A El Outline June 2007

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THE "ALAN E. LINDSAY ECG TUTORIAL"

V6.0 (July 2007)

Frank G. Yanowitz, MD

Professor of MedicineUniversity of Utah School of Medicine

Director, IH !G Services"DS Hos#ital

Salt "ake ity, Utah

INTRODUCTIONThis tutorial is dedicated to the memory of Alan E. Lindsay, MD (1923-1987)master teacher of electrocardiography, friend, mentor, and colleague. Many of the

excellent ECG tracings illustrated in this learning program are from Dr. Lindsay'spersonal collection of ECG treasures. For many years these ECG's hae !een used inthe training of medical students, nurses, housesta" physicians, cardiology fello#s,and practicing physicians in $alt La%e City, &tah as #ell as at many regional andnational medical meetings.

t is an honor to !e a!le to proide this tutorial as #ell as an interactie ECG #e!siteon the nternet in recognition of Dr. Lindsay's great loe for teaching and for

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electrocardiography) http)**li!rary.med.utah.edu*%#*ecg. This tutorial and the ECG#e!site presents an introduction to clinical electrocardiography.

ECG terminology and diagnostic criteria often ary from !oo% to !oo% and from oneteacher to another. n this tutorial an attempt has !een made to conform tostandardi+ed terminology and criteria, although ne# diagnostic concepts deried

from the recent ECG literature hae !een included in some of the sections. Finally, itis important to recogni+e that the mastery of ECG interpretation, one of the mostuseful clinical tools in medicine, can only occur if one acuires considera!leexperience in reading ECG's and correlating the speci-c ECG -ndings #ith thepathophysiology and clinical status of the patient.

The sections in this tutorial are organi+ed in the same order as the recommendedapproach outlined in the Method of ECG interpretation/see Chapter 0, p12.3eginning students should -rst go through the sections in the order in #hich they arepresented. 4thers may choose to explore topics of interest in any order they #ish. tis hoped that all students #ill !e left #ith some of the loe of electrocardiographyshared !y Dr. Lindsay.

$%&"! 'F '($!($S(. The $tandard (0 Lead ECG/p. 52 1. 6trial Enlargement/p. 702

0. 6 Method8 of ECG nterpretation/p.12

9. :entricular ;ypertrophy/p. 7


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encouraged to study this list and !ecome familiar #ith the recognition of these ECGdiagnoses. Most of the diagnoses are illustrated in this tutorial.

Basic Competency in Electrocardiography

NORMAL RA!"N#

=ormal ECG

E!$N"!AL %RO&LEM

Lead misplaced

6rtifact

'"N' R$$M'*ARR$$M"A'

$inus rhythm /7?>? !pm2

$inus tachycardia />? !pm2 $inus !radycardia /7? !pm2

$inus 6rrhythmia

$inus arrest or pause

$inoatrial exit !loc%

O$ER 'V ARR$$M"A'

6C's /nonconducted2

6C's /conducted normally2

6C's /conducted #ith a!erration2

Ectopic atrial rhythm or tachycardia /unifocal2

Multifocal atrial rhythm or tachycardia

6trial -!rillation

6trial Hutter Iunctional prematures

Iunctional escapes or rhythms2

6ccelerated Iunctional rhythms

Iunctional tachycardia

aroxysmal supraentricular tachycardia

VENR"!LAR ARR$$M"A'

:C's

:entricular escapes or rhythm

6ccelerated entricular rhythm

:entricular tachycardia /uniform2

:entricular tachycardia /polymorphous or

torsades22 :entricular -!rillation

AV !OND!"ON (stdegree 6: !loc%

Type 0nddegree 6: !loc% /Benc%e!ach2

Type 0nddegree 6: !loc% /Mo!it+2

6: !loc%, adanced /high grade2


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6nterior M

6nterolateral M

;igh lateral M

=on K#ae M

Aight entricular M

!L"N"!AL D"'ORDER'

Chronic pulmonary disease pattern

$uggests hypo%alemia

$uggests hyper%alemia

$uggests hypocalcemia

$uggests hypercalcemia

$uggests digoxin e"ect

$uggests digoxin toxicity

$uggests C=$ disease

%A!EMAER E!#

6trialpaced rhythm

:entricular paced rhythm

6: seuential paced rhythm

Failure to capture /atrial or entricular2 Failure to inhi!it /atrial or entricular2

Failure to pace /atrial or entricular2

5


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1. THE 'ANDARD12 LEAD ECG

The standard (0lead electrocardiogram is a representation of the

heart's electrical actiity recorded from electrodes on the !ody surface.This section descri!es the !asic components of the ECG and thestandard lead system used to record the ECG tracings.

$he dia)ra* ill+strates !G waves and intervals as well as standard ti*eand volta)e *eas+res on the !G #a#er.

E!# 4AVE' AND "NERVAL'5 4a/ d /y an

% a:5 sequentialdepolari+ation of the right and left atria

+R' ;l


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OR"ENA"ON O= $E 12-LEAD E!#5

"/ is i;/an/ / > /a/ / 12-lad E!# ;:ids s;a/ial in?a/ina>u/ / a/@s l/ial a/i:i/y in 3 approximately/nal di/ins(/inB5 ,C)5

Ri/ L?/ (,)

'u;i "n?i () An/i %s/i (C)

Ea ? / 12 lads ;sn/s a ;a/iula in/a/in in s;a as india/d>l (RA i/ aF LA l?/ a LL l?/ l)5

Bipolar limb leads (frontal plane):

Lad "5 RA (- ;l) / LA (G ;l) (Ri/ -/- L?/ di/in)

Lad ""5 RA (-) / LL (G) (s/ly 'u;i -/- "n?i di/in)

Lad """5 LA (-) / LL (G) (s/ly 'u;i -/- "n?i di/in)

Augmented limb leads (frontal plane):

Lad aVR5 RA (G) / HLA I LL (-) (Ri/ad di/in)

Lad aVL5 LA (G) / HRA I LL (-) (L?/ad di/in)

Lad aV=5 LL (G) / HRA I LA (-) ("n?i di/in)

Unipolar (+) chest leads (horizontal plane): Lads V1 V2 V35 (%s/i -/- An/i di/in)

Lads VK V V65 (Ri/ -/- L?/ di/in)

Behold: Einthoven's Triangle! Each of the frontal lane or "li#$" leads has a negativeand ositive ole %as indicated $& the '' and '(' signs). *t is i#ortant to recogni+e that lead* %and to a lesser e,tent a-L) are right (to( left in direction. Also lead a-/ %and to a lessere,tent leads ** and ***) are s0erior (to( inferior in direction. The diagra# $elo f0rtherill0strates the frontal lane hoo0.

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3ote: the act0al ECG avefor# in each of the li#$ leads varies fro# erson to erson

deending on age $od& si+e gender frontal lane 456 a,is resence or a$sence of heartdisease and #an& other varia$les. The recordial leads are ill0strated $elo.

1

%dial lad ;lan/

:() 5thintercostal space /$2 adacent toright sternal !order

:0) 5th$ adacent to left sternal !order

:


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2. A "7ETH8D" 8/ ECG *3TE595ETAT*83

This method is recommended #hen reading (0lead ECG's. Li%e the approach todoing a physical exam, it is important to follo# a standardi+ed seuence of steps inorder to aoid missing su!tle a!normalities in the ECG tracing, some of #hich mayhae clinical importance. The @ maor sections in themethod should !e consideredin the follo#ing order)

(. Masun/s

0. Ry/ analysis


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This is the conclusion of the a!oe analyses. nterpret the ECG as

Nal, or A>nal. 4ccasionally the term >dlin is used ifunsure a!out the signi-cance of certain -ndings or for minor changes. Listall a!normalities. Examples of a!normal statements are)

nferior M, pro!a!ly acute

4ld anteroseptal M Left anterior fascicular !loc% /L6F32

Left entricular hypertrophy /L:;2

Aight atrial enlargement /A6E2

=onspeci-c $TT #ae a!normalities

$peci-c rhythm a!normalities

E;F %R0.16 sF +R'0.09 sF +0.36 sF +R' alB

8! ./"5A%,$/& 2,' 5%#3,/U$ #.7:

f there is a preious ECG in the patient's -le, the current ECG should !e

compared #ith it to see if any signi-cant changes hae occurred. Thesechanges may hae important implications for clinical managementdecisions.

$O4 O MEA'RE $E +R' A,"'5

"NROD!"ON5 ?n/al ;lan +R' a


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:n/iula a/i:a/in (.. l?/ an/i ?asiula >lB) i/ an > anindia/ ? yadial daa (.. in?i yadial in?a/in).D/ina/in ? / +R' als us /:isualiP /is."n / diaa >l / nal an is sadd (-30 / G90). "n /

adul/ l?/ a


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f there is no isoelectric lead, there are usually t9oleads that are nearly

isoelectric, and these are al#ays


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L?/ A


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(. Lead a:A is closest to !eing isoelectric /slightly more positie than negatie20. The t#o perpendiculars are @?P and J(0?P.


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. CHA5ACTE5*6T*C6 8/ THE 3857AL ECG"/ is i;/an/ / > /a/ / is a id an ? nal :aia/inin / 12 lad E!#. ?llin nal E!# aa/is/is /?a n/ a>slu/. "/ /aBs nsida>l E!# adin y ?llin a s/u/ud "ethod of #.7,nterpretation and la/in / :aius E!# Sndins i/ / ;a/iula

;a/in/@s linial s/a/us ill / E!# > a :alua>l linial /l.*. 3or#al 7EA6;5E7E3T6

$a/ Ra/5 0 - 90 >;

%R "n/:al5 0.12 - 0.20s

+R' Dua/in5 0.06 - 0.10s

+ "n/:al (+ 0.KKs)

5oor "an;s 7uideto the upper limit of KT) Q 1? !pm, KT ?.5?s foreery (? !pm increase a!oe 1? !pm su!tract ?.?0s, and for eery (?!pm decrease !elo# 1? !pm add ?.?0s. For example)

KT ?.


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n reerse, the s#aes !egin in :@ or :7 and increase in

si+e to :0. $:( is usually smaller than $:0.

The usual transition from $A in the right precordial leads to

A$ in the left precordial leads is :< or :5.

$mall septal #aes may !e seen in leads :7 and :@.

' 'n/5 n a sense, the term $T segment is a misnomer, !ecausea discrete $T segment distinct from the T #ae is often not seen. Morefreuently the $TT #ae is a smooth, continuous #aeform !eginning #iththe Ipoint /end of KA$2, slo#ly rising to the pea% of the T and follo#ed !ya rapid descent to the isoelectric !aseline or the onset of the & #ae. Thisgies rise to asymmetrical T #aes in most leads. The $T segment occursduring hase 0 /the plateau2 of the myocardial action potentials. n somenormal indiiduals, particularly #omen, the T #ae is more symmetricaland a distinct hori+ontal $T segment is present.

The $T segment is often eleated a!oe !aseline in leads #ith

large $ #aes /e.g., :0


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Nal :aian/ (%R 0.10 - 0.12s)

Din/ial Diansis ? %lnd %R5 U0.20s

=is/ d AV >lB (%R in/:al usually ns/an/ ?

>a/ / >a/)F ;ssi>l la/ins ? / ndu/in dlayinlud5

ntraatrial conduction delay /uncommon2

$lo#ed conduction in 6: node /most common site ofprolonged A2

$lo#ed conduction in ;is !undle /rare2

$lo#ed conduction in a !undle !ranch /#hen

contralateral !undle is totally !loc%ed i.e., (stdegree!undle !ranch !loc%2

'nd d AV >lB (%R in/:al ay > nal

;lndF s % a:s d n/ ndu/ / :n/ils anda n/ ?lld >y a +R')

Type /Benc%e!ach2) ncreasing A until nonconducted

#ae occurs

Type /Mo!it+2) Fixed A interals plus nonconducted

#aes AV dissia/in) $ome A's may appear prolonged, !ut the

#aes and KA$ complexes are dissociated /i.e., not married, !utstrangers passing in the night2.

2. +R' Dua/in (dua/in ? +R' ;l< in ?n/al ;lan)5

Nal5 0.06 - 0.10s

Din/ial Diansis ? %lnd +R' Dua/in (U0.10s)5

+R' dua/in 0.10 - 0.12s

ncomplete right or left !undle !ranch !loc%

=onspeci-c intraentricular conduction delay /:CD2

$ome cases of left anterior or posterior fascicular !loc%

+R' dua/in 0.12s

Complete A333 or L333

=onspeci-c :CD

Ectopic rhythms originating in the entricles /e.g.,

entricular tachycardia, accelerated entricular rhythm,pacema%er rhythm2

3. + "n/:al (asud ? >innin ? +R' / nd ? a: in /

?n/al ;lanF /d + + asud + sQ-/ RR in sndsF

&aP/s ?ula) Nal + is a/ a/ d;ndn/ (u;; lii/ ? + 0.KK s) Ln + 'ynd - L+' (>asd n u;; lii/s ? a/ a/F

+ 0.K7 s ? als and 0.K8 s in ?als is dians/i ?

di/ay L+' in a>sn ? / auss ? ln +)5 This a!normality may hae important clinical implications since it

usually indicates a state of increased ulnera!ility to malignantentricular arrhythmias, syncope, and sudden death. The prototypearrhythmia of the Long QT Interval Syndromes (LQTS)is Torsadesdepointes, a polymorphic entricular tachycardia characteri+ed !yarying KA$ morphology and amplitude around the isoelectric!aseline. Causes of LQTSinclude the follo#ing)

(1


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Drugs /many antiarrhythmics, tricyclics, phenothia+ines,

and others2

Electrolyte a!normalities /=RJ, =CaJJ, =MgJJ2

C=$ disease /especially su!arrachnoid hemorrhage,

stro%e, trauma2

;ereditary LKT$ /at least 1 genotypes are no# %no#n2

Coronary ;eart Disease /some postM patients2 Cardiomyopathy

'/ + 'ynd (+ T0.32 s)5 =e#ly descri!ed hereditary

disorder #ith increased ris% of sudden arrhythmic death. The KT criteriaare su!ect to change.

K. =n/al %lan +R' Anali/is in / +R' A


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$ome cases of entricular tachycardia

(>


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>. ECG 5H?TH7 AB3857AL*T*E6

,&'%/0U.',/& '/ #.7 %*'" A&A*$,$:

$"N#' O !ON'"DER 4$EN ANALC"N# ARR$$M"A'5

6rrhythmias may !e seen on (0lead ECGs or on rhythm strips of one or moreleads. $ome arrhythmias are o!ious at -rst glance and don't reuire intenseanalysis. 4thers, ho#eer, are more challenging /and fun2 They reuiredetectie #or%, i.e., logical thin%ing. Ahythm analysis should !egin #ithidentifying characteristics of impulse formation/if %no#n2 as #ell asimpulse conduction. ;ere are some things to thin% a!out)

Descriptors of impulse formation/i.e., the pacema%er orregion of impulse formation2

$ite of origin i.e., #here is the a!normal rhythm coming fromO

$inus =ode /e.g., sinus tachycardia #aes may !e

hidden in the T #aes2

6tria /e.g., 6C2

6: unction /e.g., unctional escape rhythm2 :entricles /e.g., :C2

Aate /i.e., relatie to the expected rate for that pacema%er location2

6ccelerated faster than expected for that pacema%er

site /e.g., accelerated unctional rhythm2

$lo#er than expected /e.g., mar%ed sinus !radycardia2

=ormal /or expected2 /e.g., unctional escape rhythm2

Aegularity of entricular or atrial response

Aegular /e.g., paroxysmal supraentricular tachycardia

$:T2

Aegular irregularity /e.g., entricular !igeminy2

rregular irregularity /e.g., atrial -!rillation or M6T2

rregular /e.g., multifocal :Cs2 4nset /i.e., ho# does arrhythmia !eginO2

6ctie onset /e.g., 6C or :C2

assie onset /e.g., entricular escape !eat or rhythm2

Descriptors of impulse conduction/i.e., ho# does the

a!normal rhythm moe through the heart cham!ersO2 6ntegrade /for#ard2 s. retrograde /!ac%#ard2 conduction

Conduction delays or !loc%s) i.e., (st, 0nd/type or 2,


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". $upra=entricular Arrhythmias

5remature Atrial .omplexes (5A.;s)

4ccur as single or repetitie eents and hae unifocal or multifocal

origins.

The ectopic #ae /often called '2 is often hidden in the $TT #ae

of the preceding !eat. /Dr. Marriott, master ECG teacher and

author, li%es to say) .herchez le 5 sur le '#hich in Frenchmeans) $earch for the on the T #ae, and it's clearly sexier tosearch in French2

The 'A interal is normal or prolonged if the 6: unction is partially

refractory at the time the premature impulse enters it.

6C's can hae three di>erent outcomesdepending on the

degree of prematurity /i.e., coupling interal from preious #ae2,and the preceding cycle length /or AA interal2. This is illustrated inthe ladder diagram #here normal sinus !eats are follo#ed !y

three possi!le 6Cs /a,!,c2)

4utcome S(. =onconducted /or !loc%ed2 6C i.e., no

KA$ complex !ecause the 6C -nds the 6: node stillrefractory to conduction. /see 6C 'a' in the upperdiagram la!eled (, and a nonconducted 6Cs in ECGsho#n !elo# after


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sometimes called anAshman beat/see 6C '!' in theupper diagram la!eled (, and ECG !elo# sho#ing a 6C#ith A333 a!erration2

4utcome S


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Atrial 4ibrillation (Ab):

6trial actiity is poorly de-ned may see course or -ne !aseline undulations

/#iggles2 orno atrial actiity at all. f atrial actiity is seen, it resem!les theteeth on an old sa9/#hen compared to atrial Hutter that often resem!lesa cleansa9tooth patternespecially in leads , , a:F2.

:entricular response /AA interals2 is irregularly irregularand may !e

?as/ /;A (?? !pm, indicates inadeuate rate control2, da/ /;A W@?(?? !pm2, or sl/;A @? !pm, indicates excessie rate controlmedication, 6: node disease, or drug toxicity2.

6 regularentricular response #ith 6-! usually indicates complete or


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unctional escapes indicating highgrade 6: !loc% due /note constant AAinterals2.

The di"erential diagnosis includes atrial Hutter #ith an irregular entricular

response andmultifocal atrial tachycardia /M6T2, #hich is usuallyirregularly irregular. The di"erential diagnosis is often hard to ma%e from asingle rhythm strip the (0lead ECG is !est for di"erentiating these threearrhythmias.

Atrial 4lutter (ACutter):

Aegular atrial actiity #ith a clean sa9toothappearance in leads , ,

a:F, and usually discrete '' #aes in lead :(. The atrial rate is usuallya!out


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The entricular response may !e 0)(,


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conduction /i.e., rate related 3332. There are seeral types of $:T dependingon the location of the reentry circuit.

AV Ndal Rn/an/ ayadia (AVNR)5This is the most common form

of $:T accounting for approximately 7?Z of all symptomatic $:Ts. Thediagram !elo# illustrates the pro!a!le mechanism inoling dual 6: nodal

path#ays, alphaand beta, #ith di"erent electrical properties. n the diagramalphais a fast path#ay !ut #ith a long refractory period /A2, and betais theslo# path#ay #ith a short A. During sinus rhythm alphais al#ays used!ecause it is faster and there is plenty of time !et#een sinus !eats forrecoery to occur. 6n early 6C, ho#eer, -nds alphastill refractory and mustuse the slo#er betapath#ay to reach the entricles. 3y the time it traersesbeta,ho#eer,alphahas recoered allo#ing retrograde conduction !ac% tothe atria. The retrograde #ae /called an atrial echo2 is often simultaneous#ith the KA$ and not seen on the ECG, !ut it can reenter the 6: unction!ecause of beta;sshort A.

n the a!oe ECG 0 sinus !eats are follo#ed !y 6C /in the $T segment2 andonset of $:T. Aetrograde #aes immediately follo# each KA$ /little dip atonset of $T segment2

f an early 6C is properly timed, 6:=AT results as seen in the diagram !elo#.

Aarely, an atypical form of 6:=AT occurs #ith the retrograde #aeappearing in front of the next KA$ /i.e., A' interal (*0 the AA interal2,implying antegrade conduction do#n the faster alpha, and retrogradeconduction up the slo#er beta path#ay..

0@


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AV Ri;a/in ayadia (Ey;ass ;a/ay)5This is the

second most common form of $:T and is seen in patients #ith the BBsyndrome. The BB ECG, seen in the diagram on p. (5, sho#s a short A, delta#ae, and some#hat #idened KA$.

This type of $:T can also occur in the a!sence of the BB ECG if the

accessory path#ay only allo#s conduction in the retrograde direction /i.e.,naldBB2. Li%e 6:=AT, the onset of $:T is usually initiated !y a6C that -nds the !ypass trac% temporarily refractory, conducts do#n the6: unction to the entricles, and reenters the atria through the !ypass

trac%. n this type of $:T retrograde #aes appear shortly after the KA$in the $T segment /i.e., A' (*0 AA interal2. Aarely the antegrade lim!for $:T uses the !ypass trac% and the retrograde lim! uses the 6:

unction the $:T then resem!les a #ide KA$ tachycardia and must !edi"erentiated from entricular tachycardia.

'in-A/ial Rn/an/ ayadia5This is a rare form of $:T #here the

reentrant circuit is !et#een the sinus node and the right atria. The ECG loo%s li%esinus tachycardia, !ut the tachycardia is paroxysmal i.e., it starts and endsa!ruptly.

@unctional %hythms and 'achycardias

Jun/inal Esa; &a/s5These are%assive, protectie !eats originatingfrom su!sidiary pacema%er cells in the 6: unction. The pacema%er's !asic-ring rate is 5?@? !pm unctional escapes are programmed to occur#heneer the primary pacema%er /i.e., sinus node2 defaults or the 6: node!loc%s the atrial impulse from reaching the entricles. The ECG strip !elo#sho#s sinus arrhythmia #ith t#o unctional escapes /arro#s2. ncomplete 6:dissociation is also seen during the unctional escapes.

01


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Jun/inal Esa; Ry/5This is a seuence of < or more unctional

escapes occurring !y default at a rate of 5?@? !pm. There may !e 6:dissociation or the atria may !e captured retrogradely !y the unctionalpacema%er.

Ala/d Jun/inal Ry/5This is an acti=eunctional pacema%er

rhythm caused !y eents that pertur! pacema%er cells/e.g., ischemia,drugs, and electrolyte a!normalities2. The rate is @?(?? !pm2.

Nn;a


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:Cs may occur as isolated single eents or as couplets, triplets, andsalos /5@ :Cs in a ro#2 also called !rief entricular tachycardias.

:Cs may occur early in the cycle /AonT phenomenon2, after the T #ae /as seen

a!oe2, or late in the cycle often fusing #ith the next KA$ /fusion !eat2. AonT :Csmay !e especially dangerous in an acute ischemic situation, !ecause the entriclesare more ulnera!le to entricular tachycardia or -!rillation.

n the example !elo#, late /enddiastolic2 :Cs are illustrated #ith arying degrees offusion. For fusion to occur the sinus #ae must hae made it to the entricles tostart the actiation seuence. 3efore entricular actiation is completed, ho#eer, thelate :C occurs, and the resultant KA$ loo%s a !it li%e the normal KA$, and a !it li%ethe :C i.e., a fusion KA$ /arro#s2.

The eents follo#ing a :C are of interest. &sually a :C is follo#ed !y a completecompensatory pause, !ecause the sinus node timing is not interrupted one sinus

#ae near the :C isn't a!le to reach the entricles !ecause they are still refractoryfrom the :C the follo#ing #ae occurs on time !ased on the sinus rate. ncontrast, 6Cs are usually follo#ed !y an incomplete pause !ecause the 6C canreset the sinus node timing this ena!les the next sinus #ae to appear earlier thanexpected. These concepts are illustrated !elo#.

0>


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=ot all :Cs are follo#ed !y a pause. f a :C occurs early enough /especially ifthe heart rate is slo#2, it may appear sand#iched in !et#een t#o normal !eats. Thisis called an inter%olated:C. The sinus #ae follo#ing the :C usually has a longerA interal !ecause of retrograde onealed ondution!y the :C into the 6:

unction, slo#ing su!seuent conduction of the sinus impulse.

Finally a :C may retrogradely capture the atrium, reset the sinus node, and !efollo#ed !y an incomplete pause. 4ften the retrograde #ae can !e seen on theECG, hiding in the $TT #ae of the :C.

6 most unusual post:C eent occurs #hen retrograde actiation of the 6: unction/or atria2 reenters /or comes !ac% to2 the entricles as a entricular echo. This isillustrated !elo#. The ladder diagram under the ECG helps us understand themechanism. The #ae follo#ing the :C is the sinus #ae, >u/the A interal istoo short for it to hae caused the next KA$. /Aemem!er, the A interal follo#ing aninterpolated :C is usually longer than normal, not shorter2. snVt that coolO


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:Cs usually stic% out li%e sore thum!s or funnyloo%ing!eats /FL3Vs2, !ecausethey are !i+arre in appearance compared to the normal complexes. ;o#eer, not allpremature sore thum!s are :Cs. n the example !elo# 0 6Cs are seen, S( #ith anormal KA$, and S0 #ith A333 a!errancy #hich loo%s li%e a sore thum!. alln /? is / niP s /u>s ? a/ /y a and/a/@s / ny Ds. Alan Lindsay =anB ani/P and J. Dulas Ridsin / 1980s. 'li/ diSa/ins ? / iinal a: >n ad)

A&ERREN VENR"!LAR !OND!"ON


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"NROD!"ON

6!errant entricular conduction /6:C2 is a ery common source of confusion ininterpreting (0lead ECGs and rhythm strips. 6 thorough understanding of its

mechanism and recognition is essential to all persons #ho read ECGs.

3efore #e can understand a!errant entricular conduction #e must -rst reie# ho#normal conduction of the electrical impulse occurs in the heart. 4a/ aaniSn/ dsinX mpulses from the fastest center of automaticity /$6 node2are transmitted through the atria and oer speciali+ed -!ers /3achmannVs !undle tothe left atrium and three internodal tracts2 to the 6: node. The 6: node proidessuXcient conduction delay to allo# atrial contraction to contri!ute to entricular-lling. Follo#ing slo# 6: node conduction high elocity conduction tracts delier theelectrical impulse to the right and left entricles /through the ;is !undle, !undle!ranches and fascicles, and ur%ine net#or%2. $imultaneous actiation of the t#oentricles results in a NARRO4 NORMAL +R' !OM%E,/?.?@?.( sec KA$duration2. $hould a conduction delay in one or the other of the !undle !ranches

occur then an A&NORMAL 4"DE +R' !OM%LE,#ill result. /6 delay in a fascicle ofthe left !undle !ranch #ill result in an a!normal KA$ that is not necessarily #ide !utof a di"erent morphology /i.e., a change in frontal plane KA$ axis2 from the personVsnormal KA$ morphology2.

=iu 1

Figure 0 !elo# illustrates a !asic principle of 6:C. 6:C is a tem%orary alteration ofQS mor%hology when you would have ex%eted a normal QS om%lex*ermanent!undle !ranch !loc% /3332 is NO AV!.

n this discussion #e #ill concentrate on 6:C through normal !undle !ranch andfascicular path#ays and not consider conduction through accessory path#ays /e.g.,as in BB syndrome2. The ECG illustrated in Figure 0 from lead :( sho#s t#onormal sinus !eats follo#ed !y a premature atrial complex /6C, -rst arro#2. TheKA$ complex of the 6C is narro#. Follo#ing the usual incomplete pause, another


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sinus !eat is follo#ed !y a slightly earlier 6C. =o#, !ecause of this slightlyincreased prematurity /and longer preceding AA cycle2, the KA$ complex is a!normal/rsAV morphology of A3332. f you #ere not careful you might mista%e this #idepremature !eat as a :C and attach a di"erent clinical signi-cance /and therapy2.

The %ey features to recogni+ing 6:C in this tracing are)

(. dentifying the premature #ae /V20. Aecogni+ing the typical A333 KA$ morphology /rsAV in lead :(2

Lad V1

=iu 2

A&ERRAN VENR"!LAR !OND!"ONA / /a/ dsi>s /;ay al/a/in ? +R' ;ly undndi/ins a nal +R' i/ > adyadia

2. u assy ;a/ays (.. n/ >undl)

6s seen !elo# -e features or clues help identify 6:C of the i/ >undl >an

>lB ariety. t should !e emphasi+ed that although A333 morphology is thecommonest form of 6:C, L333 or interruption of one of its fascicles may also occur,particularly in persons #ith more adanced left heart disease or those ta%ingcardioascular drugs. n healthy people the right !undle !ranch has a slightly longerrefractory period than the left !undle at normal heart rates and, therefore, is moreli%ely to !e [sleeping8 #hen an early 6C enters the entricles. The [secondinaro#8 phenomenon #ill !e illustrated later in this section.

=EARE' =AVOR"N# R&&& A&ERRAN !OND!"ON1. %din a/ial a/i:i/y (;a/u % a:)2. 'R sR ;ly in lad V13. QRs ;ly in lad V6K. 'a ini/ial a: as nal +R' ;l< (in lad V1)

. Y'nd-in-a-Z ;nnn

The Asan %nnnis named after the late Dr. Aichard 6shman #hodescri!ed, in (>51, 6:C of the A333 ariety in patients #ith atrial -!rillation.6shman reasoned from o!sering ECG rhythms in these patients that the refractoryperiod /during #hich conducting tissue is recoering and cannot !e stimulated2 #asdirectly proportional to cycle length. The longer the cycle length /or slo#er the heartrate2 the longer the refractory period is. n Figure < a premature stimulus /$2 can !econducted if the preceding cycle length is of short or medium duration !ut #ill !e


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!loc%ed if the preceding cycle length is long. 6shman o!sered this in atrial-!rillation #hen long AA cycles #ere follo#ed !y short AA cycles and the KA$terminating the short AA cycle #as #ide in duration.

Loo% at the ECG rhythm strips in Figure


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=iu K

KA$ S( and S0 are [classic8 A333 morphologies #ith rsAV or r$AV triphasic KA$shapes. Bhen either of these is seen as premature !eats in lead :( #e can !e atleast >?Z certain that they are a!errant A333 conduction and not entricular ectopy.Examples S< and S5 are notched or slurred A #ae KA$ complexes. BhereVs thenotch or slurO Thin% of ra!!it ears. f the notch or slur is on the do9nstroDeof the

KA$ /little right ra!!it ear in Example S52, then the odds are almost (??to( that the!eat is a entricular ectopic !eat /or :C2. f, on the other hand, the notch or slur ison the upstroDeof the KA$ /little ra!!it ear on the left in Example S


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=iu 6

=o#, letVs loo% at some real ECG examples of the preceding KA$ morphology rules.

Be #ill focus on the :( lead for no# since it is the !est lead for di"erentiating A333from L333 and right from left entricular ectopy.

Figure @ /a!oe2 illustrates t#o premature funnyloo%ing !eats /FL3s2 for yourconsideration. FL3 U6V has a small notch on the upstro%e of the KA$ complexresem!ling Example S< in Figure 5. Aemem!er, thatVs only a 7?)7? odds for 6:C andtherefore not helpful in the di"erentiating it from a :C. ;o#eer, if you loo%carefully at the preceding T #ae, you #ill see that it is more pointed than the other

T #ae in this :( rhythm strip. There is ery li%ely a hidden premature #ae in theT !efore U6V, ma%ing the FL3 a 6C #ith A333 a!errancy. Dr. Marriott li%es to say).herchez le 5#hich is a sexy #ay to say in French Y'a ? / %Z !eforethe FL3 to determine if the FL3 is a 6C #ith 6:C. FL3 U3V, on the other hand, has asmall notch or slur on the do#nstro%e of the KA$ resem!ling KA$ S5 in Figure 5.

ThatVs almost certainly a :C.

6las, into each life some rain must fall Aemem!er life is not al#ays(??Z perfect. nFigure 1 after 0 sinus !eats a !igeminal rhythm deelops. The < premature FL3shae %"!AL R&&& MOR%$OLO#/r$AV2 and yet they are :Cs ;o# can #etellO They are not preceded !y premature #aes, !ut are actually follo#ed /loo% inthe $T segment2 !y the next normal sinus #ae #hich cannot conduct !ecause theentricles are refractory at that time. The next #ae comes on time /completepause2. Bell, you canVt #in them all.

=iu 7


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The ECG in Figure 9 #as read as [:entricular !igeminy8 in our ECG la! !y a tiredphysician reading late at night. Try to see if you can do !etter. The -rst thing tonotice is that all the early premature FL3s hae A333 morphologyNalready a (?)(odds faoring 6:C. =ote also that the T #aes of the sinus !eats loo% [funny8 particularly in Leads (, 0, and :0. They are small, short, and pea% too early, a erysuspicious signal that they are indeed hidden premature #aes /Cherche+le2.

The clincher, ho#eer, is that the premature !eats are follo#ed !y "N!OM%LEE!OM%EN'AOR %A'E'. ;o# can you tellO 4ne lead /a:F2 has no prematureFL3s, so you can measure the exact sinus rate. Ta%ing 0 sinus cycles from this lead/#ith your calipers2, you can no# tell in the other leads that the #ae follo#ing theFL3s comes earlier than expected suggesting that the sinus cycle #as reset !y thepremature #aes /a common feature of 6Cs, !ut not :Cs2. The correct diagnosis,therefore, is atrial !igeminy #ith A333 a!erration of the 6Cs.

=iu 8

The diagram illustrated in Figure > helps us understand the di"erence !et#een a[complete8 compensatory pause /characteristic of most :Cs2 and an [incomplete8pause /typical of most 6Cs2. The top half of Figure > sho#s /in [ladder8 diagramform2 three sinus !eats and a 6C. The sinus #ae after the 6C comes earlier

than expected !ecause the 6C entered the sinus node and reset its timing. n the!ottom half of Figure > three sinus !eats are follo#ed !y a :C. 6s you can see thesinus cycle is not interrupted, !ut one sinus !eat cannot conduct to the entricles!ecause the entricles are refractory due to the :C. The next #ae comes ontime ma%ing the pause a complete compensatory pause.


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=iu 9

The top ECG strip in Figure (? illustrates 0 6Cs conducted #ith 6:C. =ote ho# thepremature ectopic #ae pea%s and distorts the preceding T#ae /Cherche+le2.

The -rst 6C conducts #ith L333 a!errancy and the second #ith A333. n the secondstrip atrial -!rillation is initiated !y a 6C #ith A333 a!erration /note the longpreceding AA interal follo#ed !y a short coupling interal to the 6C2. The a!errantlyconducted !eat that initiates atrial -!rillation is an example of the [secondinaro#8phenomenon #hich is freuently seen in atrial tachyarrhythmias #ith 6:C. tVs thesecond !eat in a ro# of fast !eats that is most often conducted #ith 6:C !ecause ofthe longshort rule /6shman phenomenon2


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=iu 10

n Figure (( you can see 6shman !eats at their -nest. A333 !eats in lead :( follo#the long cycleshort cycle seuence. $ince the atria are -!rillating, you canVt identify[preceding atrial actiity8 so you hae to presume that all !eats are conducted. =ote

that the 0nd

6shman !eat in the top strip is follo#ed !y a uic%er !ut narro# KA$ !eat the right !undle is no# responding to a short cycleshort cycle seuence and !ehaesnormally. Dr. 6shman noticed this in (>51

=iu 11

f youVre ready for some fun, consider the next example illustrated in Figure (0. Thisunfortunate man su"ered from palpitation and di++iness #hen he s#allo#ed. Bhat yousee is an ectopic atrial tachycardia #ith intermittent A333 a!errant conduction. Thearro#s point to ectopic #aes going at nearly 0?? !pm. =ote ho# the A interalgradually gets longer until the 5th#ae in the tachycardia fails to conduct/Benc%e!ach phenomenon2. This initiates a pause, and #hen ()( conduction resumesthe second and su!seuent KA$ complexes exhi!it upright KA$ complexes in the formof atypical A333. This has to !e a truly coolECG rhythm strip


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=iu 12

3undle !ranch !loc% a!erration can occur during a [critical rate8 change #hich meansthat 6:C comes #ith gradual changes in heart rate and not necessarily #ith a!ruptchanges in cycle length as in the 6shman phenomenon. Thin% of a [tired8 !ut not[dead8 !undle !ranch. This is illustrated in Figure (


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Things can really get scary in the coronary care unit in the setting of acute myocardialinfarction. Consider the case illustrated in Figure (7 /lead :(2 #ith intermittent runs of#hat loo%s li%e entricular tachycardia. =ote that the !asic rhythm is irregularlyirregular indicating atrial -!rillation. The #ide KA$ complexes are examples oftachycardiadependent L333 a!erration and not runs of entricular tachycardia. =otethe morphology of the #ide !eats. 6lthough there is no initial [thin8 r#ae, the

do#nstro%e of the $ #ae is ery rapid /see Example ( in Figure 72.

=iu 1

Finally #e hae an example in Figure (@ of the rarest and most perplexing form of 6:C deceleration or !radycardiadependent a!erration. =ote that the KA$ duration isnormal at rates a!oe @7 !pm, !ut all longer AA cycles are terminated !y !eats #ithL333. Bhat a paradox You hae to !e careful not to classify the late !eats ventriularesa%es, !ut in this case the KA$ morphology of the late !eats is classic for L333 /seeExample ( in Figure 72 as eidenced !y the [thin8 r#ae and rapid do#nstro%e of the$#ae. This type of 6:C is sometimes called [hase 58 6:C !ecause itVs during hase5 of the action potential that latent pacema%ers /in this case located in the left !undle2!egin to depolari+e. $inus !eats entering the partially depolari+ed left !undle conductmore slo#ly and sometimes are nonconducted /resulting in L3332.

=iu 16

The rhythm in Figure (@ may !e diXcult to determine !ecause sinus #aes are hardto see in lead :(. #aes #ere more easily seen in other leads from this patient. Therhythm #as sinus arrhythmia #ith intermittent 0nddegree 6: !loc%.

5(


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The ECG strips in Figure (1 summari+e the important points made in this lesson. nstrip U(V intermittent A333 is seen #ith atrial -!rillation. The -rst t#o A333 !eatsresult from an accelerating rate /tachycardiadependent A3332 #hile the later triplet ofA333 !eats are a conseuence of the 6shman phenomenon /long cycleshort cycleseuence2. $trip U0V from the same patient #hen in sinus rhythm sho#s t#o prematureFL3Vs. The -rst FL3 has a KA con-guration similar to Example 7 in Figure 5 and is most

certainly a :C as the pause follo#ing it is a complete compensatory one. The 0

nd

FL3has the classic triphasic rsAV morphology of A333 6:C /see Example ( in Figure 52. Thepause follo#ing this !eat is incomplete #hich is expected for 6Cs.

=iu 17

'MMAR

The di"erential diagnosis of FL3s is intellectually challenging and has important clinicalimplications. This section proides clues that help distinguish #ide KA$ complexesthat are supraentricular in origin #ith 6:C from ectopic !eats of entricular origin/:Cs and entricular tachycardia2. Bhen loo%ing at single premature FL3s al#ayssearch for hidden premature #aes in the $TT #ae of the preceding !eat /Cherche+le2. Measure #ith calipers the pause after the FL3 to determine if itVs compensatoryor not. Aemem!er the lead :( morphology clues o"ered in Figures 5 and 7 thatproide the !etting odds that a particular !eat in uestion is supraentricular orentricular in origin. These morphology clues may !e the only #ay to correctly

diagnose #ide KA$complex tachycardias.

DonVt !e fooled !y -rst impressions. N/ all =L&s a :n/iula in iinX

n


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3entricular 'achycardia Descriptors to consider #hen considering entricular tachycardia)

$ustained /lasting


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easily recogni+ed if the rate of tachycardia is (7? !pm. Faster heartrates ma%e it diXcult to isuali+e dissociated #aes.

Fusion !eats or captures often occur #hen there is 6: dissociation and

this also strongly suggests a entricular origin for the #ide KA$tachycardia.

KA$ morphology in lead :( as descri!ed on p. ?

degrees or =B uadrant2 suggests entricular tachycardia

KA$ morphology similar to preiously seen :Cs suggests

entricular tachycardia

f all the KA$ complexes from :( to :@ are in the same direction

/positie or negatie2, entricular tachycardia is li%ely

Mostly or all negatie KA$ in :@ suggests entricular tachycardia

Especially #ide KA$ complexes /?.(@s2 suggests entriculartachycardia

6lso consider the follo#ing =u-s/; Ali/ reported !y

rugada et al, #irulation ++!-./+01/

'/; 15 6!sence of A$ complex in all leads :(:@Os5 D< is

:n/iula /ayadiaX

'/; 25 N5 s interal from !eginning of A #ae to nadir of $

#ae ?.(s in any A$ leadOs5 D< is :n/iula/ayadiaX

'/; 35 N5 6re 6: dissociation, fusions, or captures seenO

s5 D< is :n/iula /ayadiaX

'/; K5 N5 6re there morphology criteriafor :T present !oth

in leads :( and :@Os5 D< is :n/iula /ayadiaX

NO5 Diansis is su;a:n/iula /ayadia i/

a>a/inX

The ECG sho#n !elo# illustrates seeral features of typical :T) (2 KA$morphology in lead :( loo%s li%e KA$ S5 on page


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The next ECG illustrated !elo# sho#s another typical :T, !ut this time comingfrom the right entricle. =ote the :( KA$ morphology has all the features of leftentricular :T origin including (2 fat, little A #ae 02 notch on the do#nstro%e orthe $#ae and


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Accelerated 3entricular %hythms (see #.7 belo9) 6n actie entricular rhythm due to enhanced automaticity of a entricular

pacema%er /reperfusion after throm!olytic therapy is a common causalfactor2.

:entricular rate @?((? !pm /anything faster #ould !e entriculartachycardia2

$ometimes called isochronic =entricular rhythm#hen the entricular rate

is close to underlying sinus rate

May !egin and end #ith fusion !eats /entricular actiation partly due to the

normal sinus actiation of the entricles and partly from the ectopic focus2.

&sually !enign, short lasting, and not reuiring of therapy.

5@


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,dio=entricular %hythm

6 passie escape rhythm that occurs !y default #heneer higherleer

pacema%ers in 6: unction or sinus node fail to control entricular actiation.

Escape rate is usually


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6: seuential pacing #ith entricular pacing /note tiny spi%e !efore each

KA$2 and atrial sensingof normal sinus rhythm /note) pacema%er spi%es aresometimes diXcult to see2)

6: seuential pacing #ith !oth atrial and entricular pacing /note pacingspi%es !efore each #ae and each KA$

=ormal functioning entricular demand pacema%er. $mall pacing spi%es are

seen !efore KA$ S(, S


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decremental conduction that means that conduction elocity progressiely slo#s!eat !y !eat until failure of conduction occurs. This is the form of conduction !loc% inthe 6: node. Type !loc% is all or noneand is more li%ely found in the ;is !undle or!elo# the ;is !ifurcation /i.e., in the !undle !ranches2. The term exit blocDis usedto identify conduction delay or failure immediately distal to a pacema%er site. $ino

atrial /$62 !loc%, for example, is an exit !loc%.This section considers conduction

disorders in the anatomical seuence that de-nes the cardiac conduction system solets beginEEE

,! $,&/A'%,A #F,' B/.G ($A BlocD): 2ndD 'A &lB) this is the only degree of $6 !loc% that can !e

recogni+ed on the surface ECG /i.e., intermittent conduction failure !et#eenthe sinus node and the right atrium2. There are t#o types, although !ecauseof sinus arrhythmia they may !e diXcult to di"erentiate.

Type /$6 Benc%e!ach2) the follo#ing < rules represent the classic rules of

Benc%e!ach #hich #ere originally used to descri!e Type 6: !loc%. Therules are the result of decremental conduction #here the incrementinconduction delay for each su!seuent impulse gets smaller untilconduction failure -nally occurs.

(. interals gradually shorten until a pause occurs /i.e., the !loc%edsinus impulse fails to reach the atria2

0. The pause duration is less thanthe t#o preceding interals


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,,! A'%,/3#&'%,.UA% (A3) B/.G:%ssi>l si/s ? AV >lB5

6: node /most common2

;is !undle /uncommon2

3undle !ranch and fascicular diisions /in presence of already

existing !undle !ranch !loc%2

1s/D AV &lB5 %R in/:al U 0.20 sF all % a:s ndu/ // :n/ils.

2ndD AV &lB5 diaa >l illus/a/s / din

>/n y; " (4nB>a) and y; "" AV >lB.

7?


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n classic Type (2encDebach) 6: !loc% the A interal gets longer (by

shorter increments)until a nonconducted #ae occurs. The AA interal ofthe pause is less thanthe t#o preceding AA interals, and the AA interalafter the pause is greater thanthe AA interal !efore the pause. These arethe < classic rules of 2encDebach/descri!ed a!oe for $6 !loc%2. n Type ("obitz)6: !loc% the A interals are constant (for at least 2 onseutive &

intervals) until a nonconducted #ae occurs. The AA interal of the pause ise


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the nonconducted #aes are !loc%ed in the other !undle. n Type !loc%seeral consecutie #aes may !e !loc%ed as illustrated !elo#)

!;l/ (3dD) AV &lB5

&sually see complete A3 dissociation!ecause the atria and entricles

are under control of separate pacema%er !osses.

=arro# KA$ rhythm suggests a unctional escape focus for the entricles

#ith !loc% a!oe the focus, usually in 6: node.

Bide KA$ rhythm suggests a entricular escape focus /i.e.,

idio=entricular rhythm2. This is seen in ECG '6' !elo# ECG '3' sho#s thetreatment for


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! 6cceleration of a su!sidiary pacema%er faster than sinus rhythm i.e.,ta%eoer !y usurpation:

-! 0ndor


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,,,! ,&'%A3#&'%,.UA% B/.G$ Ri/ &undl &an &lB (R&&&)5

Complete A333 has a KA$ duration

?.(0s /(0? ms2 Close examination of KA$ complex in arious leads reeals that the

terminal forces /i.e., 0ndhalf of KA$2 are oriented right#ard and anteriorly!ecause the right entricle is depolari+ed afterthe left entricle.

Terminal A' #ae in lead :( /usually see r$A' complex2 indicating late

anterior forces

Terminal $ #aes in leads , a:L, :@ indicating late right9ardforces

Terminal A #ae in lead a:A indicating late right9ardforces

The frontal plane KA$ axis in A333 should !e in the normal range /i.e.,


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illustrated in the ECG !elo# in addition, poor A progression from :( to:< is common.

The normal $TT #aes in L333 should !e oriented opposite to the

direction of the terminal KA$ forces i.e., in leads #ith terminal A or A'forces the $TT should !e do#n#ards /negatie2 in leads #ith terminal $forces the $TT should !e up#ards /positie2. f the $TT #aes are in thesame directionas the terminal KA$ forces, they should !e la!eled

primary $'' 9a=e abnormalities!n the a!oe ECG the $TT #aes arenormal for L333 i.e., they are secondaryto the change in theentricular depolari+ation seuence.

ncomplete L333 loo%s li%e L333 !ut KA$ duration W ?.(? ?.(0s, #ith

less $TT change. This is often a progression of L:;.

L?/ An/i =asiula &lB (LA=&)\.. / s/ n

in/a:n/iula ndu/in d?/ Left axis deiation in frontal plane, usually 57 to >? degrees

r$ complexes in leads , , a:F /i.e., small initial r, large $2

$mall #ae in leads andHora:L

$ in $ in A in a:L A in a:A

Apea% time in lead a:L ?.?5s, often #ith slurred A #ae do#nstro%e

KA$ duration usually ?.(0s unless coexisting A333

&sually see poor A progression in leads :(:< and deeper $ #aes in leads

:7 and :@

May mimicL:; oltage in lead a:L, and masDL:; oltage in leads :7, :@

77


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n the a!oe ECG, note 57 degree KA$ axis, r$ complexes in , , a:F,

tiny #ae in , a:L, $ in $ in , A in a:L A in a:A, and late $#aes in leads :7@. KA$ duration is normal, and there is a slight slurto the A #ae do#nstro%e in lead a:L.

L?/ %s/i =asiula &lB (L%=&)\. Vy a in/a:n/iula

d?/X

Aight axis deiation in the frontal plane /usually J(?? degrees2

r$ complex in lead

A complexes in leads , , a:F, #ith A in lead A in lead

KA$ duration usually ?.(0s unless coexisting A333

"ust rst exclude (on clinical or other grounds) other causes of

right axis de=iation such as cor pulmonale? pulmonary heartdisease? pulmonary hypertension? etc!? because these conditionscan result in the identical #.7 pictureI

&i?asiula &lBs A333 plus either L6F3 /common2 or LF3 /uncommon2

Features of A333 plus frontal plane features of the fascicular !loc% /axisdeiation, etc.2

7@


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The a!oe ECG sho#s classic A333 /note r$A' in :(2plusL6F3 /KA$ axis

W @?P, r$ in , a:F and small in and a:L2.

Nns;iS "n/a:n/iula !ndu/in D?/s ("V!D)

KA$ duration ?.(?s indicating slo#ed conduction in the entricles

Criteria for speci-c !undle !ranch or fascicular !loc%s not met Causes of nonspeci-c :CD's include)

:entricular hypertrophy /especially L:;2

Myocardial infarction /so calledperiinfarction blocDs2

Drugs, especially class 6 and C antiarrhythmics /e.g., uinidine,

Hecainide2

;yper%alemia

4l-%aBinsn-4i/ %


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7. AR"AL ENLAR#EMEN %ight Atrial #nlargement (%A#? 5pulmonale? 3iagra 59a=es)

#ae amplitude 0.7 mm in and*or (.7 mm in :( /these criteria are

not ery speci-c or sensitie2

3etter criteria can !e deried from the KA$ complex these KA$ changes

are due to !oth the high incidence of A:; #hen A6E is present, and the A:displacement !y an enlarged right atrium.

KA, Kr, A, or As morphology in lead :( /in a!sence of coronary heart

disease2

KA$ oltage in :( is 7 mm and :0*:( oltage ratio is @ /$ensitiity

W 7?Z $peci-city W >?Z2

eft Atrial #nlargement (A#! 5mitrale)

#ae duration ?.(0s in frontal plane /usually lead 2

79


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=otched #ae in lim! leads #ith interpea% duration ] ?.?5s

Terminal negatiity in lead :( /i.e., terminal force2 duration ?.?5s,

depth ( mm.

$ensitiity W 7?Z $peci-city W >?Z

BiAtrial #nlargement (BA#)

Features of !oth A6E and L6E in same ECG

#ae in lead 0.7 mm tall and ]?.(0s in duration

nitial positie component of #ae in :( (.7 mm tall and prominent

terminal force

8. VENR"!LAR $%ERRO%$

,ntroductory ,nformation:

The ECG criteria for diagnosing right or left entricular hypertrophy are ery

insensitie /i.e., sensitiity 7?Z, #hich means that ^7?Z of patients #ithentricular hypertrophy cannot !e recogni+ed !y ECG criteria2. Bhen indou!tN.#/ an E!$OX;o#eer, the criteria are ery speci-c /i.e., speci-city>?Z, #hich means if the criteria are met, it is ery li%ely that entricularhypertrophy is present2.

,! eft 3entricular ypertrophy (3)

General ECG features include)

KA$ amplitude /oltage criteria i.e., tall A#aes in L: leads, deep $

#aes in A: leads2 Delayed ntrinsicoid deHection in :@ /i.e., time from KA$ onset to pea% A is

?.?7 sec2

Bidened KA$*T angle /i.e., left ventriular strain %attern, or $TT oriented

opposite to KA$ direction2. This pattern is more common #ith L:; due topressure oerload /e.g., aortic stenosis, systemic hypertension2 ratherthan olume oerload.

Left#ard shift in frontal plane KA$ axis

Eidence forleft atrial enlargement /L6E2

7>
http://var/www/apps/conversion/tmp/scratch_6/LESSON7.html#LAEhttp://var/www/apps/conversion/tmp/scratch_6/LESSON7.html#LAE


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E$TE$ Criteria for L:; /diagnostic, 7 points pro!a!le, 5 points2

JE!# !i/ia %in/s

:oltage Criteria /any of2)(. A or $ in lim! leads 0? mm

0. $ in :( or :0


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Example 0) /E$TE$ Criteria) < points for oltage in :7, < points for $TTchanges also L6E and L6D of 5? degrees note also the :C2

,,! %ight 3entricular ypertrophy

General ECG features include)

Aight axis deiation />? degrees2

Tall A#aes in A: leads deep $#aes in L: leads

$light increase in KA$ duration

$TT changes directed opposite to KA$ direction /i.e., #ide KA$*T angle2

May see incomplete A333 pattern or A pattern in :(

Eidence of right atrial enlargement /A6E2 $peci-c ECG features /assumes normal cali!ration of ( m: W (? mm2)

6ny one or more of the follo#ing /if KA$ duration ?.(0 sec2)

Aight axis deiation />? degrees2 in presence of disease capa!le of

causing A:;

A in a:A 7 mm, or

A in a:A K in a:A

6ny one of the follo#ing in lead :()

A*$ ratio ( and negatie T #ae

A pattern

A @ mm, or $ 0mm, or r$A' #ith A' (? mm

4ther chest lead criteria)

A in :( J $ in :7 /or :@2 (? mm A*$ ratio in :7 or :@ (

A in :7 or :@ 7 mm

$ in :7 or :@ 1 mm

$T segment depression and T #ae inersion in right precordial leads is

usually seen in seere A:; such as in pulmonary stenosis and pulmonaryhypertension.

Example S() /note A6D J


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Example S0) /more su!tle A:;) note A6D J(?? degrees A6E Kr complex in

:( rather than A is atypical2

Example S


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,,,! Bi=entricular ypertrophy (diJcult #.7 diagnosis to maDe) n the presence of L6E any one of the follo#ing suggests this diagnosis)

A*$ ratio in :7 or :@ (

$ in :7 or :@ @ mm

A6D />? degrees2

4ther suggestie ECG -ndings)

Criteria for L:; and A:; !oth met

L:; criteria met and A6D or A6E present

9. MO!ARD"AL "N=AR!"ON

,ntroduction to #.7 %ecognition of Acute .oronary $yndrome

(A.$)

The ECG changes of 6C$ are the result of a sudden reduction of coronary

!lood Ho# to a region of entricular myocardium supplied !y a coronary artery#ith a ruptured atherosclerotic plaue and intracoronary throm!us formation.Depending on ho# uic%ly the patient gets to the hospital for de-nitietreatment /usually percutaneous reasculari+ation or throm!olytic Ax2myocardial necrosis /infarction2 may or may not occur. The diagram !elo#sho#s four possi!le ECG outcomes of myocardial ischemia in the setting of anacute coronary syndrome. 4n the left no myocardial infarction occurs !utthere is either su!endocardial ischemia manifested !y reersi!le $T segmentdepression or transmural ischemia manifested !y reersi!le $T segmenteleation. 4n the right are t#o %inds of myocardial infarction, one manifested!y $T segment eleation /'EM"2 and one manifested !y no $T segmenteleation /N'EM"2. reiously these t#o M types #ere called K#ae Mand nonK#ae M respectiely. 3ecause K #aes may not appear initially,early treatment decisions are !ased on the presence or a!sence of $Tsegment eleation, and if reasculari+ation is accomplished uic%ly K#aesmay neer appear /[time is muscle8 says the interentional cardiologist2.

@


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?llin disussin ill ?us n E!# ans duin / :lu/in ?a 'EM"

Most M's are located in the l?/ :n/il. n the setting of a proximal right

coronary artery occlusion, ho#eer, there may also !e a component of i/:n/iulainfarction as #ell. Aight sided chest leads are usually needed torecogni+e A: M.

n general, the more leads of the (0lead ECG #ith M changes /K #aes and$T eleation2, the larger the infarct si+e and the #orse the prognosis.

The left anterior descending coronary artery /L6D2 and it's !ranches usually

supply the anterior and anterolateral #alls of the left entricle and theanterior t#othirds of the septum. The left circumHex coronary artery /LCx2and its !ranches usually supply the posterolateral #all of the left entricle.

The right coronary artery /AC62 supplies the right entricle, the inferior/diaphragmatic2 and true posterior #alls of the left entricle, and the posteriorthird of the septum. The AC6 also gies o" the 6: nodal coronary artery in 97>?Z of indiiduals in the remaining (?(7Z, this artery is a !ranch of theLC`.

The usual ECG eolution of a $TEM #ith K#aes is illustrated in the diagram!elo#. =ot all of the patterns may !e seen the time from onset of M to the-nal pattern is uite aria!le and related to the si+e of M, the rapidity ofreperfusion /if any2, and the location of the M.

6. =ormal ECG prior to M3. ;yperacute T #ae changes increased T #ae amplitude and#idth KT prolongs may also see $T eleationC. Mar%ed $T eleation #ith hyperacute T #ae changes /transmuralinury2

=oM$u!endocardial schemia

Transient $T

=e# onset angina

=onK M=on$T eleation M

$T depression orT#ae changes or

normal ECG

=oMTransmural schemia

Transient $T

:ariant 6ngina

K#ae M$T eleation M

/$TEM2Typical eolution of

$TT changes

Myocardialschemia

@5


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D. athologic K #aes, $T eleation decreases, terminal T #aeinersion /necrosis2 this is also called the fully eoled phase.E. athologic K #aes, T #ae inersion /necrosis and -!rosis2F. athologic K #aes, upright T #aes /-!rosis2

,! ,nferior ", 4amily of $'#",Ks (L9a=e ",;s)M includes inferior? true

posterior? and right =entricular ",;s

"n?i M"

athologic K #aes and eoling $TT changes in leads , , a:F

K #aes usually largest in lead , next largest in lead a:F, and smallest inlead . K #ae


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Example S0) 4ld inferior M /note largest K in lead , next largest in a:F, andsmallest in lead 2. 6xis W 7?P /L6D2

u ;s/i M"

ECG changes are seen in anterior precordial leads :(


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Example S5) 4ld inferoposterior M) =ote tall pathologic A in :(< /K #aeeuialent2, upright T #aes and inferior K #aes2

Ri/ Vn/iula M"/only seen #ith proximal right coronary occlusion i.e.,

#ith inferior family M's2 ECG -ndings usually reuire additional leads on right chest /:(A to :@A,

analogous to the left chest lead locations, !ut in opposite direction2

Criteria) $T eleation, (mm, in right chest leads, especially :5A /see

!elo#2

Example S7) 6cute inferior M #ith rightsided ECG leads sho#ing mar%ed $Tsegment eleation in :


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,,! Anterior 4amily of $'#",KsM includes anteroseptal? anterior?anterolateral? and high lateral

An/s;/al M"

K, K$, or r$ complexes in leads :(:< /:52

Eoling $TT changes

Example S@) ;yperacute anteroseptal M mar%ed $T eleation in :(< !efore K#aes deeloped

@9


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Example S1) Fully eoled anteroseptal M /note K$ #aes in :(0, r$complex in :


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!n/5 The precise naming of M locations on the ECG is eoling as ne# heartimaging /e.g., MA2 !etter de-nes the entricular anatomy. =e# terminology has!een suggested /see #irulation 2330!++1/+455). Bhile not uniersally accepted,the follo#ing [ne#8 K#ae M patterns hae !een de-ned for left entricularsegments)

$eptal ",) K /or K$2 #aes in :(0

"idAnterior ",) K #aes in a:L, sometimes in lead , :0, :


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Example S(() Extensie anterior M #ith A333 J L6F3 note K's in leads :(:7,terminal fat A #ae in :(5, fat $ #ae in :@2. 6xis W 9?P /r$ in , , a:F) leftanterior fascicular !loc% or L6F3.2

M J Left 3undle 3ranch 3loc%

4ften a diXcult ECG diagnosis !ecause in L333 the right entricle is

actiated -rst and left entricular infarct K #aes may not appear at the!eginning of the KA$ complex /unless the septum is inoled2. $uggested ECG features, not all of #hich are speci-c for M include)

K #aes of any si+e in t#o or more of leads , a:L, :7, or :@ /$ee

ECG S(< !elo#) one of the most relia!le signs and pro!a!lyindicates se%talinfarction, !ecause the septum is actiated earlyfrom the right entricular side in L3332

Aeersal of the usual A #ae progression in precordial leads /see

a!oe2

1(


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=otching of the do#nstro%e of the $ #ae in precordial leads to the

right of the transition +one /i.e., !efore KA$ changes from apredominate $ #ae complex to a predominate A #ae complex2this may !e a K#ae euialent.

=otching of the upstro%e of the $ #ae in precordial leads to the

right of the transition +one /another K#ae euialent2.

r$A' complex in leads , :7 or :@ /the $ is a K#ae euialentoccurring in the middle of the KA$ complex2

A$ complex in :7@ rather than the usual monophasic A #aes

seen in uncomplicated L333 /the $ is a K#ae euialent2.

rimary $TT #ae changes /i.e., $TT changes in the same

direction as the KA$ complex rather than the usual secondary $TT changes seen in uncomplicated L3332 these changes may reHectan acute, eoling M.

Exaggerated $T deiation in same direction as the usual L333 $T

changes in L333 /see Example S(02

Example S(0) 6cute anterior M #ith L333. =ote conexup#ards $T eleation in:(< #ith exaggerated $T depression in :@.

Example S(


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,3! &on$' ele=ation ", (&$'#",)

ECG changes may !e minimal, may sho# only T #ae changes /inersion2, ormay sho# $T segment depression #ith or #ithout T #ae inersion.

6lthough it is tempting to locali+e the nonK M !y the particular leads

sho#ing $TT changes, this is pro!a!ly only alid for the $T segment eleationpattern

Eoling $TT changes may include any of the follo#ing patterns)

Conex do#n#ard $T segment depression only

Conex up#ards or straight $T segment eleation only

$ymmetrical T #ae inersion only

Com!inations of a!oe changes

3! 'he 5seudoinfarcts

These are ECG conditions that mimic myocardial infarction either !ysimulating pathologic K or K$ #aes or mimic%ing the typical $TT changes ofacute M.

BB preexcitation /negativedelta #ae may mimic pathologic K #aes

see ECG on p702

;$$ /septal hypertrophy may ma%e normal septal K #aes fatter

there!y mimic%ing pathologic K #aes2

L:; /may hae K$ pattern or poor A #ae progression in leads :(nali/is

"NROD!"ON) The T #ae is the most la!ile #ae in the ECG. T #ae changesincluding lo#amplitude T #aes and a!normally inerted T #aes may !e the resultof many cardiac and noncardiac conditions. The normal T #ae is usually in thesame direction as the KA$ except in the right precordial leads /:(< !elo#2. 6lso, thenormal T #ae is asymmetri#ith the -rst half moing more slo#ly than the secondhalf. n the normal ECG /see !elo#2 the T #ae is al#ays upright in leads , , :


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,! 0i>erential 0iagnosis of ' 2a=e ,n=ersion

K #ae and nonK #ae M /e.g., eoling anteroseptal M see !elo#2)

Myocardial ischemia

$u!acute or healed pericarditis

Myocarditis

Myocardial contusion /from trauma e.g., steering #heel accident2

C=$ disease causing long KT interal /especially su!arrachnoid hemorrhagesee ECG !elo# #ith giant negatie T #aes2)

19


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diopathic apical hypertrophy /a rare form of hypertrophic cardiomyopathy

#ith giant negatie T #aes2

Mitral ale prolapse

;ereditary long KT syndromes

Digoxin e"ect

A:; and L:; #ith strain pattern /pressure oerload2

"iscellaneous $'' .hanges

Electrolyte a!normalities

;ypercalcemia /a!!reiated $T segment #ith short KT interal

;ypocalcemia /long $T segment #ith prolonged KT interal2

;yper%alemia /pea%ed T #aes, prolonged KA$ duration see ECG !elo#2

;ypo%alemia /$T depression, lo# T #aes, large & #aes2

3rugada type ECG /seen in the hereditary 3rugada syndrome2 this is

an unusual pattern of $T segment eleation #ith or #ithout T #ae inersion

1>


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in the right precordial leads. 6n example is seen in the ECG !elo#. Li%e thelong KT syndrome, there is increased incidence of malignant arrhythmias inthis condition2

12. 4a: A>nali/is

"NROD!"ON5The & #ae is the only remaining enigma of the ECG, and pro!a!lynot for long. The origin of the normal & #ae is still in uestion, although manyauthorities correlate a!normal & #ae #ith electrophysiologic eents called

afterdepolari+ations in the entricles. These afterdepolari+ations can !e the sourceof arrhythmias caused !y triggered automaticity including torsade de %ointes*Thenormal & #ae has the same polarity as the T #ae and is usually less than onethirdthe amplitude of the T #ae. & #aes are usually !est seen in the right precordialleads especially :0 and :


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0i>erential 0iagnosis of U 2a=e Abnormalities

rominent upright & #aes

$inus !radycardia accentuates normal & #aes

;ypo%alemia /remem!er the triad of $T segment depression, lo#

amplitude T #aes, and prominent upright & #aes2

:arious drugs including antiarrhythmics

L:; /may see prominent upright or inerted & #aes in left : leads2

C=$ disease and other causes of long KT /T& fusion #aes2 see ECG

!elo#.

9(


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=egatie or inerted & #aes

schemic heart disease /often indicating left main or L6D disease2

Myocardial infarction /in leads #ith pathologic K #aes2

During episode of acute ischemia /angina or exerciseinduced

ischemia2

ost extrasystolic in patients #ith coronary heart disease

During coronary artery spasm /rin+metal's angina2

=onischemic causes) some cases of L:; or A:; /usually in leads #ith

prominent A #aes2 $ome patients #ith LKT$ /see !elo#) Lead :@ sho#s giant negatie

T& fusion #ae in patient #ith LKT$ a prominent upright & #ae isseen in Lead :(2

A El Outline June 2007

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Transcript of A El Outline June 2007