• Regular atrial tachyarrhythmia with atrial rate between 250-350 bpm.

• Flutter waves are seen as saw-tooth like atrial activity


Atrial Flutter

• Atrial Flutter is a form of atrial reentry localized to right atrium.

• Typically the ventricular rate is half the atrial rate, but the ventricular response may be 4:1, 2:1, 1:1 etc.


Atrial Flutter Circuit


Atrial Flutter



Atrial Flutter• Most often in patients with organic heart

disease

• Usually less long-lived than AF and may convert to AF.

• Control of ventricular rate is difficult in atrial flutter

• The most effective treatment is DC cardioversion


Paroxysmal Supraventricular Tachycardia (PSVT)

• Usually at a rate of 150-250 bpm

• No organic heart disease in the majority

• Presentations– Palpitations– Chest discomfort,dyspnea, lightheadedness– Frank syncope– SCD


PSVT



PSVT Mechanism

• Reentry in the vast majority

• Reentry may be localized to sinus node, atrium, AV junction or a macroreentrant circuit involving a bypass tract (WPW)

• In the absence of WPW, more than 90% are due to reentry through AV node or a concealed bypass tract


AV Nodal Reentrant Tachycardia(AVNRT)

• The most common form of paroxysmal supraventricular tachycardia (about 70%)

• More common in women (66%)• Usually a regular narrow QRS complex

tachycardia• No P wave is usually evident during the

tachycardia. Retrograde P waves may occasionally be seen at the end of QRS.


Longitudinal Dissociation Within AV Node

Slow Pathway

Fast Pathway

Atrium

His Bundle


AVNRT


Preexcitation


Wolff-Parkinson-White Syndrome



AV Reentrant Tachycardia(AVRT)

• Incorporates a bypass tract as part of the tachycardia circuit.

• Surface ECG:– Manifest with short PR interval and delta wave

(preexcitation)– Concealed with normal ECG

• Prevalence of ECG pattern: 0.1% to 0.3%.


AVRT


Concealed Accessory Pathway



PSVTTreatment

• Vagal maneuvers particularly carotid sinus massage

• AV nodal blocking drugs– Adenosine– Verapamil– Propranolol– Digoxin

• DC cardioversion if hypotensive

• Radiofrequency ablation


Electrophysiologic Study (EPS)


Catheter Positions at Fluoroscopy


Intracardiac Recordings


Radiofrequency Ablation (RFA)

Through femoral vein and right atrium


Loss of Delta during RF Burn



Loss of Delta during Burn


Ventricular ArrhythmiasDefinitions

• Premature Ventricular beats– Single beats– Ventricular Bigeminy, the appearance of one PVC after each sinus

beat– Couplets, two consecutive premature beats– Triplets, three consecutive premature beats– Salvos, runs of 3-10 premature beats

• Accelerated Idioventricular Rhythm (Slow VT), rate 60-100 bpm

• Ventricular Tachycardia (VT), rate over 100 bpm • Ventricular Flutter, regular large oscillations at a rate of

150-300 bpm• Ventricular Fibrillation (VF), irregular undulations of

varying contour and amplitude


Ventricular TachycardiaClassification

• Duration– Sustained VT defined as VT that persists for than 30 s

or requires termination because of hemodynamic collapse

– Nonsustained VT, 3 beats to 30 s

• Morphology– Monomorphic

– Polymorphic


Salvos


Sustained Monomorphic VT


Sustained Polymorphic VT


VT, Holter Recording


VTPresentations


VT Etiology

• VT generally accompanies some form of structural heart disease most commonly:– Ischemic heart disease– Cardiomyopathies

• Primary electrical abnormalities– Long QT syndromes– Brugada syndrome

• Idiopathic VT


Electrocardiographic Differentiation of VT vs. SVT with Aberrancy

• Clinical history

• AV dissociation

• QRS morphology

• QRS axis

• Fusion beat

• Capture beat


A-V Dissociation, Fusion, and Capture Beats in VT

Fisch C. Electrocardiography of Arrhythmias. 1990;134.

ECTOPY FUSION CAPTURE

V1 E F C


Fusion and Capture Beats in VT

Fisch C. Electrocardiography of Arrhythmias. 1990;135.

F C C

C C


VTPrognosis

• Depends on the underlying disease state– 75% first year mortality in the first few weeks

after MI– Poor prognosis in patients with left ventricular

dysfunction– No increased risk in those with idiopathic VT


Ventricular Fibrillation


Sudden Death Syndrome

• Incidence– 400,000 - 500,000/year in U.S.– Only 2% - 15% reach the

hospital– Half of these die before

discharge

• High recurrence rate


Underlying Arrhythmia of Sudden Death

VT62% Bradycardia

17%

Torsadesde Pointes

13%

PrimaryVF8%

Adapted from Bayés de Luna A. Am Heart J. 1989;117:151-159.

Tehran Arrhythmia CenterTehran Arrhythmia Center

Snapshot of Death

Tehran Arrhythmia CenterTehran Arrhythmia Center

Return of LifeNot the usual case !


Clinical Substrates Associated with VF Arrest

• Coronary artery disease• Idiopathic cardiomyopathy• Hypertrophic cardiomyopathy• Long QT syndrome• RV dysplasia• Rarely: WPW syndrome


VT/VFTherapeutic Options

• Antiarrhythmic drugs

• Anti-tachycardia pacing

• Radiofrequency ablation

• Implantable defibrillators


Earliest Defibrillator in Clinical Use, 1899


First Implantable Defibrillator 1970


Thoracotomy Lead System, the technique

used at the beginning


Nonthoracotomy Lead System


Pectoral ImplantationThe Current Technique


Tiered Therapy Defibrillators


Defibrillator Function


Interrogated ICD EventVT, treated appropriately by burst pacing therapy


Interrogated ICD EventVT (CL 320ms), no response to burst pacing therapy


Interrogated ICD EventVT (CL 320ms), cardioverted by DC shock


Clinical Uses of Defibrillator Therapy

Congenital Long QT Syndrome

A Frequently Missed Diagnosis


Long QT Interval


Clinical Manifestations

• Long QT syndrome is characterized by the presence of a long QT interval (usually over 440 ms) and emergence of ventricular arrhythmias.

• The presenting arrhythmia is a polymorphic ventricular tachycardia called ‘Torsade de Pointes’.

• Patient present with recurrent syncope or sudden cardiac death.

• Early diagnosis by ‘looking at ECG’ is critical!


Torsade de Pointes

• Prolonged QT interval associated with a polymorphic VT characterized by QRS complexes that change in amplitude and cycle length, giving the appearance of oscillations around the baseline

• Congenital or acquired


Brugada SyndromeDefinition

• Clinical-electrocardiographic diagnosis based on:

- High incidence of sudden cardiac death

- Structurally normal heart

- Characteristic ECG pattern


ECG Abnormalities

• ST segment elevation in V1-V3

• QRS complex resembling RBBB

• J-point elevation


Brugada ECG Pattern


History• First time in 1986: a 3-year polish boy• First presentation at NASPE meeting in

1991• First paper by Pedro and Josep Brugada in

1992• In the Philippines as “ bangungut”• In Japan as “Pokkuri”• In Thailand as “ Lai tai”, SUDS Circ. 1997

• Thai men correlated to Brugada, SUNDS Hum. Mol. Gen. 2002


Brugada Syndrome Prevalence in men (8:1 ratio males: females)

Familial incidence (autosomal dominant with incomplete penetrance ranging between 5 and 66 per 10 000)

True prevalence is difficult to estimate as the ECG pattern is often concealed.

It is endemic in Southeast Asia including: Thailand, Japan, Laos, Cambodia, Vietnam, the Philippines, and China.

Appearance of arrhythmic events at an average age of 40 years


Clinical ManifestationsSudden cardiac deathSyncope, seizure, agonal respiration, Episodes at night during sleep with labored

respiration, agitation, loss of urinary control, recent memory loss

Most commonly occurs during sleep, in particular during the early morning hours

Early diagnosis is of utmost importanceThe only treatment is currently implantation of an

‘Implantable Cardioverter Defibrillator’.



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