abnomalites of ecg

8/3/2019 Abnomalites of ECG

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Arrhythmias and

Conduction Disorders

Professor V. Syvolap


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Standard ECG Components

By convention, the

ECG tracing is divided

into theP wave,

PR interval,

QRS complex,

QT interval,ST segment,

T wave, and

U wave


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Normal rhythm

The resting sinus heart rate inadults is usually 60 to 100

beats/min.

Normally, a marked diurnal

variation in heart rate occurs,with lowest rates just beforeearly morning awakening.


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Normal rhythm

A slight increase in rate duringinspiration with a decrease in rate

during expiration (respiratorysinus arrhythmia) is also normal;

it is mediated by oscillations in

vagal tone and is particularlycommon among healthy youngpeople.


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Normal rhythm

The oscillations lessen but do notentirely disappear with age.

Absolute regularity of the sinusrhythm rate is pathologic andoccurs in patients with autonomic

denervation (eg, in advanceddiabetes) or with severe heartfailure.


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Normal rhythm

Most cardiac electrical activity isrepresented on the ECG, although SAnode, AV node, and His-Purkinjedepolarization does not involveenough tissue to be detected.

The P wave represents atrialdepolarization. The QRS complexrepresents ventricular depolarization,and the T wave represents ventricularrepolarization.


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Normal rhythm

The PR interval (from thebeginning of the P wave to the

beginning of the QRS complex) isthe time from the beginning ofatrial activation to the beginningof ventricular activation. Much of

this interval reflects slowing ofimpulse transmission in the AVnode.


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Normal rhythm

The R-R interval (time between 2QRS complexes) represents the

ventricular rate.


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Normal rhythm

The QT interval (from the beginning of the QRScomplex to the end of the T wave) representsthe duration of ventricular depolarization.

Normal values for the QT interval are slightlylonger in women; they are also longer with aslower heart rate.

The QT interval is corrected (QTc) for influence

of heart rate. The most common formula (allintervals in sec) is:


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Sinus bradycardia

Slower rates (heart rate less then60 b/m) occur in young people,

particularly athletes and during sleep.


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Sinus tachycardia

Faster rates (heart rate more then100 b/m) occur with exercise, illness,

or emotion through sympatheticneural and circulating catecholaminedrive.


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Pathophysiology

Rhythm disturbances result from

abnormalities of impulse formation,

impulse conduction,

or both.


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Bradyarrhythmias

result from decreased intrinsicpacemaker function or blocks in

conduction, principally within theAV node or the His-Purkinjesystem.


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Tachyarrhythmias

Most tachyarrhythmias are causedby

reentry;

some result from enhancednormal automaticity

or from abnormal mechanisms ofautomaticity.


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Reentry

is the circular propagation of animpulse around 2 interconnected

pathways with different conductioncharacteristics and refractory periods


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Reentry

Two pathwaysconnect the samepoints. Pathway A

has slowerconduction and ashorter refractoryperiod. Pathway B

conducts normallyand has a longerrefractory period.


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Reentry

I. A normal impulse arriving at 1 goes downboth A and B pathways. Conduction throughpathway A is slower and finds tissue at 2already depolarized and thus refractory. A

normal sinus beat results.


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ReentryII. A premature impulse finds pathway B refractory and

is blocked, but it can be conducted on pathway Abecause its refractory period is shorter. On arriving at 2,the impulse continues forward and retrograde uppathway B, where it is blocked by refractory tissue at 3.

A premature supraventricular beat with an increased PRinterval results.


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ReentryIII. If conduction over pathway A is sufficiently slow, a

premature impulse may continue retrograde all the wayup pathway B, which is now past its refractory period.If pathway A is also past its refractory period, theimpulse may reenter pathway A and continue to circle,sending an impulse each cycle to the ventricle (4) and

retrograde to the atrium (5), producing a sustainedreentrant tachycardia.


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Atrial premature beats

Atrial premature beats (APBs), or prematureatrial contractions (PACs), are commonepisodic impulses.

They may occur in normal hearts with orwithout precipitating factors (eg, coffee,tea, alcohol, pseudoephedrine) or may be a

sign of a cardiopulmonary disorder.They are common in patients with COPD.


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Atrial premature beats

Diagnosis is by ECG APBs may be normally,aberrantly, or not conducted and are usually

followed by a noncompensatory pause.

Aberrantly conducted APBs (usually withright bundle branch block morphology) must

be distinguished from premature beats ofventricular origin.


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Atrial tachycardia

Atrial tachycardia is a regular rhythmcaused by the consistent, rapid atrial

activation from a single atrial focus.Heart rate is usually 150 to 200beats/min; however, with a very rapidatrial rate, nodal dysfunction, or

digitalis toxicity, atrioventricular (AV)block may be present, and ventricularrate may be slower.


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Atrial tachycardia

Mechanisms include enhanced atrialautomaticity and intra-atrial reentry.

Atrial tachycardia is the least commonform (5%) of supraventriculartachycardia and usually occurs inpatients with a structural heart

disorder. Other causes include atrialirritation (eg, pericarditis), drugs (eg,digoxin), alcohol, and toxic gasinhalation.


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Atrial tachycardia

Symptoms are those of othertachycardias. Diagnosis is by ECG; P

waves, which differ in morphologyfrom normal sinus P waves, precedeQRS complexes but may be hidden

within the preceding T wave


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Atrial tachycardia

This narrow QRS tachycardia arises from an abnormalautomatic focus or intra-atrial reentry. P waves precedethe QRS complexes; it is a long RP tachycardia (PR 300/min notalways apparent in all leads),

and irregularly irregular R-R intervals


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Atrial fibrillation


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Atrial flutter

Atrial flutter is a rapid regular atrialrhythm due to an atrial macro-

reentrant circuit.


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Atrial flutter

Classical atrial flutter is due to a largereentrant circuit involving most of the rightatrium. The atria depolarize at a rate of 250

to 350/min (typically 300/min). Because theatrioventricular (AV) node cannot usuallyconduct at this rate, typically of theimpulses get through (2:1 block), resulting ina regular ventricular rate of 150 beats/min.

Sometimes block varies from moment tomoment, causing an irregular ventricularrhythm. Less commonly, a fixed 3:1, 4:1, or5:1 block may be present.


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Atrial flutterSymptoms and Signs

Symptoms depend primarily on ventricularrate and the nature of any underlying heartdisorder. If ventricular rate is < 120

beats/min and regular, there are likely to befew or no symptoms.

Faster rates and variable AV conductionusually produce palpitations, and decreasedcardiac output may produce symptoms of

hemodynamic compromise (eg, chestdiscomfort, dyspnea, weakness, syncope).Close inspection of the jugular venous pulsereveals flutter awaves.

Atrial flutter


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Atrial flutterThe diagnosis is by ECG, which shows continuous and regularatrial activation with a sawtooth pattern, most obvious in leads

II, III, and aVF


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Conduction Disorders


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Atrioventricular (AV)block

is partial or complete interruption ofimpulse transmission from the atria to

the ventricles. The most commoncause is idiopathic fibrosis and

sclerosis of the conduction system.Diagnosis is by ECG; symptoms and

treatment depend on degree of block,but treatment, when necessary,usually involves pacing.


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First-degree AV block

First-degree AV block may bephysiologic in younger patients

with high vagal tone and in well-trained athletes. First-degree AVblock is rarely symptomatic and notreatment is required, but further

investigation may be indicatedwhen it accompanies another heartdisorder or appears to be causedby drugs.


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First-degree AV block

All normal P waves are followed byQRS complexes, but the PR interval is

longer than normal (> 0.20 sec)


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Second-degree AV block

Some normal P waves are followedby QRS complexes, but some are

not. Three types exist: In Mobitz type I 2nd-degree AV

block,

Mobitz type I 2nd-degree AVblock,

M bi I 2 d d


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Mobitz type I 2nd-degreeAV block

In Mobitz type I 2nd-degree AV block, thePR interval progressively lengthens with

each beat until the atrial impulse is notconducted and the QRS complex isdropped (Wenckebach phenomenon); AVnodal conduction resumes with the next

beat, and the sequence is repeated

M bit t II 2 d


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Mobitz type II 2nd-degree AV block

In Mobitz type II 2nd-degree AV block,the PR interval remains constant. Beats

are intermittently nonconducted and QRScomplexes dropped, usually in arepeating cycle of every 3rd (3:1 block) or

4th (4:1 block) P wave

Hi h d 2 d d


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High-grade 2nd-degreeAV block

In high-grade 2nd-degree AV block, every2nd (or more) P wave is blocked


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Third-degree AV block

Heart block is complete.There is no electrical communication between the atria

and ventricles and no relationship between P waves

and QRS complexes (AV dissociation). Cardiac functionis maintained by an escape junctional or ventricular

pacemaker.

L ft B dl B h Bl k


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Left Bundle Branch Block(LBBB)

Left bundle branch block (LBBB) resultsfrom conduction delay or block in any of

several sites in the intraventricularconduction system, including the main leftbundle branch, in each of the two fascicles,or, less commonly, within the fibers of thebundle of His that become the main left

bundle branch.The result is extensive reorganization of theactivation pattern of the left ventricle.


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ECG ABNORMALITIES LBBB

LBBB produces a prolonged QRSduration,

abnormal QRS complexes, and ST-T wave abnormalities.

C l t d


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Commonly accepteddiagnostic criteria for LBBB

Basic requirements include a prolonged QRSduration to 120 msec or beyond;

broad, sometimes notched R waves in leadsI and aVl and the left precordial leads;

narrow r waves followed by deep S waves inthe right precordial leads; and absent septalq waves.

R waves are typically tall and S waves aredeep.

C l t d


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The mean QRS axis with LBBB is highlyvariable; it can be normal, deviated to theleft or, less often, deviated to the right.

Left axis deviation is associated with moresevere conduction system disease thatincludes the fascicles as well as the main

left bundle, whereas right axis deviationsuggests dilated cardiomyopathy withbiventricular enlargement.

C l t d


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In addition to these features, someelectrocardiographers require a delayed intrinsicoiddeflection (60 msec or greater) to diagnose LBBB.

ST-T wave changes are also prominent with LBBB.In most cases, the ST wave and the T wave arediscordant with the QRS complex; that is, the STsegment is depressed and the T wave is inverted inleads with positive QRS waves (leads I, aVl , V5 ,

and V6 ), while the ST segment is elevated and theT wave is upright in leads with negative QRScomplexes (leads V1 and V2 ).

ECG ABNORMALITIES


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ECG ABNORMALITIESLBBB

CLINICAL SIGNIFICANCE LBBB


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LBBB usually appears in patients with

underlying heart disease. It is associated with significantly reduced

long-term survival and with 10-year survivalrates as low as 50 percent, probably

reflecting the severity of the underlyingcardiac disease.



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Among patients with coronary arterydisease, the presence of LBBB correlateswith more extensive disease, more severe

left ventricular dysfunction, and reducedsurvival rates.

The duration of the QRS complex in LBBBcorrelates inversely with left ventricular

ejection fraction. Patients with associatedleft or right axis deviation have more severeclinical manifestations.



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In addition to the hemodynamic abnormalitiesproduced by these underlying conditions, theabnormal ventricular activation pattern of LBBBitself induces hemodynamic perturbations, includingabnormal systolic function with dysfunctionalcontraction patterns, reduced ejection fraction andlower stroke volumes, and abnormal diastolicfunction; reversed splitting of the second heart

sound and functional mitral regurgitation arecommon.

ECG patterns of LBBB, including low R waveamplitude in the midprecordial leads and ST-T wavechanges, can simulate anterior infarct patterns.

Ri ht B dl B h Bl k


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Right Bundle Branch Block(RBBB)

Right bundle branch block is a result

of conduction delay in any portion ofthe right-sided intraventricularconduction system.

Ri ht B dl B h Bl k


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The delay can occur in the main rightbundle branch itself, in the bundle of

His, or in the distal right ventricularconduction system.

Right B ndle B anch Block


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The latter is the common cause ofRBBB after right ventriculotomyperformed, for example, to correct thetetralogy of Fallot. The highprevalence of RBBB corresponds to therelative fragility of the right bundle

branch, as suggested by thedevelopment of RBBB after minortrauma produced by right ventricularcatheterization.

ECG ABNORMALITIES


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ECG ABNORMALITIESRBBB

As with LBBB, the QRS complex durationexceeds 120 msec.

The right precordial leads show prominentand notched R waves with rsr', rsR', or rSR'patterns, while leads I, aVl , and the leftprecordial leads demonstrate wide S waves

that are longer in duration than thepreceding R wave.

ECG ABNORMALITIES


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ECG ABNORMALITIESRBBB

Septal q waves are preserved because theinitial ventricular activation remainsunchanged.

The ST-T waves are, as in LBBB, discordantwith the QRS complex, so T waves areinverted in the right precordial leads (andother leads with a terminal R' wave) and

upright in the left precordial leads and inleads I and AVl .

The mean QRS axis is not altered by RBBB.


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RBBB


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CLINICAL SIGNIFICANCE

RBBB is a common finding in the generalpopulation, and many persons with RBBBhave no clinical evidence of structural heart

disease.In the group without overt heart disease,the ECG finding has no prognosticsignificance.However, the new onset of RBBB doespredict a higher rate of coronary arterydisease, congestive heart failure, andcardiovascular mortality.


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CLINICAL SIGNIFICANCE

When cardiac disease is present, the coexistence ofRBBB suggests advanced disease with, for example,more extensive multivessel disease and reducedlong-term survival in patients with ischemic heartdisease.

An entity known as the Brugada syndrome hasbeen described in which a RBBB-like pattern withpersistent ST segment elevation in the right

precordial leads is associated with susceptibility toventricular tachyarrhythmias and sudden cardiacdeath.

abnomalites of ecg

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