How to read the ECG — Part 2

How to read the E C G - Part 2

B. Feneck and F. Duncan

In this article we shall consider the effect that alterations in conduction and rhythm have on the ECG, and the changes that are seen in patients with myocardial ischaemia and infarction. Finally, we shall consider the effect of a number of other conditions on the ECG, and the value of the E C G in patients undergoing anaesthesia and surgery.

Arrhythmias

• Conduction blocks: electrical activity originates in the SA node but conduction is unexpectedly slowed or blocked altogether. • Pre-excitation syndromes: electrical activity is conducted via an abnormal pathway that effectively bypasses the normal pathway.

Arrhythmia means the absence of normal sinus rhythm. I The abnormality can be a disturbance of the rate, regularity, site of origin or conduction of the ~lectrical impulse in the heart. Arrhythmia detection is one of the most important aspects of electrocardiography, and no other test performs the task of arrhythmia detection as well as the ECG. Many factors may be involved in the generation of an arrhythmia, including myocardial hypoxia or ischaemia, activation or inhibition of the autonomic nervous system, neuro-endocrine disorders, anaesthetic and antiarrhythmic drugs, and abnormal biochemical or physiological states. Arrhythmias are mostly caused by abnormalities of automaticity or conductivity or bothY The further classification of the causes of arrhythmia are complex, but for the purposes of this article, we shall consider there to be four types of arrhythmia:

Arrhythmias of sinus origin The (SA) node normally fires 60-100 times/min. Rates occuring outside these limits are defined as sinus bradycardia and tachycardia, although clearly these supposed abnormalites are commonplace. However, extremes of sinus rate at rest may have pathologic significance. Sinus arrhythmia is a slightly irregular sinus rhythm in which the heart speeds up in inspiration and slows down in expiration. It is normal in children and young adults. The SA node is the fastest pacemaker and therefore normally drives the heart. Sinus arrest may occur if the SA node fails; usually, other pacemaker cells take over. These other pacemakers which are normally overridden by the SA node may be affected by a number of factors, including the autonomic nervous system. Under normal conditions, atrial pacemaker tissue can depolarize at 60-75 beats/min, atrioventricular junctional pacemakers at 40-60 beats/min and ventricular pacemakers 30-45 beats/min. If none of these other endogenous pacemakers takes over then the result will be asystole (Fig. 1). Fortunately the most common occurrence is for the junctional pacemaker cells to discharge leading to a junctional

• Arrhythmias of sinus origin: electrical activity follows the usual conduction pathway but it is either irregular or has an abnormal rate • Ectopic rhythms: electrical activity originates somewhere other than the SA node. This origin may be atrial, junctional or ventricular.

Dr B. Feneck,FRCA,ConsultantAnaesthetist,F. Duncan,FFARCSI, Research Fellow, The London Chest Hospital, Bonnet Road, Bethnal Green, LondonE2 9JX, UK Current Anaesthesia arm Critical Care (1995) 6, 29-40

© Pearson Professional Ltd 1995

29

30

CURRENTANAESTHESIAAND CRITICALCARE

escape rhythm (Fig. 2). Normal atrial depolarization does not occur, and sometimes there is no p wave, or the p wave is shown conducted retrogradely as the wave of depolarization spreads from the AV node to the SA node (Fig. 3). The retrograde p wave can occur before, during or after the QRS complex depending on the timing of atrial and ventricular depolarization. If they occur simultaneously the p wave may be completely obscured by the QRS complex. One variant of sinus arrest is sinoatrial block, or sinus exit block. The SA node discharges but further transmission of the impulse into the atrial tissue is blocked. Depolarization of the SA node produces no effect on the ECG, and so both sinus arrest and sinus exit block produce the same silent picture. However, whereas sinus arrest will usually produce either an escape beat or ventricular standstill, sinoatrial block is often incomplete and will therefore usually produce a pause equivalent to 2 or more cardiac cycles, depending on the frequency of the block (Fig. 4). The abnormal SA nodal activity referred to above is a manifestation of the sick sinus syndrome. Episodes of

~'~.~

tachycardia, often atrial flutter or fibrillation, are often seen as well as episodes of bradycardia; hence the name 'brady-tachy' syndrome. The important issue here is a therapeutic one, as drug treatment of atrial flutter or fibrillation will usually inhibit SA nodal activity and make complete SA node arrest more likely. The appropriate treatment is a cardiac pacemaker, preferably with an atrial or sequential system.

Ectopic rhythms Ectopic rhythms usually occur as a result of enhanced automaticity or re-entry. We have been above how failure of the SA node may produce an escape rhythm. However, under abnormal conditions pacemakers other than the SA node may become accelerated until they take over as the source of electrical activity, not in response to SA node failure but as a pathologic defect. The disorder may be said to be one of impulse formation, with normal transmission thereafter. The electrophysiological conditions for re-entry may be complex, but essentially it relies on an impulse being

;', ~ !', , -~ L;I ; : I ~ ' ~ T ~ 7

~

~

,'~'~'g~-,, , ~ ' ~

Fig. 1 - - Sinus arrest with no escape rhythm causing a period of asystole.

l:i!ldi!if!ii[li!';tt!:i !l~!;;lt:ii t~i i!i :,',! i:ii ~,~i iii~;~:iliiliti~iil i4 : 4! ~/it~ i, 'f~ ~:!i ii!:1 ~,!~i::i ]~i ; i~ ~:i ~ii ~1 ~:~!: ; 4 '~ Ii:I :i i i

Fig. 2 --

Sinus arrest with a junctional escape beat.

...............

. . . . . . . . . . . . .

.- ¢ ..............

2..

I...... I.................... ~! ...... .......... !...........

'I

............ .................

-

I

Fig. 3 --

: ........ i

...............

.

~

i

'

"

~ . . . .[ . . . . . . . .

..... i

Junctional escape rhythm with a shortened PR interval and retrogradely conducted p

waves,

~ ! - ~ : ~ . , ! ~ I ~ t ~

i~......

i

~ ~,

!~! i~t.. :i

~T~:~ :~i~: !:!~i!

:i :!.~[7:

F i g . 4 - - Second degree sino-atrial block. P waves and QRS complexes are dropped. The pause is equal to t w o R-P intervals.

:~

i

HOW TO READ THE ECG - PART 2 conducted to a circuit in which there is a unidirectional conduction b l o c k ? The i m p u l s e is then conducted in a circular fashion and is seen to re-enter the conduction pathway (Fig. 5). Interruption of the circus pathway would terminate the arrhythmia. The original concept of circus re-entry due to an anatomical block has b e e n expanded to include c o n d u c t i o n block due to variability in refractoriness or other m o r e complex mechanisms. However, the result is that the impulse m a y be conducted rapidly in a circus fashion, re-entering the conducting circuit instead of being conducted n o r m a l l y through it. As the impulse spins in this re-entry loop, waves of depolarization m a y be sent out in all directions which m a y overide the sinus m e c h a n i s m and drive the heart. Sustained supraventricutar ectopic rhythms are a c o m m o n and important group of arrhythmias, and it is important to be able to diagnose them accurately. They can be differentiated b y asking the four questions described in Table 1. Ectopic arrhythmias m a y vary from sustained arrhythmias to single beat ectopics. Supraventricular ectopics are usually either atrial Or junctional in origin. Atrial ectopics are best identified by the timing of the beat and the contour of the p wave. The beat occurs earlier than normal, as identified by comparison of the R - R interval. Also the contour of the p wave is different from normal, reflecting the altered pattern of depolarization within the atria. Junctional ectopic beats resemble j u n c t i o n a l escape beats, but the important difference lies in the timing. Escape beats occur after a lengthy pause, which m a y signify failure of the SA n o d e or at least a sufficiently slow SA nodal rate such that the A V pacemaker tissue takes over as the source of depolarization. On the other hand j u n c t i o n a l ectopics occur early, and in comparison the R-R interval is shorter than normal. Paroxysmal supraventricular tachycardia (PSVT) is a regular arrhythmia, but its start m a y be irregular as it ' w a r m s up'. It m a y occur in normal hearts, associated with exhaustion, excitement, caffeine or alcohol. The m e c h a n i s m is a re-entry circuit at the A V node, hence the alternative n a m e of atrioventricular re-entry tachycardia

Table 1 - - Factors identifying supraventricutar tachyarrhthmias P a r o x y s m a l S u p r a v e n t r i e u l a r tachycardia (PSVT)

p waves ? - rarely seen. Maybe seen retrogradely conducted in lead I1 are the QRS complexes normal? yes; unless there is aberrant ventricular conduction due to transient right bundle branch block relationship between p waves and QRS complexes? - if p waves are seen, 1:1 regular or irregular? - absolutely regular. Rate between 150-250 beats/min. Atrial Flutter

p waves? - yes, but abnormal. Often seen as sawtooth flutter waves. Best seen

in lead II or III. Rate 250-300/rain. are the QRS complexes normal? yes relationship between the p waves and the QRS complexes? - may be 2:1, 3:1, 4:1. regular or irregular? regular, except where block is variable and it may change e.g. from 2:1 to 3:1. Rate usually Atrial Fibrillation.

p waves? no. Baseline may undulate slightly as f waves. Rate 500/rain are the QRS complexes normal? usually. If they are wide and slow then there is AF with total AV block and a ventricular escape rhythm. relationship between p waves and QRS complexes? - -

no

regular or irregular? - irregularly irregular due to inconstant re-entry mechanism Multifoeal atrial tachycardia.

p waves? - yes, but no uniform appearance as several foci may be responsible are the QRS complexes normal? - yes relationship between p waves and QRS complexes? - yes, 1:1 regular or irregular? - inegular. Rate variable, usually 100-200/min. (Fig. 6). It m a y be abolished or slowed by vagal stimulation (i.e. carotid sinus massage) or b y drugs i n c l u d i n g verapamil or adenosine (Fig. 7). Atrial flutter is also susceptible to carotid sinus massage and adenosine, which induces a b r i e f total A V block (Fig. 8). The m e c h a n i s m is a single constant re-entry circuit. A l t h o u g h atrial flutter is easy to detect w h e n there is a 3:1 or 4:1 block, it m a y be difficult to differentiate b e t w e e n atrial flutter with 2:1 block and P S V T i i

A

l

i:K

B

•i-!!~ ix.i

il

iE!i

il rl •:;ill;..

I.ll.il':;.

:

~i~

. . . . . .

;~.!.i.~. ,,,:

!,.i..i

~:~r i:i;iii

. . . .

:i;.ll..:.i:| 4!.. ;

In the top panel (1), conduction passes normally via channels A and B. In the lower panel (2), antegrade conduction at B is slowed and retrograde conduction into the loop occurs, causing re-entry. Fig, 5 --

31

L :i

i. i : l i

:

.!2_ i _,_.=;l;': !~'i;

-i- :!i ! : ~?:

F i g . 6 - - Paroxysmal supraventricular tachycardia. Leads shown are V1, V3, V6.

32

CURRENTANAESTHESIAAND CRITICALCARE

..........................

" ..........

:~::: :.~ff~

.............................

'--r'-

:

.............

I ''

'~

'~

~

......... ~....

Fig. 7 - - T h e e f f e c t o f a d e n o s i n e o n A V n o d a l r e - e n t r y t a c h y c a r d i a . followed by a period of slowed conduction with AV block.

', ....................

~ ...........

Four ventricular

.....

:

extrasystoles

•

are

i !llii:lil!iiiil, i lliii11!',!iiii!lll liii!'i }l!iiUll ii'ii'

Fig. 8 - - T h e e f f e c t o f a d e n o s i n e o n a t r i a l f l u t t e r . C o m p l e t e p e r i o d o f A V b l o c k is u s u a l l y s h o r t - l i v e d .

(Fig. 9). Although it can occur in normals, atrial flutter is more usually found in patients with cardiac disease. A re-entry circuit may also be responsible for atrial fibrillation. However it is not a single constant circuit but a constantly changing and chaotic re-entry pattern. Atrial fibrillation is probably the most common stable an'hythmia and is frequently seen in patients with either cardiac or pulmonary disease (Fig. 10). It is often treated with cardiac glycosides which produce their own characteris-

AV block reveals flutter waves.

The

tic ECG effects. Occasionally patients with atrial fibrillation show evidence of complete AV block, which may also be a consequence of overdose with digoxin. Here the QRS complexes may be wide and slow in rate, suggesting an idioventricular escape rhythm (Fig. 1 l). Single ventricular ectopic beats (also called premature ventricular contractions or PVCs) occur commonly in normal individuals and have no significance. However, frequent PVCs (more than 5/rain), a run of three or more

-H+ff.H.H-{-H4H+t+H+H.i-H-L, ' ' ' ' ' ~' ' • , . ,',m , , T. .m , , ~, .m , , ,T, r, t T ] ,. I I ~~: I I I i i I ~~i ~i FFH+½'H:FFH'FFgFFT~:|:IT-FT-FFFFFfTF] II

"~1111

II

II

[I

III

I ~1 I I II

Ill

11 [ II

I I IIIIlt

III

IIII

I [ ill

Ilil

I

I

"tIH'H+H-I+ttH4+H-H~H+|.I-I..H-HIH+H-FH.

I

IFFHH-H-H~'I'H-t

~ |,~ ,~, ~ } ~ |

~ [~ r, n,

~ ! ~! ~ ~ , i ~ - ~ ! ' : ' ~ ' i "~'~ v ' ~ " '''' "' , ~ v u ~ - . . ~ - ~ + . ~ ~' ., m' .................. ::::;:::::~;ml ,~÷:, i~" 1 ~ ~ 1 ¢ 1 ~ ':::":':':'::': . . . . . . . . :::::::::::::::::::::::::::::::::::::::::::::: • ~tm " ' I ; HI't .......................................... • .. -H . . . . . . . . . . . . . . . . . . . . . :;IHIH=H H H:';IH;HHIHHIHHIflIt~ " ~ . . . . . . . . . . +H-H.ft +H+H+~t+t+H4+FH+FH.fH 1t ;' 1' 1; I ,' ': :' : 1' I' : l ' ' I I ~1' 111; ; 111 ', ', ~ 1,~,,~, 1~; 1~1~1t 4 . H + H + ~ H , ~ .............. .... ~I~I~|~,r

[ : ; : : : : . . . . . . . . . . . . . . . .

.....

~L~,,

. . . ~ ~ ', ~ ~ ~l~ ~ ', ', ', ', : ~ ~,,,H ~. .~ .', .~. ',. ',. ~. |. ~. .', .~. ~. :. ',. ~. ',,~

+~t ................................... ~.~.~.~,..,,,,,,.~.~.~ ............ ::::::::::::::::::::::

Fig. 9 - - A t r i a l f l u t t e r . T h e c l a s s i c ' s a w t o o t h '

. . . . . .

[[~

II~H

'

'' ........ . I~ . . . . . . :::, [1 ::':~H:t~,, ~.~ ~[J .

appearance.

~ ~ t l ,~, ,.v~ .,-~, i i ~ ..t .~,T~, i,7 i~,~i .!,-,-~,+: ~t ~,..+'~'?'i?~"'~","~'~**~'°"~rlrrm"?~+"m"*": ! ~ ! . ~ ~ ~ t ~ : t

~t'ff'tt' fllt'btlff"ll-t

•

4,

~'

...

~ - ~ , ~4...... . 1i .L.I...L[LL

Fig. 1 0 - - C l a s s i c ' n e w '

atrial fibrillation.

Note the rapid ventricular

~4..t.~J..~..L~.~.,,t.4

~-.I

response.

N~NN~ Fig. 11 - - A t r i a l with complete

fibrillation AV block.

showing

'f' waves.

The slow regular

ventricular

escape

rhythm

suggests

AF

HOW TO READ THE ECG - PART 2 33 consecutive PVCs (technically a burst of ventricular tachycardia), multifocal or multiform PVCs or a PVC whose R wave falls on the T wave of the preceeding beat are all potentially dangerous and need to be treated (Fig. 12 & 13). As we have seen earlier, a depolarization originating in the ventricle will be conducted abnormally throughout the ventricles. A p wave is rarely seen. On occasion the p wave may be conducted retrogradely, and in conditions of transient AV block, a normal p wave is seen followed by a pause and then a wide QRS complex. The shape of the QRS complex confirms that, whatever atrial activity is seen, ventricular depolarization is occuring as a result of an impulse originating from within the ventricle and not conducted from above. Multiform PVCs have a changing shape, reflecting the fact that there may be a number of ectopic foci within the ventricles. This may rapidly progress to ventricular tachycardia, and should be treated urgently, as should the R on T phenomenon which may precipitate ventricular tachycardia or fibrillation. It has been suggested that the mechanism of ventricular arrhythmia due to R on T may be due to a re-entry circuit within the ventricles) Sustained ventricular tachyarrhythmias are life-threatening. Ventricular fibrillation is a pre-terminal arrhythmia requiring resuscitation and defibrillation. However, ventricular tachycardia (VT) may be more subtle. It may be difficult to differentiate between ventricular and supraventricular tachycardia, and it would be quite wrong to assume that simply because the patient is concious or still has an acceptable cardiac output that the arrhythmia must be supraventricular. However, a ventricular tachycardia with evidence of an adequate cardiac output is not benign, and in addition the treatment for ventricular and supraventricular tachycardia may be

markedly different. It is therefore important to distinguish between the two. Usually, one may assume that a broad QRS complex tachycardia is ventricular and a narrow complex tachycardia is supraventricular. However, if a supraventricular complex is aberrantly conducted through the ventricles a broad complex tachycardia may result. The mechanism is simple; the atrial rate is so fast that the ventricle is bombarded with impulses before it has time to fully repolarize in preparation for the next impulse. This may particularly affect the right bundle, and the resulting complex resembles a tachycardia with right bundle branch block. As we shall see, left or right bundle branch block produces a wide QRS complex, and therefore a broad complex tachycardia which is supraventricular in origin may be formed. How do we distinguish the two? It may be difficult, but there are a few clues. Firstly, carotid massage may slow or terminate an SVT but will have no effect on VT. Secondly, approximately 75% of cases of VT are accompanied by AV dissociation, resulting in sporadic venous cannon waves which may be visible. The ECG may show p waves with an independent rate and no relationship between the p waves and the QRS complexes, whereas in PSVT there are either no p waves visible or they may be retrogradely conducted. Also, VT is usually irregular, whereas PSVT is regular after a 'start up' period. In PSVT aberrancy, the initial deflection of the QRS complex is usually in the direction of the normally conducted beat, whereas in VT the initial deflection of the QRS complex is in the opposite direction. Finally, in ventricular tachycardia one may see a fusion or capture beat - resulting from a supraventricular beat that has managed to pass through the AV node to produce a QRS that is part supraventricular and part ventricular in appearance (Fig. 14).

+iH::i: -:': ~ l-414.. 4-I..~

Fig.

12 --

M u l t i f o r m or multifocal ventricular extrasystoles.

1 3 - - The R on T p h e n o m e n o n . A ventricular extrasystole occuring on the T w a v e of the preceeding beat initiates ventricular fibrillation. Fig.

34

CURRENTANAESTHESIAAND CRITICALCARE

Despite these differences it may be hard to differentiate between VT and SVT with aberancy. In the acute setting the diagnosis may be made in retrospect by the response to drug treatment. In the chronic setting, His bundle electrocardiography may be helpful, but further discussion is beyond the scope of this article. Not all ventricular arrhythmias are fast. As we have seen, when there is no other electrical source available to act as the stimulus for depolarization, ventricular pacemaker tissue may serve to initiate ventricular depolarization. A ventricular escape rhythm occurs, usually at 30-45 beats/rain. In certain circumstances, such as following acute myocardial infarction (MI) an accelerated idioveventricular rhythm may develop, with a rate of 50-100 beats/rain. This is rarely sustained, does not progress to ventricular fibrillation and is therefore usually considered a benign arrhythmia.

degree or third-degree (complete). In first degree block, there is a delay as impulses are held up at or near the A V node but they always penetrate the node to depolarize the ventricles. There are p waves present, the QRS complex is of normal width, the relationship between the p waves and the QRS complexes is 1:1 and the rhythm is regular. The only abnormality is the delay in conduction. As we saw earlier, the P-R interval includes the time for both atrial depolarization and for conduction delay at the A V node, so we would expect the PR interval to be increased in first degree block. It is - to greater than 200 ms (Fig. 15). The second degree block, not every impulse is conducted through the A V node. The relationship between the p waves and the QRS complexes is more than 1:1. Second degree block is divided into two types. Mobitz type 1 (also known as Wenkebach) block is seen as a progressive lengthening of the P-R interval as the conduction delay at the A V node is increasing until finally the conduction block is complete for one beat, and we see a p wave with no ensuing QRS complex (Fig. 16). There are p waves and the QRS complexes are of normal width, but the relationship between the p waves and the QRS complexes is not 1:1. Often it is 4:3; that is, after every 4th p wave there is no QRS complex. This may make the rhythm regularly irregular. The progressive lengthening of the P-R interval and the dropped QRS complex is the key to the diagnosis. Mobitz type I block occurs high in the A V node. It is now clear that Mobitz

Conduction block Conduction block can occur at the following sites: SA node - as we saw, SA node exit block is indistinguishable from sinus arrest. A V node - this now includes blocks that occur below the SA node. • Bundle branch block - this refers to conduction block in one or more bundle branches. A V block is described as either first degree, second

rr-

;;:}, • i

.ii

:i.1:i' ::-:)1

•Ei

!i

i.=}X"

:i ~.+:i ........ 77i: ii:! ............

• L.~'t

..=k LI,~

7]7 ~i.!~

i~4: ); i:J!:i:~L7 77;

i;il

! : 777 :!:f

: ti:

:i~" ........

..I,,.I..

..i.Lii .:..L .

•., .~.i; !~!~::l,+: J~ill : :~

.

.

.

.

!>~+ +,

: ;'~' ; ; : '~'.i.ii o :~:;~

.,...

t ~ '

:!~i~11 i

......... l+ ii, ,..

;

'i

~"..J3*; .

-.;.:

Y,; L -

:~!;

4 - , I ~..÷I

LI :..;: ~;t;j

i!:,'2.1

7;i;i:l~

::..:i: : c.L;~:: ,=~. . . . . i,~4~,-11,1,1,I : 7 ': '~:~: ...........i~}l........ • "t + ...........

=I

....

Ftt

:.~t:l~:I:~.:l::l.icl~cH;t471.~!ij~:l:t::,::l.i:~:~:l::~:i:,:~:l:tl:~:~:~: I ~ i:i::.:!!: .'H:?i ,-t]~:i} ~ll :~!:.~:I:~:?#11141~lgllil~ltllgil~lll?,;iJ4

"" '" '+~! ' ' . . . . . . •.

'. . . . . :

~:.~

I~~

,::~" :i:

.

-~

........ ll-'~,{ .h'~= I~::~ .........

.

.

~

.

~,.... .....

t...,,.~.~.+

:' ...........

]..i..

!!~;~ iii~iii~: '~i=: ~ :~ ~,'....... .~i ::i-7777l:: ~,ll~"~' ;,' .iili .1];: ::::: "~ +*+='*'+-

-~"t'i-i't't t I

t]++

#v++,

Fig. 14 - - (a) It a p p e a r s t h a t t h e r e is a p w a v e p r e c e e d i n g each Q R S c o m p l e x in lead II (top trace)• H o w e v e r , s i m u l t a n e o u s r e c o r d i n g of lead III s h o w s this to be artifact. T h e r h y t h m is v e n t r i c u l a r t a c h y c a r d i a , (b) T h e s e v e n t h beat is a f u s i o n or c a p t u r e beat. T h e r h y t h m is v e n t r i c u l a r t a c h y c a r d i a .

~.4,4

HOW TO READ THE ECG - PART 2

,' ' .. :~:~ ' i:~::';:;;; ::::i:~:::: : :':E '~:]::~:' : :~ :: :'~$~:T"" : " ¢

:iJ..Id..~,4.~ :~...

,~ ~H.~..i,.t.i.*~.~.**.~.. .]:~::i::l¢~:~t±:i:~.~:: i~,i;:~:tI::~..i~t¢:t:;:

t ~'M t~:', ~- rt'l'H

;1 "r'~"~'(

First

degree

=='= :=====,= :[ ====;====:~. ,'-;..-'

heart

Mobitz

type

t ........

:. :' .:~:~: :,~ !..

:i:il: "':t:~::~:; :" :~.:i:: .""': ;::::r::: ,' ::*:. "~.......

::::~::': ;: : . . . . . . .

~

"..~:i:. . . .

"~" :: ~k"

J.

i¢:!:~::!f!:

:.

:;4 : [::

'

Fig. 16 --

: . : ::~'~.~::]:::}:'::~',',::z:~T.z."

........ ~...................

block.

4. !,: .. ,~

:T:

: h ,,,,

d...! !:.t..."

i~:.!'[,~:!l~ : , [...!~ ~ , ~ , , ..,,,~,

I:ig. 15 --

..... , ............... ~....................

I or Wenkebach

::;F

block.

type II block occurs below the AV node, in the bundle of His or lower. Not every impulse is conducted to the ventricles, but in contrast to Mobitz type I, conduction is an all-or-none phenomenon, resulting in normal beats followed by a p wave that fails to conduct to the ventricles. The ratio of p waves to QRS complexes is usually constant, often 2:1 or 3:1. The QRS complexes are normal width, but because of the dropped beats the rhythm is regularly irregular (Fig. 17). The differential between Mobitz type I and II is easy if the p:QRS ratio is high, but if it is low (e.g. 2:1) it may be difficult to differentiate, since progressive lengthening of the P-R interval is difficult to see with so few normal beats. The severity of the blocks described above can be classed in ascending sequence; first degree the least important, then Mobitz type I, finally Mobitz type II. This reflects the change of each block progressing to complete or third degree heart block. Third degree heart block results from a lesion at or below the AV node. There are no normally conducted beats. Every atrial depolarization is blocked, and the

ventricles respond by spontaneous depolarization of ventricular pacemaker tissue at 30--45 beats/min - a ventricular escape rhythm. If this were to fail there would be no ventricular depolarization or contraction, and so treatment is essential. Occasionally drug treatment may be successful, and isoprenaline may serve either to speed up the rate of spontaneous ventricular depolarization or to help conduction through the AV node. However, often it serves only to speed up the inherent atrial rate, with no other beneficial effect. The most effective treatment is an external pacemaker. This should also be considered in patients with Mobitz type II block who are at risk of developing third degree block. The diagnosis of third degree block rests on the relationship between the p waves and the QRS complexes. The p waves are unconnected to the QRS complexes and the p:QRS rates are completely different. The QRS complexes are usually wide due to the ventricular escape rhythm which is often quite regular (Figs 18 & 19). Conduction blocks may occur lower down in the conducting system, at the level of the bundle branches. Left or right bundle branch block may occur. However, the

iii iii!iii]iii i!]iiii! iiiiiiii i i i]iii i i ii:iiiii iii iii !ii!i i ]iiiiii Fig. 17 -- Two

:

normal

"7-'rr:~T--r'~:

i

Fig. 18 --

Complete

beats

........

followed

~r ................

~ *!

,

:

•

heart

35

block.

~

QRS

by Mobitz

:,;'t',r~p'-~'~

.

]

!

complexes

type

•

11AV block.

Conduction

is 2 : 1 .

r

F

,

are unusually

~,

~':;itli~it narrow.

P-i.

~i-¢: t t~" i I::, :!-i: r .ix: ~:d:,~'~t!iiitlh It f ~ [ ¢

36

CURRENT

ANAESTHESIA

:::t,-:................./ : t

AND CRITICAL

CARE

.....

::2 ~ : i:ii :~if?]' --:............ :i ~ '

=:=: =/if:

:; ~ : : V ~

.[i3::~ii~S;l: ~:~(i! ~. *~h ' ::. ;

~:Li.L~i::~2.[!.; .Li2~::::r:E :t;:2[

i!

:

i!:i:! ~5

.~F-

!',;'. ::'i

:I:i ~i:~t: ];,:i: !~i!=::::~til:!:~! !:!: ~

'~:

~

1

1

:

l

:

I . i , 1 ,t

t:!!~i!

Fig. 1 9 - - Complete heart block with more typical broad QRS complexes.

left bundle has an anterior and a posterior fascicle. If one of these is blocked as well as the right bundle, atrioventricular conduction may continue but the patient is living on a knife-edge, having only one ventricular conduction system working. Furthermore the diagnosis of left anterior or posterior hemiblock may be quite subtle. In right bundle branch block, the left ventricle may depolarize normally, but the right ventricle has no working conduction system and will therefore depolarize much more slowly. We will still see an R wave representing LV depolarization, but this is followed by a second R wave (an R'wave) as delayed right ventricular depolarization occurs. There are therefore two obvious defects, best seen in the leads that overlie the right ventricle (i.e. V1 or V2): an RSR' pattern, representing a second but delayed spike of depolarization • a wide QRS complex (greater than 120 ms) reflecting the delay in total ventricular depolarization. There is also a deep S wave in the lateral chest leads (Fig. 20). In left bundle branch block, the reverse happens. The right ventricle depolarizes quickly, but the left ventricle depolarizes slowly, producing a prolonged positive deflection in the leads that overlie the left ventricle (the lateral chest leads). The LV contains the main myocardial mass, and so the delayed depolarization is not seen as a second R wave but as a single sustained slow rising R wave. Again, the QRS complex is wide (greater than 120 ms), and because of the prominence of left ventricular depolarizing forces, left axis deviation may be seen (Fig. 21). Repolarization is also affected in bundle branch block, and those leads showing tall R waves will show inverted T waves and ST segment depression in both left or right bundle branch block. Right bundle branch block is often benign, and may occur at fast heart rates during an epi-

sode of PSVT. Left bundle branch block nearly always reflects underlying cardiac disease. The left bundle divides into an anterior and a posterior fascicle thereby ensuring even distribution of depolarizing forces throughout the left ventricle. Either of these fascicles may fail, and the effect may be seen on the ECG. Let us consider left anterior hemiblock. If the anterior fascicle fails, current will be conducted to the posterior surface of the left ventricle by the posterior fascicle, and then depolarize the anterior surface more slowly progressing in an inferior-to-superior, right-to-left direction. The vector of depolarizing forces is shifted leftwards, and we see this as left axis deviation. We should check that there is no other explanation for left axis deviation, such as left ventricular hypertrophy. In left posterior hemiblock, the left ventricle is depolarized by the anterior fascicle, and current flows in a superior-to-inferior, left-to-right direction, thereby shifting the vector of depolarizing forces to the right and causing right axis deviation. In both situations, the QRS complex is normal in width and there are no repolarisation changes in the ST segment or T wave. Left anterior hemiblock is the more common of the two and is frequently benign, in contrast to left posterior hemiblock which always signifies cardiac disease. The significance of either hemiblock is that when they co-exist with right bundle branch block the possibility of developing complete heart block is high. There has been some controversy about which combination block has more potential for danger, 6 but it would appear to be sensible to treat both combinations as potentially dangerous and fit a pacemaker (Fig. 22). It is clear that different conduction blocks may coexist in the same patients. These are often more significant than one block alone. For example, the combination of first degree heart block and left or fight bundle branch

ifttittfff:i:It:: ttfttt::N:tt

F i g . 2 0 - - Right bundle branch block shown in leads I, V1 and V6, There is a deep widened S wave in the lateral leads. The RSR' pattern in V1 is diagnostic.

Left bundle branch block in leads I, Vl and V6. The deep Q wave in V1 is suggestive. The RSR' pattern in the lateral leads is diagnostic. Fig. 21 --

HOW TO READ THE ECG - PART 2 37

.t,, ,, t~,I., ....i, .t,. . .~I.I-,. t~t h t~,l~ .~.h Hti~t ~ ~hHt,.I U.i,~:l.~.+.~ .~.h~, . ~ .I,,. .h. h mt ~ , ....... : tT~+ttl . . . .tt.H].] +

Itiiiliti!t~ill~iitii~.,t!iltltiiitiiilt ftt1,ttl~ ~tttiil~.~4,qtttltttittl

. :~:~i:.~ ~i::~::t:: :~,::':i,~:.~. i~-~

:

~: !~; ~:~,t :L ! !::: !! it: :!.. !:illi!l: i~tll

fI~ti~tt~ tttttttitlI tttt~tttit~-~ttt~if ftttttttttttt I

II

III


AVL

.~ ~-z-!-:.=.~-~.-':-:~7-.'.-"~~-~

~

Iltfittiittltilt!ililtt~IiiIilUttttttftttttl 72

73

tllllllttttftttltttttttt tttttttfl tftlttlittltltttttfit!tttt!ttltti111t1111

l]]tifttitttlttttiitltlttttltlttttltltttttUit Ittttt!l!ttttlittilifttttftltlltttllflitlltlti

IIUIIUIIIIIIIIUIUUIUUUtUIIIIIIII

V4

V5

¢;i!ti

t,fHJi

In WPW, the accessory pathway is called the bundle of Kent. This aberrant conducting pathway connects either the right atrium to the fight ventricle of the left atrium to the left ventricle. There is little or no delay in conduction at the AV node as it is partially bypassed. Therefore the P-R interval is seen as shorter than normal (less than 120 ms). However, ventricular depolarization is initiated by both the accessory pathway and by AV nodal conduction. We would expect to see a QRS complex that appears to start as a deflection a little earlier than normal due to the accesory pathway. This would then blend into and continue as a normal R wave as normal AV nodal conduction continues. The QRS complex is shaped as a delta wave due to the early start to ventricular depolarization and the QRS complex is widened to more than 100 ms. Delta waves are diagnostic of WPW, but they may be not be seen in every lead (Fig. 23). In L G L syndrome the accessory pathway is intranodal. This bypasses the delay at the AV node but does little else. Ventricular conduction, though initiated early, proceeds as normal. Therefore there are no delta waves or widening of the QRS complex, and the only abnormality is a short P-R interval of less than 120 ms. Pre-excitation syndromes, and particularly WPW, may predispose to re-entry tachycardias. The bundle of Kent and the AV node often have different refractory periods, the bundle of Kent usually being the longer of the two. If an atrial ectopic is conducted through the AV node, by the time ventricular conduction is complete the bundle of Kent is no longer refractory and can pass the wave of depolarization back into the atria via the accessory pathway. It can then pass straight to the A V node, generating a perfect re-entry tachycardia, usually PSVT. Atrial fibrillation may be particularly serious in WPW, as the

Ittitt~ttttttitiiiittt~li,itflfttfllttltttttt Iltlftlft!tttt!t~ii';ltttttiiitl|tttttltitlftt

Fig. 22 - - There are 3 conduction What are they?

;l ~I', ! ! ;t I i ~; l !' rff:~ I ~ I ~:i t].i¢I4fttflfl H l.~l:17 I1

AVF

~!,t¢:.;~it~IttfHi't!ilt ~iiPiitiI~ t Vi

........ ' ........~:'-~ .......

Fig. 23 - - W o l f f - P a r k i n s o n - W h i t e syndrome. In this example the accessory pathway conducts intermittently. The first and fourth complex demonstrate delta waves.

lttifi,ttttibia!tilt ~tttttttfP~ II tttttttti~ ~tttttltfltlltlftlli AVR

i:

. .tl':il ~H:: : :l!.~:~{!:: :ft!H:HI: :i~t!

'" '

V6

abnormalities

on this ECG.

block, both relatively trivial in isolation, may progress to complete heart block. This is easily seen early after cardiac surgery since many factors may provoke conduction abnormalities following cardiopulmonary bypass.

Pre-excitation syndromes In contrast to conduction block, some patients suffer from a process whereby depolarization is conducted to the ventricles too quickly. Normally conduction is held up at the AV node, but if the AV node is bypassed by accessory pathways then the ventricles may be stimulated too soon, or 'pre-excited'. Such accessory pathways exist in approximately 1% of the population, usually in men, and may occur in isolation or associated with other cardiac disease. The two main pre-excitation syndromes are the WolffParkinson-White syndrome (WPW) and the LownGanong-Levine (LGL) syndrome.

:ti:tCCt:~,:ill=i:~li~:

i iiihi ¢ :

~+~"~..~, ~I#: i i i i i ~i~¢;.,!.tii~.~ ,~,,. ..... •tHllF.~4.t.ll, ~

....

~..i+lli

+..,-LIt, :i !tti;t:l:t:i

.*..- ~ . . . . ~

:i..~¢~.,...~L~.~~!.:11.~.~.

lt¢ itti

tt[tt4+~t":i: t..[: :I::.:::'L

.41t-;t

-i

rot:7

.I ,+..:.........

i!}ii

Fig. 24 - - W o l f f - P a r k i n s o n W h i t e and atrial fibrillation. N o t e t h e n o r m a l l y c o n d u c t e d beats in the centre of t h e trace and the v e r y fast ventricular re s p o n s e in the r e m a i n d e r .

38

CURRENT ANAESTHESIA AND CRITICAL CARE

Hiiiiir ili llllH llliiiii,,iiil!!lIiH iiiiiiiiiit!iiiiil~q

llllllllllltHllillll lllllllilllllllllllll

iiiiiiiilii!!!!!ttltl

E l l E l l / l l l , J t l l [ , I , I I

IIIIItHIIIIIII,, Fig. 25 - - The changes seen in ischaemia and infarction. Peaked T waves, symmetrical T w a v e inversion, ST s e g m e n t elevation and pathologic Q w a v e f o r m a t i o n .

bundle of Kent may transmit the majority of the atrial impulses (up to 500/minute) to the ventricles (Fig. 24).

Myocardial ischaemia and infarction The ECG changes of myocardial infarction are both well documented and easily recognised. However, they are often simply learnt by pattern-recognition and we should remind ourselves why they occur. The earliest sign of ischaemia is peaking of the T waves (Fig. 25). This occurs within seconds of the onset of ischaemia as has been documented in studies of percutaneous transluminal coronary angioplasty (PTCA). 7 T wave changes are common during ischaemia and infarction, but they also occur in other situations, some non-pathological. One other cause of peaked T waves is hyperkalaemia. However, in ischaemia the T waves are peaked only in areas overlying the ischaemia whereas in hyperkalaemia they are peaked throughout. In subendocardial ischaemia the pattern of repolarization is not disturbed and the T wave is positive in leads with positive R waves. However, in subepicardial ischaemia the pattern of repolarization is reversed and the T wave inverted. ST changes also occur early, but the exact cause for the changes seen is controversial. Ischaemic injury causes the leakage of K + and C1- ions from the affected area, and an electrical imbalance develops at the border of the ischaemic and non-ischaemic area. Thus a current of injury is established, which flows from injured to uninjured tissue during repolarization (electrical diastole) and from uninjured to injured tissue during depolarization (electrical systole). With diastolic currents, the P-Q segment is deflected downwards and the ST segment, though isoelectric, appears elevated compared to the depressed baseline. With systolic currents, the P-Q segment is isoelectric but as the injured area repolarizes more quickly the ST segment is elevated. In patients with subendocardial injury, ST depression occurs in those leads overlying the affected area, whereas ST segment elevation occurs with subepicardial or transmural injury. Subendocardial infarction is also associated with T wave inversion, which may occur as an early change only hours after the onset of injury. An important point is that T wave inversion due to ischaemia or infraction is symmetrical in contrast to the T wave inversion of bundle branch block or ventricutar strain. T wave inver-

sion by itself may only indicate ischaemia and may revert to normal, but where infarction has occured T wave inversion may persist for months. The appearance of pathological Q waves indicates full thickness myocardial infarction, and when these waves appear they are diagnostic. They may appear within hours or days, or sometimes never, but when they appear the ST segment has usually returned to baseline. Pathological Q waves are wide (greater than 40 ms) and are one-third the height of the R wave in the same lead (except aVR). They appear because infarcted tissue does not transmit a wave of depolarization, and therefore the electrode over the affected area records no approaching electrical forces, only forces moving away to depolarize other areas of the myocardium. Thus a deep Q wave deflection is recorded, and the electrical axis may also be shifted. Reciprocal changes including tall R waves may be seen in leads overlying other areas of myocardium. The localisation of an area of ischaemia or infarction is important, since it identifies which coronary arteries are diseased and may need cardiac intervention. The changes described above are localised to groups of leads that view the different areas of the heart. Thus inferior changes are seen in leads I[, III and aVF, anterior changes are seen in leads V1-V4, and lateral changes in aVL, I, V5 and V6. The inferior surface of the heart is supplied chiefly by the right but also by the left coronary arteries via a rich collateral network. The anterior surface is supplied primarily by the left anterior descending (LAD) artery, and the lateral surface by the LAD and circumflex vessels. The interventricular septum is also supplied by tributaries of the LAD. The posterior surface of the heart is supplied by the right coronary artery, which also supplies the SA and AV nodes. As there are no leads directly overlying the posterior surface, posterior infarction is diagnosed by identifying reciprocal changes in the anterior leads. The most specific is a tall R wave in VI, being the opposite of a large Q wave in a posterior lead if one were present, but there must be no right axis deviation, which would otherwise suggest right ventricular hypertrophy. The diagnosis of myocardial infarction neccessitates identifying abnormalities in the width of the QRS complex, and the nature of the ST segment and the T wave. Other conditions may also cause similar ECG abnormalities, but it is generally recognised that the ECG similarities are such that myocardial infarction cannot be reliably

HOWTO READTHE ECG- PART2 39 diagnosed from the ECG in the presence of left bundle branch block.

Other abnormalities As we have seen, electrolyte abnormalities may produce characteristic ECG appearances. Hyperkalaemia causes T waves to peak across the 12 lead ECG; further hyperkataemia causes p wave flattening, P-R interval prolongation, and finally severe widening of the QRS complex. Arrhythmias including ventricular fibrillation may result. In hypokalaemia, ST segment depression and T wave flattening occur. A U wave, a small discrete wave with the same polarity as the T wave and appearing shortly afterwards, may also be seen. The U wave is the most characteristic feature of hypokalaemia, but it is not diagnostic and may have little pathologic significance whatsoever. In hypercalcaemia, the QT interval is shortened, whereas it is prolonged in hypocalcaemia. Prolongation of the QT interval for any reason may predispose to a variant of ventricular tachycardia, called torsade de pointes. Hypothermia may produce general and specific abnormalities. The heart rate slows and J or Osborne waves, a characteristic variant of ST segment elevation, may be seen (Fig. 26). Arrhythmias are common whether the cause of the hypothermia is iatrogenic or the result of accidental exposure. As both impulse formation and conduction are slowed, hypothermia is a perfect setting for ventricular escape rhythm which often ends as ventricular fibrillation. Peficarditis may cause ST segment elevation and T wave flattening. These tend to be diffuse, in contrast to the changes seen in infarction. Furthermore, T wave inversion usually occurs after ST segments have returned to baseline, in contrast to infarction. A large pericardial effusion may produce a low voltage appearance and alterations in electrical axis as the heart rotates within the fluid filled sac. Chronic lung disease may also produce characteristic changes. Chronic airflow limitation leads to gas trapping and hyperinflated lungs, leading to a vertical position of the heart within the thorax and right axis deviation. If right heart failure occurs then right atrial enlargement and right ventricular hypertrophy and strain may be seen. Acute pulmonary embolism may also produce right ventricular strain and right bundle branch block. In addition, the classic 'St Q3 T3' pattern may be seen; that is, an S wave in lead 1 and an inverted T wave in lead III.

H-~+tfHI-N-

NtN NNt Fig. 26 --

~i:,ii:,iiiiii,:fii!,:!!!!!~/,iiii:,~ i i , ? : i i , / / : i i i i i i i : , i L , J wave or Osborne wave.

lililillllllialllllOlllallllll IIlllll|lglillillglillnOOiligl mlmoilllmlimliilllillOililllll ilOnUlmlWlmlmllllUlmllUillllmn linilolmilmnmimlminmmmlilnlill OllUOOlmllmllllllllllllllllmmi IIIIIIIIllllllllllllllllllllll I l l l l l l l l l l l l l l l l l l l l l l l l l l l l l I I I l l l l l l l l l l l l l l l l l l l l l l l l l l l IIlIIIIIIIIIIIIIIIlllIPIlIIIII IllllllllllllllllllllllIVIIIIII I I I l l l l l l l l l l l l l l l l l l l l l l l l l l l I l l l l l l l l l l l l l i / l l l l l l l l l l l l l l IIIIIIIIIIIIIIlillllllllllllll I I I l l l l l l l l l l l l l l l l l l l l l l l l l l l IIIIIIIIIIIIllllllllllllllllllJ Illll IIIIIIlllll Illll Ill IIIIIII lilll Illililllll IIIII gill Illl %,I I lit. IIIIIIIIIIlllqllllllllt~lll iPlllllOllliillll ,' I I I I I | I P %d i l l illltl 11WJIllll • d lilllllll IIIIIIIk Ill Illlllilldllllll Illllllllllllllllllllllllllllll IIIIIIIlllllllllllllllllflllllll lllllllllllllllllllllllllllllll I I I I I I l l l l l l l l l l l l l l l l l l l l l l l l IIIIIIIlllllllllllllllllllllll l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l I l l l l l l l l l l l l l l l l l l l l l l l l l l l l l I l l l l l l l l l l l l l l l l l l l l l l l t l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l

Igg|l|||gg|~ll|||ll|l|g[|||ll| l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l I l l l l l l l l l l l l l l l l l l l l l l l l l l l l l

I

III

Changes o f acute p u l m o n a r y e m b o l i s m - S in lead I, Q w a v e and inverted T w a v e in lead II1.

Fig. 27 --

The Q wave seen in lead III is usually not seen in any other inferior lead, in contrast to patients with inferior myocardial infarction (Fig. 27). Drugs including anti-arrhythmic drugs may cause a number of ECG changes. Therapeutic levels of digoxin cause ST segment depression and T wave inversion and are predictable ECG changes that should be considered normal in patients taking digoxin. However, toxic levels of digoxin may cause first, second or third degree block or tachyarrhythmias. Sometimes these occur in combination, for example paroxysmal atrial tachycardia with 2:1 block, which is a well described consequence of digitalis toxicity. Many other antiarrhythmic drugs have the potential for changing the ECG, either as a result of overdosage or pro-arrhythmic effects. Anaesthetic drugs may also cause ECG changes, usually by an effect on cardiac rhythm or rate. An anticholinergic effect will cause the heart rate to increase; whereas an anticholinesterase effect will potentiate the effects of acetylchotine and thereby reduce the heart rate. Similarly, some volatile anaesthetics and opioids may reduce the rate of SA nodal discharge and cause a bradycardia, which may lead to a sustained or non-sustained arrhythmia at atrial, junctional or ventricular level. Furthermore, halothane (and possibly enflurane but not isoflurane) may make the heart more receptive to the arrhythmogenic effects of catecholamines leading to ventricular arrhythmias.

Anaesthesia and the ECG The ECG should be taken as simply one step in the process of patient evaluation. The presence of a normal ECG does not exclude the possibility of significant cardiac disease. The value of the ECG in identifying patients who are likely to suffer an adverse outcome from anaesthesia and surgery has been reviewed) There is considerable evidence both to support and to refute the observation that the ECG is able to identify factors that predict outcome? Also, scoring systems that use ECG data to assess risk have been developed. 1°,11 In patients undergoing non-cardiac surgery, a routine pre-operative

40

CURRENT ANAESTHESIA AND CRITICAL CARE

Table 2 - - Indications for pre-operative ECG

Chest pain, angina or equivalent Congestive heart failure symptoms History of/or high blood pressure Diabetes History or symptoms of arrhythmia History of shortness of breath History of myocardial infarction Age > 40 males, > 50 females History of smoking Unable to exercise without SOB or chest pain Major surgery, including cardiothoracic, neuro-, vascular. From: Roizen MF, 6th Annual Soc. Ambul. Anesth. 1991

ECG appears to have most value in those patients who have symptoms of cardiac disease or significant risk factors, including age. s32,13 However, overeliance on symptoms particularly in ischaemic heart disease may not be wise, as many patients have ischaemic episodes which are silent. One suggested protocol for ordering a preoperative ECG is shown in Table 2. Recently attention has focused on intraoperative ECG monitoring for myocardial ischaemia. Intraoperative ischaemia may herald perioperative infarction, 14 and infarction or re-infarction carries a significant mortality. 9 Furthermore, pre-operative patterns of ischaemia my be reproduced in the perioperative period, j5 and multilead monitoring systems may be most effective at detecting perioperative ischaemia.16 Given the time course of adverse perioperative events, monitoring in the early postoperative period may also be useful in detecting postoperative ischaemia and infarction. 17 Despite all its limitations the ECG is one of the most effective diagnostic tests we have, whether it be as a pre-operative screen or as an intraoperative and postoperative monitor. Future developments may enhance its value even further, but even the current technology is able to generate

a wealth of information which hopefully this article has been able to identify and explain.

References 1. Krilder D M. Arrhythmia prevails. (Editorial) Anaesthesia 1988; 43:1003-1004 2. Atlee J L, Bosnjek Z J. Mechanisms for cardiac arrhythmias during anesthesia. Anesthesiology 1990; 72:347-374 3 Chung E K. Parasystole. Progress in Cardiovascular Disease 1968; 11:64-81

4. Mines G R. On circulating excitations in heart muscles and their possible relation to tachycardia and fibrillation. Transcripts of the Royal Society of Canada (section IV) 1914:43-52 5. Davis R F. Etiology of perioperative cardiac arrhythmias. In: Kaplan J, ed. Cardiac Anesthesia, 3rd ed. Philadelphia: WB Sannders 1993; 170-209 6. Rooney S M, Goldiner P L, Muss E. Relationship of RBBB and marked left axis deviation to complete heart block during anesthesia. Anesthesiology 1976; 44:64-66 7. Chambers C E, Skeehan T M, Hensley F A. The cardiac catheterization laboratory: Diagnostic and therapeutic proceedures in the adult patient. In: Kaplan J, ed. Cardiac Anesthesia, 3rd ed. Philadelphia: WB Sannders, 1993:42-87 8. Mangano D T. Perioperative cardiac morbidity. Anesthesiology 1990; 72:153-185 9. Mangano D T. Preoperative assessment of cardiac risk. In: Kaplan J, ed. Cardiac Anesthesia, 3rd ed. Philadelphia: WB Saunders, 1990:3-42 10. Goldman L, Caldera D L, Nussbaum S R et al. Multifactorial index of cardiac risk in non-cardiac surgical proceedures. N Engl J Med 1977; 297:845-850 11. Didolkar M S, Moore R H, Takita H. Evaluation of risk in pulmonary resection for bronchogenic carcinoma. Am J Surg 1974; 127:700-703 12. Mulcahy D, Fox K. Therapeutic implications of ischaemia in the ambulatory setting. Progress in Cardiovascular Disease 1992; 34:413-420 13. Katz R L, Bigger J T Jnr. Cardiac arthythmias during anesthesia and operation. Anesthesiology 1970; 33:193-211 14. Slogoff S, Keats A S. Does perioperative myocardial ischemia lead to postoperative myocardial infarction? Anesthesiology 1985; 62:107-115 15. Knight A A, Hollenberg M, London M Jet al. Perioperative myocardial ischemia: Importance of the preoperative ischemic pattern. Anesthesiology 1988; 68:681-689 16. London M J, Hollenberg M, Wong M Get al. Intraoperative myocardial ischemia; localization by continuous 12 lead electrocardiography. Anesthesiology 1988; 69:232-241 17. Rao T L, Jacobs K H, E1-Etr A A. Reinfarction following anesthesia in patients with myocardial infarction. Anesthesiology 1983; 59:499-518