ECG Dr Osama Mahmoud

(1)

(2)

ECG

Cardiac cycle. Basic cardiac cycle (P-QRS-T) repeats itself again and again.

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BASIC ECG COBPLEX

EeGpaper. ECG paper is a graphic divided into millimeter squares. 'lime IS

measured on the horizontal axis. Each small millimeter box equals 0.04 sec, and each larger (5 mm) box equals 0.2 sec with a paper speed of 25 mm/ sec. the

amplitude of any wave is measured on the vertical axis in millimeters.

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Measurement of tbe.P-R interval.

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Positive and Negative Complexes. P Wave Here Is Positive (Upright), and T Wave Is Negative (Downwards). QRS Complex Is Biphasic (Partly Positive, Partly Negative) S-T Segment Is Isoelectric (Neither Positive nor Negative) rf

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P wave represents atrial depolanzation. P-R mterval represents time from initial stimulation of atria to initial stimulation of ventricles. QRS represents ventricular depolarization .S-T segment, T wave, and U wave are produced by ventricular repolarization,

(3)

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Characteristics of normal S-T segment &T

wave .. J junction, marks beginning ofS-T

segment.

S-T segments. Top, normal S- T segment.

middle, abnormal

s..

T elevation. Bottom.

abnormal S-T depression.

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Standardization mark. Before taking an ECG, the machine must be calibrated so that thli standardization mark, A, is 10 mm tall. Electrocardiographs can also be set at one- half

standardization, B, or 2 times standardization, c.

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Multiple chest leads give a three- dimensional VIew at cardiac electrical acnvity.

Sample ECG mounted for interpretation showing 12 standard leads.

(5)

NORMAL CHEST LEAD PATTERNS

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Normally, the R wave in chest leads becomes relatively taller from lead VI to len chest leads.

A,

Normal

R

wave progression with transition zone in lead V3

B.

Somewhat delayed R wave progression with transition zone in lead V5. ('. Early transition woe in lead \ ' These ,II"( II normal variants.

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_-Pattern of QRS in limb leads

The normal pattern (the complex illboth I, AVF) =normal axis

RIGHT AXIS DEVIATION _{LEFT AXIS DEVIATION}

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III

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Right axis deviation (RAD)-mean QRS axis more positive than

+

lOO°--ean be deter-.

mined by simple inspection of leads I, II, and III. With RAD, lead III will show an R wave taller than the R wave in lead II.

Left axis deviation (LAD), mean QRS axis more negative than -30°, can also be determined by simple inspection of leads I, II, and 111 With LAD, lead 11 will show an rS complex, with the S wave of greater amplitude than the r wave.

II

RIGHT AXIS DEV IATION

III oVa oVl

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Example of right axis deviation. Note R waves illleads II and III, with the R

wave in lead III greater than that illlead II.

LEFT AXIS DEVIATION

Example ofleft axis deviation. Note rs complex illlead II.

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P wave measurements. Normal P

wave is less than 2.5 mrn tall and less than 0.12 sec wide.

Tall narrow P wave indicate nght atrial enlargement

( P pulmoale pattern).

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Note tall P waves. best seen here in leads II,ill,aVF, and V1. in patient with nght atrial enlarqernant (P pulmonale).

LEFT ATR 1

AL ENLARGEMENT

(AB;-~OKMALITY)

P Mitrale Biphasic P waV$ in lead V1

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Left atrial enlargement may produce.

A. wide, humped P waves Inone or

more extremity leads (P mltrale

partern) and j or, B, Wide, bipnasrc P

WCives in lead V1.

A B

Example of broad, humped P waves In

pauent

with left

atuat

enlargement

(P rnitrale

pattern)

6

(8)

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Example of wide, biphasrc (initially positive. then negative) P wave in case of left atrial enlargement.

RIGHT VENTRlCULAR

HYPERTROPHY

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Note tall R wave in lead V1 (with inverted T wave caused by right ventricular strain).Also note right axis deviation (R wave in lead III taller

than R wave in lead II). Patient had tetralogy of Fallot.

(9)

RIGHT VENTRICULAR

HYPERTROPHY

".

RV

strain

Sometimes with RVH lead V1 shows tall R wave as part of qR

complex.

Note peaked P waves (leads II, III, and

V1)

because of right atrial

enlargement. Also note prolonged

P-R interval (O.24 sec),

indicating

first-degree

AV block.

(10)

LEFT VENTRICULAR

HYPERTROPHY

II III

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Patient with severe hypertension with left ventricular

hypertrophy

with

strain pattern. Note tall voltage in chest leads, with strain pattern in leads I,

aVL, and V4, to V6. Also note tall voltage in lead aVL, (R

=

16 mrn), In

addition, note pattern of left atrial enlargement,

with biphasic P wave in lead

VI and broad, notched P wave in lead II (P mitrale).

(11)

+

Questions.

1. Answer these questions about the following E&G

a) What

IS

the approximate heart rate?

b) Is sinus rhythm present?

c) Where is the transition zone in the chest leads?

d) Cite three signs of LVH.

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(12)

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2. In the following ECC:

a. What is the heart rate?

b. Name two abnormal findings.

II

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Answers:

1. a) About 100 beats/min.

b) No. Notice retrograde

P waves, positive in lead aVR and negative in

lead II, owing to AV junctional rhythm.

c) Around lead V4.

d) Tall voltage in chest leads (SVl

+

RV6> 35 mm); tall voltage in

lead aVL. (R wave> 13 mm); left ventricular strain pattern in leads

I, aVL, V5, and V6.

2. a) About 75 beats/min.

b) The P-R interval is prolonged (about 0.22 sec) because of

first-degree AV block. Also, the P wave in lead II is abnormally wide and

notched (notice the two humps) as a result of left atrial enlargement.

(13)

ECG SEQUENCE WITH ANTERIOR WALL INFARCTION

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Sequential QRS and ST-T changes seen wit'" anterior wall infarction Note reciprocal ST-T changes in inferior leads (11111.and AVF).

A. Acute phase' S-T elevations and new Q waves.

B. Evolving phase: deep T wave

inversions.

C. Resolving phase.

ECGSEQUENCE WITH INFERIOR WALl INFARCTION '" "'I,

A Acute phase S· T elevations and new Q waves

B Evolving phase. deep Twave mversions C Resolving phase ~ _~

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Sequential QRS and 5T -T changes with infenor wall infarction Note reciprocal ST-T changes in antenor leads.

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S-T segment elevations seen with acute infarction may have variable shapes, as shown in

A

to

D.

(14)

A

'B

Chest leads from patient with acute anterior wall infarction. A, Note tall positive T waves (hyperacute T waves) seen in leads V2 to V5 in earliest phase of infarction. B, Recorded several hours later, shows marked S-T segment elevation in same leads (current of injury pattern) with abnormal Q waves in leads V1 and V2.

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Hyperacute T waves with anterior wall infarction, Patient was complaining of severe chest pain. Note very tall, hyperacute T waves in chest leads. There is also slight S-T segment elevation in lead aVF with reciprocal S-T depressions in leads II, III, and aVF. Note premature atrial contraction (PAC) in lead V4.

(15)

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Anterior wall infarction. Note

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complexes in leads V1 and V2 indicating anteroseptal infarction. Also note characteristic notching (arrow, V2) of QS complex often seen with infarcts. In addition, ECG shows diffuse rscherruc T wave inversions in leads I, aV1, and V3 toV5. indicating generalized anterior wall ischemia.

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Evolving anterior wall infarction. Patient sustained anterior wall infarct 1 week earlier. Note abnormal Qwaves (leads I, aV1, and V2, to V5) with

slight S-T segment elevations and deep Twave inversions. Left axis deviation resulting from left anterior hemi block is present as well.

(16)

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,-_.-t.--::-.t-.r-:tc:;;r..±d-=t==-Evolving anterior wall infarction. Infarct occurred I week earlier. Note poo.·

R wave progression in leads VI to V5along wjth Q waves IIIleads I and a V I.

T waves are slightly inverted in these leads. Right axis deviation 111this case IS

the result ofloss of lateral wall forces, with

(J

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Posterior

infarction.

Note tall R waves in VI and V2. In addition there IS

evidence of prior inferior Ml (Q waves 111 II, Ill. a VF) and probably lateral

infarction (T wave inversions 111 V4 to V6).

IS

i

(17)

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Old inferior wall infarct. Note pronuncnt Q waves ill lonl-. II. II/, ami <1\ j. 1:',11I

patient with infarct I vear previouslv. ST-T chanaes have t"'l'llll;llh rev crt cd 10

uurmal.

Subendocardial infarction. Patient with severe che ••, pam who subsequently developed cardiac enzyme elevations. 1\01(' marked S-T depressions best seen III chest

Il'ads \'2 to \ S. Pa nern ., consistent with subendocardial infarction. NOlI.' premature ventricular conrractiou (1'\ C) in I"',ld I. SlighIreciprocal S-T elevation is seen in le.id

a\'R and lead III.

(18)

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---Subendocardial infarction (ant. wall):

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• T wave is inverted in I, aVL, V2~

V6 •

• S-T segment depressed in V3, V4

subendocardial

• Finding V2~V6.

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(19)

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• Elevated S·T segment is V2, V3. V4-~ transmural.

• Finding in V2, V4, V5= anterior wall

mfarction

• Segment elevated>

recent.

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(20)

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Antero-lateral

infarction

with

left

aXIS deviation:

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.,'"'r'

0J--, I ..l ..' _

I

v

• QS Pattern in VI ~ V5 transmural infarction.

• Elevated

SoT

segment In V3, V4=anterior

wall.

• Finding m VI, V5, I, and avL =anterior wall infarction.

!:fJ 'r'I'"I,. ,.'

:!!: ''''~1!;: (':: '!

, t , I I " ill;

;p. ::;; :;:

'I" ~ ~

l

I

i

: I: :,;:

:':l.-+i: ' ...:.._." .:

:~~:~

~2~,~~

~~I~A

., r I'j 1 ~. .: • ::.r: .::::,:.1.,.:': ':"

t

i-

I (~;

i .-',

~:~:~::~....~!!;..~:

r .' '. ';': , Wi ::1: .. .; "I::; ..•... ;."r" .. :

'j'

~:-t: ut. ;tr :.l;t

:d:;:

·11~... :~ ••.1':· .~.: !

I

II

.;;

19

i

,

, "

.

~

-..

.'

--:

... I I ... ....

_-,--I

T-I I-i

i

-- f" I 't ..,.,,-'

(21)

l-r-·--'. I

!

I.· I. t j " I I

, r-\

]

r

J

I ...: ~!!;. ; I

~~~~

r"":'~ ~ •.,

;~'f':

.,

'j' .."]'

...• [1:,"i'

tlr

ft::! _ :..

II

~"

Notice leads II, ITI, aVL =infenor leads

Elevated

S·T

segment ::.recent transmural inferior wall

infarction

J I

1

.J

(22)

I,

-

",

";; Ii!; , , I

~~!

r"":"

;a'f' :

t •., ""

'1'

j' :- r-4. .rt-:' l-~ --; ,

rEr-

I::;:

I . l. _

II

~"

Notice leads II, ITI, a VL <infenor leads

Elevated S-T segrnenr

>

recent transmural inferior wall infarction

Development of

inferior

infarction

1,1'-1-11"

I

I '

I ' I

,"!

I

,

, I - • I '

-~

! -1 __

j

" "

,--j!

t

-:

-;-,

l I

, . J

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--r----, I

!

I 1_ - I , ! I i

I

1

20

(23)

I

~

Questions:

1. Answer the following questions about

the

ECG below:

a) What is approximate heart rate?

b) Are there any 5- T segment elevations?

c) Are there any abnormal

Q

waves?

d) What is the diagnosis?

.

(24)

2. Answer the following questions about the ECG below: a) Is sinus rhythm present?

b) What is the approximate mean QRS axis?

c) Is the R wave progression In the chest leads normal? d) Are the T waves normal?

e) What is the diagnosis?

I

\

3. With an acute anterior wall infarction. the 5 -T segments In leads II.

m.

and aVF are likely to be

4. Persistent 5- T segment elevations several weeks or more after an infarct may be a sIgn of... . .

5.

A patient with severe chest pain shows per-sistent diffuse 5- T segment depressions with abnormal elevations of the ccrdrcc enzymes The most likely diagnosis is:

a) Prinzmetal's angina. b) Subendocardial infarction c) Hyperacute infarction. d) Angina pectoris.

6. What ECG abnormality is shown and what symptom might this patient have complaining about?

v.

: t

(25)

7.

I I ! ;"11 ' . I

+

Answers:

1. a) 100 beats/min.

b) Yes. Leads II, III,

and aVF (with reciprocal S-

T

depressions in leads

V2 to

V4, I, and aVl).

c) Yes. Best seen in leads

m

and aVF.

d) Acute inferior wall infarction.

2. a) Yes. Positive P wave in leads II, negative in lead aVR.

b) About +90°. (Between 80° and 90° is acceptable.)

c) No.

d) No. Note inverted

T

waves in leads V2 to V6, I, and aVl.

e) (Evolving)anterior wall infarction.

3. Reciprocally depressed.

4. Ventricular aneurysm.

5. b.

6. Marked S- T segment depressions. Patient ha9 severe ischemic

chest pain

and had a subendocardial infarct.

7. Yes. There is evidence of anterior wall infarction with loss of

R

wave

progression in chest leads. There is also evidence of inferior wall

infarction with large Q waves in leads III

and

aVF.

Also note tall R

wave in lead aVl. (14 mm) with strain pattern

in leads I and aVL.

Patient had prior history of hypertension, producing left ventricular

hypertrophy.

(26)

EFFECTS OF HYPERKALEMIA ON ECG

Normal 4 mEq/L 7 mEq/L p IJ mEq/l 10 mEq/t

t

Ii

ts

mfql

L

~LA.

12 mfq/l

Earliest change with Hyperkalaemia IS peaking ("tentmg" I of T wave. With

progressive increases lD serum potassium (K+). there ISWidening of()RS

complex. loss of P waves. and. finally, ventricular fibrtllauon I hese changes do not necessarily occur with a specific serum K+ level. fur l'\.tlUple .•• unit" panents

may have a normal E.<(J with a K+ of 7 mEq/L. othe •.••111..1\ devetop ventrrcular

fibrillanon at 9 mEq/1.. II III

I

I \ I

Note peaked T waves. Wide QRS complex, and prolonged P-R mterval. At other times, junctional rhythm IS present with no P

(27)

HYPOKALEMIA

I _II _III

oVa oVI

_oV

_f

I

i:!l ..': !I" :!:: ",

!!;I ':11 "II 'JII

:11' I, ,.

,',' " ,

'I"

Ii

1:1 I" I'll

':11:1:: I::: ".1 "I .."I' i\:1 " '

,I ~' !

:::1

III' "I 1 ; : ~ I!: \11: II: I_I "'1 I' 1::\ >,,1 I" ,I _'

..

:1.

:ji

:;" : 11:::11

I

i

~!!

;ilj I::i il!i

" , .. ₁₁₁₁I .• ,

1111;:1:'!II i'il:' II~;;;1

:!

:::: :lj: :111:" _I: " :'1: I'" ,

,

,II. "I I .• I" T: 1 t:i~

c~~ttn~

"! ",I

I

\:1\ ;1 ,I

il!!

I ,I" I!r ;ii'ili I .. , ", " _{I !I} _I",pill

II

_:ill

'" II:~j 11

I

I: ', " " ,I _:1 ,.. " 'I" '\ I' , , ~~ ',;'\" " ~. ~" .: I ", 1 In ,

::::~

nn

I:;:

rm

,,!::1:, _,1;1

!Il!

:i

l

\, II: Ii;: I_

I

\.. " _{!1 :} I

I::::

,'" _,j"! ~'" :

I:' !:i'

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::!'Ifl:1

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1

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,

;~.,ill

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i:!

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I •• I :;11,;i;'I',

:

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,I

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il

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l.

• _I ,'I !:II! ~.: ~~I I 'I" t 11 .l.l"',1,1, , .I •..•I" "

I

" ,', I" .. , _I jr.

'I:

11 " " I '11'1

I

1;:1 :" ill ! I II:I::: :

~:!

.:1: :1,: T,

~H

!I:: I

!

I~

,.1:Ii!,

:::,

I" iii

Y

1)1, _Iii;

_:::!

_li:!lIil

~"," _: "I ttr, ',,1 "I 1 : .:

~!:

j :, : ••• . •I _I :' '

'.

II, J • , I '. "IJ 1 "

..

" ,

I

V,

': :!:I ii:

Ij'!i i

," •• I 'I I

V,

'1""1" ~I

'fflii

II II ,'~ 'I ~~ IU

~*

Mn

l,: :, ~' , I: I I

tn

~Ijl , ':I:

".

"'1,1,,, rm !'mIl '/'J, '1111

':;11;"1

11

HnI:'II':,I,1

friH

II

'I

i

I 111,

I I

!I:

:IIWI

:1/, F I

~1:IIJ~1t;

I, III ,!III,

I, I' :::11

1:' II 1;, ,:. :" ,:1 .. ; ,', '1,111 '1'1'1 y.

I!

~ I. I I I' m T ,U

Normal T wov. Serum K+ was 2.2 mEq/L. Notice

prominent U waves.

Nonspecific ST· T chong os

\1

Flattening of the T wave (left and middle) or slight T wave inversion (right) are abnormal but relatively nonspecific changes that may be caused by numerous

factors.

IS

(28)

-J II III oV oil,

"j"'"-; -' ..••

~-.Jr-

r

4

'.

!

i

I

1

I

".

I 1 I ; .

J

t --y--y-~

~~~r-J.

:.r ,/"";,-

·..J,,--~.Jr·

• •• : I

t;

l-

1; ~

I ~!. ' r

".

I •

:Jc+,Al.

, ,

J

I . " !

I

."7""r:--r- ----,-'--,- __".;

~~i-;-II \~lt lIft-.• ...' lIft-.••. lIft-.•. of ~ • 1 , L.

Nonspecific Sl·T changes Note drrtuse I wavefldll~ rung

Subendocardial Digitalis effect Ischemia

.Jftlt~

uu

It It

Hyperkalaemla I I ,

··u·

Acute Infarct ,.,

Relatively specific ST-T changes. ST -T changes depicted are relatlnly but not absolutel) specific for abnormahnes show n.

(29)

Calculation of heart rate

Measurement of heart rarefbeats per minute)by counting number ofiarge(0.2 secjrime boxes between two successive QRS complexes and dividing 300 by this number. In this

example, heart rate is 300"'3 = 100 beats Imin.

I

Measurement of heart rate per minute by counting number of cardiac cycles in a 6 sec interval and multiplying by 10. in this example, there are 10 cardiac cycles/6 sec.

therefore, heart rate is lOx 10= 100 beats/mill .

•

.

~~ _0·' _•

Measurement ofQ -T interval. p. R interval is interval between two consecutive QRS complexes.

(l.,

D~

l.

o.•..l

Abnormal Q·T prolongation. Note that Q·T interval (0.6 sec) exceeds one- half the R-R interval (1/2 xO.92=O.46sec.).

(30)

1.

Calculate the heart rate in each of the examples

2.

Name the major abnormality IFI each example.

A II

3. A block in the AV node IS most likely t.:

a. Prolong the P·R .nterv .11

b. Prolong the QRS width c. Prolong the Q·I interval.

d. None ot

the above.

4. A block in the left or rIght oundle branch IS most likely to

a Prolong tr« t f..' .nterv.u b. Prolong tne ~k~ width

c. Shorten the V- I intervat.

d. None ot the above

(31)

5 Name the component waves of the QRS complexes shown. 1

i

I

A B c o

ll1-~'

1:!:

,. ,'

_J

i

.

:

I

ANSWERS:

1. a, 50 beats/ nun. b.I50 bears/nun. c. 60 beats/ min.

d. Approximately 160 beats/min (There cW' 10<..!RS vcle ...in o '1.'1.: )***

2. a.Abnormallv wide QRS complex (0 14V" ,

b Abnormally long P·R tnl('fval (approx»: j~fl\ e "'. I

( Abnormally iongQ-l IIIt·I val

«.Ff

.nur v». .;'< .I:,till'~ U·1 'C:l. l'w fI I,'

Interval measures 06 sec dod the heart fall' I.'>!U\J'!JL: d 4, b S. a. R b.QRS L.QS

D.RSR

e.QR

t-*** Notice the IrregularIty of the QRS complexes and the absence of

Pwaves. The rhythm here IS ctrrcl frbrttlcnon.

(32)

NORMAL SINUS Rh 1fHM

II

I

Each QRS complex is preo it'd by a P

wave that is negative in lead aVR ano positive in lead II

\' 1 \

Sinus tachycardia.

Sinus bradycardia.

(33)

Phasic sinus arrnythrrua Norrnatly melt:: i::'sugnr increase in he an rate witt

inspirauon ana ::'JJgI.lldecrease Will. .xpuauon.

Nonphasic sinus arrhythmia. Monitor lead shows markedly Irregular rhythm Each QRS complex ISpreceded by P wave with constant P-R interval. Marked nonphasic smus arrhythmia in this case resulted from viral mvocardms IT waves are blpl1d::.1. LD

this tracing j

Sinus pause in panent WIth "sick smus syndrome" Monitor lead shows marked sinus bradycardia with long sinus pause Patient had sinus node disease and required a

pacemaker

Junctionaj escape beat. Monitor StrIP shows SInUSpause WIth runcnonal escape beat.

(34)

Premature ventricular contraction, PVC, PVC is recognized because it comes ht'lUIC

the nex~ normal beat is expected and has a wide, aberrant shdpe (Als» note lung I'R

inrcrval in the normal ,l!1US beats indicating firstdegree r\ V block

A

1'"'I+;t7:

f ~t-;'~'F:~

B

PVC\ ,,)mp,llt:'d I~)PACs Note wide, J.bt'iLIl11 S~.iPt' IIIfl\'1.

A \

»rnpared II'

l1<ifl\)\\ PAl

B

Premature ventricular contraction

Note that the same PVC (marked X) 1l:'~OJlkJ

(35)

Monitor lead

.

,

t

FVCs. Two PVCs (marked V)10a row a.c called "paired Pv'Cs "

I've,

hn," r, )W "R on Til phenomenon.

PAROXYSMAL

ATRIAL TACHYCARDIA

(PATj

PAT is a run of three or more consecutive PACs. ThJS stnp shows F:\T wul: . ~::' of about 167 beats/rum. Note marked regula my of rhythm. No P w.r.:-. ,1:1.' \~:>:h\t"

PAROXYSMAL

ATRIAL TACHYCARDlt\

PAT with rate of about 200 be ,us ,r ; .,'

PAT

u

Carotid Sinus massage

Paroxysma! ·1tna;l.iChvuuJJ.l: !'Xi, ':t',ti','" with C:ll,,~;d '.,111\1', PUSq,},l' I'h\' tlr~l 14 bedls In ih:', rhvthrn ~,t:-1P"lhY"'- }:"T wuh r,Ht' of about J50 beats. mill

Carotid 'lnt'" mJ)~ag~ :c':ultt'J Hlabr upt terrr.mauon of the tachycardi., with

,I

ppearan,c or 1'1,'(':'1.\1xinus rhdhr.l

(36)

I

r+.

PAROXYSMAL VENTRlCULAR TACHYCARDIA j1'\ 1'\\1;'\PH~H

n.';

lilt ;i!i\iiF Y1Q ul!BuHiW}

'1t,l.in

:It: 'to' ,:1,Li:!EI

:,~;'!lii ; !i'l',\

"PHI!'1i ~

lii!,!' 'l1\lUltiJ It lfii 'i1}R!! I!h,'l!ll jUo'

, ;1:Ilil 'Ii I X '1

,Tfl1 ,"

!~~lJ\1ll111,~

ll~i j,11:1.'; '" :1 ill,' ~'~, I I"

l:I!!T":'

l;

:w

l~

'!I;ltRmf,.,~::

:if;:~

t~

f

:M'm

,I

I!'I ' lit'· ,.~ffTj j'l '1, ':.' ,: : • olj 1 ~I I ' ill' 1;' I I 'I II II' 1:111 j' I' 1'1il r:1 'I'

1'1 ,;

II I ' j 4':. !flt I' t':· H

:iI, '":f:t.,, !1 It! fin11I'd 11;Jf I; "01 l; n II:

"'I'~

,!.II 11

;',:; .:,; :!l1'If

iii.

'q

It '111'1t li1J

f

n!ll1tH~

j' I! Wf tid H JJ

:':: ,:,: ;:J','w;.,. :1'., il,l' 11:HI' I,~ .

'tin

t r

·

'illJ mmj. t, jj:I. i,li. 1i i'::i~1l:.;: '\' I J"

I'i,."

'r~!

p

:: ~fi.i

I ,: . , 1.1

l'

I,: '!Ir:' "

I,!;! IV! ,I, !, !i' ·i" ,f

~g

un •

:~: i;!'"I ; ,: ' 'n I' '" ,I " td'1 f

f

lli! 11 , Ij

r..: [\" r:Ijill"j'll ; l:TitllI , II ~

n

,1(\\\11jti. J'

,'" •.• 1 II. ""11 WIH 1 IIJ It ,Ill '1i1"'JlI, J 1

#j

!'lili...

I'g' pi tf,'!J"1 . "

I,' :,'

I •• ,,~ . ifr 'I ' •• I It ' Ii'Ii!!i, :,

II

11: ::: ' • • , : f· H: I 'J.:. : " ,,"j'f: : i J}L,i;~. I! ~ , t I " :'1 1 'it

1'!

1 , '[ . 'I J. IiI,f .ii,' . f l' 1 : t I '1;, • l

.nmtl1Hllll

1 ,

Monitor lead shows bursts of ventricular tachycardia.

VENTRlCULAR TACHYCARDIA TERMINATED RY DC SHOCK

A

I

\ I \

I

\ I 11 \ '~ t i T , , 1

I

,I

j , " , I I" : 1 :

..

1 'ii,

i:~'

it I ' t B

'd

II

A. Long run of ventricular tachycardia. B, Normal SInUSrhythm restored after

DC shock (cardioversion).

II

Ventricular tachycardia terminated by thump on chest (thump version)

54

rf ,•.•...

(37)

Atrial flutter with variable ventricular rate.

55

't

••

(38)

ATRIAL FIBKlLLA I

iUN

II

' ••1••••• 1..1,1.., IlJldllb:hUl of1,.•,,·1,," 11~·\.11l'.' of hili,II,I."

...• ~ .1 •• ' \, llill' .il.If VB •.•· \lc' I· ."'''':111.11

Note irregular undulation of basel me because ot fibnllau» v waves (t wa ves). 'then' ,1ft>

no rrue P waves. Veruncular (Qj{~) Jdll' I:> '/1('gU(,H

RAPID

ATR I

AI. FIBRIL! /\

rf( 1:\J

Note coarse flbnl I atorv WilV'?S and rapid ventruula: !"\~Jl!li\' !',,;:Cl: n.a1 hyper

thyrordism. (The commonly used term "rapui atnar nbnltauon" ISactually d mISO,HIWI

"mel' the word "rapid refers to [he veruncular rate, not lhe .u:;,J! (.ilt' Ih« \dllle IS{rut'

tor the term "slow atrial fibnll.iu.«. I

ATRIAl FIBRILLATIoN

Fibnllatory waves may be hard to find with rapid atrial tibnllation. A la, tlycardia

ISpresent WIth ventncular rate of about 140 beatsImin (14 R wave cycles 0sec) The

ventricular fate is irregular. No P waves are seen. The rhvrhrn here IS atrIal tibnllauor.

alrhc ...•f.h no :'kar tibnll.Hi::, '""<1\0 "iI. Pt .\ i, .11 lni;, 1,lll

(39)

ATRIAL FIBRILLATION , _: "

..

, ,

.

: II

.

t

\'I'r~ iln·).:1I1.lIvrutriculur r,lll' is pn'\I'II{ ~IIdl'ar I' wa\I" ,liT \t'I'II 1111\th'lI Ill'rl',

a, ill Fi!: )1·Ii, i, alrbl fiJ,rillatioli with rapid \('lItn('lIlar ral ••

Very irregular ventricular rate is present. No clear P waves are seen. Rhythm here IS

atrial fibrillation with rapid ventricular rate,

VENTRICULAR

TACHYCARDiA

- '- -, ...~---,j-.----1- - '-1

1 11'1'-r\'

-i'-\-+-++'\

't"l-t-f-t-'

j'"

..-'- .-f- u .- --

i

-'1.

-'1,

,-1'1 ' .~-

i ,J, --" r-j---"

·\·-t~

-'-'--

•

--h~'

w' ,-''-~

' (-A!."

tl -~_\.

I-Wd' ,--

tf!'ff-

, I' II -~-- \- :.: .; ..

i ';'..

,'.'."

""ir--\"+-

;'" '--,

L '. . '--,',,' r~- -) - .. - -!.,,' _.. -- ' ' 'T '. ' .. -" _. \.

_...- ~l\,

,iJ ...

J

\--I'r-+9"·

-l'I!-\

\.1

t''',-l'

---,

~-

...-.., -,--I'-I-lt

fL, ." \

t

I

.jji ,I

, , , ,i Iii i " ' __I I I I i.

Ventricular tachycardia is, by definition, three Or more consecutive PVCs, ECG shows. two short bursts of ventricular tachycardia.

,--, -" .•'_'0 ., r'. "'''-'

I .: : r:i: .. ,' .•. , .. i:':

::<

\jH \i;; 1~;1iL' ~j!l ~~;l !,. I: ;;j I I' .._.

'\ ; ~;! '''' :'" ;! d. 1!H~IPn~!I1~;~jill ;;~~1::1 .t )i.t.: :'1 :q! '.L< .~:

A "':,,,::,;:

,I!' ~ ',::, :,:: ,;,: :::: ','

,i" ~,~;

lliL:~

:li:;;:; ,::,

!~ ~ :;: ,::' ,;::

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

::: ,iI:I;':TIl, :!!i!,!~ilL ... If! HI: !!:i till iI

,n

:~l 1:'1 liiH aii

;,iJ

:!!f ii!i ilii i4:~;ii!11i!tliIi'!

:i'j 1:,::!:I,!rlnil ,:Hlii!:1ii ;'1:,,!!!!;::m iI· il!·iii !pi lliH!IJIII

iii'

n

IIiii '!lllHiHii1

ili'

ill! ."',,:

B

'i;; 'it.m~ii~'l .,

In,

m:

ill

ii!' 1

::11iFI!iI!

mil

II !>;;1iU t!i :' , " :!l!iul li'l I

...

I I

1lli" '.

f . .. I

Ventricular premature contractions.

A,

Ventricular bigeminy. Each normal sinus beat is followed

by

a premature ventricular contraction (marked X).

B,

Ventricular trigeminy. A premature ventricular contraction occurs after every two sinus beats.

(40)

[=tJ

I I I j j I \ I ,

I

i

i i i

!

, I ! i I i

FULLY COMPEN~AlUKY PAUSl: f i '\ ~~C. 'I r

t

1,! I

: . 'i·1Ili'; II

r-H

r . ': Ii IIi:I ! i·

, ,,~I, \P:!~'; p "p 1"'1.

"' .•••_r "\~ ["I;'t'!"~",:~_'

_v,

_,'Ii' _{,,;:t ~,} .i"!'-"':'_~_I:_W; : •••••_{I' .,}

,it,_':V l.' Ill'_111' I ,_.

t"

I I I 'II' ;

'J

.. :i':- I·· , I, I ' IfL- I I ...• " ~ r

_.

II 1,-1, 520msec

Some Pv'Cs cause a tully compensator" pause sucn I.tldl the uuervai between the

vwo sinus beats that surround the PVC (}{} anu R4 HIuus "'d~t')!:> exactly two urnes

the normal interval between sinus bC,HS :Rl and R2 In trus Case) Nonce that the P waves come on nme,except that the third P \.'v.lyt·l~ Hlll'Il'-l~lcuby IIIl'P\C and

therefore does not conduct normally through rhe A V-iuncuon Tile next (!l-urth) P

wave also comes on tune The fact thai ine SIIlU) ll11dt' l\J:H:t;un 1,\: p,Kt: uvspue the

PVC: results 10 the lullv rornperisa« lTV prtlJ:>e

MULTIFt,)( At. PVl.._'

II

PVCs here have different shapes In same lead, Imlll<iUllg uuuu tUt <11ongin

S8

't I

I

I I

i

I

! i I I I \

,

! I ;

!

, !

(41)

VENTRICULAR FIBRILLATION (VF)

1 1

Ventricular fibrillation may produce coarse waves or fme waves. Immediate defibrillation should be perfcrmed

B

FIRST-DEGREE AV BLOCK

,:1..

A

First-degree A V block, P-R interval is uniformly prolonged above 0.2 sec WIth each beat.

A

and

B

are from different patients.

WENCKEBACH (MOBITZ TYPE I) SECOND-DEGREE AVBLOCK

I

P

I

With Wenck:ebach block, P-R int val lengthens progressively with successive beats until one P wave

is

not conducted at all, Cycle then repeats Itself.

(42)

WENCKEBACH tMOBITZ TYPE 1)SECOND-Uh.d<U AV BLOCK

'·R '·R P

'·i

P·I P P·I P·R P P·R P·R P P·I

Notice nrogressive mcrease in P-R interval, with tlurd P wave Ineach sequerv-: nor followed by QRS complex, Wenckebach block produces charac tenstically irregular

rhythm with grouping of QRS C01l11' ,.,',

MOBITZ TYPe 11Sr.CONU·D.l:.1 .KEI \ V iH.Ul:K

W •.th Mobitz type II Av block there is a series ot nun .unducted I' waves tollowed

by a P wave that ts conducted In this diagrammatn example .~! t.,I block

I'

present

wrth three P waves tOI each VI{:> .;"n:;'IO

Complete heart block IScharacterized by independent atrial (P)and ventncular

(QRS) activity. The atrial rate IS always faster than the ventr n ular rate The P-R

intervals are completely variable. Some P waves tall on the T wave. distorung the shape ofthe T wave Other P waves may fall in the (JR2. ,-UIlIP,l\ .1nJmay he "lust"

Note that QRS complexes are normal Width, mdicaung that the ventricles are being paced trom the A V junction

THIRD-DEGREE (COMPLETE) AV tiLUL K

Another example ot complete heart block. showuu; slow .druvenu ',1.11 invthrn

and taster. uidependent dlfldi ihvthm

(43)

't

RIGHT BUNDLE BRAN('}T

nT

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Example ofRBBB. Note wide rSR complex in lead VI and qRS complex III lead

V6.Inverted T waves in right precordial leads (VI to V3) are common with RBBB and are called "secondary T wave Inversion, "

LEFT BUNDLE BRANCH BLCk

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Example of LBBB. Note characteristic wide QS complex III lead VI and wide R wave 10

lead V6 with slight notching at the peak. Note inverted T waves 10leads V5 toV6, which

are also characteristic ofLBBB (secondary T wave inversions).

r ;.,

41

(44)

BeG appendix

II

AVjunctional beats

II

aVR

_II

A

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.

c

This Fig.: A V junotional beats produce retrograde P waves that are

upright in lead aVR and negative in lead II, just opposite of pattern seen

with sinus rhythm. The junctional P wave may precede the QRS complex

A; follow the QRS complex. B; or occur simultaneously with the QRS

complex, in which case no P wave will lie visible. C

To summarize, AV junctional heats can be (recognized

on the ECG by one of the following three patterns:

1. Retrograde P waves (positive in lead aVR, negative

in lead II) preceding the QRS complex.

2. Retrograde P waves following the QRS complex.

3. Absent P waves, so that the baseline between QRS

complexes is fiat.

(45)

HOW TO INTERPRET AN EeG

In Parts I and II we described the-fundamentals of the normal ECGandlht'

major abnormal patterns and arrhythmias. Part III is a collection of test questions to help you review these topics. We will conclude Part II wuh J lJi'LI

summary of how to systematically approach any ECG.

ECG INTERPRETATIGN

Accurate interpretation of ECGs requires, above all, rltoroughness andc.u , Therefore, it is essential to develop a systematic method of reading ECGs I lid ,~

applied in every case. There are 13 points that should be analyzed m every

EeL;

Standardization:

Make sure the electrocardiograph has been properly calibrated so that the standardization mark is 10 mm tall (1 mv

=

10 mm).

xx

In special cases. the ECG may be intentionally recorded at

1/2

standardization

(1 mv

=

5 mm) or 2x standardization

(1 mv

=

20 mm)

Heart rate:

Calculate the heart rate. If the rate is faster than 100 beats/min, a tachycardia is present. A rate slower than 60 beats/min means a bradycardia IS

present.

Rhythm:

Decide whether normal sinus rhythm (NSR) is present or whether some arrhythmia is present.

P-R interval:

The normal P-R interval (measured from the beginning of the P wave to the beginning of the QRS complex) is 0.12 to 0.2 second. A consistently prolonged P-R interval means first-degree AV block is present. A short P-R interval (with wide QRS

complex

and delta wave) is seen with the

Wol((-Parkinson-White syndrome. A short PR interval with a normal width QRS may

represent Lawn-Ganong-Levine type pre excitation.

P

wave size:

Normally, the P wave is less than 2.5 mm tall and 3 rnm wide in all leads. Tall peaked P waves are a sign of right atrial enlargement (P pulmonale). Wide P waves are seen with left atrial abnormality.

QRS width:

Normally, the QRS width is 0.1 sec or less in all leads.

Q-T interval:

A prolonged Q-T interval may be a clue to electrolyte disturbances (hypocalcaemia, hypokalemia), drug effects (quinidine, procainamide), or

myocardial isrhernia. Shortened Q-T intervals are seen with hypercalcemia and digitalis effect.

QRS voltage:

Look for signs of left or right ventricular hypertrophy. Remember that thin-chested people and young adults frequently show tall voltage without left ventricular hypertrophy. Do not forget about low voltage which may result from pericardial effusion, Myxoedema, emphysema, obesity, or myocardial disease.

(46)

Mean QRS electrical axis:

Estimate the mean

QRS

axis in the frontal plane. Decide by mspecnon whether the axis IS normal (between -30° and +100°) or whether left or right axis deviation is present.

R wave progressIOn m chest leads:

Inspect leads VI to V6 to see if the normal increase in

R

waves is seen as you move across the chest. Poor

R

wave progression may be a SIgn of myocardial infarcnonsbut It may also be seen with left ventricular hypertrophy, chronic lung disease. left bundle branch block, and

other conditions in the absence of inrarcuon. ".

Abnormal

Q

wave:

Abnormal Qwaves m leads 11, Ill. and aVF may indicate transmural infenor wall infarction. Abnormal

Q

waves in the anterior leads (I, a V I , and VI to V6) may indicate transmural antenor wall intarcnon .

S-T segment:

look tor abnormal SoTsegment elevations or S·T depression,

T wave and U wave:

Inspect the T waves. Norrnallv lht' I wave IS always

positive (up-nght) in leads with a posiuve

QRS

complex

The T wave ISnormally positive in leads V3 to v6 in adults. It IS normally negative in lead aVR and positive in lead

n.

The normal polanty of the T waves in the other extrermty leads depends on the QRS electrical aXIS.

Also look for prominent U waves, which may be aSlgIl of hypokalemia or drug effect (as With quinidine).

ECG

for interpretation:

1- Standardization: Note normal (10 mm) standardization mark

recorded at end of leads I,

VI,

and

V6.

Standardization mark

need be recorded only once when taking ECG.

(47)

2. Heart rate: 88 beats/min.

3. Rhythm: Normal sinus.

4. P-R interval: 0.16 sec.

5. P waves: Normal size.

6. QRS width: 0.08 sec (normal).

7. Q- T interval: 0.36 sec (normal for rate).

8. QRS voltage: Normal.

9. Mean QRS axis: About -30

0

(biphasic QRS complex in lead II

with positive QRS complex in lead I).

10. R wave progression in chest leads: Normal.

11. Abnormal Q waves: Pathologic Q waves in leads

n, m,

and

aVF.

12, S- T segments: Isoelectric.

13. T waves and u waves: Ischemic T wave inversions in leads n,

nI,

aVf, and V6.

Impression: ECGconsistent with inferolateral

wall myocardial

infarction of indeterminate age.

Comment: You cannot determine the age of an infarct from the ECG.

The ECGchanges here:

(q

waves and T wave inversions) could have been caused by an

infarct that occurred the day before or the year before.

After you have analyzed these 13 points, you should formulate an overall interpretation. For example, an ECG might show sinus tachycardia, first-degree A V block, and

Q

waves and

T

wave inversions consistent with an evolving anterior wall myocardial infarction. Part III contains other examples for practice. We would like to emphasize that every ECG abnormality you identify should summon up a list of differential diagnostic possibilities. The ECC is a clinical tool, and you should search for a clinical explanation for any ECC abnormality you find. For example, if the ECG shows sinus tachycardia, then the next question to ask is what caused this arrhythmia? Is the sinus tachycardia a result of anxiety, congestive heart failure, shock, Sympathornyrnetic drugs, or other causes? If you find ventricular tachycardia, what are the diagnostic possibilities? Is the ventricular ectopy caused by myocardial infarction or some potentially reversible cause, such as acidosis, hypoxia, digitalis toxicity pr other

drugs, hypokalemia, or hypotension? If you see signs of left atrial enlargement or left ventricular hypertrophy, what is the cause: valvular heart disease,

hypertensive heart disease, ischemic heart disease, or cardiomyopathy? In this way, the interpretation of an ECG becomes an integral part of diagnosis . and patient care. Finally, we will conclude this section with a brief discussion of some important ECG artifacts.

(48)

ECG

artifacts:

The ECG, like any other electronic recording, IS subject to numerous artifacts that may interfere WIth accurate interpretation Some or the most common of these ECG artitaets are described here.

60 cycle (Hertz.) mterterence: Interference from alternating current generators product's the characteristic pattern shown in Fig. below Note the fine-tooth comb 60 cps (Hz) artifacts. By switching the electrocardiograph plug to a different outlet or hy turning off other electrical appliances in the mom, 6Ucycle mterference can

usu~y be eliminated. J

Muscle tremor: Involuntary muscle tremor can product' undulations in the baseline that may be mistaken for atrial fibnllauon or flutter

Wandenng ba8chne: Upward or downward movement ot the baseline may produce spunous SoT segment elevations or depressions

Poor electrode contact or patIent movement. Pour electrode •.ontact or paueru movement can produce arnractual deflections m the baselme I WhIChmay obscure

the underlying pattern or be mistaken for abnormal beats

Improper standardlzanon: The electrocardiograph. as mentioned, should be stan-dardized before each tracmg so that d Imv pulse produces dsquare wave 10 mm high, Failure to properly standardize will result m complexes that are either spu-riously low or high. Furthermore, most electrocardiographs are equipped with half standardization and double standardization setnngs. Inadvertent recordmg of an

ECG on either of these settmgs will also result mspunously low or high voltage

A

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. I

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A, Muscle tremor artifact produces wave baselme resembling atrial flutter. B, Same pattern Without artifact showmg normal P waves

(49)

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,

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,Wandering baseline resulting from patient movement.

:n~o

:In~'nll

tV~ittJ

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11Jtt~1lj~~

i :

II

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. Vii

t '

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Patient movement artifact produced deflections simulating Pv'Cs. 60-cyc1e artifact is also present.

++

Remember:

The following 13 points should he evaluated in ever)'

ECC;:

1. Standardization

2. Heart rate

3. Rhythm

4. P-R interval

5. P wave size

6. QRS width

7. Q- T interval

8. QRS voltage

9. Mean QRS axis

10. R wave progression in chest leads

11. Abnormal

Q

waves

12. S- T segment

13. T wave and U wave

Any ECG abnormality should be related to the clinical status of the

patient.

The ECGcan also be affected

by numerous artifacts,

including 60 cps

(Hz) interference,

patient movement, poor electrode contact,

muscle

tremor, and so on.

lAHMED RAMZY

(50)

Test questions

_.~4."_._ ...

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...'.

v~ ~r .,.,

II

.

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1:·

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r

----1

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1) A 40-year-old woman is referred to the Out-patient Department because of

increasing breathlessness. What does this ECG show. what physical signs might you expect. and what mIght be the underlYing problem? What mIght you do?

Comment

QRS or chamber enlargement,

-...-,

-_

.... • ""l ~ ._,.---~.". _ ••.•. - .•..•--r .•- • ~ .•

.-:--II ...__~:-_..~_~

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...

. ---

_{---_}

..--. ,"7':-"-' .- .._,.-' ._.,...- _. ....

---

...•....

-

---

,-_. -.-.-.

2) This ECG came from a 40-year-old woman who complained of palpations. which were present i\

rhythm.

rhe

recording was made. What abnormality does It show?

Comment on

48 I

I

\ I

(51)

-.-····...r-_' __ .,._.._...__,~._...

:.~~.

:"j-- ~~

:~·~!;·T~-:~r:~··::_":~·~·-!3:~:~.~,~.~:~~::.-:~

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;

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3) A 50-year-old man is admitted to hospital as an emergency, having had chest pain

characteristic

of a myocardial infarction for 4 hours. Apart from the features

associated with pain there are no abnormal physical findings. What does this ECG show

and what would you do?

Comment on

$-

T segment.

l··..~

...•...,... , t' . , .•. )j

R .. ~-.... "1"-

n¥i ..··'"•...

.

,..,....

'V.•...•...'.•...•...~

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:..n ..,',."..

u"J~. . -..

-

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._

:..-...•...

__

...•

--_

...•

_.

_

-.'_

.._.

__

- - : I ••_ •.•'""'!'- •••"~--_._--;...-~--:._._._.- .,_ • " : ,

_

-

..- '.'...•..•... . .•-:' •...•..•,.. •. -_ _._ ..•.... _.•...._ .•_ ..'·0 _ ,_ .

4) This ECG was recorded from a 75-year-old

woman who complained of attacks

of

dizziness. It shows one abnormality: what is its significance?

Comment on P-R

interval.

(52)

...;.

~N.· •

i.:

~ U\A.Jvw III -. . ._. _.. .-!.-. _.~.

_._..---.--:-.----.

- ..-

_·__·_;-:-'-····_--···--···f-,····-+-•. ~.. ~ .••. 00+-- • •. ..•• .• • •.•.• ~ .~.. . . .. -,.-: . ·1' ,-'r .'''': I .- _ .••••• -._ •.••-- ''''''f--''' •• - •.- _.. . •.•••.• -_. '.o • j". <... t· .< ."

- - ---_._"

..

_~

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--,_.:-

__

....•

-.-

.- ...;-...- ~

.

,

5) A 75-year-old woman complained of central chest discomfort on climbing hills, together with dizziness; on one occosron she had "fcmred'' while climbing stairs. What abnormality does this ECG show and what physical signs would you look for?

Comment on QRS.

----._.

-_._--.

_._--

---.-. ----,

---. '\J \./'2,"--- - ._.-.-. - ...5.. .•..I " . \11 .. -.-.- . ..,tt· ..•.

-

,

6) This ECG was recorded from a 60-year-old man being treated as an out-patient for severe congestive cardiac failure. What might be the dIagnOSIs of the underlying heart condition and what would you do?

Comment on fate

&

rhythm.

so

I

'\

I

\

(53)

I !

---~.7

.

I ._:_~~...:...._ •• ~ , I. I 1 : .! . .'- __ ~ ~..1 .,...:..,~~-1.-' -'-'-. ,

-..-.~

...JlhJ---t.

I-,' ~~.,

A-' -,(-,~.~'_._.,

·1·-:-- . -

.

T" ,r;""-- . - ... "

...'.-.-.-.-. ...,...,.._- '-I ,-:oJ-; ]'1

--J-,-rl...,-l-C-·--~-r:r-q:::;:p~..,-,,_ ..~.

,~I_IL':..__,-•...•._.,_.

I • j ..•.._~-:.. ,... :...._..:_~..L.~... .:.._ :.i. :_. __; .•"i_._--.: ... _ ..._....J-_L..L~_ •...,L~ .._..4_~ ._._.; 1_••• : j. .••• ~,_ •

7) A 60-year-old man, who 3 years earlier had had a myocardial infarction followed by mild angina, was admitted to hospital with central chest pain that had be.sn present for 1 hour

and had .not responded to sublingual nitrates. What does his ECG show, and what would you do?

Comment on QRS

&

S- T segment.

-

-_.

__

...

-

--.

'-.--_._._---...··_,·--:0·-:;-.~

-·..·~T,r·-fi'

. . ... : '. ,--to ,.;' VA', ,.

.' "~';~:

~i·-:-!_t·~---::-T.r-r-f : '. '; -; ..

, v "'. v: I 1 4· -r..., ...··· .._-V2-~-.~~-

--_:-.=.-:: _~~;

v~

~::L~:.~,~~·

'~~.:.--

..

,--

.'.~-··r

~r·;-..~

j.-~'~::-

.~-.:

..~:-. i.j,; I","'., ••.-••••,•• -,._-_...•....__ .

-

.. .- .._..

.. .--~.~~

-:-.:-..-~.:=-.~~-=-~=~~~_.:=:~-_:=-~==-:-~-=~~::.~=-=-~.:.._.=~=-.

_:-~: ..

~._'--~~~-:~~=-," .. !., ;--,_ _..

,-.,'--~-:::_;II:::_~;::~;~~==:_:VF._::,:

=:~::-~::::;y.~;~k;:~!:::

::iJtHi

--,--- - ..-i---_._- ._-_'_·I·,...:.- ·.__ -:~- __

, I'

"-'-'-r- -.__ . ·..·-..·---~-- ..i'-;_-M- ;_;_; __ -;--. ..

- •..- .-- j-i"~'-- .--- ---' : ,....o.

8) A 15-year-old boy was referred to the Out-patient Department because of a heart murmur. He had no symptoms. What does this ECG show and what physical signs would you look for?

Comment on QRS.

(54)

~.

I ~2'

--_._.---L.L--.--: ...

v;--~-:-r~ ,

•...

-..-.;..;---:--._._~---. 1 •• ~.••• _4._

~~'1.J.-~:-:-T:.·.-~--_.·

I.,_{•__}_{._",_.,.. 0..} I 'p'

9) This ECG was recorded in a Coronary Care Unit from a patient admitted 2 hours

previously with an acute anterior myocardial infarction. The patient was cold and clammy, he was confused. and his blood pressure was unrecordable. What does the

ECG show and what would you do?

Comment on complex.

I·

VA

II _VL

1lI

. VF ..I

.

-.--,--10) A 50-year-old man is admitted to hospital as an emergency, having had chest porn for 4 hours. The pain is characteristic of a myocardial infarction. Apart from signs due to pain, the examination is normal. What does this ECGshow and what would you do?

Comment on S- T segment.