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CHURCHILL LIVINGSTONE An imprint ol Elsevier Science Lirnated @ Longman Group

Linriled 1973, 1980 Group UK Limiled 1986, '1992, assigned to Pearson Prolessbnal 1995 @ Pearson Prolessional 1997 @ 2003, Elsevier Science Limited. All righls reserved. @ Longman

The right ol Protessor J. B. Hamplon lo be identitied ae arrlhor ol lhls work has been asserld by him ln accordance wilh lho Copyright. Doslgns and Patenls Acl 1988. No parl ol lhis publicalion may bo reproducod, slorod in a relrieva! Syslsm, & [ansmilled in any lorm or l,y any m€ans, eloclronic, mochanical, pholocopying, rocordng or olhonrriso, withor.lt eilhor the prior permission ol the publishers or a licence psrmitling restricted copying in lhe Unitod Kingdom issued by lhe Copyrighl Licensing Agerrcy, 90 Toller*ram Coun Roaq London WIT 4LP. Permissions may be sought direclly lrom Elsevior'e Heahh Scieinces RigtrB Oepaftnonl h Ptriladeptia, USA: phone: (+1) 215 238 7869, lax: (+1) 215 238 2239. e-mail: h€alttpormbsiorpOelsryier.com). '/ou may also complele your request on-line via the Elsevier Sdence hornepage (http://www.elsevier.com), by selecling 'Cuslomer Support'and lhen 'Obtahing Pennissirxrs'.

Firsl edilion 1973 Second edition 1980 Third edition 1986

Fourth edilion 1992 Fllth orlilion 1007 Slxllr oditlon 2003 'Floprintod 2003 Slandard editlon ISBN 0 443 072523 lnternallonal edltion ISBN 0 4tl3 072531

British Llbrary Catalogulng ln Publlcatlon

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A catalogue record lor this book is available lrom lhe Bdtish Library

Llbrary ot Congress Cataloglng ln Publlcatlon Data A catalog record lor this book is available lrorn the Ubrary

ol Congress

Note Meciical knowledge is constantly changing. Standard safety precautions must b€ tolbtfled, hll ae new research and clinical experience broaden our knowledge. charqos in lrealmont and dnrg therapy,may become nocersary or appropriate. Roaderr art advltsd lo chcck lhe mosl cuncnl producl inlormalion provided by the manulactursr of each drug lo be adrninictered to vedly the rocommonded doso, lhe msthod and duration ol adminlrlrrlion. rnd conlnlrdcalbru. lt b the rosponsibilily ol th€ praclilionor, rolying on oxpodonce and knov{cdgc ol lha pslhnl. lo delennlnc dosngos and tlre bost lroalmonl lor each lndivlduel pallonl. Nellhcr tha Pub{cher nor lhe autttor assumos any liabilily lor any iniury and/or damage lo porsoos or propeny artsing lmm this publicalion.

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Prefoce: in 1973, and over a langLrage versiotr English quarter of a million copies of the of the first five editions have bcen solcl. The book has been translated into German, French, Spanislr, Italian, Portuguese, Potish, Indonesian and Japanese.'['hc airrrs of this new edition are the same as before: the book . is not intended to be a comprehensive textbool( on interpretation, but ECC electrophysiology, nor even of it is designed as an introduction to the ECC for medical students, nurises and paramedics. In addition, it nray provide useful revision f6r those wlro lrave forgottcn wlrat they learned as students. There really is no need for the ECC to be clar-rnting: just as'most people drive a car without knowing much about engines, and gardeners do not need tcl be botanists, most people can make full and proper use of tl're ECC without getting submerged'in its complexities. This book encourages the reader to accept that the ECG really is easy to understarrd, antl that its use is just a natural extension of tlre history arrd the physical examination. This is the sixth edition of tlrc book. Ttrc tc'xt l'ras becn changed a little, but the changes to the illustratiorls are morsimportant. There is a neiw emplrasis on fult (12-lcacl) ECGs, presented in as realistic a way as possible. Examination of a L}-lead ECC gives tlre best chancc of making a diagnosis, and a ctinician needs to get into the habit of looking at ECCs presented this way. At the encl of the book there is a new section so that you can test yourself The ECG Mnde Ensy was first published

The ECG Mnde Ensy shotrld hclp the student to prepare for examinations, but for tlrc clcvc'topnrcnt of clinical

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and confidence - there is no substitute for reporting on large numbers of clinical records. Two conlpanion texts may help those who have masteredTlrc ECG Nladc Easy and waut to progress further. The'ECG irt Prncticc deals with the relationslrip between the pttient's l'ristory ancl physical signs and the ECG, and with the many variations in the ECG seen in health and disease.150 ECG Problants dcscribes 150 clirrical cascs arrd gives their full ECGs, in a format that encourages the reader to interpret the record arrd decide on a course of treatment before lookirrg at the allswers. The title Tlrc ECG Mctle Easy was suggested 30 years ago by the late fbny Mitchell, Foundation Professor of Medicine at the Univcrsity of Nottirrgham. I am grateful to him and to the many pcople who have helped to refine the book ovcr lhc Vcat's, culd partictrlarly to many students for the.ir constructivc criticistns and hclpful comnrents, which have rcirrforcccl nty Lrclicf l,lrat tlrc I]CC rcally is casy [o uudcrstaucl. cornpetelrce

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Contents I.

Whor rhe ECG is

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2. Condirction ond its problems

29

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3. The rhythtn of the heorf

53

4. Abnormoli?ies of P woyes, ond T rnroves 88

5. Reminders I l0

QRS cornplexes

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"l Whot fhe ECG is obout Wfrit to expect from the ECG The electricity ol the

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1

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The shape of the Regrording an

The shdpe of the OnS complex 12 How to report an

ECG

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ECG lntorprolatlon 23

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Things to remember 28

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ECG stands for electrocardiogram, or electrocardiograph. Irr some countries, the abbreviation used is 'EKC'. I{enrember:

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By the time you have finished this book, you should be able to say'The ECC is easy to urrderstand'. Most abnormalities of the ECG are an'renable to reason.

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ECG;i$SiF

Clinical diagnosis depends mainly on a pratient's lristory, and to a lesser extent on the physical examinatiorr.'l'hc, llCC

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it is crucial for pratient managcment. [t is, however, inrp'rortant to see the ECC as a tool, and not as an end in cases

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\IltEcilDcssential for the cliagnosis, ancl therefore r'rlilrlagenrent, of abnormal carcliac rlrythms. It hglps witl'r the cliagnosis of the cause of clrest ['roin, a{td the-proper use of thrombolysis in treating n'lyocardial inffrction depends Ltpoll it. It can help with the diagnosis of the cause of brca thlessness.wittr practice, interpretirrg the ECG is a nratter of pattern rccogrrition. l-lowevcrJhe ECG can be analysed frpm first prirrciprles if a few sirrrple rules and basic factJtre retnembered. This chapter is about these rules and facts.

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The conlractiorr o.!ar:+-nueslc is associated with electricaf a changes called 'Qpolarizatioi\', and,these changes can be detectcr{ by clectroidcs aTfached to the surface of the body. d '- Since all muscular contraction will be detected, the electrical OwAt ci---,',g"s associated with contraction of the heart muscle will =;#r , .only be clear if thc pal.icnt is fully rctaxed and no skeletal are contracting. i Jur[nuscles ,o Although the heart lias four chamberr,fro* the electrical €W TlZ, poirrt of view it can be thought of as having only two,

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discharge for each cardiac cycl: normally ,*r:*trical irla spccial area of the right atrium qalledrthe futaiti Gffiat 1bn; rrode'. D/ltolar[,atiorr their spreads

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through thc atrial mguftle fibres. Tlrcrc is a delay while thc clJpolarization;lireacls througlr anotheisp".iut ur"i irt the atriun{dtl're'afiioventricular node){ulro called the AV

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THE ELECTRICIW OF THE HEART/THE SHAPE OF THE

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Bundle of His Atrioventricular node Left bundle branch

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node', ot sometimes just 'tl're node'). Thereafter; the electricat discharge tiavels very rapiclly,Eiln specializecl conduction tissug: first a single pathway, the 'bundle of His', which thei*dividep in tie ieptunr between the ventrictes into right or'r.l luft bundle brancher.Fi-e leftr bundle branch itielf divicleffn-b two. Within tir,ffiof ventricular muscle, concluction spreaclffiewhat n'lore slowly, through specialized tissue called 'Purkinje iibres'.

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The rhythm of .the_heort As we-ihall see laterflectrical activatio:r of the heart can ro*gdi*6 begin in ilaces other than rhe SA rloa{rnu wod 'rhythm; is used to refer to tl're part of the heart which jq dqtrtreIulg^he-_ a ctiva fi ffieq u o r* n I li ei.i ifiiet,', ;rrj,'it'tnt, t"itT6ieciriial activation".r." bet'inning in the sA rrocre, is called 'sinls rhythm'. q(

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" vQ, The muscle mass of the atria is small conrpared with that of J F', the ventricles, and the clcctrical change agcon'lpanyirrg thc' I ts\v contraction of the atria is therefore small.fContracticrn of the atria is associated with the ECC wave-called 'Pf The ventricular mass is large, and so there is a large deflection of

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the ECG when theyentricles are depolarized. This is called the 'Qt{S' comple*frn" 'T' wave of ihe ECG is associated, with the return of the ventricular mass to its rcstingfi electrical sta te ('repolarization'fi * Tl're basic shape of the noundf ECG is shown in Figure 1.2. rhe letters I Q, R, s and r were selected in the,eiily days of ECG history, and were chosen arbitrarilyrThe'B Q, R, S and T deflections are all called waves;lthe Q, R and S waves togetherffiGrp a comple$nd theTnterval between the S wavc ancl thc T *arc ii cffied tlre ST'segmenil eQ ':'i::::] i;

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The different parts of the QRS conrplex are labelled as shown in Figure 1..3elf the first deflection is downward, it is called a Q wave (FiS. l.3alAn upward deflection is called an R wave (FiS. 1.3b) - whether it is precedecl by a Q wave or not (Fig. 1.3clA.y deflection below the basq,llne fcillowing a; R wave ii called an S wave (FiS. 1.3ct) *rt6[Lu. therdhaJbeen a prececling Q wave o, ,.oi (r,ig. 1.3e).

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Times ond speeds ECC. machfies record changes in electrical activity by drawingd qqe on a moving paperl$p.All ECC machines

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(s), or 200 milljseconds (rnt)fu9there are' five large squnres /\\ )jl-9J per second, afid 300 per minlite (rninfl So an ECC even-t, r (*,j ,p such as a QRS complex, occurring once per large square YJ ,,'ri* r,r/ is occurri^g at a rate of 300/nrin (Fig. I ..1). The heart rate Yr\ "' '--' '

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Flg.1.4 Relatlonshlp between the squares on ECG pirper and time. Het€, there ls one ORS complex per second, so the heart rate is 60 beats/mln

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JtrsI as tlrc lcrrgtlr of l)('lpcr be twccn R wavcq gives the lrearl, ratc@the distancc bctweerr thc cliffcrcsni'parts of the P-QRS-T conlplcx shows the Linrc taken for conduction of

the electrical dischargc to spread Lhrough the different parts - (;r,,,q;;t a,Rs ) of the heart.

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Tlre I'}R irrterval is nteasured fronr the beeinnins of the P wave to the begirrning of the QRS'."*pt"*I@if tt',e time takerr for excitation to spread from the SA node, fhrough the atrial nruscle alrcl tlre AV node,.Iowf the burrclle of His arncl intt) vgltricular nruscE

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Tlre normal PR interval is 0.'lZ-0.2 s (120-200 nrs), representecl by three to five small squares. Most ol'[re time is taken trp by clelay irr the AV noclc (lrig. l.S;@tlrt, I,R irrterval is veryshort, t'i[lrer the atria have [r.]err .ltfttariz.t,clol from close to tlre AV norlc, or thcrt, is alrnorrnltly l'irst L'oh(lLrclion fronr tlre rrtrin lo tlrt' vt'nlriclcs. cr+3 $tl I
-:=' RECORDING AN ECG q{

Ttre wrtrcl 'lcacl' srlnretirncs cAusos c()nfrrsirlrr. Sonrctinrcs it is used to nrean the pieces t'lf wire that connect tlre patient to the ECC recorclegr?roperly, a leacl is an electrical lricturc "rble** of ttre heart. {rr,),re;; q The electrical sigr[al frcinr the heart is cle,tc.ctccl trt thc {g surface of tl're bocly through five e.lectr"ocles, w,hich are ' P. joined to the I1CC recorder by wires.Aldelc.ctrocle is r(f attache'cl to eaclr linrb,(ffiLEis lrelcl by strctiorr to tlrt, ,ra++r .t-l: front o[ the chcst,r,r.l ,]r.,v.,,l t r rlifl'ercrit 1-r1r51tions. (]oorl

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electricarl contact bcl.rvccn tlrc clcctrt-ldes arrd skir-r is esscntial. It nray be neccssary to shave the chest.

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Thc ECC rccorclcr conrparcs the clcctrical activity J-"wl2r detcctecl in the c{if.fcrcrrt elcctrodcs, arrd lhe elcctrital \ e-a'.f 1 picttrre so obl.airred is callec-l a'lcad'cThe different s,. conrparironrGk at' the hcart frorn different directions. e'3 i Iior cxample, when thc recorder is sct to'lcarl l' it is corllparrirrg tlre clectrical cvents dctccted by the electrodes LA drc. attachcd to the right irncl lcft arnrsrEach lead gives a Rl -.,* , cliffcrcnt'iew of [hc clcctrical activity of thc h"eart, uni rt ete

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The l2-leod ECG ICC irrtcrprctatiotr is casy if you rclncmbcr

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fronr.which the various lcads look at the hcart. The six 'statrclat'd' leads, rvhich are recorclccl from the electrodes attrtchetl to tlrc linrbs, carr bc tlrouglrt of as lookirrg at thc hcarrt iu a verlical pl.rne (i.e. frorn the sides or the feet) (Fig. 1.7). Leacls l, lI anc{ VL look at the lcft lateral surface of the hcart.lcacls III ancl-l/F at tlre infcrior surfacerancl leacl VRlooks at Lhe right atriunr. 'l'lrc V lcacls arc attachccl to Llrc clrcsl wall by nrcans of a strctiorr clcctrcclc, arrd recorc'lings arc madc from six

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positions, overlyirrg thc ftlurth arrcl I'iltlr rib spaces as shown in Figure 1.t1. The six nnmbere'd V lcacls look at thc'hcart in a horizontal pla.rre, from tht' front arrcl thc lcft sicle (ltig. 1.9). Thus, lcads V1 and V, lt-lok:rt tlre riglrt ventricle-V1 and V4 look at the s€p'r[11111 Lretwccn the verrtrick's arrcl thc arrtcrior ;>( wall of the left ventricle.and Vq, ancl V,, look at thc atrtcrior z' JtJ t and lateral walls of the lcft verrtricle/As with thc'linrl-r k'acls, $FY, the cl'rest leads each show a diffcrent I:CC prattern (ltig. 1.10). In each lead the pattern is characteristic, bcinl; sirnilar irr different individttals who htrve nornral lreirrts.

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*HATTHE ECG rsABouT

Fig. 1.8 Positioning of the chest V leads. Note that the 2nd, 3rd, and 4th rib sl)aces are numbered

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@ colibrorion

S\6-nd qr tzq+ ioa = timitect amount clf infornratiorr is prurviclccl Lry tlre hcigtrt

f-n \J of the I'waves,

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QIIS cornplexes ancl T waves, pr.ovidecl the machine is properly catibratr:4.@frDb r,l-tt conrplexes may indicate, a L'rericarclial effusioir, arrd tall R waves may indicate left venlricular hypertroprlry (sce Clr. zt). A stanc-lard sigrral of 'l rnillivolt (nrV) shotrld nlovc the sjylus

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(Fig. 1.11), antl this 4 -*:*yertically 'calibratlon' siglral slrould be includcd with every record. F x Moking o recording Y

Whcrr nrakirrg a rccortling:

patient tnust lie down and relax (to prevent muscle Ir'clnor) 2. Conuect up the limb electrodes,, making certain that they are applied to the correct linrb 3. Calibrate the record with Lhe L mV signal 4. Record tlre six standard lcads - three or four complexes 1. The

5. Record the six V leads. 12 lead recorders do this au tonratically.

@

THE SHAPE OF THE QRS CON'IPIEX ,.'

.*: .7.

,-a'

Wc trorv treetl to consiclcr why the ECC has a characterisl.ic appcarancc in eaclt lcac!

The QRS complex in the limb le^ods Thc ECC nrachirrc is arrirngcd$frTrf,rhen

' 12

a

tlcpolarizationwa\,e,p,"ni,thffialeadtlrcstylus nloves upwards, ancl urhcn it spreads away front the lead thr: stylus lnoves clownrvards.

a e

A\\<: F Avr ; Lf A

AWL;A

{

(a)

\L;t--

A//v lHk

SI1APL

Ol- IHE Ql(s LOA^rtbX

(b)

rc

(c)

Fig. 1.12 Depolarization and the shape of the QRS complex. Depolarization moving (a) towards the lead, (b) away from the lead and (c) at right angles to the lead

X

Depolariz,atiorr spreacls tlrrotrl,,h Ihc lrtart irr r]tiuty clirections at once, [-rut llrc strapc ol'tlrc Ql{S crlrn;rtc;x shonrs tlte average dire'ction in wl'rich tlrc wAVc of clcpolariz.atiorr is spre.acling through the ventricles (Fig. 1.12). I tflttre QRS conrplex is predornirrantly rrpwarcl, or positive (i.e. the R wave is grt'ater tharr the. S wave), thc' dqolarization is moving towards tlrat leacl (f,ig. 1.t2a). (Ifl Pt".lonr i rrir tr t ly clow rt wA rcl, () r' r'r cl',a t i vc (S wa vc 13r'ea tt. r' tharr R rvave), the depolarizal.ion is nrovirlg away fronr that

rel{Iig.

1.72b).

\UVhedthe depolariz.ation wave is moving at right angles to the leacl, the R and S waves are of cqtral size (Fig. 1.12c). Q waves have a special significArlce, which lve shall discuss Iater.

x

.

The cordioc

oxis

lP.l

P'-q,-G l

Leads VR and II look at the heart fronr opposite c-lircctions. @from the front, tlrc clepolarization wave rrorrnally lQreads through the ventricles frorn 11 o'clock to 5 o'clocl<, (ry) tne deflections in lcad VR arc norrnally rrrairrly clownwarcl (negative) and in leacl ll ntainly trpwarcl (positive) (FiS. 1.13).

I3

Wrl,tt IllE

A-X

15

)t fi,3

rs

Ll qbr-AC) Cp:cV) L/ aX is

AUOUT

! ^vL (g

J- -,1,=/'-

)

I

_;{u

ECG

l,^

I lr-/l _,f\_

a'

(.;,

,

GCG

,4,(

Ficl. 1.13 The cardiac axis

(-

g'o x

The average directiorr of sprcarJ of the depolarization wave l.lrrough thc ventriclcs as scell frorrr thc front is called the

,carcliicu*i',@decidewhetIrertlrisaxidisina

rrorrnal directiorr or not.'Ihe direction of thc axis can be clerived nrost easily fronr the QRS corrrplex in leads I, II and III. A rrornral 11 o'ik:ck-S o'clock axisGG@LBttre rleprelillizing wavc is s1-'rrcading towarc-ls leads [, II and III arrrc{ is thercfore associatec{ with a predominantly upward tlt'l'lt'r:tiorr irr all Ihcsc lcatls; thc clcflcction will bc grcatcr in lcacl I[ tlran in I or III (Fig. 1.14). CBtlrc riglrt verrtriclc beiomc's lryl'rertrophied, tl're axis will svllg towards the right: the deflcction in lcad I becornes ncgativc (predorninarrtly dowrrwarcl) and the deflection in lcacl III will bcconre nlore positive (predorninantly upward)

(I'ig.1.15).Tlrisiscallct[,riglrtarxisclcviation,.@

tr

rrr.rinly with l'rulrnorrary conditi
J-

/v

o\

,)

-/

n-ls

zul-,ll Jr\ E-#

THE SHAPE

LUri(-/ -

oF lHt oRS CoMPLtx

ruryI I

-

ffiffif, I

rt

;p il

ilr

,/

Le.o

-lr

Fig. 1.14 Tho normal axis

-:--jrr

JT

AvF t

_4'n

:\s

+\Aq

t,

I

a'f-

JV

r{

\

-+w

{

u Aeco-srd r

t

I

t,

',

-\a

I

,l

62

l

I

V

I I

I

\t I

(1""1

ita I

Jr",

liL

+-,tD 'ill v

Fig. 1.15 Right axis deviation

?LrC

3

I5

T;)l

-

tfl;riii*Ecc,s

);,fr 4 Al 'u4-p

4f-4 /0,, 4/'

,a ABOUT

,11 .o\)r ( I!r ctSi'r) \ ( t;tt +r- )a{ /r,/

d7'

i

I

ttiittiLl.uil

C-y'

4 -o ri!

lt I

II

Figr. 1.16 Left axis dcviation

-

o

;/*iS # !,,?t'

5e

e:b:

3,lJL

cr4
,y;i@tlreleftventriclebeconresJrypertroplried,theaxisl --:I ma-ffing to the le[t, so that the QRS cornplex becomes -l/

-

1 ):F L : ? G. t{

-

? , 9Z

prt.l,rrnirrlrrlly rreliative irr lt:acl III (Fi1;. 1.16),'l,eft axis rlcviatiur'is rrot si[rrilicanl. unl.il tlrc QttS tleflecl.ion is

;rrt'clorrtirrarrtly rrt,gativc in lcatl II, arrd the problem ig uriui'rlly cluc [o a concluction dcfcct ral.hcr tlran to increascd lrrrlk oI lhr lr'[l vcrrlt'irul;rr trrtrsclr' (srt' Clr. 2).

An'olrernotive explonqlion of the cordioc

oxis V

Sourc pcoplc find thc cardiac axis a difficult concept, and ^' atr irltcrtrativc approaclr to working it out may be helpful. 'l'l're r:arcliac axis is at riglrt angles (90") Lo the lcad in wlrich the R and S waves arc of equal sizc (Fiq. lJn. It is, of course, likcly tlrat the axis will rrot be precisgly at right arnglcs to any of the lt'ads, but will be somewhere Lrctwct'rr Iwo of thcr-rr.'l'hc axis poir-rts lowards alry Iead rarlrcrrr thc I{ \vavc is largc,r tlran thc S wave. lt poirrts away l't'ott't ttl)1r 11';1.1 wltcl't: tlrc S wilvC is largcl'tlrap tlre I( wavc. '['hc ,.iircliirc axis is sornc'tinrL's n'lcasr,r..cl i,', clcgrces (Fig. 1.1.3),

I6

ecG [-in

{

alsr-r

f L

L

Jr4\ c-"P.- P,

l'1 \

--- lrt s. I-

'i

THE St-tAPE OF THE QRS C()MPTEX

ut$ I

I

ara

S

I

Aa

fa es

Fig. 1.17 The cardlac axts tg at rlght angtes to thls leact./slnce rlrc -

and S waves are o[ equal

.l

\[, \'(, V*

size

r-L

uf 4

/

-

l-l

-

---on"

VR --

lliO'

vtIJU'

-

-1 B0' +1 80"

-

*i X '

Limit of the normal n r--'| cardiac axis

Flg. 1.18 The cardtac axls and loact angte

t7

ffi*

ECG IS

^BOU>

t>r') t----/

though tlris is not clinically particularly trseful. Lcad I is

takerr as lo.-rking at tlrc heart frorn 0"; lead l[ fronr +60"; lead VF fronr +90"; and leacl III from +120". Leads VL arrd VR

are said to look from -30" and -150", rcspectively. Tlre normal cafdiac axis is in the range -30o to *90". For cxa:-rr1-rlc, iI irr lcad Il tlrr: sizc of tlre I( wavc cquals that of the S wave, the axis is at right arrglcs to lcad ll. ln tl'rcory, the axis cotrkl bc al. citlrcr -30" or * l5(f. If lcacl I shtlws atr R wavc greirtcr thirtr thc S wavc, thc axis tnusl point Lowards lcad I ratlrcr tlratr lcad III. Tlrercforc tlre trr"re axis is at-30"- this is thc linrit of nortnality towarcls what is called the 'left'. l( wavc, tlre @irr lt:arcl II tlrc S wavc is greatcr tlratr tlrelc(L aiilir at arr anglc of grcatcr than -30", and axis clcviation is pt'cscnt. Sinrilarly, if tlrc siza of tlre l{ wave equals that of thc S wavc irr lcad I, the axis is at right angles to lcacl I or at +9(f. This is tlrc linrit of nornrality towards thc'ri.t;ht'. [[ thc S wavc is grcater Lhan tl're l( wave in lead I, thc axis is aL an atrglc tlIgrcatcr thatr +90", ancl right axis ' clcviatiotr is prcsctrt.

Why worry obout the cordioc oxis? l(ight anrl lcft axis clcviatiotr itr lhcnrsclves are scldonr sigrrificarr t - tninot' clcgrc"t@G, l]rg, Uin irffiluals and

irislr.lt.l,[.ttirrclivitlrtals,,...,1,"ffiiy@tlrr'1.lt.cscncerrf

% I x

axis clcrriatiorr shotrlcl ale rt yott tt-r lotlk for otlrer sigrrs of right anc[ lc['t vcntricrtl.rr hyp'rcrtrophy (scc Ch. 4).lA chair$C irf aiis to tlrc righl. lnay strggcst a ptrlnrollary cnrbolus, 1lI.{ € a changQ to thc lcYt irr.lic'atcs alorrclucl.ion dcfcct. i

W

,

Xt I-''

r/nrt'ah The QR5 cornplex in the V in thc chest (V) leads is Thc shape The septunr betwectr the vetrtriclcs is depolarized before Ilrt: w.rlls tt[ [lrt' vctrtt'it'lt:s, arrtl Iltc dcpolariz,atitllr wavc sprcacls acr()ss thc scPttttn frtltn lcft ttl riglrt'

^)

THE SHAPE OF Tt-tE QRS COMPLEX

uflre

\

V o In tlic normal lriart lltt'rc is rnt)r'(, r'r'rusctt: irr tlrt,wirll o[ thc lcft vc'ntriclc tltan in tlrat o[ thc right vcrrtriclt:, itncl , @tlrt' tt'[t vcntrictt.(,x(,r'ls nrort irr[trrr,n('(,()rr llrt. tr('(; f t _ pattc,rn than does thc right vcrrtricle. l---: { I-*u.ts V1 arrcl V, took at ttrc ffi,vt:rrtriett.llt.atls V,

*

'f V ( -' '

\and

Vo took at the

L-' leacls V",' ancl Vor'at tlrc ttiftY:

septu,lr;[I,fl

y:!11:F (ry* ris. 1.0i.

In a right ventricular leacl the'cleflection is first sl)wi1'rls (R wave) as tlre septtrm is tlt,pota riz,,tl (Fig. l.1qf ln ;r lt,[t ventricular lead the opposite patterrr is seerr: there is a small downward deflection ('septal' Q wavc) (ltig. 1.19). / t', a right ventricular lead (V, and V,) there is then a downward deflection (S wave) as tlre nrain rntrsclc rrrass is d"polarized (Fig. 1.20)- thc electrical cl'fccts in tht' Lrigger left ventricle(in which clepolarization is spreaclirrg away from a right ventricular leacl) otrtweighing tl'rose irr the smaller right ventricle (in wliich clepcihriz.atiorr is rnoving I..-.^,

/ yf

F''r \.Lt

zv>

lilfi .illll VC

Flg. 1.19 Shape of the QRS complex: lirst stage

I9

ffi-ilili';ri

i.orsArlour

' !i

!i

"rX "-*\lp'i;rr,,, ,r diLfir- Fb:Lirt& Fig. 1.20 Slrapo ol tho Q[lS complox: socond etogo b

iF rf-* qvR

@ \ ----

,51? .H

il

.:.,

,S

Cl

P

"\t 3e

/1

\^' 3

AorMt( 20

Fig. 1.21 Shape of the QRS complex: third stage

q. e

\

)

IHE SHAPT

*

ol- lHt

QRs LoMPLLX

EEei

towarcls a riglrt vcrrtricul.rr lcacl). Irr l lc[t vcntrictrlirr lcltl tlrere is an trpwarcl cleflection (l( wavt) as the vcrttricular nrusclc is clc;:oltriz.vcl (l'if,. | .20). 4 Wlren the wholt. of thc myocarcliunr is cle;rolarizccl ttrc ECC rcllrrrrg to lrir:;t.lirru (lli1,r. l,2l). tD The QRS complcx in tlre chest leacls shows o l-rrollrcssion {rom tcarcl V1, wlrcrc it is prc.dorrrirrarrtly tlt)wnwirrrl, to lcirrl -1.22). 'l'lrc V6,, where it is preclorninarrtly upwarcl (l;ig.

/,/,

v/

;Y'7 l

0

\l

a

1 --z

=)

Z

b @

F Flg. 1 .22 The ECG patterns recorded by the chest leads 21

'2/

G6fJ 3A

I

fffi

WHAT THE ECG IS ABOUT _--. _a

,J

It)thc riglrl, vcntrlclc ls cnlargerl, attcl ttccuplcr morc of tlra prccorcliunr tlran is nortnal, t'lre trarrsitiorr point will move sorrretinrcs leacls V {V n, Llroughl. of as havlng rotatcd ln a 'Cloctwise rorat,P:l,NT ECC lunu tliscase. _*__=(<_uD)

I

I

*

.-r

' ' , ,L? ' ' .'

rJ\ sit -r r/'{ P,,\ 4
\*i/(-:

(tr.-'i'f

g[gc!g$l

heart can be dlrcctlon.

ir@ronic \____-:_

j'Xil"lW,J),;J,

I I

l-

--__]

i 'transition point', where the t( and S waves are equal, : position of the interventricular s-ephrm. f i"ii..,.r'ifi" i\----= ic::c P, ll G; f \ , {o rr.q p. l"t qi3 r . 2 Z -!(Vhy worry obout the tronsition point?

trlw-r*ffiponraN'ic

D

ft.

Ytru now know cnough about the ICG to understand the lrasis of a rcport. Tl'ris slrotrld take the form of a description, ' "' followcd by orr inte rprctation . Tlle .lescriptiorr sliotrlc-l always bo giverr-in the;same

-scqucnsg; t - ?etsan,cl D. L-c^l iL,"Ll.,r 3 r. nl',ytt',rr', < Rcgute{ oE a'l- ,9t'At*Jf d a"l^ ) ?' L4 HR gSBtsS ii z.E,;ffi

, '_,- i: FTllffil:.fof ,,?qfF:.f^r:I:f ?"€Kxaileb T waveg. tlrc ^L

S.

u> AKie

ST segnrcnts and

A tlescripl,iorr

f l(cportirrg a series of totatly nornra[ findings is possibly [ ;rr:rl,rrrlic, irrrtl irr rcirl lifr.r in frcrlucntly not donc, Hctwcvt'1 / \ yotllust tl'rink al:out all ttre findings every time you I i,'rlcrrrrcI arr ECC

i : Y*:;l: \

-

{,oo fy

r;

S P.Q^1, : li a't ;(" G., .;*,cgp$d, E-*.,ii,l;;

r

AAe ,

M

+4

Dal<

.-

a

R

JT

I

G

uF/eK

!^rof'u.^ 5c3en L.X.\Ae

R<€(-;

ECG INIERPREIATION

ruT l-

,Y'

The interpretation indicates whethcr the record is normal the underlying pathology needs or to be id . Examples of 12-lcacl llCCs are showtr itr Figures 1,23 and "1.,24,

I

a-

-

._-.-

_-

) ,V*ili, J,er- J f -Ur)

,+.-

i;,

-r

-

-aa

l;;inu r.o

rs

Arrou'

-

]- / nvL ./ r,) (y"AS

J

Lr,r.z rt..,

e \ttrr-.h eA a

Lt.,t(LlA,L,{

II

A,-^l^

1 -' .r {Pj:i,Lal . Qln,;t-hylhm, q1 olr-ift --- 3 Xr' J ., Normal PB intorvai{tao rns) -\ .. r NormallQHs duration (1?0 ms) -- [ . . Normalrcardiac rrir +

F1g.1.23 lZ-lgad.ECG: exar4plo .'' ' Descqlloi "il{ {-c7 -"-'.n I

.,

-t' :lr

o Normal ORS complexes

I

orNqrrnalT waves (an lnvorted T wave in lead VR ls normal)

B

_

.

lnlerprelallon o Normal ECG

t'//(Y 9,?

V 4aI

46 ,v; S

-n-

lI I

- lI

25 -l -4

f,ry

wllnl llll l((.lrr'.t',rtttl

I

F

_L I

I I I

I I

I

j 7ti o,nl, 26

An

l
4

fi 4/\

.

;.

P

N,, a'rrr ,J AJ, F

/rwt

a.L

Uovtl

-

-T

[<. [^

L

lr, ,t

atuJ

g. ( ^._-',! s.4. \ll. J \'',., EcG rNrERpnrrarLNlitr

€o*t1a

Q RS

1.-'

''(\^!

u\

snlo.tutu

s-F#i'a.at

b.2 o)seca)

F--a4lA tztf4F19,1.24 1?.laad ECG; oxamplo 2 Descriplion

. Sinus rfrylhm, rala 75lmln . PR interval 200 ms . ORS duration 120 ms r Flght axla devlallon, (promlnont ) \=.., : e lead l) r Normal -! ORg eornploxoo .

cf.r-F ryC.e-cr{ -1

S werve

ln

'\ \ \ I

I

Nolmal ST segments and T waves

lnterprotallon

o Normal ECG

- apart lrom right axis devlatlon, whlch could be normal in a tall lhln person.

L

Unfortunately, there are a lot of minor variallons in ECGs which ars consistont with perfectty normal hearts. Recofrizlng the limits of normality is one of the main dilflcultles of ECG intorpretation

V^rf

@ E^r\,

p,l-

@,

lh\

lK(

|

l-. l\s

S€c

o-,J

o

T\- s@t-

?o(ese^/l'

n f€C

2o-

+ir*

-r

y0 lnf f

I.\

t\

\.._ \.\

/

e %t "

\. -.--

\\ \

-r

27

I

-

WHAI

II

II

,

-t-

Ii N BUU

I

X

I I

LCU

THING{

'o

nrmrmBEi

'l'lrc ICC rcsults frorn clectrical charrges associatecl with actival,ion firsl of tlrc atria and l.hen of the vcntricles, 2. Atrial activation causcs tlrc P wave. 3. Vcntrictrlar activatiorr causcs thc QI{S complex.'$ the first tlcflt:cliolr is downwirrcl it is a Q wave. Any'upward deflection is an I( wave. A downward deflection after an

I

1.

I

I

t_--

o 4. Wlren the depolarization wave sprcads towards alead, the deflection is predominantly upward. When the wave sprcads away from a lead, tlre dcflection is prcdt-rnr i rra rr tly downwa rd. 5.'l'lrc six linrb leads (1, Il,lll, VR, VL and VF) look at the hcart fronr the sidcs and thc fcet in a vertical plane. (r. 'l'lrc carcliac axis is tlrc avcrage direction of rpread sf clepolarizal,ion as scen from the front, and is estimated l'r'onr lcads l, ll and Ill. 'l'hc 7. cl'rcst or V leads look at the hcart from'the front and the left side in a horizontal plane. Lead V, is'positioned ()vcr thc right venl,riclc, and lead V,, over the left vt.t'r I r'iclt:.

ti.'l'lrc scpttrrtr is dcpolarized from tlre left side to the right. 9. ln ir n(,r'rnal lrcart llrc k:ft vcrrtriclc cxcrts nrorc irrflucnce orr tlrc I1CC tlrarr tlrc riglrt vcntriclc.

28

2

\5

Conduction ond its problems Y"j (;'uG,uus qqr=t

l>I

,f\ l-5;^

d,

€;

-t Conduction problems in the AV node and His bundle 30 Conduclion problems ln the rlght and lelt bundle branches btrndle branch

blocf

-

36

Conduc{lon problems ln the distal parts of the lelt bundle branch 44 What to

do

50 -,'

Thlngs to remember 51

-

-t.

electrical activation normally begins in. the sinoatrial (SA) node,ffi OefYmr to tlre atri6ventricular (AV) nocle, arrcl /@*+ eA mn hiorrof this wave front can be dclayecl or blockecl at arry ;roirrt.

*.t)

J4 -

X . Conduction

problems are simple to analyse proviclecl you kuup_te wiring diagram of tlre heart corrstantly in mind (Fig,Y.l).,

,

We can ttiir',t of conduction problems in tlre orcler in whiclr the, depolariz.alion wavc normatly sprr,a(ls: ',. node -> AY node -+ His lrurtclle -r lruncltc-bralrctres. ,-

\',,

-

SA

2q

t .i rrne.

...,r

r

" B!..56.r

CONDUCTION AND ITS PROBLEA4S

tr 4

)( -/'

/rs

-*l

J\

3- S 5c--r\\

o(

Sqr.

/

;.' ;':

,l.J*or*,.,,b\o.-,ln

|2,?

Sinoatrial node Bundle of His

)'

Airioventricular node

-'H

;

nf,'

--:

Left bundle branch

i

Right bundle branch

Flg.2.1 The wlrlng dlagram ol ths heart

f, ?B 4/ 3 -c, 3

f.r..

^

\\

e1/* or

I(enrernbcr in all tlrat follows that we are assuming clcpxrlarizatiotr bcgilrs in l,hc ntlrnral way in the SA node, The rhythm of the heart is best interpreted from whichever ECG lead shows the P wave most clearly. This is usually, but not always, lead II or lead Vr. You can ilrinurnr. llrnl nll lhr''rlrytlrm ntripn' in thir lrook were recorcled frotn one of these leads.

L, F-

:\.

CONDUCTION PROBLEMS IN HIS BUNDL1 i'111"' "",' """'' ":i')'''''""

"

TIre tin're taketr for the spreacl of depolariz.ation from the SA node to the ventricular muscte is tto*"i-y'ti.-ii'>---' irrlcr.vnl (see Clr. 1),i,.Q4d is not rrormally Sfeater than 0,2s (one large squarclEcG events are usually timed in irrilliscctln.ls ,o*{r, tlratr scconcfu, no tlrc limit ni'[t * pn interval is 200ins. Interference with the conduction Process '", causcs tlrc ECC phcrr.r,rrcnon callcdlhcart blocK. \s - 2, V

'*rV

a---

-^,t1 i

First degree heort blocli If each /rave of depplarization that oftinates in the SA node is corlducted to thy'ventricles,-b.y[ there irdelay sornewhere = ,, at,,,',1ftt',c conclrrction patlrway, thenjlhe PR intcrval is lr ro

((

,

i

lrr

n gt: t|

,'^

.

1'

po

l' [r

is is

ca Hcil''

(,qat-i,n.,

fi

rs

t tlEfirce hesrt bloc k'

il

{

Fi

g, 2.2),

*^-jv,, L* '1e

Secrrl

Ja

':_^*_HHHT,

s1*
r*-pre:<_r/L gr 2

@r 2oo o,^t \\t Lar3e Sa = 2oo Ms

j,ft'-.n-i

t

.

t

t,e

CoNDUCTION PROrrtEMs rN THE AV NODE AND HtS truNDLE

4A

PR

^A

ft

?

360 ms

Flg.2.2 Flrst degree block

Note '1.? . One P urave per QRS complex--;v r

.

Q,

rvnr o

fj '-Sno,^,

5

,,

S

'uG

*r?'>-,

r* a \7l S',,

#

First degree heart block is not in itself important, but it may be a ilgn of coronQry 0rtery tliscase, acutq rh-curnatic ca rd iti s, a igo-^,lli,xi ci tytl'ei dc t ro iy t.. i s t ir rba n?ei. I z_r

l_ L

CRD€**);" ,-L'

Sccond dcgree heort block

- Soffi* excitation completely fails to pass tlrrorrl,,tr tlrt' .-.AV node or ttrc bundle of I'lls. Wlrcn tlrisl.,.-ct:r.,s / . ' intermittenHy,' 'seeonel- clegree h€art-hta€{4-irsnit}-to exist . 'l'here are tlrree varlatlons ol' tlrls: l'-'^"'t-

,,--'

-t',

-L'4 /

'lt:"

'l

dnL+\ -

t'

fl. . *'.|, Most bcatr flrc cotlchrclccl wilh n r'onslturl l'l( irrlrrvirl, #LG brltrrecasiOnally tiiA'e is an atriat corrtraction willrorrt a

Y --''

subsequglt.ventricular contraction. This is callcci the

'Mobitz.type2'phenomenon(l?ig.2.3). i,

.i-.

E.There may be progressive lengthening of thc, Pli irrtc'rvnl and thcn fallu rc of concluctlon of arr atrial Lreat,.follcrrmcrcl b,y.a conducte*trcat with a slrortgrPl iFtervftI and tlren a rcPetlflon of thli Cycle, Thlr lfl llrs'Wurrckubnlrlr' s ( phenohgnon (Fig. 2.4). fvlc b,iz '7:// 3 I ,P. ;?) il'b-&, There mA v be nl,felnR l g'con cl u cl prl u r rl l rrn r -r,o r h l l ct r,t l at|'* raffa@ais (o7on'b conclucted atrial beatzand t/rcn two )' o n )/ 7aL,
e*##-e**-*

r

3-=T-

-

r

ara

-t

dloJr: ?

3I

W

+AP€-'L CONDUCIION AND lTs Pi(OB!,{iMs

21:1

I

r

I

_L I

I

i

LYt*rb a--

Fig. 2.3 Second degree heart block (Mobltz type 2)

l\

Nole

7

. G) .

I

l

PR interval of the conducted beats is constant One P wave is not lollowed by a QBS complex, gnd here gecord L+ X tJogroo bloek lo occurrlttg

?

\

-2-00 ms

4 -z

11 ---\

280 ma, 320

ms P

iiitillt';IiTl,i:i

Flg. 2.4 Sscotttl dogroo hoart block (Wonckobach typo) Note

. . .

\

L *

-/

7

7r7\

i "'t IZ

*jPo,

Progressive lengthening ol PR interval g ff^rA drj. r.; $ One non-conducted P wave Next conducted beat has a shorter PB lnterval than the precedlng conducted beat

T

n(,n-c()rrclrrclr-'ct ttcitls), triivilrg twicc (orthrce tirncr) ar nr.u'ry {' wavcs arE}t(S complcxcs. Tlris is called '2:'l'' ('twtt

to orrc') (or'3:1' ('tlrrcc [o orre')) concluction (Fig,2,5).

('J

G

32

o-.-

; \r\-

with any other itself as a distortion of a rlrytlrnr, i I' *u,re nlay only show -.-_'f wavc (ttig. 2.6). €F'ff Qt ll. is impor'tant to rcmcmbcr that, as

l.*^rr- \". t, Ji \-

t-!\P

,.r-l=i'*z-'+,1- ?

'l

^,

1

CONDUCTION PROBLEMS IN THE AV NODE AND HIS I]UNDIE

i'

l

\x

,l

Flg,2,6 Eccond dogrce hrart block (2:1 typo) l.tole

r

Tfvo P wsvoo por OnB cornplox

o Normal, and constant, PB interval in the conducled

5R=e

beats o

a^

gt-e21

Flg.2.6 Second degree heart block (2:1 type)

Note.

o

J-

P wave in the T wave can be identified because ol its regularity .

, u(J'

.U

/- 2-/ s

underty lng, cau3rrl scconcl r,f",pq-IU11I-UI!gk 1f qqltrqs_q_qf first dcgree pheFbmenon ie usually benign, but tvilfiitz typc 2 block yf 2l block may llglLlg 'cornptete//or 'ttriril clegree', lrearr blhck, /.il,tt 7 l.l ,t g,- ,''r\,{ ,

...*o llil tE 93.u

btock.m

' '-'n

"r;,'A'heort Third a&i","

!.

' ./,.i

-\,

block

-

,

'\'a

'

'*',

t' Complete heart block (third degree t,lock) is said to occttr when atriat contrilclion is nornul lrrrl rro lrcirt$ ilr.u :it! conducted to the ventricles (Fig. 2.7). Wlren this occtrrs the 33 i

\'-

..H:effi'.:.

#E"

k--

F:--

5iry

LONIJUL IIUI

t

..l

NI {1,

I

Ib I,RUIJLLMS

d r (;l

5<

>.@w

y c|

I

Z.

Abnorrnally-slraporJ QRS comploiog bocauso ol abnorm al apread ol dopolarlzation from a vontricutar focus

upbt<- D{ >so.{^!to n te,} ,h|,".9 C'o

uG

orb ^-Al e >t_

nn'

34

.,

ttir:

1.

,

LUNUULIIUN PRUUIEMS IN II.IL AV NUUI /\I\IJ I-II5 IJUNUII:

rer

vendictes are excited by a slow 'escape mechanism' (see Ch. 3), from a depolarizing focus witlrin the ventricular

musctg.

(

u

.

.,

Complete block is not always immecliatety obvious in a lLlead ECC, where there may be only a few QRS complexeo per lead (e.g. see lrig. 2,8), Vru have to krol< at the I'}R interval in all tlre leads. r Complcte hcnrt block mny occur nH nn nculq phenomenon in patients with nlyocarclial frffirction (w'hen it is usualty traneient) or it may be atlrrorrie flllclUsunlly due to fibiosis around the bundte of l-li--slTffiffilIo be caused by the btock of botlr bunclle lrranches.

€

#

Flg.2.8 Complete heart block Nole Slnus rhythm, but no P waves aro

.

conductod

I o Blght axle dovlallon

L . 3 .

I

.

-ra,vf-?(duration

^(v/*

Broad ORS complexes 160 ms) Blght bundlo hranch block pallorn Ths cause ol the block could not tlo determlned, though ln most pationts it rcsulla lrom llbrosls of lhe bundlo ol Hls

de)Y t'Y

^

In

I

_-, J

i-t I

I

g. 31

II I I

-l 35 F1

-ws cpR

r x r1*i

x

L a6s D

LUNLTUi-Ilrl't /rl ii.r lll> l'ltUtlLLMlr

s,T or zcv

u-)

/4

Rvu

P€

'

If llrc dcpolariz.ation wavc rcaches the interventricular scptunl nounally, the irrterval between the beginning of 'thc I'wave arrd the first deflection in the QFS complor (the l'lt inl.crvat) will bc nornra-! fowevet if theie is abnormal conduction through either the right or left bundle branchcs ('bundle branclr block') there will be a delay in Ilrc clcPttlarir,ation of part of tlrc vcntricular mugcle. Thc extra time taken for depolarization of the whole of the ' vcrrtricular rrrusclc causes widcning of tlre QRS complcx, lrr tl're rrorrrral heart, tlre tirrre taken for the depolarizr,tion

wavc to spread fronr tlre irrtervcntricular septurn to the fu:'i.lrest part of the ventricles is less than 12D m,s, re prcscnted by three rti?tt squares of ECG paper. If the QI$ duration is greater tl'ran L2,0 ms, then conduction .' wi t hi n the ven tricles musthawloeeuri:e*byran abnormal :--' -'i nlow l]lthwny, ; > !- r1\- (1. --- -^]\ t-, -*r+r+[-rMtrrc - '-Although a wide bHs complex can indicate bundle bianch bltrt:l<, wiclcrrirrg nlso ()ceur$ if dcpola ri'tatiott bcginr within thc vcntricular musclc itsclf (sce Clr. 3). t{emem6er that in sirrus rhythnr witlr l.rundlc branch block, lrormal I, waves arc preserrt with a colrstant PR intenral, Wc shall see that this is rrot the case with rhytlrms beginning in the ventricles. Illock of both bundle branchcs has the same effect as block of the His bundle, and causes complete (third degree) ': lrc,rrt trlock. l(iglrI bturcllc branclr lrlock (l(Ul]lJ) ofte_lr indicatee l.rroblcrrrs irr thc {gl,t sidc of thc Lteartrplt ITBBB patterns willr a Ql(S on are quite common irr lrcal!l1y pcoplc. * l,cft burrdle brarrclr block (LBllB) is always an indication (r"blep )n of lreart disease, ustrally otthe lgfi side .W important to rccogrrize that bundle branch block is p,/csent, because

L-r

{r

iso

V5'Vg

DUNDLE

BRANct{ BLocK

ufl

't. LBBB prevents any further interpretation of the cardiogram, and RBBB can make interpretation clifficrrlt. The mechanism underlying tlre EC(i pratterns of I{l}l}ll and LBBB can be worked out from firsl prirrciplcs. Remembep (see Ch. 1):

i'

\

'

.

The eeptum ie nornrally clepolirriz.ccl I'r'onr lcft to riglrt. o The left ventricle, having the greatcr rnlrsclc rrrass, r'xerts more influcnce on thc ECC tlrarr clous the right vr.,ntriclc. . Excitation spreading towards a leacl caLlses an uprward

Right bundle bronch

bloqk

i'/

':

)

{

No conduction oge1ntgdol4{r\fire riglrt bunclle branch,

\ 1L,

cauoing an n wave tn a rilh+ventricrrf.rr leacl (Vr) arrcl a small Q wave in a left ventrieular leacl (Vo) (Fig .Z.g).

R6@@ {\ t\4/

ffiffi E-plbt -/ vo

/'ju rQ\- /Y{

rvaLrUl:

I

t /,.'-,2 )t {^e-z 1' Flg,2.9 Conductlon ln rlght bundlo branch block: flrst stage

37

\-*

W

coNDUCuot{ Ar.{r nb

r.,r(otJLLMl

u),d ',*.4'

Ir

v1

Fig.2.10 Conduction in right bundle branch block: second stage

?RI

SR,

vo

!=,, Jee

1 u-r1a a l'71 Vz

V.'t: ri"' 38

,"''

Fig. 2.11 Conduction in right bundle branch block: thlrd etage

I

r)

t*gGg

j NJ D

Co,.&qHo

G.4 t--LI- !--,^J.^\a

! GLl-iRe(39

'

?., f3,

BUNDLE BRANcH

,..i'

-1 BrocK

AW

Excitation tlren spreacls to tlre left ventricle, causinll arl in lead V1 and an R wave in tcacl V6, (Fig.2.l0). It takes longer than in a nornral Ircart for excitation to reaclr tlre righ"t ventricte bccausc of tlrc faiturc oI ltrc normal conducting pathway. The right ventriclc, thert,forc' ctepolarir,esafter ttrc lcft. Tlris causr,lr il !rcr'()n!l t( wnvr'(lil1 irr lead V1, and a rvide ancl deep S wave in leici V.1rtig. z.:tti: An'RSRr' patlein, but wiilr a QnS conrp["* iir rrii,.nral. width (less than 120 ms), is sometimes called 'partial right bundle branch blocK. It is seldom of significance, ancl can be congidered to be a normal variant. S wave

\' I

''/,

'

_

I

c- (

l' )t

l( conduction doh

the left bundte branch fails, the septunr rlglrt lo lo[t, cnuulng rurnr,rti (-l wave in lead V,, and an R wave in lead Vr, (Fig. Z.1Z).

lrpcornpn +lepoln rlnpcl frotn

]

(

t \s

'i

,,V, 't

*-

F1g.2.12 Condficilon ln left bundle branch block: first stage

39

*--EAffi

'W

coNDuctt(rr{ nt'ltr ltu I'RCJI}LI;MS

;

ffi .v6

Fig.2.13 Concluctlon ln lelt bundlo branch block: gecond etage

F

LB {'G,\i

"A

/ .t

..16

'(

<-

\\,

\t1

v6

RsG

ffi

e

vl

40

^{s Fig. 2.14 Conduction in left bunclle branch block; thlrd stags

.

1.: i

\

-l BUNDLE BRANCH BLOCK

UT

a

/

Tlre right ventrlcle is clepolar.izecl bel'ore thc lcft, so _ despite the smaller musctc, mnss tlrerc is an R wavc i^ tt,.rt V, and an s wave (oftcn ar,pearlng,rrty as a nrtctr) irr lead V, (Fig. 2.lg). Subrequent depolarization of llrc tcft vcrltrictc causes nn lead V1 and another R wave irr leacl V6, (trig. 2.14). y1l1il \___-S LBBB is associated with T wave inversion in the Iateral leads (1, Y zand V5:-Vu). \+

+:

Whqt to romember RBBB ig begt Been

in tead Vs where ttrerc is an RSR, Pnttt,rn

$tig'-2a,!5)' .) v LBBB is best seen in leacl v"

-.

:^t

€

P

where ttrere iJ a broacJ complex wltlr a notcltcd top, wlriclr rescrnblcs llrc lcttcr.'M' and ii thus known as an'M' pattern (Fig .2.16)..ftre gomptete picture, with a'w'pattern in ilad v,, is often not

t-r.

fully developed.

\

' 'o l/l

\tA,

t,\-, i=L

e

QRS

- (3[ \5

I

.t

-

41

.;'xE[rcltigr:{R-

-e ryry

tt

42

coNrruc,ot*

AND tls t't{olrLEMs

;2

\J+ 95o. BC5R -T1

'S

Ao

is

i

(v

i'Jx-^e / 1;'

21

V

3

QRS

RrR

RBBca

-

ru

9a olA t^---

(ug--

."lt

|

L>1

i..

r

-lr --- ._.l*

BUNDLE rlRANCt-t BLOCK

? qA e

r+t&

/A'i rn

l?,,ffiffiT

6,-L

Rv o( LfF1g,2,16

i.

Nole

Elnuiitrythm rtfrtr nAna

--i:'

,-,--= H /a t

o Sinus rhylhm, rate 7Slmin 1 o Normal PR interval

r - . Normal cardlac axls

1 r Z. ' ,X

o

Wlde ORS complexoe (1S0 ms) RSBI paltern in lead V, and deep, wido S wavde ln loacl Vu Normal ST segmenls and T waves

-a

43

,ffi (,OI.lDtJ(.ll'I IAl

lt,r

l',

l,l((,llilL/vlS

,I

\ )\/

I

,,i ,l

',1

il .riI

bt\

i

:

;l

I

',1

lo .'1

ri 'l

v

il li

,i i

:l ,i

.:l

ri I

ii

LAD 2( ft

ftqY

*

r

,1

?.. =L t'o N D ii aii6iiih R,b, d'tE iii3"iff

:,

oF

THEI LEFT,

v{v =

BuNDLrlgnaNcH

Ant ' lw t14i;'pr*nrl. iLis wdr@i{ittld-riloje.,fuail

th,g an urrdtr€. The right burrdlc branch has no main divisions but the left bundle branch has two - tllc anterior and posterior'fascicles', The dcpolarizalion *nu"\eEfore spreads into the ventricles I'y llu't'r,r lrrrlltwrtyn (llig,.-2..17), \=tt 3' -.!\,.','!."'r.:-t. The cardi.rc axis (sce Ch. 1) d"p@s ol"l the average t l i rt't' l i o r o t' r l c poli r rit,irl iorr of t lrc vcnTFic-tss{ 5i ncc\ tlrc lcf t ventricle corrtains ntore muscle than the rigHfi-lhas more irrflucnt:c ()n llrc cirrrliirc axir (llig,2,L8), r

44

+" s'ci Ae

-4-\

-(

.a

Iti

''l

-s =-:fgtt"-( PROBTEMS rN THE DISTAL PARTS

oF

BRANcn

THE LEFT BUNDTE

llrl

F19.2.16 Slnus rhythm wlilt LBB[]

Note . Sinus rhylhm, rate 100/min -r

\ o Normal PR'lntorval

\

o Normal cardlac axls

\ .

Wide ORS complexes (160 ms) M pallern ln the ORS cornploxos, bost soon }= ln leads l, VL, Vs,Vu ? o lrwerted T waves in leads l, ll, VL

.

4l Ji

{

t*

*.E ,*.----

-\ Bundlo of l'lis Left bundle

-

-,-

- \

branch

w-tyrl AruV" -f,-, +'k

Anterior fascicle Blght bundls branch

l'osto

rlt-r

d,)\ , ,

fne Urile pathwaye ol the depotarizatlon wave

.ts

r lusr:lcltr A

't: Fl,g.2.17

f-

45 as

.frffin

Col{UULllul.l nl.ltr

lli

l'ltulrLlMi

tlrc antcrior -- \e -. corlduct, left Il'

-e v-,

-;

^a - \-99\2, 'ly,J\,Y

fasciclc-of tlrc lcft bundle branch fails to verrtricle lras to bc depolarized tlrrough the llrr: lrrrrtr.r'ior' (unclclc nrtr,l ro tlta eardlac axb foldtst ''. Upr,vards (Fig. tr.L7). uP'/YdlLlD \I'15. 2.19). /" \ -,-.\' ' '' \ " l,r-:f[ axis rlcviirtiorr is tlrcrcftlrc cluc to left antcrior -t-' IcicuJar bi-ock. block, or'lc[t anterior hcmibloclC (Fig. Z.Aq. t8. z:, -fafcicrilar

4nL f,

,l

",.

\ -,' AL'- o';.h)A ./. ,

qv nyu

b,

Normsl axlg Fig. 2.18 Eftect o[ normal conductlon on the cardlac axle

qo

PROBI.EMS

lN THE DISIAL PARIS OF I HE LEr I BUNDLE IJRANCI-I

'l'r"

[.

( f][

i -ii \t

rq

-,'

- -\'-_>

of tlre lcft [:trrtcllc trot TIre posterior \g selectively the IICC blocked, but if tlris is

fapclcle

does occLtr

e

oftc'tt slrows

riglrt Qx!s-aev!4!ion. - "' ' \{ _{hEf, the right bundle branch is blocked, the carcliac axis usGlly remaiis normaL Wp"i there is normal depolarization of tlre left ventricle wit| i6 large_ tnu-scle mass (lti,g. ry). 1 (-C'.rY

,/,

,

Left axis devialion

F19.2.19 Ellecl ol lelt anterlor laeclcular block on tho cardlac axls

i ^r lo?"<-\--.1'r'.^

<-

F19.2.20 Slnus rhythm with left

devhllon(olherwlre normnl)

Note

1 1 i

.-}-e

t

axis C e, "., .a vu'i'/r k'r':-' -

-

l-..-

ail.
lead l, but downward (dominant S wave) in leads ll and ltl Normal ORS complexes, ST segments and

-

T waves

-r-

,LJt

47 **

m*m.-.*ifrE*"d".*,-

-

,m \'r'i-!'!'

r-YrulW

/J*

: 4

t

--_\-

,:

t-lowcvc[ if bot!1 tlre riglrt burrclle branch ancl tlre left antei'ioifaiA6i6 aic trlockt'd, thr' ECG shtrlt'S riglrt l'undle hrffih blocJt and lc.ft ari< dtri:t..r rL{D) tF.5.:f- ThL<

\)2'r.Dr

\c\

a

>P

- d

_-.J n?) b.{

!Kn

I

:-*

HL 6,il)

?

?,ot-^3< h'. "

Fitg.2.21 Lack ol elloct ol RBBB on lhe cardlac

*r,

48

\.tn"1

./

sl-,rA-?-)

axlr

'tt

;

t PROB.EA,TS

tN IHE

DTSTAL ,ARTS

OF THE LEFr rluNDtE

'*ANCH

"^ licc.pattern

obviously ilcli^c.ates wicrcsrrr.cacr '

crarna1,,t.

\ >

f,rffi

r. trr.

_ "uljucting ru\ t,bunalg u1affii, anct bortr fascictcs.f rrrr. refr bv,-.,I.1,1*,:igf as if the ma'in His buncilc rracl Faitea to concruct. sysrem (I?,g.

RBDB + LDBI

:

Loft axls rlcvlirtion LJ

F19,2,22 Efiscr of RBBB and rcrt antorror homrbrock on uro cnrcilac axlg

Flg. 2.2J Bllasclcutar btock Nole

o Sinus rhylhm, rate g0/min r o Lolt axls dovlallon (rlornlnant S wave ln leads ll and lll) ,.1 a o BBBB (RgR poltorrr ln loacj V1, ancl ctoop wide S wave ln tead Vu)

-i

49

-

L1;I llrtJ(.ll(rl

l/rl

ll.r

ll;, l,l{(_rlilll,Ai,

\NN ?^ce^^alr.e/

([

plo lp<-s\ gr,.

Always remelnber that it is the patient who should be treatt:cl, not tlrc IICC. I(elief of symptoms always comes first. I lowcvcr; sotllc gcrrcral ptlintr can bc made about the action that rnight bc takur if tlrc liCC shows conduclion arbnornra litics. First degree block

. .

Often sccn in nornral pcople, Think about acute myocardial infarction.and acute rlreunratic fevcr as porsible caureg. No specific action needed.

a-,.

Second cJegree

>,

block

,

.

Usually indicates heart diseasc; often seen in aeute

.

Mobitz typc 2 and Wenckebacl'r block do nst need specific

nryocatrdial

infarctitllt.

i

,'

'

treatmeut.

ftlr tempor?ry or Pc'rnranent pacing, especially if the ventricular rate istlow. ,

ANNp 2:1 block nlay irrdicatc a need

Third degree block Atwnyn inclicntcn conductirrg timue diseasc - lrlor€ often fibrosiE tlrarr isclracnric. Consider a temporary or Pcrmanent pacemaker.

( .

,.A,lro

4

Risht buncllebronch block t?B t3E . Think about an atrial septal defcct. No spccific treatnrent. Left

. ' 50 .

buncJ

le bronch btock

':

I S lj \S

'tl'rirrk about aortic stenosis atrd ischaemic diseasc. tf tlrc Patictrt is arymptonralic, no action is nei?ded,

WHAT To Do/THltlGS To REMEMBER

fffil

'\

.

P0irr, I-ll lil i may indicate. an acute myocardial irrfarction, attd ' ' thrombolysi:.shoulil bc' considerecl.

If the patient has recently Irad scvcrc cltcst

_

Left oxis

deviotion ''

j*

o Tlrink about left ventricular hypertroPhy.

. '

tf ri

No action needed.

*ri,l

lS'',';'

{-t$

illl

Left oxis d"r,iotion olia ,rnt',t bundle bronch btock o lndlcafclr severe conductllrg tisstrc cliscttsc. No specific treatment needed. Pacemaker rgquired if the paticnt ltas synrptoms suggcstive of intermittent complctc heart block.

ilfnfpO'i TotflEfliiiligin'l;1i."h*ii

-V

',ui"*1iff,,!fi't ';

'r'tj.i,.'lirrl-'

;

in tlre SA node, atrcl spreacls to the ventriclcs via tlrc AV ttttclc, the I lis Lrtrrtrllc, the right and left branches of tl're I-lis buncllc, and thc anterior and posterior fascicles of tlrc lcft btrncllc' l'rrarrclt. 2. A conduction abnormality citn dcvclop at arty of tltesc

I

1. Depolarization normally begins

-

points.

,-,/'

/i

in the AV nocle ancl I-lis burrcllc may be partial (first and second degree block) or comptetc (third dcgrc'e block) 4. lf conduction is normal tlrrotrgh tlrc AV noclc, tlrc I'lis btrrrdle and one of its brarrclres, brrt is abrrornral in the other branch, bundle branch lrlocl< exists and thc' QIIS complex is wide. s.The ECG pattern of RBRB and LRRR can be workt'cl out if you rcmember (a) tlrat thc-sgptunr is clc;rolariz,ccl I'irst from lef.t.tci right; (b) that lead V, looks at the rigl'rt ventricte ind lead V. at tfte left ventricle; and (c) that when depolarization spreads towards an electrode thc' stylus moves upwards. 3. Conduction problems

-\ -

.

,t

/ CONDUCTION AND ItS PROI}LEMS t I

(r. lf you can'I rcnrcrrrbcr all tlrir, remcmbcr that RBBB hag ,-/ /d r or1 RSI([ pattern in lead vl, while LBBB has a letter'M' { 7. IJlock of the anterior division or fascicle of the left bundle

bralrch causcs lcft axis dcviatiolr, i

.Ur",

i)il^i)\

Vr

t { *R tigB "t :

LVz

|

i.'

{ E,

<;fu 52

rl,

?.3\ "

_,

t,,\,

,.!

6-r)l

./:,

)

"
Ai

4

Lit

,,.? { "n/l

2,1)ls

->G

--2

t-c-/

\

c

2

-'1-: ,/ (,J

3",\

, fThe rhythm of fhe heorf

I

(

i,{;,.-/ ,J1-1-

i | '.ri

J5'*t/

The intrinsic rhythmicity of the Typee ol abnormal

heart

Ltz\;

54

Z.:

Its,!!

rfrythm 57

Exlraayalolor g2 The laclrycardlas

x

-

lhe fasl rhythms

Fibrillation 78 Wolff-Parkinson-White (WPW) syndrome

B1

Tho orlglne ol tachycardlas tl4 What to

\

do

84

Thlngs to remembor Bo

-

far we have only consiclerccl tlre spread of xL depolarization that follows the normal activatiorr of tlre So

si@,Wlrcnclcptllaril.itlitlrrbcgitrsitr!tr.:S4

r\

node thO heart is said to be in sinus rhythm. Depolarization can, lrowever, bcgirr in otlter pllccs.'f'lrcrr tlrc r'lrytlrrrr is named after the part of tlre lrc,art where tlre depolariz.atiorr ae'el;ldncc clriginatc:1, Ancl an 'iu'r'lryllrnrin' is sirirl lo lrt, present. Remember:

.

ffi

Abnormalltlcs of carcliac rtrythnl ilrc casy: to worl< or.rt. The two things to look at are the P waves and tl're widtl-r of tlre QRS conrplexes.

I

a-

4-f

\

lllt. l(l t(ttttAt-.tt

$iruW

lllt

llt /rl(l

Wlrcn attcrnl;tirrg to alralyse a cardiac rlrythm rernember: t/.

\r''

.

'---^

O

Atrial contractiorr is associated wil.lr the P wave of tl're ECC. Vcrrtricular contraction is associated with the Ql$ conrplex. Atlial corrt ractiorr nornrally ;-'rrcccdes ventricular corrtraction, and lhcrc is nontrally
THE INTRINSIC

f' / \'

of thc hcart can clepolarize spontaneously ancl r'lrytlrnrically, arrcl tlrc ratc of conlraclion of tlrc vcntriclcs rvill bc controllcd by thc part of the heart tlrat is rlr,;rulrrt'izin11 rrronl fi',,rgu,,irlly,'l'ltc SA nocle ttornrnlly lran Llrc hi1;lrest frequcncy of disclrarge. Tl'rerefrlre the rate of t rrrrlr',rt'liorr of llrrt vt,rrtrir:lt'tr will r.rrlttal tlrc rrttc of dirclrar6c ol' tlrc SA norlc. 'l'hc raLc of discharge of thc SA node is influenced by the villlLrs nct'vcs, also affcct [lrc lrcart rate. Cl'ranges in hcart rate assscia+effihVtr.,s[ gr.rr'ts

'.-rcSt

S

:, callccl 'sitrus arrlrytlunia'(Fig.3.1). + j i-, :, c '-\ , '{* '- " " n slow sirrus rliythrn ('sirrus braclycarclia') is associatecl ^.*p 1 .1\ D' *'/rvillr ifllrlclic Ir'airrirr1l, [ailtintf"!$-.kr, lryl:ol,lrcnnia and ,r. -_r .]i )i-..''i-,l)l,y^.,"jilffi..TitisoftffifrrmecliateG_ftc}alrcart\.-',.|r .:s

.

r.

t

'

J\---+

'

(-\

,,ti.,if, /\ [asI sirrus rlryl.lrn'r ('sinus tf,chycarclia') is associatccl . \r/itlr cxcrci:;c, {gg; pj-1!1, lracmol{pgc and thylgti;;;;;,---; 't"t ,) 2 't'tr.','c[lt ' 1',ni[L:.,iiil:ntc i]Giffiilcd'bradycildi?6r ), ' / V f 'l,lt'lr1,q';1r'tliir'- tlrr:se iu'(: nlcrt:ly dcscriPl,ivc lgrlng, ". L :, 1,,, ^\ Abnornral cardiac rhythr',',s io,r bcgiir in t[il'e places - '1,1t' . \ .tlrc atn**U,sclc; thcri'giorl aroun.titlg1f6oclc (this I ,:J , r,,', , ^;;), rhythin IsCallcd 'nocl5l' of nrore propeil-y, functional'); a-1,\^\, -'-

1

-

s4

.lw

* ':'e ,1,4-o O

' [+*

or tlrc vurtricular rrrusclc. In Figure 3.2 the stars suggest , -

r ,c3

;i
rAyfh*t

L,a

l-

frR

.,- o/

t

60

t tgo

--.

_i

)cl tNTRtNStC Rt-tyTt-tMtctTy

/x t*

iA

oF

w

HEARr

t,\(-

-z/

k*

Tr.lE

ffi&U

./\f lr

ll,lllii I

t'l

fr

i:

I

iillii

Ir

Fig.3.1 Slnus

arrhythmla

lri

-/

Nolo . One P wave per QHS complex tJc17o,t . Conslant PR interval . Progresslve beal-lo-beat change in R-R interval

,13

K

3in'r<

; A t Vtt lh 7.-__ i 4 The star in thls and other figures tn lhls chapler indicates the part of lre hearl where lhe aclivatlon sequenco began

' qlt

SA node Atrial muscle

AV node

Ventricular muscie

.I

-

FIg.3.2 Polnts where cardlac rhythms can begln 55

-r

tHE Rnylt-tM

e;}ffi

or rHr uuARr

)\

€(\

'?f/''

I

VJT

-;-spccrfic points withiu the;rtrial and ventricular muscles which clectrieal ircl.ival,iorr nright begin, but abnornral ''/ at rhytlrnrs can begin trnywhcre within tiie al.rial or L- vcrrtricular musclc. A y,.- [ Sirtus rhythrn, al.rial rhy1hm, and junctional rhythm 1 tog,e ther corlstituLc Lhe'supravelltricular' rhytlrnrS (FiS. 3.3). lrr Lhe supraventricular fhytl-uns, the depolarization wave spreads to the ventricles in the normal way via the His btrndle and its branches (Fig. 3.4). The QRS complex is therefclre llorrral, arrd is the salne whcther depolarization n/ g tfrave^lric ,A. ,rP \1. (e A f ,rot supraventricutar .>, N "J*l ./^P' i Ventricular [>, roll ;-

\+

>\; Yr Jt

Pa

*

q-< c\ [r<\n.'

t"+

V ea\ t'<\ e

Q+T

:

g

o, n

uQ,-o-g*"+r(frfl

or

-J

c-,,

A

Lri.,! u ( QRt)

Fig.3.3 Division of abnormal rhythms into supraventricular and ventrlcular Sv prav *.Jr,
,-\,Lrao Qfr,al = e'5 fit
GlV"tl

br.

sL.La

11

J.J

F*r

b

--,1

Da

#

ut

suUT *,'J*-)

Fig.3.4 Spread of tlre depolarization wave in supraventricular .il l,

-;i

N-J \?

' ri IL t;

li

li

56

{

rhytlrrns c,t)

1

e^Ft c' A.

G.-L* ,) NJ.,

(-- ,.[

x) c: i) ,- 4.\A-. +

A\.Aor- -r\ sq^aJ \

V> ,^

r'' )'l

zC-

e€w

z- So o,a Gl hJPhJ Ph+l*- C4ze*arysl *Q C(]

"

\

o, ( bt- J*\.) / N)., P *.r','.^-

} fiLnorr.',''} QQS

<,,,Lrtc

t-r 1

a

e\\ ^(se A=

C

(cr'oq*t*S)

__42-

tNTRtNslC RHyTHMtclTy oF THE HEART/wPEs oF ABNoRMAL RHYTHM 44 -4

Aq

YL'.

4+,-/i )wr;' *e-L"(-*

-r{

\

G-a

'*

> (5.--"-/;)

P* \ t,*Gr Ph ..l

2?''

uai

t'.

r ,i r.*{*o

t l---'\ erC-ta-1

\

!ffifl@

i 4'-a. f3 tr

,

cQT 4p

tlrrb\.....^.-,

(>.o

)\ /,\

\"^7o,J

Fig. 3.5 Spread of the depolarization wave in ventricular rhythms

sl,'r-,.Lqh

9/

r--

(, \2

;

---!r

I

tl-

-'\)\

was initiated by the SA node, the atrial muscle, or tlre junctional region. . - In vbntricirlai rhyilims, on tlre other lrand, tlre depolariz-ation wave sprcads through the verrtriclcs try an abnormal, and tlrerefore slower; pathway through tlre Purkinje fibres (l'ig. 3.5).Tl're QRS complex is therefore wide and abnormal(Repolarization is also abnorn'lal, so the T wave is of abnormal shape) ( - v,- ' _ -+ ;'1't_,st^' ,P i;.j,-,r\ 1, sl,,przrV. 1-L^.\i6.t at , ,$em.ell9glt , -

4\r

G'a

,)i) . .( >t -/' *P;J* EI

-

ia-5a;'{' +r' .)l/r'r..n, ! \-1. Supraventricular rhythms

have narrow QRS complexes. 2. Ventricular rhythms have wide QRS complexes. 3. The only e*"eption to tl'ris rute occllrs when there is a

supraventricular rhythm with right or left btrndle branch will be wide.

bk-rck when the QRS complex

>--a

ffi TYPES OF ABNORMAL RHYTHM

-r

1

.I

Abnormal;ftythms arising in the atrial nrttscle', thc iuncfionrdl resion or the ventricular rDrtscle can t're slt-lw arrd 'sustgy'ne.t or the;adan occrr as early singtc

@;

07:/E i

.=,'

57

ffiilffi

il.tr Rr]Yil1M ut- IHL t1rARr

bcirrrr(*^r,,'a.ysil* i, or'{lrcy can bc fast

7

J-./Y {rL

\_

arrcl sustainccl

\(tachycartlias). Whclr activation of the atria or ventriclcs is Iotrrlly tlisor'1ialr.izccl,'fibrillatiorr' is saicl to occur, Wc shall corrsirlcr caih o[ thcsc typcs of rhythnr ilr turn.

12 Tlre escqpe rhythrns - the brodycnrdiqs It is clcarly advantagcous if different parts of the heart

r

are able to irritiate thc depolarization sequence, because this 1;ives the heart a series of 'fail-safe' nrechanisms that will kecp it goirrg if the SA node fails to dcpolarize, or if conduction of thc depolarizatiorl wave is blocked. However; the protective rnechanisrns rnust normally be inactive if conrpctition bctwccn rrormal and abnormal sites of sponlaneous c{epolarizatiorr is to be avoided. Tl'ris is erchit:vccl by thc sccorrdary sites lraving a lower intrinsic fr'ccltrcrrcy of clepolarization than the SA trode. 'fhe heart is controllcd lry whichcver sitc is sFror,taneously depolarizing most frequently: nomrally tlris is tl're SA node, and it gives a normal heart rate of about 7O/rnin. If the SA node fails to depolarize, control will bc i.rssunred by o focus citl'rer in the atrial tnuscle or in thc regiorl ar'ourld Lhe AV node (the junctional region), both ot' rvhich have spontatrcous depolarizatiorr frequencies of about S0/nrin. If tl'rese fail, or if conduction througll tl're His bun,lle is blocked, a ventricular focus will take over and givc a ventricular rate of about 30/min. These slow and protective rhythrns are called escape rhyl.l'rlls, becaruse tl'rey occlrr when secondary sites for irritiatirrg depolarization escape from their normal inhibition by lhc nrore active SA node. Escape rhythms are trot primary disordcrs, but are the rcsporlsc to problcrlts Irighcr in thc'conducting pathway. 'Ilrcy are con'rmonly seen in the acute phase of a heart

I

\--,

\

- .\ rl

.a\n

, L c

u\nl

I n

? AVt'"\'

; 5 ta'l_I.-

IYPES OF ABNORMAL RFIYTHTJ,\

;

X

sffiffi

attack, when,they may bc associated with sinus bradycardia. tt is important not to try to supprcss an escape rhythm, lrecause witlrout it tlre heart might stolr

I altogether./'

\ ;ib;, r

\

fc

:A ,atriol escope t-- tf the rate of depolarization of the SA node slows down and a focus in the atrium takes over control of tlre hear't, tlte rhyl.lrrn is describecl as'atrial c'scapc' (Fig. 3.(r). Atrial t'scaire beats can occrrr singly.

Alri..\

br,t{

fio2.,\-l'rc

,J'J

il

tltt

r\

.

-\

.' ...'

After one sinus beat,the SA node fails to depolarize. After a delay, an". abnormal P wave is seen because excitation of the atrium has begun somewhere away from lhe SA node. The abnormal P wave is followecl by a normal QRS complex, because excitation has spreacl nor6_.1lly down the His bundle. Thd remaining beats show a return to sinus

-

arrhythmia

Qto)'r +

P

59

IHE RrrTHM

=.. ffiiffi

NO

-

ol-

IHE HEART

(

+ VroLa

,?j Fig.3.7 Nodal fiunctlonal) escape

i I ,/. ,/-) ( (-a r..4 ..--{.r :."a r *< , -.

I

Nole Sinus rhytlrm, rate 100/min:junctional escape rhythm (following arrow),

. .

rate 70/min

No P tvaves in junctional beats (indicates either no atrial contraction or P wave lost in ORS complex) ' n o1 Norinal QRscomplexes I >> c ,/ | r-J'-/ ' I t a r.fiU-fal

t,;;.r"

e ^?b)t

^ Nodol (iunctionol) escope ? _ if the regiorl around the {YXg{dhkes overas the focus of - clepolariz,ation, the rhythffi c-iilecl 'nod al' , or rnore froferly, 'junctional' escape (Fig. 3.n.

;

-Ventriculorescope 3 -rntls+eorrmrrrrrty s c e n w h c n conduction bctwcen the atria and ventriclcs is interrtrpted by cornplctc hcart block (FiS. 3.8).

'

60

Ve+rt

rietr*at-eseapel

-is

(

crt

J-)

N\"

A

b

('--

a\ TYPES

OF ABI.JORMAL RHYTHM

v1 €,ag^,\ar

?

QRS

\E

Flg.3.8 Complete heart

r

---> o,o.t( '! e'"Lt i t al^t 4 sc-a,le--) - 'r'.. U ';'.u!^t \'=' '

Nole . Regular P rlvaves (normal atrlal depolarization)

5 eu€^€

o P wave rate 145/min

.

QRJ

b*s3

QRS complexeg highty abnormal because of abnormal conduction

. &t?1"::;lJ#iJ:;:1";15,min .

;v_€

/"

sRs

t-

No relationship between P waves and QRS conrplexes

^-.f

l,te.-.u !.P\1.a.P:,_.^t.,

-I

Ventricular escape rhythms can occur withotrt conlpletc heart block. Ventricrrlar e'scapc beats carr be single (i.ig. 3.9). --i The rhythnr of the heart calr occasionally be controtlecl by a ventricular focus with p*iltrinsic frcq,rerrerof d ischa rr;e '; faster than tl'rat seen in complete heart L-rlock. The rlrl,tlinr is called'accelerated idioventricular rhyth rn' (Fig. 3.10).'l"lr is is often associatecl with acute myocardial irrfarction. Althougl'r the appearance of the ECC is sinrilar to ttrat of ventricular tachycardia (descriLred la ter), accelcra [c.c{ U _idioventricular rhytlrnr is bc'nign andistroutd not be treatt,cl. Vc'ntricular tachycarclia shoulcl not trc-rliagnosecl rrnlcss tlrc heart rate exceeds 120lnrin' e

-r

,i

6I

*gnilnritd

Cq

rr rr- r\r

lt

tt t/vt

r--ir

>^/

rs

1{K ,..,

a{zt ,-/, Y-{

Jrr,+l."

4a\" (o

A4te, =

"L';',"'

t------'

\

u!

r, gb3

b

\ t\_

il.ii iit

iil

Fig. 3.9 Ventricular

escape

t.J6 \, t:'" -

Notc ' AIlr:r llttotl iittltt:i

,.-/

- -j{-

.-)

-V

lrt:trl:;. tlro SA rrorltl lirils to tlist:lr;rrt;g]N.r.,t,r.ll pr = 1.tl.ll t4
-\

\''-)\

n: t

alv-

fo

..L''

o, L>r.J-f )p (po(-l .= tJ i,s -t*^ lrr'<--0,-; (h1Lh,

j]

;.v*..'

i

Fig. 3.10 Accelerated irlioventricutar rhythm '- -l

' _

;.lo

q \r'J <\7L<

74c

Nolt.,

62

;.ilii

l:t

-;/

Alter tltree .1rt(.ir trrruu brllut) sinus L.,uclts, beats.tir.e tlle

noclr: lalls fails tO SA no(lc )A to Oepolaftze. clipolarize.tAn An escape IOCUI focus "..npe in lhe vr:nlrir:lc lak6nffiilcarrsirrr; .r regular rlryilrnr of 75lnrn wrth wrde

QllS

corl,*:r

itrrd abrrorrrr.rl 'l-

waves

+r- = =

?

5"+

\

-^1

?f^,J

e:>.tLf

l.

At

,^ U/

1(u-:^

'icu\ o , t.

A I l(/\S y tr

I

Ul

t.5

Spfq*n-*,rp_r,ti

t:

\

',';:

-

lre'.t't carr tlcl'rol.rizc' e'a.lir.r' r'arr-iI s'.trttt, lteartLreat is callccJ an ,_ .,.*'ti).";;;;,, _ 1^_.__ l"l-tnn-yirl8 t, l e' -'l'lr e ter rn'ectoiric' ir r!n',. t i,res u sect,ll";1;:j,ll''')sYs tleP6fnrization or.ir,,irratecl irr rrn ntr,_,.r,rral locatiorr, arrtl Itrtr a t rr r-r, t.,. I rA c t i.., Irr'er. r. r,a rrs I t. ,:_.t.':1],' I'tre lrcc appea, n,',."'.r tlre :,, "I,rnryr,lt,,::ll:,llr'1,',,,,r rrt,r. arrial rrrtrr.i", rtrt, jtrrrcti.,ar f.r,-,it,.rar r.t,1;i.rr,.r.rtrt. L-vL'r'rtric,rar nrtrsctC, iS trrc sa,lle as rtrat .f ttrc c.r.r.csr.,.rtri.r,, esrn.c lreat - rrr. tri[[t'errce i.s rrraI a^ extr.asysr.t(, (..r]l(,s early ancl an (:scaPc, lrcal corncs Ialt,. \ il ni-lf{ extrasystt'rlcs lrave a[.rnr.rrnrat P

.^,lll,iHJJlte .r.l_-

(-

r'.1

n

;,,,i@;;

.;i,;ffi:ll,,l

;,J;TlT.yj#],1,: rfrilr rffil i., t"l-v [rt,f.r(, n,. ;,rrr,"tl i, I t,ty a ft cr. I Ir t QIis c()rrpl") (rrig. J.r-r). 'r'rre er(s cor,;rr"r.., .I atri;rr arrtr jtlrrctiort.l extt'ilSv5[11t1ts ar'(', .I c.tr,.rc, r'r.,., sArl(, .s rrr.st. .r. sirrtrs rlrytlrrtr. ( O::r r..,tt\, 4':frc{tr

i

t a ppel

lr

ll

ili l l-U I lil I ll;l il i-lll llt irlr'lll-llii liil

'l l it

I

il

I

l,tl

t,li

ll,l

it

rfiffi Sinus

illtllfl c/llllffi1/]1fl1il+flll+h/flllfiL

I

ntriui

1'11,,.1,"j11""'* l:"iH,ffi:[,'J]ilil;;]n:* t ' An n,ar exrrasysrolo has nn L

],yi['#c,io,rar

;,,,,r a,ri;rr

A'r

^ a\

rof-.

",,,,,,,r,i],,,,1,

ntrnornrnry s^apcrr p wav. r,ave

1c!d uunJie;1ffi',,111"",

;T;*x';::1,r:r:.,':':':'.r:rls condu,ion rn and rrcyond tno

irRS conrproxcs

r r

fiJ

,/ siiE$it*r&l

/-l

-*. _=_ .

r"-

lr rL r\r ll lr utt

vr

rt rL I rL/\r\l

Vcltli'icula1c1[ty.Istrilcs,*rwrever, have abnormal QI{S c.,,',ffiGffiricirT;:b$pically wide but can be of atmost ;u'r)r 5;11;1;rr' (lli1i. 3,12), M,ntricular trxtl'nryrkrles arc co,nrnot'l dntl irrt: usuirlly of no inrFrortaulcc. Llowevct; when thcy ()('('ln't'ar'ly in tlrc'l'wilvLr of a prcccdirrg bcat they can ilrrlucc vctrtt'iculeir fibrillation (described latc$, and are thus

o'li,'r',t.;'ilj,l,:r:i',ll

particurarty if a bcirt of suprave ntricular origin is couductcd abnonnally to thc vcntricles (bunclle branch block, sec Ch. 2). It is 1{vi5nlrle to gcl. into thc lrabit of asking five qucstions every tinrc an ECC is being analyscd: rre as easy as rlris,

-=-

.[. Does an car:ly QI{S complcx

follow an early P wave? If

so,

it rntrst bc alr atrial cxtrasystole. 2. Can a P wave be scell anywhere? A

-

junctional

cxtrasystolc nray cause the appearance of a P wave vcry

:1".:i,il;;'1,*.:l:l:l:"JJ1",.?Ii;'#lT,,T::il:

-

vcrrtricles.

throughout (i.e. has it thc sarnc initial dircction of deflcction as the normal beat, arrct has it the same eluration)? Supraventricular beats look thc sanre, velrtricular beats look different. 4. Is tlrc T wave the sanre way up as in the normal beat? In sa'|l.e wav up; in

3. ls thc QRS conrplcx thc same shapc

-

xli:fi"'ll;:lt,Tljilll::,:l:

-

-

,.

\

64

5. Docs thc rrcxt P wave aftcr thc cxtrasystole appear at an cxpcctcrl tirnc? lrr both supravcntriculirr arrd vcntricular cxtrasystolcs thcrc is a ('conrpc'nsatory') pausc before the rrt:xI lrcartbcat, but a supraventricular cxtrasystolc usually u1:rscls llrc trorrnal pcrioclicity of thc SA rrodc, so tlrart the.. .ti qr9xl. SA noclc clischarge (and P wrrve) collles late.

.

I'l'rc effccts of supralqj],lSylar and vg$fg-glr exLrasystolcs on the following P wave are as follows: . _l rr, l> ,/i]..,1 ,i

a

Ar(

a

\

f--- A

/ l" L^lr(AsYslolts

)--,

Gtcr

tl

L'^ z-'qq-/ 1-

ffiile{ - ./

C4L,

\

o+

--

)

Ue,

Grs u?- 0*-

'-24

aa

*-ih

;A 4

iilllllil I

R on T phenomenon:

'

I

[}€( .-a

'.\,' I '')(-'' =r r-..-.\ R\"f Note . Illrppertrc shows five sinus beats, then an early beat witl' a__ wiFl .QRS complex and an abnormal T wave: this is a ventricular ertrasystole.i L o ln the lower trace, the venlricular exlrasystoles occur larrowil ai tne ' ,R Flg.3.l2Ventrlcutarextrasystote

\-- *

P, )-------+

.,1

peak of the T waves of the precccfirrg sinus beats: this is the phenomenon

\n^".-,

on T,

-

A supraventricular extrasystole rcsc,ts tlre p wave cycle e

(1tig.3.13).

A ventricular extrasystolc, orr the othe.r lrancl, clot's rr6t affcct the sA node, so tlre ncxt l'wavc appc.rrs at rtrc prerlictecl tirne (Fig. 3.14). ,':

: f'

65

L

G

lHr

Hr

RHYTHM

ur rnL HhARt

Pj

No P wave

:_

$o Ce

n^!e^

o/1

Pn^t" )

Fig. 3.13 Supraventrlcular extrasystole Note

. Three sinus beats are followed by a junctlonal extrasystole. No P wa\r€ is seen at the expected time, and the next P wave.is late

)\

;/

JuanA;^*\ r\tt#t* :.9

sr{ q ra! s,^.\-t( c-<\.-z

4

s,s

-"

No P wave Expected P wave

-

Fig. 3.14 Ventricular extrasystole Note

. 66

-

Three sinus beats are followed by a ventricular extrasystole. No P wave is seen after this beat, but the next P wave arrives on time

s^ql_ I

ll-lb IALHYCARDIAS

-

IHL rA5l

RHYylHMs lHM5

Lrad-va |g!!ft

(.Jr Foci in the atria, the junctional (AV nodal) region, and ventricler.mqy depolarize repeatedly, causing a sustained tachycardia. The criteria already descritrt'd carr ['re trsctl to decicle the origin of the arrhythrnia, ancl trs before tht nrost important thing is to try to identify a P wave. L-

Suproventriculor tochycordios

j

br^

I

lI

,-

E

Atriol tochycordio (obno rmol focus in fhe otrium) In atrial tachycardia, the atria clepolarize faster than 150/nrin (rig. 3.rul.

q

-

.*;j L.< ,ft

Flg. 3.15 Atrlal tachycardla

/'8

Note After three sinus beats, atrial tachycardia develops at a rate of 150/min. P waves can be seen superimposed on the T waves of the prececling beats. The QRS complexes have the same shape as those of the sinus

.

beats

..

'J

./

r

ron

67

.- ryf

Ja-

,l ;,i iL

lHt

RI-{YIHM

ur

tHL HLARI

I I

\

lir I

x

The AV nocle cannot corrduct atrial rates of discharge grcater than about 200/min. If the irtrial rate is faster than this, 'atrioverrtricular block' occurs, with some P waves not followcd by QRS complexes. 'l'hc diffcrence between this sort of atrioventriculai block and se_cgnd deglee heart block is ttrat in atrioventricular block associated with a taclrycardia the AV node is functiorring properly - it is preventing the ventricles from being activated at a fast (and tirerefore irrefficient) rate. In first, second or third ctcgree block associated with sinus rhythm the AV node arrcl/or the I-lis bundle are not conducting nonnally.

r)

.< When the atrial rate is greater than 250/min, ;ind there is no flirt basclinc bctwccn the I' waves ,'atrial fluttci' is present (l'ig. 3.16).

i,

\,-

/u*.te L-* E

F

-

Fig. 3.16 Atrial

flutter

-

.i.'',.: -,,./ii,::':

.'--'-,r-..

Note I *ii., . P waves can be seen at a rate of 300/min, giving a sawtoothed 68

appearance. There are four P waves per activation is perfectly regular at 7Slmin

,

Qns comptffi,entricular

THE TACHYCARDIAS

-

THE FAST RHYTHMS

f \-

rcry

\

; -: ,L-

When atrial tachycardia or atrial flutter is associatecl with 2:1 block, you need to look carefully to recognize tlre c.xtra ! y*"t $ig.3n.6 rarrow complc'x tachycarclia with a te;triculelrati of l,p(lmin should always alert you to the possibility of dtriqk'flutter with 2:1 block. Any arrhytlrfiia should be identified from the lead in which P wlfus can most easily be seen. Full 12-lcacl ECCs are thgre-fore better than 'rhythm strips'. In the record in Figure 3.18, atrial flutter is most easily seen in lead II, but it is also obvious in leads VR and VF.

?/1;

Flg. 3.17 Atrlal llutter wlth 2:1 block

)

I -' , 't r' ; 't.,'! " .) NOtg . Atrial flutter with an atrial rate ol 300/min is present, and tlrere is 2:1 block, giving a venlricular rale of 150/min. The lirst ol the two P waves associated with each ORS complex can be mistaken lor the T wave ol the preceding beat, but P waves can be identilied by their regularity. ln this trace, T waves cannot be clearly identified i

\a

gt t

'^'{i.-

?

Ir

'

69 o

-

Hlfiffi

THE RHYTHM

oF

THE HEART

t -fj,.+

rl

il

il

,l

-

il\ rl i,

-

'

I

t,

70

IHE IACHYCARDTAS

-

THt l-ASl RHYTHMS

trq

r

.!

Flg.3.1S Atrial llutter with 2:1 block Nole P waves at 300/min (most easily seen in .,,""' -l leads ll and VR) r: ): ,:- r . Flegular QRS complexes, rate 150/min . Narrow QBS complexes of normal shape . NormalT waves (best seen in the V leacls; ln the limb leads it is dilficult to distinguish

.

betweenTandPwaves)

-

t

-

7l

atF

ltlb l(lli ll rivt \l ltlt- llr-nlil

,*E*#*tr

CSP

jlliiilii

ffilli Fig.3.19 Atrial flutter with carotid sinus pressure (CSP) Note

.

f'

'

,! i

ln this case, carolid sintrs pressure (applied drrring lhe period indicated by tlte arrows) has increased the block betlveen atria and venlricles and has made it obvious that the underlying rhythm is atrial flutter

Caroticl sirrus pressLlrc ntay havr: ir uscful therapeutic effcct or1 sr.rpravcntrictrlar Lachycardiars, arrrl is always rygftll trying because it rlay make the nature of the arrhythmia i nrorc obviotrs (Lig. 1.lg).Cnroticl sirrtrs prcssurc rrctivates a icflex thai lcar.f.t ro stimulartion ol'thc, SA ancl "igii 'l'his AV rroclcs. ciluscs a recluction of thc frcqucncy of clischargc oI tlre SA nocle, artci irrr incrcasc in the tlclrry ol' conctuction in the AV node. It is the latter which is important in the cliagnosis ancl treatment of arrhythmias. Carotid sirrtrs pressnre slows thc ventricular ratc in sonle s!!praventricu l;rr a rrhyth nrias a rrcl completely ab@eq_ ) <:l}terc, Lrut it has ncl cffcct on vc'rrtricular arrhythnrias. Junctionol (nodol) tachycordio arci'l art)t,u1cl thc AV rrorlc dcpolrrrizcs. f"c.qtrcrrtly, tlre P

lf iirc

72

wavcs nlay bc sccn vcry close to the QI$ conrplexcs {arwittrtlrc €r)rresFr)nr ), or llray no[ be sccn at nll (ltig. 3.20).'l'he Ql{S conr;rlex is of normal shape because, as

IHE IACHYCARDIAS

-

IHL l-Asl ltllYll-lrnS

ffiEe

illa,,itt', the other supraverrtricular arrhytlt tttias, the vctr tricles activatetl via tlre truntllc of I-lis in tlrt' trortttal wily. 1 arel'he 12-leacl ECG irr lrigtr ra 3.2t shows that irr a itttrctiotral tachycardia rro P lvAvL's cnrr bc seen irr arly lc.acl.

;r

^&

x )-

d)

x

?-ea*\r

r

aQs

Junctional tachycardia:

Sinus rhythm:

Fig. 3.20 Junctionat (nodal) tachycardia

Note . ln the upper trace there are no P waves, and the ORS complexes are

completely regular. The lower lraco is lrorn lho same patienl, in sinus rhythm. The ORS complexes have esscnlially llrc same slrape as tltose ol the junctional tacltycardia

-

73

\

ll ll- l{-t I

I

I l,vr

\Jl

I

I

lL I lLl\l(

I

JaI !

a

I

i

i I I I

I :

li

,

:!

ii :

Ventriculqr tochycordins If a focus in thc ventricular muscle dcpolarizes with high f re-elue ncyrGu si rU, in e ffec t, ra pidly repea ted ven tri.rIu. extrasystoles), the rhythm is called'ventricular tachyc ardia' Fg tZD. Excitation has to spread by ql qbnolmql palh t[rotlgh the ventricular mus_gIe,. anQthe QRS complex is tlierefore wide and abirormil. cl. -... .\ ,-,;:, i 1..,J wicle and abnornral conrprlexes are seen in all 12 leads of tlre standard ECG (Fig. 3.23). Rcnrentber that wide anr{ abnormal complexes are also seen with bundle branch block (Fig.t.*).,*t a'

74 arta

THE IACHYCARDIAS

-

Sr..t

THE FAST

f

RHYIIIMS

\

ffir

Flg. 3.21 Supraventrlcular tachycarclia ,/P I

. NoPwaves ,r /-' / ', . Regular ORS complexes, rale 180/min o Narrow QBS complexes ol normal sltape o Normal T waves

r

Trealment: carotid sinus pressure, then adenosine il necessary

@.

-Y

F.--a!d

,y,t)atb*

f5:r.3

Ats,^'P

S{
a. Fig. 3.22 Ventricutar tachycardia Note

.

After two sinus beats, the rate increases to 150/min. The QBS complexes become broad, and lhe T waves are ditlicult to identify. The final beat shows a return to -sinus rhythm

l^

|:."1;;

l::

llllllr.,l,

-

I

1,,,

75 F-

ll-lt RHYIHM

iilgtr

rl,Z

rrrrYY to rl, LrJrrrr:, distiinguish 1,rJrr befween ventriculcrr ,, How q/-l tochycordio ond suproventriculorfochycordilct

rnrith bundle bronch block is essential to remcmbcr th.rt thc ptrtient's clinical / state - whetl'rcr goocl or bad - docs not help to cliffcrentiatc .r , .bctwccn thc lwo p-rossiLrlc causcs oI a tachycardia with l5roac{ QI(S conrplcxes. lf o [r,',l.icrrl, with an acute myocardial iufarctit'rrr has a broatl-conlprlcx tachycarclia it will almost .1 t - always be vcntrictrlar t;rchycardia, but a patient with A cPisocles o[ strch .r tachycirrr,li.r witlrourt an infarctiotr cor,rld be havirrg either a ventrictrlar tachycarc{ia or a I strpraventricular tarclrycirrdia with bunclle branch block. such circtrnrstanccs thc following proirrts nriry lre -tJrtcler \, . hclnful: .v",r

flt

I

i I

76

'i I

ur lHt HSARI

THE TACHYCARDIAS

-

Tl'tE FAST RHYTHMS

!I[83]

Fig. 3.23 Ventricular tachycardia Note

. . .

.

No P waves Regular ORS complexes, rate 200/min Broad ORS complexes, duration 240 ms with a very abnorrnal shape No identitiable T waves

q

\,

.a

*'x

n-'9s -2'

t

r^ tti! Fig.3.24 Sinus rhythm witlr LBBB Note Sinus rhythm: each ORS complex is preceded by a P wave, with a constant PR interval. The QRS cornplexes are wide and the T waves are inverted. This trace * was recorded from lead Vu, and the M pattern and inverted T wave clraracteristic ol LBBB are easily identifiable

.

-.^t I

( Z\ arL)

)-"trl

J rr V e

77

ll tL

i,.jd[kdssffi#

.-

t(l

tr lr l/r'r (,l ll

tr_ I

rt./\l(

I

H

(- L l;irrtlirrl; t'w.lvcs a,,.t ,,-l"irrq lrow tlrty r-clatc to thc et(S col'l'lPIt:xcs is alw;rys Ilrt' kry to irlcrrtil'yirrg ar-rtrythrtrias. {'\- Alrvirys lr.li r'.r'L.r'rrlly .rl .r r'rrll r2-lc.rtl l:,C(.].

r-2. Il'ptlssiLrlc, coltrL)arc thc Ql{S crlrnplcx tlur.irrg t6e taclrycartli.r rvitlt lh.rl tltrrirrli sirrtrs rlryttrnr. it t1.," paticrrt K has Lrtrrtcllc Lri'alrt'h [rtrrck rvlrcrr in si,rus rlrythnr, tlie elts c()lllplcx cltrl'irr1i tltt'l.tt'lryt'.rrrli.r as clur.irrg nor-n1al r.h1,tlrnr.

t.3- lf thc QI(S cottlplcx ir; witlcr' W- -- ( l(r0 nls), thc rhythnr rvill

rrriqin.

rvill lrar" il,".s.ulrc s5apr,

tlrirn [our snrall s(lLrar-cs 1'rrolraLrly Lrc vcntriculirr- irr

+ .[. I-t'l'I axis tlcvi.rtiorr tltrr.i'-r1j tlrr.t.rt:ll)/car.tti.r ustrally

bi

irrclicates.tvt'tt[t.icttl.rr.trr'itirr,iis_

5.

Il'tltrrirrl; thc t.rclrl,c.rrtli.r tlrc Ql(S conrPtcx is vcry i.r'csul.r; thc is 'lrytlrrr P'.babty ,tr-ial fibr.illatiori with Lrrrrrcllc brarrclr block (scc [rclon,).

'1 ;9

FTBRTLLATION

x

1-ntl tlrc.u't'trlrttrrrri.rs tlist'trsst,tl so l'.rr. lr.rvt.invol\,(,(l Ihc I /\ \., \ tytrcltt'tltrt)Lrs contracli
4, ' l. vctttricr.rl.u' nrrrsclc. . €---\,'ncn Ilrt: tlrc atnal rrrrrst lc li[lrcs conrract intlc;rcrrclc intlcpcrrclcrrLly . u,'itr:tr *[ji!rrrrst l'i[rrcs corrlract tlrcrc at'c rro I'wavcs orr Ilrc I]CC, orrly y an arr irrcgtrlar ir.r.cgular line (l;it;. 3.25).frl tinrcs tlrct't' nr.ry Lrc t'lrrttcr-tikc wavcs [or 2 V- tlr :t sc.-rxrcl.s. 'l'lrc AV rrt,.tc is t:orrtintrotrsly bgqlsrrtlqtl

n

/-

tlt'1-r1rl.1r'iz.rliorr s1-rrc,ltls,rl it.l.crirrl.rr.irrtcr.v.lls Llorvrr tlte

lrtrtttlle ol. llis.'l'lrc AV rrot]t'corrtlrrt'[s in i'u'l'all or.nonc' firslriotr, so tlr,rt tlrc tlt.;-,ol.u.iz.,rli
7B

Ng

=

e- \rretn(n, A f trit,',,h'*-l @ 6,,tt-

.P

r

R[l

A,.

l,'t "

pc b

(\€s'n

(o.

Aq

{t )v \

(d{\^-(-

I IIJRILLA

t{ t7 +)1.n?)".*o fu-


1\o

IION

;(

+

,6fi

{-z^-\"1

Lead ll:

A

\ I

ili

I

ri tl I

ll li

I

il

I

I

I i_.

llt

llil,'ll,

Lead V,:

lilt iili ril, l: t,

i

I

I

iliili

i

r:ig. 3.25 Atrla! fibrillation ,Vole

. . NU .

No P wavcs - irreuul;rr ltir:,clirro lrregular ORS cornplexes \a t^! l.lorm;rlly slraped f)llSl corrrJrlexr:r; llt ltlittl V, witves cittt Ilc st.r..lr wrllr:;orno ]os(inrlrl;u)r;t-, Io tlro:;r::;r]t-,rr irr alrtal lluller - lltis is con'trlrr-rrr irr alriirl Iitlillirtrorr -...,..+

's-)

':

-,;.-'> -

-,

\

!

'-..-

-

li -''.;

e,irr{$ttlrtr-fiTrl

(L'

: - ,- l'

,

1tl[rTfi]r'L' ('( ) r'r t r',r r: t Iy.iitr.itii* c,iiilTffi rr i rr Io a+++I-il+*r+++rJ+ t |11, ventricles is Lry tll(' rr()r'nr.rl r'[trtc) t'aclr Qlili (-()nrl)le.r is ol' |)()r'n)rrI sha1re. lrt it ll-lcirtl rccot'rl, Iilrr ill,rtit)r'r \\/ir\/('s ('rrrr oltt'rr Lre sr'('n rtrtrclt L'lctlcr irr sonrc lr'.rrls tlr.trr olltr'rs (lrr1,j 2tr). u

i

IIr

e

v c r r t r i r-l c s

rrt'1irr Ia,

79

I

-

t1L hl-l r

I

r l/Yt

L.,r

If

lL r t[Al(

I

-

iI lr

1t

-

'F,"L

tiliitii

1i

,,'Iloh'n ,, y,.

Fig. 3.27 Ventricular fibrillatlon

A\ /r

)\ i,' \ A\

(c.. \

rlBRlLlATloN/WoLl'l--PARKINSoN-wHl

I

L SYNDROME

ffififl[

Fig. 3.26 Atrial librillation Nole No P waves lrregular baseline lrregular ORS complexes, rale varying bolwoolr 80 rrrrcl ltlO/rrrlrt . Narrow QnS complexcs of normal shapo . Doprossorj Sl' soglrtcrrts in lontls Vs-V,

. . . tl ri

.

NormalT wavas

e*n

- Ur

/'r1

e jrnJro^n

L

C

When the vcntricular rnuscle fibres contract inck'petrdently,-lro QRS conrFrlex carr Lre iclerrtifiecl arrcl the ECC is totally clisorgarriz.ctl (ltig. 3.27). -" -, .- -.-: , ?..)- L- a f nt the patient will usually have lost corrsciousrless by the ri I time yott l'ravc rcalized that ttrc charrgt irr the IrCC pattern iit not just cittc to a loose connection, the cliagnosis is easy.

IFF-PARK|NSON-WH ITE (WPW SYNDROME

( ( ,

'['he orrly trortrral eltctrit'irl colrrrcctiorr lrg[11,1-'g1r thc atria atrel verrtricles is thc [-lis buncllc. Sonre peol'rlc,, horvever, lrarrc ntr cxtt'a 'rr'ilcccss()r'y' concltrcting lrtrirr'!lc. Acccss()r'y burrclles fornt a clircct corurcctiorr Lrctwcen atriurn and vc-rtt,icrc" ,suaily orr thc lt'f( sic{c of (lrc lrcni-t, antl irr tlrc

BI

rr'-*'t t A A<^ost'AvIHL RHYlt1&( t/r- tHE HtAr( , 4 '.f ( De-\l ., \\.*' A{ N o l-e- \-\'&"'

*ffi

?

-

\ c'14to^

<--

6 \Ar

-

ft:'^U -1L.L

-

J\"

*-'

a\Ve^rL

- sq& A\

E

i\

\-.{3.{1r., I

I I

f}stFa

L)\9t

J

*V €-

-.\, I

,,4

X T_:,..cssory Lruntllc Iht'rt' is rro AV notlc to tlclay cotrtluctiotr. A clcpollrization wovc t+rc#e*Jre rcachcs llrc vcntriclc cirrly ,) "-9: FPf,,,/rri'urcl 'prc-cxcitatiorr'()ccrrrs.'l'he l'l( interval is short anc{ \ , -i: re tlrc QRS conrplcx shom An cirrly sltrrrccl u1r51111kc callcci ir ,'.)L\ 4-'clclta wave' (FiB. 3.2ti),'l'he secorrcl part ol' thc Qt(S contplex . .,,-\j i,l_ir.norrlal, as concluction through the l-{is bttnclle catchc-s up -:^ with the pre-excitation. ; 'Ilrc only clirricarl irn;-rortancc of this anatornical abrrornratity is that it can causc pilroxysmtrl tachycardia. f Depolariztrtion ciur spread down the His bunc{lfirtl back r\ trp the acccssory prathway, and so reactivate the atriurn. A '\_ _'r'c-cntrv'circuit is tlrus sct up, arrcl a sustained tachycardia occLrrs (ltig. 3.29).

--=-

r

82

+ U

(nr)

t.-zJ

t-r

-^

P C^J

'^r l"tb=,-=-J ] .-!(*

,e'a't

/a'4t

E.pl 9\

G"

t-.-{l--a-- -,' z-n

{c>

A r.'nrt-o

A

Aa

c-ll

O^ k, A ,r\'^-Jo,r.- al

D'aocaioca^

'

(J-*

W'JLI-I---PARKINSUN-wHI I L sYI{DRQML

ffie*

/l

-

Fig. 3.28 WPW syndrome Nole Sinus rhytlln

. . . . .

-fF

Right axis

Shorl PR inlorval

-

Slurred upstroke of the OFIS complex, best seen in leads V" and Vn. Widened QRS comlilex rJue to this'delta'wave Domininant R wavc in lead V,

e-

Fig. 3.29 Sustained tachycardia in the WPW syndrome Note

o f)uring re-entry lachycardia, no P waves carr be seen B3

F

iqrlhr#l

N

ll-lt

Ri

\

li ll lrv\ t/l ll lL I lt-r\l(l

THE ORIGINS OF TACHYCARDIAS We-have colrsidered the tachycarc{ias up to now as if all were due to an incrc,ased spontaneous fretluency of depolarization of somc part of the heart. While such an 'enhanced atrtonrat'icity' ccrtainly accounts for somc tarchycardias, others are due to re-errtry circuits withirr the heart muscle. It is not possible to distirrguish enhanced automaticiLy from re-entry tachycardia on standard ECCs, but fortunately this c-liffcrcntiation has no practical

ll

importallcc. I

rP

C,

-fl-I*

WHAT TO DO

r.-- Accuratc interpretation of thc ECG

is an essential part ol'arrhythnria rltanagenrent. Althotr13,h this book is not interrclecl to discuss thcrapy irr any dctail, it seenrs appr'opriatc [o outlinc sot'ltc sinrp-rlc a-lpproaches to paticnt nlanagernent tl'rat logictrlly follow interpretation of an IICC;

L_ recorcling:

L:

i-, *J "t l. -. 1. For fast or slow sinus rhythnr, trc;rt tlte r,rnderlying callsc

r' obG li

li

,lr

i,ll

-

2. Ilxtrasystc'llcs rarcly neccl treatlnent. 3. Irr patients with acute heart failure or

low bloocl prcssurt due to a tachycardia, DC cardioversion should be corlslcl.cl'cct eafly on. 4. Patier-rts with arry bradycarrdia tlrat is affectirrg the circulatioll catl be trcatec-l with atropine, but if this is incffc,ctivc thcy will ncccl tcnrpt@or lrcrntanent p".^g (ttig. 3.3t)).

rii

a

,iii' :ll l;. I t;

iii

B4

wl-lAl l,JDo

HG,t:{

-

l.

ii ll

I

lr

il rl

ti

ri

Fig.33O Pacemaker

'L

f- f Note . Occasi6nat P waves are visible, but are not related to the QRS complexes. Tlre OnS conrplexes are precedcd by a brief sJliltt', representing lhe pacemakcr stimulus. The ORS comptexe-ar': broad, because pacemakers stirnul;rte the rigltt verrtricle and cause', entriculilt' *{

beats

/'

/

D. €K)\

first treatnrent fot'rrny abrrortnal tachycardia is carotid sinus prcssure.'l'his slrotrlcl L're perfortncd r,vith tl're ECC running, attcl rnay help nrake the diagnosis: - Sinus tachycaioiu -..roii.t siirus press,re ca,sf :s temporary slowing rrf the heart rate and junctional tachycardia - carotid sinus Atrial pressrrre t)tay tc.rrninate the arrhythnria r:r'n"la-y have no effect flutter - caroticl sirrus pressrtre usLrllly catrses a Atrial temporar-y increase in t'rlock (e.g. from 2:.1 to 3:l) - Atrial fibrillation and ventricular tachycarclia - caroticl

5. Tlre

f (

!-^ {6r t

l-t

sinus I'rft'ssttre has no e[fr'ct.

rrow conr'p-rlex with adenosine. Ntr

taclr yca rcl ia s slrtltt

ld bc' trc.r t ecl i n i tia I Iy

e cotrt l'rl q'x tnch yc;r rrl iirs slrott tl [rt' tt'cit t'tl U Witl with lignocaitre. l

l

i rt i t

ia

l

ly

B5 4

\,

.F

#jllJ$U

I

I

lL lil ty ltlM

L/r

I

I

lL t1l-At(

I

b

z^t' f

*-\\/

l--.

/ (-

A

THINGS TO REMEMBER 1. Most perrts

of the hcart arc capable of spontaneous clepolarizatiorr. 2. Abrrormal rhythms can arise irr tl're atrial muscle, the region arourrd the AV node (the f unctional region) and in tlre ventricular muscle. 3. liscape rlrythnts are slow and are protective. .1. L)ccusional carly clcpolariz;rtion of any part of the heart ca uscs arr cxtrasystolc. Ii. lircrlucnt clcpol.rr.iz.rtion of rll.ly F)art of l,hc heart catrscs A l,rchyc;r rtliit. (r. Asytrclrrotrous cr.rnlraction of tnuscle fibres ir'1 ,(\re atrirr or vcrrt riclcs is'cnllctl fitrr.illation. 7. Apal'[ fronr the rate, the ECC pfltte'rn of an escape rhytlun, an extrasystole arrcl a tachycar.dia arisirig in any one part of the heart arc thc same. 8. All sLlpravcntricular. rl'ryl.hnrs have normal eRS conrplexes provided there is rro bundle branch.block (see Ch. 2). 9. vcntrictrlar rhytl'rnrs cause wicle and abnormal eRS conrplcxes, and abnorrtral T waves. Iiccogrrizirrg ECC abrrorn'ralitics is to a large extent like ilrr clcPlrun[ - ()ncc scen, llcvcr forgottcn. l lorvt:vcr; in clscs of rlifficulty it is helPfrrl to ask l,hc l'ollowing, tlrrcstiorrs, rcl:ct.rirrg to Tltble 3.1: l'('('()1,)t'liz.in1i

ls tlrc ubrrornrality occasional or sustainccl? r\t't: llr('r'(' iu'lyr lr rvi-tvcs? l\r'u tlrt:r'c tls nt.'trry Ql(5 conrlrlu.xcs ils l, rvavcs? Are tl'rc vcntricles contracting regularly or irregularly? ls thc Qlis cornprlcx t'lf norrnirl slrape?

LB6

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4

Abnormcllities of P wcrvese QRS comPlexes clnd T

woves

Abrtorttralltlos ol tlro P

'

wavo 09

Abnormalities of the QRS complex 90 Abnormalities ol the ST segment 100 Abnormalities ol the T

wave

103

the T wave Otlrer abnormalitles ol the ST segment arrd

108

Things to remember 109

rtrythnr first' Whcn itrlct'1'rrctirrg an liCG, itlcrrtify thc i* t5c samc ask ttic folltiwirrg tltrcsti()l"ls -.lways

El

,[.5e.rr

I

sccltlellcc: 't. Arc thcrc atry abtrornralitics of thu P wave? .t t6e QRS con'rplex in 2. What is tlrc Jarcliac axis? (l,.ok ne.ces.sary) leacls I, ll, Ill - and at Chapter L if dtrration? ttorural 3. ls thc Ql(S cotnplcx of ,1. Ar.r, tlrcre nny .ril.,"r ab*orrrralitics i. the QRS wavcs? c.urplex - pJrticulirrly, are t5cre arny abtr.rnral Q

5.lstlrcsTsegrrrcntrai.se(lordepressed?..\.

-n /,^ -\

88

\

6. Is

thc'[ wavc trortnal?

l

ff*-+

--t'1illD-I.aB_,F
+

i

PPir v \

UL<

"p

I P

I

ur
cdt

,F, : c,*-/

ABNORMALIIIES

U C, LD

el- [ tr t, wnv,,

If,flry

Remember:

l.'l'lre I) w_avc clrr only trc rtor.rrrtl, tnlusLlrlitl,

'

1,11, or rrnusually broad. 2.'l'ltt'QR'S ('()tllplt'x cntr ortly lrnvr, ttrrt,c ntrrrpr.rrrllitics -- it can lre too trroad, too lirll, ancl it nray contain A11 alrnonnirl Q rvnvo. 3. The sr segment can only be rrormal, elevated or

-

rlr.pr.r-'sscrl. 4. The T

\

wave can only be the right way up or the wrong wn/ rrp. . ., ,,

'. P'^f

{

__l

-

nllronrrnlities:

cn, rigrrt atrium Hrceonre hypertrophled (such as tricusplc! v{ye stcnosis or puln'ronary l'rypertension)'cair.ses the p wave to become lrug&d (lrts.4.l). 2. Left atria.l hypertropl]y (l*,rally clur. to nritral stenosis) tiluses a broad arrtl bllg p wavc (lrig. +.6. :r)ctc\r heA ,-r.::,,, i \:\.., I.-A+rytlrint$'tlrat

-

e o( \\Oe \\3

Flg.4.1 Rlght atrlal hypertroplry

i tr{\- z t_f n] (,el

I

it

P uJ^'(<

5;

lo'"'

i

J

'tt P tt'VL

l,^ i t

89 J)'i-

'

t4

J 7_qf Jrhuer t'n

I, F

ill-{'il

ABNORMALIIITS OF P WAVES, QRs LOMPLEXTS ANU

I WAVbs

c\ crgl-#. i'

^') --

Jl

/v C
_

)

a Ab do'r '^'t '

Fig.4.2 LeIt atrial hypcrtrophy

gBB

4 s"a. or j-l

QRS

in

%

ui Ju"

ryull.ul^) h RvU

, ABNOnmaltflES' OF THE QRS'COMilfX

,, PG

i''{'',ii[rT.,i,"#$'l

'l'hc rrornral QI{S conrplux lras charactt'ristics: E!!]' l. tts cluration is no greater than 120 ms (three snrall squares) 2" Irr a rig,lrtr'ventricttlar lead (Vr), the S lvave is greater than the I{ wave 3, Irr a lcft'vctrtricttlnr lcatl (Vq or Vo), the heig,ht of the R wave is lcss thatr 25 nrnr 4. Lclt ventricular leads rnfritslrow Q waves dtte to septal .l. 'l 't {o '? tlt'1',1rlirt'iz,ttiotr, trttt lht'st' itrc loHs thttn nrtrr ttcross ntrtl a\ less than 2 mm c{eeP. '}z' L , v

\,

n

I

--.:i^-

t -),.1

q

\,,

..

l'\

i

Abnormolities of the width of the QRS complex

\ i'

^t L\

(e

br-rncllc branch block\see Ctr. 2) or when depolarization is ini[i.'ttccl by ir I'octts in thc vSB$S1$r tnttscle ci'tttsit'tg \rt, n t ri cr r l.u' ('scit pc lrca ts, Cx t rnsyittllt'S o r tnch.y\n rcl ia- (Scc C5. 3). In citlrcr citsc, tllc itrcrcttsc'ct _rvidth irr{ichtcs tl'rat :.rt: tr tr'icles try-n tt t I t. p1r I ir ri za t i tt n lra s s p rcR tl t h mrtr 6lr thc thway. sloq tlterc+il'e I an* irtr rrrrrnra '-'- --' \ lra *)t e r l1o pL,.l __ " 4

GIRS comPlcx J -''' ' "itte An increase of rnuscle nlass irr eitl'rer ventricle will lead to

lncreosecl heigfri

Ll

irrcrcasccl clcctrical activity, and to an iucrease

--

o[ thc Qf(S ctttnplex. r'

90

S 'r, i

e nh)1

+-t

-7

(

i1

-/\

t

\{

ff

\r

! '\

in the'height

'

i.

----']+a:-fE4&

-=.4:

jf-tqk!-i-*=*--*r,,.

t47f_ ,nt

-_3LJ,a

*a-11 .ur (/*1

,trtu

ABNORMALITIES OF THE ORS COMPLEX

dcl^-i

R,'ght ventriculor hyper trophy

Ri8hlve.njqlcular hypertrophy is best seen irr the right i n I ly V pr. s | ). Si+ree+hr'fffventich' rl its usuatlclom i,ralrt e ifect, ort the e RS s h a pe, t lre -nst-have eut[plux trc.co[lr.s upriglrt (1.u. tlro lruil;lrt uI tlrc l( wrryr, exceeds the depth of the S wave) - thirisrtenrtfatways i n V lbnornrnl (llig..t.3).Tlrt'rc will [ru n clct,P s wnvc irr lt,ntl v,,. verrtricttlar hypertro;-'rhy is usrrnlly ncconlparriccl by - Itight axis gevio[9] (see ch. t), by a peakec{ p wave (righr :1s!rl atrial hypertropLy), and in severe ca.ses by irrver.siorr ni't1.," T waves in leads V1 anci V2, and sonretinrls irr leacl v1 or

-

ve tt tri ctt I ni'f-l en rl s (t'spec

,

-,

-:

Lrvcrl Vo (Fig. 4.4).

" PaL

Ir

/\-

v\{

-

l,"e

\\

vl Flg. e.3 Conducilon ln rlght vorrtrlcular lryportrophy

9I

-

tps.G\(-cf t,/,

/1

i I

I i I !

rV> JU S int* f +-.chJ

\,L,3ztt? -R{H *r+L+3

,,

Pulnronory ornbolism

In pulmonary embolism the ECC may show features of rigirt vutt l rir,'trlrtr lrypcrtruphy, . When a lrrrlrrrtrrrrlry cnllrulrtg lr uttxpuclutl, ltrtllr ftrrl A _] , / o .>,/ ^

., 3[ l. I'cakccl P wtrvcs ,, .. a, l<\,.,.. ) . kr . z', Bt;ilts.ir .r"uioti"i(s *i(", in lead I) ^\ tAg.itii u-*arfs irr leacl V, * &9 S il J: '-;:,_l r"-..ti;. oitr,,i ir,.,',',dr" brarrch block ' R BBb [- n-\--" ( -' - {rr. r

\

+

92

dL,

a,

5. i,rrcrGcl'['waves in lead V, (r'rormal), spreading across to It'.rtl V.r ()l'Vr (r. A shil't ol' tr.ursitiorr point to thc lcft, so tl'rat tl're R wave ecluals ttrc S wave in leac{ Vr or Vu rather than in lead V3 or Vj (clockwise rotation). A deep S wave will persist in lead V6

.;

--C" €Cc,r

>ula)u

{U' -r\

5;qP?rrh$<6\"D

a \

\ ABNORT\AAUTIES OF THE QRS COMI

PLEXrt

Flg.4.4 Scvcro rlght vontrlcutnr hypertrophy Noles Slnus rhylhm o Right axis deviation (deep S waves in

.

. r

lcad l) Dominant R waves in lead V, Deep S waves ln leacl V6 (clockwise rotatlon)

o lnverted T waves ln leads l, ll, lll, VF, Vr-V4

1+

7.

' l

csrleqrly, a'e'wave in leacl III resemblirrg an inferior i;Tarction lsee tater;. [ ', \\:t f-r ^ ,. , v G I'loweveD clo not hesitate to trc.at thc patier.rt if ttre clinical

picture suggests ptrrmonary emborism but the ECG croes not tltc'i'lrr.ssir.'ol pntt.'.,', .if. r'ight vcntr.iculnr hypr.r.tr..,lry. lf i. tl.rrtrt, trc.at the patiurt witti rrrr arrticoagula,.,t. L__

. slttlw ^''"

\r ,u'\-), \ \ hypeqtropr-ry ca*ses a tail R wave (grearer *1lv^llricllar tlrnn 25 rrrnr) irr lend.Vc cli Vo nrrrl n tlc,ep S wnvc iri'ir.n.l V1 or vr (lig. 4.q).- byt in Practice strcrr 'voltage' changcs arorre rq un\elplgl i n g lef t vc t ri cu ra r e rr a rg.liii". t. ---4with significant 4iegrorln hypertrophy, tlrere^ are atso inverled T wnves in lcacls I, vL, vo arrcl Vn, arrd sonrctinrcs v4, flrrrl tlrcr.c 93 tefl verrtriculor -'rr-'..-f,,f lypertroplty

r

ST

*>tNH

s1np"\J L5,= 5-r,;o+*&

-,

/

31

ABNoRMALTTTES

oF

p

wAVEs, eRs coMpLExES AND

T

wAVES

I

li !l

ii it

it

-

wiJtL n).ly Lrc lcl't trxis rluvintiorr. lt is rlifficult to tliag,rr.ose trritror clegrees of left ventricular hyp-rertrophy from the ECG.

wqves G t're nT

The origin of Q Snrall (sr,ptal)'Q' w.lvcs irr the leflyglltticular lc'ads rcsult l'r'orrr r.lr,1r11l.1r'lerrllorr eif llru r*uptttttt frttttr lcft trt rlglrt (utlu 1.rr,y Ch. 1). However, Q waves greater than one sniall square in wirltlr (r't-,Pt'uriulltlug,11l rus), rtnrl greitter tltrttr 2 tuttr irr tlepth have a quite different significance. 'l'Iru vurrtlielcs ale elcprolarleecl frtttu irrsir,lu otttwttrtls (Fig. 4.6). Thereforc, crir clcctrocle placed in the cavity of a ventricle would record only a Q wave, because all the -r

*rI

-

it il

,ll .tl l!ri

-

:ii il il

I

,li rli ril li

1

't/ 4i ;"\

clcpolarizatiorr waves wotrld bc rnoving away from it. If ir rlry()cartlial infarctiorl causes conrplete death of mttscle fronr thc irrsic{e surface to tl'rc outside surface of the heart,. irrt clt'ctrir:,tl 'witrtlttw' is ('rtt,ltcr,l, irtrtl atr clcctrotlu lotlhirrg at l,trc hcart over Lhat window will record a cavity protsntialllr.rt is, ,r Q witvc.

<-'--, )\ E .!t*'-: tGffiEA-

.*a:€iG'

rfu-

i o\t

tvl,

q

wC

--=>

@

Grzlqu.6o

g*

I

r-€-

/

f^(-r'or

€-j

-\

m,

ABNORMALTilES OF THE ORS COMPLT-X

-1-

rc

es

Flg. 4.5 Left ventrlcular hypertrophy Noles o Slnus rhythm o Normal axls o Tall B waves in leads V5, V6, and deep S wa\ros ln leads Vr, Ve (R wave in lead V,, 40 mm) o lnverled T wavos ln leacls l, ll, V5, V6

(r'r

rr

,\,

Q waves grsntt'r thittr ()nc snl{rll srluare in rvic'ltlr ancl irt least 2 mtn t]eep tluefo,re irrclicirtc. a nryocarclial irr[arctiorr, ,/ i nn! Lhe h-'ntls irr wlrich tlrc e wave afrpears givc.lonlLr iindication of the part of the heart tl'rat has been damagecl. e prui, infarction of thc anterior wall of the left veirtricle

a

t /fi1 A n*erio( {'z , z t4

L-.I.^\ 1 -i

/v\L

t

A"\o

l, V

-(e

$r

i^-

5rr

io

t.i-r t'

^l'"..

\--,

1'"

\ ^\ur^ '

'..1

A,9 ?^1O

I

{** t /

at/

Flg. ()

b

J

i.0

/\\fe-l \ o /

/v\ L

MJ

7

.-( l--

The orlgln of O wavor

- s X-e.,r

FN

-\

95

ffi

J I

,.\

\ABNORMALIITLS

Lr

Ot

P

WAVES, QRS COMPLEXES AND T WAVES

causcs a Q wave in tlre leacls lookirrg at the heart from the . l'ront - Vz-Vo or Vs (see Ch. t) (Irig. 4.7). + li,rteral anterior nnd If tlrc in[,rrction involvcs lroth thc Jd C-v^aje,, surfaces of l,he heart, a Q wave will be present in leads V3 - I, J L.!-t" irntl V.1 rrntl irr tlru luntls tlrirl, lttok at tl'ru lntcral sttt'face 1... VL, itrrtl Vo-Vu (ltiH. 4,tl). lnf.rrctiorrs o[ the infcrior strrfacc of the hcart catrsc Q waves in the leads looking at the heart from below - III and VF (Figs 4.7 and 4.9). r o. P '");1/ !!\ '-J F , Whcn the postulior w.rll t1f thc lcft vcrrtricle is itrftrrcter,l, a different pattern is seen. The right ventricle occupies the l'r'trnt ol' thu lrr:art crllrrtullllcally, ond llonnally deptllariaatltln .." of the right ventricle (rnoving towards the recording r,lut'truelu V,) ls trvc,r'ulrar.lowur,l [:y tlcpolarlptrtlort uI tlre lcft r

96

.,-

-*s*. .

,6*=**==:Elrt

#'

ABNORAAALITIES OF THE QRS COMPLEX t

Flg. 4.7 Aoutc nryooardlel lnlnroilon, and prcbable old lnlerlor lnlarctlon (see

Flg. 4.13) A/oles

o Slnus rhythm with a normal rhythm o Small Q waves ln leads ll, lll, VF o Raised ST segments in leads Vz-Vs

-^

o. lnverted T wave in leads lll, VF

ja

ventricle (moving a.way'fronr Vfl. The resutt is a clontilant s wave in legrd V1 (see ch. 1). Witl-r irrfarcti.rr of ttre postc.rlor wnll o[ the left verrtrielefrlc,lrolnriznlion of rhc right ventricle * ond,a dorrylnrrt R wnvc r{cvr.lop.s in tead 5frhe appearance ofEe ffiiJsi;iiar to ttrat of rfg-h t Gtrffilcu ln r-hypr. rtro p try, t h o u g tr t lr c o t l r c r c. l r n r 1;cs

' i{ i @)-dototaiipear. ^::r'. ' n Q wnv,, rlo1,11 irol glvu nriy fiiilir.,.,ri,ii, PfttltLitlcu'ttf --l:.,/ H' trf-Ttu ('l tlre a5;e of an infarction, bccatrse r

clevc'lopccl it is usually pcrntanont.

once a.e wavc lras

e(

€nty

)ut

97

i

ABNORMALITIES OF P WAVES, QRS COMPLEXES AND T WAVES

9B

-E=

--=.E--

__4-

ABNORA

sT

D
AT'yt

{C

OF lltE QRS COMPLTX

ur

->

rll

Z .,t,-p,/ r z -s -b *_____>

an}

,-r

G

Flg. 4.8 Acute anterolateral myocardial

lnlerctlon Noles r Slnus rhythm Left axis (dominant S waves in leads il and lll) Q wave in leads VL, V3 o Ralsed ST segments ln leads l, VL, Vr-Vs

=

r

.

' Des, rieho $t \r"\€,

Ax

-U

L;

-,G)

(

Cr ,-.---,e\e+ ../ t sA -"

-\Ll [=

<::::-i.t)^g

,lf )v 99

ril

ABNORMALil|L5

sl-

CJ^

Ao

ol-

p WAVES, QRs LUMPLEXES

ANU I WAVL5

---v

/;"\1

T,

-c{"lf Pa ,'
C^I -1.3- xir1

,/),r''

il& v

roo

3..

-

-tt^---

-

a a-a--_7^r

.-

LE-, Z

-.::----1'g7 2 j-r

a-

7.I$$'r', oe-'(qLSi..

--

'l'lrc S'l' scgnrcrrt lies bctrvccn thc QIIS cornplex antl thc T \^/trVC (l,ig. 4. l0). It shoulcl bc 'isoelcctric'I tlabit; aLthe- same [eve"[ as the pirrt lrctwc'cn tlrc T wavc arrtl thc rrcxt P wave - but it rrray bc clcvatccl (Irig. 4. 1 la) or clcprcssccl,(Fig. 4.'1'1b). l il t'va t io rr f t !r gtS'!_ .:L:litm(rtl trl is n rr i rrrl icn tiorr of acrr te nryocarc{ial irilffi.,ruil! cluc either to a recbnt infarction or loJrt'r'i,'.u'rlilis,[Tl-lrc lcrrtls in rvhiclr thc ule.vntion occrlt'b inrlicatc thc part of the heart thart is danrage,l -.111$JSr \.7 tl.rnralic slrows irr thc V lcirt'ls, nrrrl irrferior danrrqge irr lends \,./ llt arrcl VF (scc Figs 4,74.9['t:ricar.iiTFFnot usually a Iocalizccl affair; and so it caLrses ST elevation in most leads.

e1---

t_r

,r$5:

L.\

a-

ABNoR

oF

THE sT

sEGMENT

^ALtTrEs

E||;

-_

Flg.4.0 Acuto lnferlor lnlnrcilon; lntoral

lrchaomla Nofes

. Sinus rhythm r Normal axls

o Normal QRS comptexes o Raised ST segments in leads ll, lll, VF

.

'...

#

QG

l Yn'

tt

ST segment

Flg.l.10 Thr ST,.Or"n,

lr^4JD

i=#V[l"

:tffin.l, '^ffi,thl- ^

l

-^-J+^-

.i-iH_,,; [j;,

(a)

Flg.4-11 (a) Etevated

-:

lnverted T waves in lead VL and in V,, which is normal

sr

segment. (b) Depressed ST segment

IOI

--

\

ABNORMALII lES OF p WAVES, eRS COMPLEXES AND T WAVES

iLfl

Bost:

Exorcise:

Fig. 4.12 Exorclas-lnduced lachaomlc changra Nole

r

lrr tlro uppor (nonnal) traco, tho heart rato ls 55/mln and the ST segments are isoelectric. ln the lower trace, the rate is 140lmin and the tiT uogntorrlu aro lrorlronlally tloPruaaod __+ , \_,

*J o p, ...d.

-
---'-

/,t-

\-\e-''q

SI g,eell en)a ssocia tcd \w-ith In, -,: en Aqplssp lp f an upright T wave, is usually a sign of isehaerrtiaas* ta

Bz

I

i

9

t

lr e

rqqr+u+tl*r irrfnrction;Whtlrr tlrc llCG nt rust ls rxrrntt{I, I S'l'segrnerrt deprression nray appear durirrg exercise, I -:-a p9q[c r r I a rl y_ I4U ] _qlt,t l_ t rrrlurfgitrrg im{!:lg" 4JQ* *---. . Dowrrskrpirrg, os' dcFrc55ed, S'I' scgnrcrrts_-EfE-dstrhlty dtu to tre.dtment lv-ith cti$dXin [dGr.-T1il.

i[

Iit t c r)

.

)r), )7),4r!,-l riuO: ;t

/'.

ie]1N\ eAi

''d

.,

t\Y

102

,t

sJ

2,:s /

I

f)r:3t.)c\

,a (=(

<.\;fJ -,-nvr' --'^J'>

L>\

.,.

,l

.:=

.j- - .*-

+..._.-.,.

--__

a(3(

! IN)

R

I

ABtlORlylAUnES Or IHE ST SEGMENT/aBNOR{ALITIES oF THE T WAIE

--

'\

v-!*

:

I

fil

I

,t ,l);p

I

'l'wttvL' ltrvc't'siott is stetr in thc follorvirrg cilt'trlrrstancr,s: ---. / l.iNonrrirlity

'

H

2.ll,pclraemia

3.$entrictrlar hyprertropfiy i 4. Bundle Lrranch block '- ''-

I

i

!

--

'?.ttr

'J Cst)llltltltttcs slrow 'blphnslc' 1' wnvc's - irritlnlly uprr.iglrt irrrtl then inverted t1 rt'olgtnl! v !^ Vt'2':' -:e--iiu /?-T ,\

_4 5

Leads adiacent to those showing inverted T waves

l,-\i

-e'n

wavl is normally inverted in leads V1&a,l.t V1 (arrcl i,l --.y flhu-T lead V2 in young people, ancl also irr lead Vr in sonle Lrlack .'_ I -\i,\ :i_ReoRle). sl^* y?3.

lsChocmiq

i, v

z

'...-iv-et - L''l,

''i'

-'V-,!-tr

]--'l-'-i-i -\- '1o'ap[t

After o myoL'orcilnl infnrctlon, ttre first nLrrrorrnntity scr.rr s 7*::-" *-: #(-;-'' orr the ECG is elevati.n of trre sr stgnlpnt (E+'. 4J3),

ll_sf,g1gqq*llty e waves appeaq

orrcr

ttrc{f'},liilJ;'r,i,Il;,.,i" cvc\n1e.

The ST segment returns to thiGseiine, tlrt whole ' n _S|}Sg -

\

o^ c

process taking a variable time'but usually within the rangLr --\ -r^ of Jl -'. 24-,48 hours. T wave invercion is often pernrarrent. *l .,;, ;p If an infarction is not full'thickness and so cloes not catrse *.,-.\jnn electrieal window, tlrere will be T wnve inversiorr trut rro Thls is cnlled a 'non-e wAvc infarcti6p, :oru.*(-Fis.,4.14). \ The ti'rm'sutrenrlocnrt'lial (-Q irrfarctiorr' pntterrr is lrattertr. \t--sotrrt'times ttsecl, but it is oftr.'n not p1[llologicalty c6rrgct. r'rrr' rvr\'air\f trrJ \\" 1

9€€ w.

t(7' rx), c \-?

V

tr,10 r03

Mf

U

AuNoRMALilrEs

rI ..c

ur

P

WAVEli, QRs LUMPLbXhS ANU r WAVL5

l.-

--o-l Ts N)IV Diso 8 8BB F

&

t

hour a fter onset

ffi ffiffi ffi

-

VR

II

-

III

VL

VF

ffi ffi ffi VR

VL

VF

24 hours altor onsot ol paln:

>

ffi ffi ffi ffi

>-

ilt

-d

l-F

r04 -rF

:j-

-firF.lQf,,tr#H-

ABNoRt\AALlTlEs oF THE T

WAVE

EiI

F19.4.13 tlevelopment of lnlerlor tnfarction

Nob

]' , : .'

I '

*:

Three ECGs have been recorded over z4hours, and have been ananged horlrontelly 9!nu! rhyrhm wlth a normar cardlac axls ln a[ ilrroo ECGs The lirst record ls essenilally normal hours uil,t,r -o (,$ rN,ur5 after the lne onset oI of paln, oaln. the sr ST segments seomente have havo risen rican in in raa-r^ leads irll, lll and vF and the sr segrnent rs dopross"od rn rcad vL. A wavo e rras developed in lead lll o 24 hours alter tho o_nset ol pRin, a small Q wavo lras crP[Irutuu nppoarod t]t ln tcuo loacl ll and more obvious Q waves can be seen in leads til ano'viiTasr segments havo returned to basellno, and ilro T wavos oro ,rofirfirtott ln leads lll and VF I

/\-/

:,

\

{1 2€ )\ g.,2'-Y @
r05

-

*&-.,.\!-

.ar-,-.-l-';

AI]NORMALIIITS OF P WAVES, QRS COMPLEXES AND T WAVES

il il

il ;I rl

+ il

rl

I

Vontricutor

/,yt' r!-'

1, thV'

ry':t L-|,

,

=

t o',9

iy' i

-'

I

! i

--

,oo

eii^ ;,6-oL***'V+, e

lrypcrtrophy *<'

':

' - '='

Lel't ventricurlar liypertrophyi,causes inverted T waves in [-c.i.ls liroking at the left vcrrtrit'ldV5, Vru II au'rd VL) (scc Fi1;. +.5) fRr g lr t v e n t ricu la r hy pic' rt roffi ha u ses T wave inversio tr in thc lcarcls lookirrg at thc right vcrrtricle ftw'.ryrtrrvercien -Vi;b ur rtr wtrttc adu*ts ir*btttrrrrrat i rr iffict

EJC;;, (

/ 4Vu5roa

llo.t

e

Bundle brcrnch 'l'lr* ulrrrorrrr,rl pri'1tlr of tluPtll,rrir.rttittt't itr bttrrr"llu brirrrch with an abnormarl path of IUtock is usuirlly associtrted

f

rl ,fl

i

!l

:l

'i

il

.rl

it

ll

ii

II

rc"€

L*L

)

{ot,' z^

^.€

ABN?RMALITIES

oF

WAVE

THE T

Iiil

F19.4.14 Anterlor non-e wave lnfarcilon IVolas

o Sinus rhythm o Normal axis e Normal QRS complexes \ o lnverled T waves ln leads

L.

Vs, V4

Biphasic T waves in leads V;, %

e sc rt'(h'

a^

&,u

15

I

\-oJs -.'I, +I{U a L_\s;t

--T-

,nt

L

J,coq

> ?rfa.* c,/\ P

*X

\-rAVc/sr.o,

-/7

2\-e a_

\ F

, invertecr T waves associated with eonrplexes wrrich rrave.a crtrratior-, PRS rrls or ,1ore h*ve-*o srg*ifrea*se lrr thr.niirerves Irr8, 2.15 a^cr 2.16). G; "ilco

-t Do-)'^

Dlgoxin

_H..::l':li:I$,tr,.il1*$,il1;iU::iiH:I.,n:,,TTXn*n,

X

['5ffi *t1i:",r,#;f, iifi ]i',T,#:i-",, Lqf'

l_

wnve changes

T

F l.*e

fitr)c,'

-f=- feo k-J

+ ; U

;

L)

Jt'oi

ave i n

€/,/4/?

ii

*

'h1tro l(. - ",

.,

i =

l07

\

-\ ArJNs)RMAUilis Ot-

rI t^

oAn Ca '-(.I-

h=)

-

WAVES, QRs LOMPLEXES AND

sl@^;f-

T

WAVES

rWdME

Ns\s*=s

)

/lAarx{ Cq.^

r I +*

P

,

te6-

Nof,. dualhffio

ca,,

Fig. 4.15 Digoxin elfect Nolo . Atrial finiiltation . Narrow QRS complexes z . Downsloping ST segmenls ('reversed tick') \ . lnvortorl T wuvgs

vcrr

\Y T (.e

'

"ai:

,-1, lA,9 Po C+ ?rt IiiofniR IHBNciffi [rriiibl6r]rHE ,, Y

.

Ll\

I ,-.*

-i..

:r I

-,

t,FaEl

i ano,THE T;i,WAVf.i:'i1

t.1 la

i ar (-

Electrolyre qbnormolities Ahrrornralitic.s of tlre plnsrnn lcveln of potns.$iumr.calciunr

{ ll,i,ilJ flliiJ.T,'l'fi::i ffi??fi..HrL'lilrui il [,i,., /

\-

L

(nrcasured from the onset of thc QRS complgx to the qnd of llrc'l'wavu) arc tno$t conrnrorrly affccted. X\?.",k3lecaiar

U' r"t?\' peaked T.waves level ciluses with lrigh potassitirn .. wavc. A the disappearance of the ST segment. The QRS complex . .. / nlny bc wiclcncr{. Thr-'.effects ttf abnornnal trtngtresiunr levt'ls 'o '16, are similan .-- \*P),-1":r--t q -,.i", -\ \-;* - A low [rlasnrir crrtc'luur levol cnusrrs prolongntlon of tl're '--level shortens it. L- .-rL_I _.,' qterval, arnd a high plasnra calcium (-,,( cuav e

E

..

:

-.- . 9'

i .-

.--I'l J\ "s

, a :-f.tog ,A'rv

i-

.l:;..

>

' ^('llt.t'

G try V U a chonges I\rli,r^r. 1,.r,rr.o.... ^f q.rlo;u'l:l*i'i;:ilfz[")'l]:ilil1fl;"?ff-*liltllHH'n.o, 'non-rp"cifi.

ofrr.-rrecific

Sf-f

anrl rrrc bcst r"poit".l as

chan{es'.

;iF.

Dn€crt'L'\,'n )\E

QT J;P1;Y<))

(D4un (4o, Ka),oj r €fa cr

Ll\'ll

*,,,

thir

A\r...,r"".,t,'1,/

t(ou

_sL",)-

e

ee- )xis.

Qry'-^

D.(0-xiat

i44€

THINGS

T>.

I

To

REMEMBER

E;T

\i.,

1. Thll P waves result

from right atrial hypertrophy, ancl brond P waves fro'r lc,ft nirial hyp*r.trtrplry. ' r' 2. Broadening of the eRS complex indicaies abnormal intraventrlcular concluctlon: it is sec.n in btrnclte branch blocRhhd in complexes originating in the ventricular

llluttl.le. ,,

-

'

3. I^creased Hqight

of the eRS complex inclicates ventrieular hy.pertrophy. Iilght ventricular hype,rtr.p-rhy is seen in lead vp and left ventricular hypertrophy is .""i", in leads V5 anct V.. 4. Q waves greater tha. 1 nrnr across arrcl 2 nrr. cleep indicate myocardial in farction. 5. 9I segment elevation inclicates acutc. r-.yocarclial irrfarctior.t or pericard itis. 6. q'r scgruent depresslon nncl 'l' wnve invcrsi.rr r.ny lrc dut' to ischaerrrin, ventriculor lryPq.111opi,y, ntrrror.nrnt in traven tricula r cond uction, or-.i i goxi ri. 7. T wave inversion is normnl in leais IlI, vrt anc{ v1. T wnve inversiotr is associatecl with truncllc't,ranclr [rtocl<, ischaemia, and ventricular: hypertrophy. 8. T wave flattening or penkinf with ni, ,in,,*ualry l.^g.r short QT intervC may be due to electrolyte abnormalities, but ma.y minor sT-i changes nro ,.,n,.,-ipecitic. Arrd finally, rernenrber:

o The ECG ls easy to unclerstnnd.

'

Most ahrrormalities of trre ECc are arlerribrc to reas.^.

el

r09

\ t'

'$r

/,L -rj*-

J;U

/R*

- --

Reminders a

Whut to look lor lrt the ECG 110 The normal ECG 1 12 The cardiac axis 1 12 Conductlorr protrlorns 113

Rhythms 114 Myocardial infarction 117 Pulmonary embolism 117 Hypertrophy ol tlto heart 118 Differential diagnosis of ECG changes 118

'l'hcsc lists will renrincl you of the features that will help you rccogrrisc thc pattcnls of uornrality and abnormality in .- the UCC.

-

CGi '1.

-

Thc rhythnr.

2. [' wave abuorrnalitics:

\. . ' .

pcakcclltnll - right atrial hypertrophy rrotchcr.l, lrrond - left atrinl hypertrophy.

r lo

:-,ilItE rr.E!Atg!+.%Ei.-&*)dEri!*.!s;l

WHAT TO LOOK t-oR tN THE ECG !l

3.

Theiardiac axis.

--

-

-

'

rcft

*

-a

4. The QRS complex:

.r . width: 'a - if wide, ventricular origin or bundle branch € block . height: t . - tall R waves in leacl vs i' right ventrictrtar . Lypertrophy 7 - tall R waves in lead V, in left ventricular

.E

rr

hypertrophy o transitlorr poirrt:

.,y,! -

.1 .-

-r

R nnd S waveg ane equnl irr tlre clrent lenrl ov(,r

the interventricular septum, normally lead V3 or Vn clockwise rotation indicates crrronic lung disease

. Q u;""r.

5. The ST segment:

\.

raised inhgute myocardial infarction ancl in perlenrdltlrr 1: a"pressed in ischaemia and_with cligoxin. 6. T wnves: \ o peaked in hyperkalaemia . flnt, prolongecl in lrypokalnanria !? c inverted: - normal in some leacls I o. t - ischaemia

- infarction. "L - lc.ft orright ventrictrlar hype,rtrophy - prulnronarl enrbollnnr - bunclle branch block g'3$

I

7.U waves:

I

o can be normal a o hypokalaenria.

III

Limits of normol durotions I'l( interval: 200 ms (5 small squares) . f o QRS complex duration: L20 *i 1a small

.

'i 'n

"-f'

3

-'S squares) *---- L/f

Rhythm

X.

Sintrs arrlrythnrit'r. extrirsystoles are always normal.

o Supraventricular

(/

D,

\'

o Normal axis: QRS complex predorninantly upward in lcarls [, II arrd III; still rroirnnl if QRS conrplex is downward in lead lll. 'L o Right irxis: QI$ complcx prcdonrinantly downward in lc'irrl l. \

Z o Left axis: QRS complex lc.tr.ls

ll

rrrrul

predon'rinantly downwlircl in

ll[.

Note: minor degrees of right and left axis deviation wit['rin the normal rairge. GIRS

i

. .

o

.

-, -

,o I

l2 .

_

comptex f

er r r r i-'

are

-....i

.

\

t-'-, ,J)

<\n.--'

srnall Q wirvcs rlornrill in leads I, vL arrd vn (septal Q

wavcs) RSRI pattern in lead V1 normal if the cluration is less than l3() rtrs (lrut'li,rl rlglrt !,ttrtrllc [rrrtttClr block). R wave smaller than S wave in lead V1. R wave irr lead Vo less than 25 mm. R wave in lead Vu plus S wave in lead V1 less than 35 mm.

Shoultl [:c isoclcctric.

\G:r+ f /

JP F-)r

::l

^.) "l r^-^-^fuL4 _/ T wtrve ' . Mny lre irrvcr.tetl irr:

-

' -

Iead III leael VI{ leacl V, leads Vz ancl V3, irr L-rlack peoprle.

^t\ :--

n

oJ

First degree block

.

o

One P wave per ell,S complex. PR interval greater than 200 ms.

'-

Second degree block o wenckebach: progressive pR lengtrre.i^g trre.

Lt

3.

non-conelucter{ P wovc, nrrtl thun rt'petiiion of thc cycle. M.bitz typ6 2: occrrsi.^ar *()^-co'rructccr bcuts. 2:1 (or 3:l) trlock: two (or three) p wavcs per elts cornplex, with normal p wave rate.

Third degree (comptere) btock

. . . '

No relationship between p waves arrcl elts comprlexes. Usually, complexes. eRS _wide

Usual QRS complex rnte less than S0/nrin. sornetinles nnrrow eRS conrplcxes, rnte s0-(r(/,rirr.

Rlght bundlc bronch block

. . .

c

.

QRS. complex duration greatcr than 120 nts. RSRI pattLrn. Usually,-dorninant Rl wave irr leacl Vs. lnverted T waves i. lead v1, and sometimes in reads

-

Vl-Vr'

Deep and wide S waves in lcad V,,.

I I3

pfll

h.'Yrrl\uE*b

Left bundle bronch block QltS conrplex duration greater than 1,20 ms. M pattcrn in lead v6,, arld sonretirnes in leacls vl-vs.

. . . .

No septal Q waves. lrr.vr:r'tctl J'lviwr.s irr lurrds I, VI_,r Vs-Vo ttrtrl, sotnctinlu$,

V4.

Bifqrcicutcrr block

. .

Left anterior herniblock (i.e. nrarked left axis with deep wilvcs in leaels Il and lll). Right bundle branch block (see above).

Suproventriqulor

rhythms

. o Irr general: - narrow QRS conrplcxcs (less tharr 120 nrs) - $dlne Ql$ courirlexes as ln sinus rhythm - normal T waves. o [xceptions: $upraventricular rlrythrns

.

have wide

complexes with - bundle branch block - Wol ff-Pa rkinson-White syndronre.

Ventriculor

. .

''

S

:

eRS

:i

rhythms

1

Irr gencr.nl: - wide Ql{S complexes (greater than L20 ms) - differerrt QRS complexes frsm those seen in sinus

rhythm

-

..-

Rlrythm qbnormolltlor o , Extrasystoles: single early beats suppressing

-

irbnorrrrnl T worvcs.

I

14

.

tl're next sirrrrs lrt'rrl. Escape beats: absence of sinus beat followed by late single l'reat.

"{#,.$,:

;''

"tf

,

iarr'fi"rT-"t----T-r.--,

alnr.r

-

RHYTHMS

H[i

"..

o racnyiardias, ..Sradycardlas.

Common suplrovenlriculor rhythms Sirrus rlrythrrr, AtriaI cxtrasystolcs. Junctlonnl (AV notlnl) extrrrsystoles. Atrial tachycardia. Atrial flutten,. Atriat fibrillatibn. tunctionnl (AV nodnl) taclrycarrlin. Junctlonal (AV nodal) escapc.

Common venlrlculor rhythms Ven tricu la r extrnsystoles.

Ventricular tachycardia. ventricular escape (single beats or comprete heart blot'k). Ventricular fibrillation.

-tl

Suproventriculor rhythms

-

Sirrrrs rlrytlrrrr: one P wave per QI{S conrprlex

-

l)-l) intervnl vnrles witlr rcispirrrtiorr (sinus rrrrhythnria). Supraven tricular ex trasystoles: - early QRS conrptex - no P wave, or abnornrally shaped (atrial) p wave - narrow and normal QRS cor.nplex

-

normall.wave

next P ri&ve is'reset'. Atrial tachycardia: - QIIS complex rnte grenter thnn l5(/rrrirr - nbnormal P waves, usually wittr slrort ltR intcrvals - ttsually one P wnve pcr QRS conrplpx, lrut sornetinl(as P wave rate 200-240/min, with 2:1 block.

I t5

!n

r\L/YUt\L/LKJ ''

'f':'

''

i"r

'

i

Atrial flutter:

- P *.are ratL'300/rrrin - sawtoothed pattern - 2:1,3:1 or 4:1 block - block increased by carotid sinus pressure.

'.

.

AtrlaI l'lbrlllatibn: the most irregular rhythm of all . \ 5o complex rate characteristically -S over 160/min witlrout treatrnent, but can be slower - l1o P waves identifiable, but there is a varying, t'o rrr plctely i rregu la r baselinr_.. Jurrctional (AV nodal) tachycardia: - colll,lo,ly, but i'appropriately, called ,SVI,

.

tacl'rvcardia]

ltJB'.]',"tJ:Ticular =G: Ce cranzrs-, ru tc usually. I S0-l80/nrin carotid sinus pressure may cause revlrsion to sinus rhythnr. Escape rhythrns: - bladycarclias, otherwise characteristics as above, except that atrial fibrillatiorr does not occur as an escape rhythnr.

-

\r eR

Ventriculor rhythmr

. .

t'

.

ts

Veutricular extrasystoles: - early QRS conrplex - no I) wave - QP.S conrplex wide (greater than 120 ms) - abnornrally shapctl QI{S complex - abnornrally shaperl T wave ncxt l'wave is orr tinre. Ventricular tacl-rycardia: tro I) warvuH - QI{S cor-nplex rate greater than 160/min - accelerated idioventricular rhythm:.3s" for ventriculartachycardia, bur eRS complei iate ld$'thanjzo/nin., ,

rq

I

t6

**-?:!l**j:e4#1*

g"z-

RHn'Hi s/MyocARDlAL tNrARcTtoN/pu[MoNARy EMBoLtsM

ffi,I

-

o Verrtricnlar fibrillation:

-

g

look at the patient, not the ECG.

Sequence of ECG chonges 1. Norrnal liCC. Raised ST segments. 3. Appearance of Q waves. ,r-4, Nornrnllzntlon of ST scgnrerrts. 5. Inversion of T waves 1*_7

.

,''

i

y'.).

.

,

t : L: '

siteof inGorctiont''

?'-'l'-j

5€

o Anteriofififarction: changes crassically in leac{s v3-va, but often'also in leads VrlVu. o Inferior infarctioh: chanfes in leads III and vF. o lratgral infarction: chang-ur in leacls I, VL, Vs-Vr,. t t$:.ilrosturitlr itrfnrctiotr: tlornirrarrt [l wnvts irr lcarl V1.

Possible ECG patterns

. . . . .

--

ir-rclude:

Normal ECG with sinus tachycardia. ttaked P waves. ltight axis deviation. \, 1", Rlght btrntlle trronclr titocli. i, (j\:.1Domirrant R waves irr lead V, (i.e. R wave bigger

t a

.

thar.r

wave). . Inverted T wavcs in lc'acls V,-Vl. o Deep.S'waves in lead V6. r lti8ht axls (s wnves ln ltntl l), prtus e wnvcs irrrrl i.vcr.rcrl T waves in lead III. S

l17 r-

.

traf

i.-r. ,,.i:,

RhMlNrrtRs

HypERTROpHy OF THE HEART';i.:lf.iii'.,

,+,ii :i:it... j**.ii:.

Right vontriculqr hyporfrophy . ?ril R waves in lead Vs. '1"

waVc itlvctlsiotr itr lc.rcls V1 and V2r nhc{ sonrc.tinres ir1 V3 and even Vo. o Dccp S wavcs in lcad V6. . Right axis deviation. . Suurctinres, riglrt bunclle braneh block. \'{';;

'

-l

i'l

Left vontrlculqr hypcrtrophy

. . '

l( waves irr lcad Vs or Vo greater than 25 mm. lt wirvcs in lc.ld Vq or Vo Plus S waves in lcar,l V1 clr V2 greatcr than 35 mm. lrtvcrtect'l'w.rves in leads I, VL, Vs-Vo ancl, sonretimes, Vo.

Left qtricrl hypertrophy llificl P waves.

.

-+2

Right otriol lrypertrophy o ltakccl P waves. i"blIqqRiifi riHlYrillffi Nos-lbvi5HrEc'tf

-

..

fi{T

.:. Wc cill'l rcrlrrilnge solne of these lists to remirrcl you of t5e possible irnplications of ECG patterns ;

:ri.

P:GIRS qppqrently lI yotr cirtrtrttt suc' ejttc thc following:

-

I

:

I

I' wave llcr QI{S conrplex, copsirler

l. P wavc llrcsctlt but not casily visible: look particularly at. lcircls

-

not

ir lar

r

, I I8

'2.1f

II nrrcl Vs.

Ql$ culttplexes at'e Irrugular; thc rlrytlrnr

fibrillation and what seem to be p

*ar*,

ls prubably atrlal uctually are not.

DI|-|'ERLNIIAL DlAGNoSls It

ai

3.

ol-

ECG CHANGES

EIt F

If the QRS complex rate is rapid and thc're flr(, no p wAv(rs, a wicle QRS cotnplex irrdlcatcs

venlricular tachycarclia arrcl o llarxlw QRS contplcx inclicntes jurrctiorral (AV rrotlal) ' tacl'rycardla. 4. If the QRS complex rate is slow it is protrably an escape

rhYthm'

1S P:GIRS more thqn I:I

;[

-

(,-;','\ -\u(,

If yotr can see more P wnven than QRS corrr;r11,;1(rs, cotlsitlu. the following:

l.If

thc'Ir wovt' ratc is 3t)O/nrln, the rlrytlrnr is ntr.inl fluttcr: trrere ar.e two e waYes per QRS complex, the rhythnr is atrial tacl'rycart'lia with block. 3. If the P wave rate is normll (e.g.60-10t/rnin) ancl ther.c, is 2:1 conduction, the rl'rythm is sinus with second degree block. 4. If the PR interval appears to be differcnt witlieacl.r bear, cornplete (third degree) heart block is probably present. 2.

If the P wave rate is ls0-200/min and

-t

-

Wide QRS complexes (greoter thqn I20 ms) Wide QRS complexes are characteristic of:

1 ! ( .' . . J Gr

.t' . ' o

Sinus rhythm with burrdle branch block. F:?r€ Sinus rhythrn with Wolff-Parkinson-White synclron1e. Ventricuiar extrasystoles. ,,-)p -.) Ventricrrlar tachycardia. Complete heartLtoct<.

woves

\ !' ' L' '' *t' "? '7 ?

:.Q

Srrrnll (neptnl) Q u'nves drr nontlfll irr lenrlri l, Vl, rlnrl \/,,, Q wave ln lead III but n.t VF is a'ornlal varia^t. Prnbnlrly incllcnte infarrtion if pr11'5c'r.rt irr nlot.r, llrnrr orrt. lead, longer than 40 ms in duratiorr, and cleeper tfiap 2 prp-r. Q wnve's irr lentl llI trut trot irr VR witlr righi nxis, rnly i rrtl icate Lrttl morra ry enrtrol u s, Leads showing Q waves indicate site of infarction.

-

I 19

l(LMtNDH(5

5T segment depression r o Digoxin: S'l'scgnrcr-rt slopcs clowuwarcls. Io lsclrat'rtri;r: [lat S-f clt,Pr.cssiorr. '

,; b.^L,rt,;/;::\

\t ,e,t-,

T rvove inversior.r , .' Nttt'ttt.tl Norrrr.rl irr lt'.rrls_lll, lt..rels lll, vli, Vl 1u,.rnel Vz-V., irr lrl.rck -'t)1rlg. lrco \ o V'rrlrit'rrl.rr Vt.nlrit'rrl.rr.r.lryllurrs. rlt'

. M.yor".rrtlial in[ar.ttion. AAt . l(illlrt or lt,l'l vt.rrtr.it.trl.rr. lr_1,1rt.r.1r.o1rlr1,. . \{oll'l-l'arkinson-Whitc syndronre.

UJ

rio

.? rr--t

\L\

6 Noru test yourself \irtr shotrltl norv ['rr- ablc ttl t'ecogrtiz,t' the cotrull()rt l]CC ['atttrrrs, arrtl this firral clragrtcr corrtains ten 12-lcacl rc'corcls for you to interprret. When reporting an ECG, remembcr: I o 'l'hc liCti is cns1,. lo A tep1r11 lras tn'o Parts a rlcscriplirlrr anc-l atr i tr t

t'

rPrt'

ti't

tio

tr.

. l,ook irl irll lltr'lt'i'rtls, nrrtl rlcsr't'il-r'llrc

I1CC irr llrr. lrilrlr(.

orrlt r ('v('r-y tittte:

rltyihrtr

-

corrdtrction - PR interval iI sintrs rhythnr carrliac axis QI{S c()ltl}rlt'xes:

'tlttt'alirlrr . ltt.ir',ltl ol l{.rrrtl li \\,ilvt,:i -

ST seqnrents 'l'\\'irvt':i.

Renrenrtrt-r \r'hat carr trt, norrnAl, esPt cially whiclr leads r'iltl sll()\v iltr itttrt't'lccl 'l'rvnvc. 0' 't 1 "-' ^t' \ Tltt'rr, irrrrl orrly llrt'rr, rrrAkt' a cliirgnosis. 'l'he tcrr ljC(ls lrcre irrc irt rro 1'rartictrtlr sc)qucncc, Lrut all a have heen clescrilretl earlier in this book. Tlreir ciescriprtions IX .[4(). f arlcl irrtcr'prL'tatiotrs.rt'c givctr aftt'rwat'ds,trp pr.

I2I

-\ sHffi$

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L-..-, r\ n

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/l

u-

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,

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i ir

lii liiiiJHll i:lril lili

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liffiLilll]iliilii

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1

: '.I

illll{

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\o r^J3 c--.rJ.'S

n\n..->

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+

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s-

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l\lrvY rLJl Y\JUKbLl.l

n -\-^rn q

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s1 D*P

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125

I

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127

i^

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r\ruKJELr

I

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YQURSELT

-t

-l

a

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rt

-

I .a\./ YY

r30

a

LJ I I \./L/t\!rLL.

NUW IE5I

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fl

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_l

rr

-

.._ I3I

ftffi

r32

Nuw tEst Y(-,UK)ELr

NOWTEST YOURSELF

ffiW

-l

_

ECG 6

_ rr-

-l

a-

1"1

. _ r33

-

ffieffi

I34

Now

TEST YOURSETF

q< ,--)\

c!f C.. /

1".

l, e-*=*\

d s\. -*rj P f

NOW

TEST YOURSELF

i^ f,-'r. ( b e- Ur, ]lnn

ffiTE

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t

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31

a

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-

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t Qc< ,t Gj

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i

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-

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-l

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rt

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i..|ra-,.t,-'ryr.','Y.',..r-,.....i1.,

i EcG' DE SC RI pil ON S'AN D', Nrr npnrrAuonislT-+'riffi t

EcG

I

-'iz'

This ECG shows:

ab'ql ,r i

i, f-

1,

I- ,

'.ii

'..,

.,:

sinus rhythm;'rhythm strip (lead !I) shows siirug'-,. arrhythnria o Norrnal PR intcrval 120 ms o Normal axis . QRS duratiorr B0 ms, njlrmalhq1ght . ST scgnrent isoelectrii in all leads\ . T inversion in lead VR but no ofher lead

'

lnterpretatiort . Normal record

>> Ap en^l

If you did not get tl'ris right, look again at pages zs-zz. ECG 2 '['his ECC shows:

. . . .4 4 . . .

Sinus rhythrn

Normal PR interval Normal axis

Wic{c QRS cluratiorr, at 1(r0 rns I{SR pattern in lead V1 Wide and notched S wave in lead V5 ST segment isolelectric T inversion in leads VR (normal), Vr-Vr

'.i.i

Interpretntiotr o IUght bundle branch block

Any problems? If so, look at pages 3Z-39 and 43.

142

t.

I\\JVY IE.)I Y()URShLT

-,

.t

ECQ 3" This ECG shows:

-l

. Sinus rhytliin . Normal PR interval . Normal axis complex - Q waves in leads II, III, VF ---. QRS ST segment :soelectric . T waves inverted in leacls II, III, VF i " Intcrprctntiotr . Inierior myocarclial irrfarction, probably olcl

-r

-

i

-

Get tl'ris orle wrong? Read pages 95-102 again. -l

ECG 4 This ECG shows:

.

Sinus rhythm '-{ Alternate conducted and uon-cotrducted beats a Normal PR interval in the conducted beats _..-a Left axis deviatiorr (deep S waves in leads II arrd III) .---a Wide QRS complex (duration 160 ms)' Rl6-95 RSR1 pattern in lead V1 i ,. , 6, ,^,- .. ).o;

2ll -t

LkD Intcrpratntiorr --. Second degree (2:1) block with left anterior hemiblock and right bundle branch block, irrdicating severe cond uctirrg tissue diseasc This was expained on page 32.. ECG 5 'fhe IICG shows:

. . . . .

Atrial fibrillatiorr Normal axis Normal QRS complexes Downsloping ST segments, best seen in U waves, best seen in leacl V,

leac'ls Vu-Vn

143

I

t\./YV lLul

r

\-/\/I\JLLI

Itilcrprctatiott . Atrial fibrillation of uncertain cause, with digitalis effecU I

U waves suggest hypokalaemia

If you made a rnistake with this one, read pages 107-108. ECG 6 This ECG shows:

.

Narrow complex (i.e. QRS duration less than 120 ms)

tachycardia at 200/min No visible P waves QRS complexes normal ST segments show a little depression in leads II, UI, VF o T wavcs nornral except in lcad III

. . .

Ittterpretntiorr

.

Supraventricular $unctional) tachycardia In case of clifficulty, Iook at pages 72-74. ECG 7 This IICG shows:

o Sinus rl'rythrn

. . . .

I.Jorrna[ PR interval Norrnal axis Wide QRS complex at 200 ms 'M' pattern in leads I, VL, Vs-Vo 1 .:. o Deep S waves in leads Va, V.5 . Downsloping ST segment in leads I, VL, Vs-Vo . lliphasic or inverted T waves in leacls I, VL Vs-Vo. Itrtr:rprctntiorr

.

l

I !

:

144

Left bundle branch block (renrember that the deep S waves and the ST/f cl'ranges have no'additional sigrrificarrce)

If you neecl to cl'reck, look at pages Sg4land

44.

NUVV IE)I YOURSLLT

ffia

.!

ECG 8 This ECG shows:

,-

. . . . .

-

Broad complex tachycardia at 160/rnin

No P waves visible Left axis QRS duration 200 ms QRS complexes all point clownwards in the chest (NB: lead V1 shows artcfacts)

leacls

^

Inter1trctqtiotr

.

Ventricular.tachycardia

Tlre cliagnosis of tachycarc{ias is coverecl orr pages T4-78. ECG 9 This ECG shows

. . . . .. .

Sinus rhythm Bificl P waves

Normal conducting intervals Normal axis Tall R wave in lead V, and deep S wave in lead V, Small (septal) Q wave in leads I, VL, Vs-Vu o Inverted T waves in leads l,VL, Vs-Vr,

Interpretatiort

o Left htrial and left ventricrrlnr hypertrophy If yotr needed help with this one,

rc'-reac-l F)ages 90 ancl 93.

ECG TO This ECG shows:

o Sinus rhythm o Normal conducting intervals

. . .

o

Normal dtrs Q wave in lead

V.,

Raised ST segments in leads I,VL, Vz-Vs Norn'ral T waves

I45

l\UW lLJl

_

I\JUlr..rLt-l

I

Interpretatiott . Acute anterolateral rnyocardial You must have got this one right

-

the ECC is easy!

i I

I

I46

\

I

€

{.

i

I

L rt.

lndex

i;'

-

Note: Page nunrtrers in itnlics refcr to figtrres arrcl tables on ilrose pages. Accelern ted irlioverrtricu

la

r rlrythrn

61,63

Bilateral bundle branch block 36

Acute infarction 100-1, 100 Anterior infarction 95-6 Anterolateral infarction 98-9

Bltrck

atrioventricular 31, 68 bifascicular 48,48,4g bundle branch i6-4], ZS, 76, Zz bilateral 36 lett 36-7, 39, 39, 40, 40, 41, 44,

Arrhythmia reminders 1flf6 sinirs 54,55 treatment 86-7

113

Atrial escape rhythm Sg, Sg ' Atrial extrasystole 6!7 Atrial fibrillation 7&9, Zg, 80, I lS Atrial flutter 69-73,68, 115 with 2:l block 69,G9,7t)

right 36,37-9, 37, 39, 41, 42_3, 49,49,113 and T wave 106 fascicular; li:ft anterior 46, 47

with carotid sinus pressure 7l,Tz Atrial hypertroplry+ left 89-911,90 right tlg, tlg Atrial tachycardia 674, 67 Atrioventricular block 31, 68 Atrioventricular (AV) node ?-3, 3, 7,29

conduction problems 3G-5 Axis carrliac 1L18, M, 4G, 42,'fiL-lz

deviation left 16, 46,46

right 14,lS,

4z,

normal 74,15,47

Rifascictrlar block 4f1,48, 113

gl

heart block 3G-5 first degree 30-1, 112 second degree 2:1 32,33

3:l

3l-3, ll}-73

32

third degree (conrplete)

33_S,

6'1,713 6,

hemiblock, left anterior 46 Bradycardias 58{12

llundle, accessory 8l Bundle brancl'r block 36-52 bilateral 36 left 3G7,394'/.,, 39, 40, 44 right 3G7, 37-9, 37, 35, 41, 4Z-3 and left axis deviation 48,49 and T wave 10(r

147

lr\ul:A

llurrdle of l-lis 3,3,6 conduction problcnrs and AV

'i

supraventricular bffi, 66, lls vcrrtricular (A4, 65, 6G,ll1

node 30-5

Cirlibration, ECG recorder 11,-lZ Cardiac axis 1L18,1,4,1.5, LG,'17, M, 46, 47,111-12 Carotid sinus pressure 72,T2 Cornplete (third degree) heart block 33-5,61 Conduction problem s 29-52, J0,

ll,Ll3

irr AV node and His brrndle 30--5 bu nc{lc brancl'res 36-152

Delta wave 82 Depolarization 2, 13, 73, 14, Zg-3[,,

l0Z

108

Differential diagnosis of ECG

llCG recorder 7-12,

1 1

0-1

1

12-lead &l9, 9, 10, 1,'1, 24-5, 26-7 ca libra tiort'1,1-12, 72

interpreting 23 rcporting 22

wavc, 108 llrr hairdt'd au

tonr.rticity 84

liscaPc rhytlrnt 5tl{r2, 115 atrial 59,59

I48

first degree 30-1, 31.,112 second degree 3l-3,32,33, ll2-13 with atrial flutter (f,68, 69, Gg causes of 33 Mobitz typeZQl;32,31 Wenckebach 3tiEZ, eS 2:1 32,33

611-2, 6'1,

atrial left g9-90, 90,117 riglrt 89,89, 118

vcrrfiicular left 93-5, 93,717 and T wave 106

ldioverrtricular rhythrn 63 lnfarction, site 116 I nferior infarction 9{7, 96 tlcvelopntcnt of 1A4-5

antl T wave 103

62

llxcrcisc and ischacrnia 102, l3xtrasystoles 62-6 atrial 62-4

junctional 62,63,&

61,61,113 Hemiblock, left anterior 46,46

lsclracnria ant{ exercise 102,102

611,60

r

third degree (complete) 33-5,34,

riglrt 91-3,97,92,177

tinres and speeds t7, 5, 6 Iictopic beat 62 Iilcctrolyte abnormalities arld T

lrr

3l,llz

lleart block 30-5

Hypertrophy 89-93, 1 17-18

changcs 118-19

vcn tricu

ventricular 80 First degree l'reart block 30-1,

3:1 32

36,45

Digoxin (digitalis), and T wave

itrnctiorral

Firscicles of lc'ft bundle branclr 44,45 Fibrillation atrial 78-9,79,80

I0l

,

fcd

it:+- jli+*.

..'..i.'

.L

ry LearlT ii" Left Left Left Left

r' l.

'

4*nrai

Chqo.L

irz' 3r.-t,;, f{ R abnormalities 90-9

39, 40,44

slrape 1,2-22, 13, 1 9, 20 in V leacls 1U22,2'l

wirlcrrirrg

Myocardinl lrtfnrction 9.1-10{, 116

: '1 . \ ,,

R

anterior95-6

tall

-

j

3(r

21

\

11

Rc.-entry 82 tachycarclia 83 RernirtcL'rs tl0-19

anterolateral9S-9 inferior gG7,gG duvelopnrent of 103

4 53-87,87

Repolarization

Rhytlrm

\

'

abnormal 114 treatment of 86-7 accelerated idioventricular escape 58-62 atrial 59,59

bitid

gg

!

UGaa eg

height

lt

Facemaker 85

Itricandial effusion

I

I

100 r ; interval6-7,6,30

pmlonged short

82

30

r:

junctional 60,60 ventricular 60-2, intrinsic 54-7

,j

sinus

,f '*,

,

.P

r

g

-;4-

53,il,73

1 76

ventrictrlar 56,57,57 Right axis cleviation 14, '15,9'l Right bundle branch block 36,37-9, 37, 38, 47,42-3,49-9, 49, 49 and left axis deviatiorr 49

):

-

GU; |f-v -\\Ag

' I

f,,, O f^a---zf,

q

19 ., 33i

S wave 4,

Pre-excitation 82

\

Second degree heart block 31-3,32,

Premature contraction 62 Pulmonary embolis m 9?-3, 117 Purkinje fibres 3,

2:,1

-

32,33

with atrinl flr.rttcr 68-9,

:i.

6t1,69

causes of 33

Q wave 4

Mobitz type

septal 19,9A

Wenckebach

2

31,32, 33

31,32,33

I49

I :

f^.,

Yn
.-

-+\^z

61, 62

supra.,,entricnlar 5G7, 56

s\i"f e

:,

6'1, 63

with lcft bunclle lrranch bkrck

\z+r,"\

llericarditis PR

i

on T plsl.rrlrnrenorr 65

l( wave 4,

acute 9G7, 96, 700-1, 100

abnormalities 89-90

-

fit

definition 3-,1,112 duration 5,7

bundle branch block 36-7,

Mitral str-rrosis 8J Mobitz tyWZ phenomenon 31,32,33

i

t

QRS complex 4

axis deviation 16,39

39-ll,

reI = Alrr'-l Srt., INDEX

l.'. ., t'

'.

Q waves, origirr 94-7,95

anterior iiscicular block 4$,47 anterior hemiblock 46, 45 "

,\

f$GB--(

I

{'e,1\

t^,

Ca

"l""cI,J,n

SX

r'1 hr

1'l

tt

trl-

-a

rr

o-11, r

-l

e(,q

flI ry -.

-

\

iL_=(

=-

\\ \ H 4")L1', -/

)\ \r\'J

-

*

'D' x/"' p a (/_n

-