ecg module basic

8/11/2019 ECG Module Basic

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Analysis and Interpretation of the Electrocardiogram

A Self-Directed Learning Module

Technical Skills Program

Queens University

Department of Emergency Medicine

Introduction

The electrocardiogram (ECG) is one of the most useful diagnostic tests in emergency medicine !t is an easy and

ine"pensive test that is used routinely in the assessment of patients #ith chest pain The ECG is the cornerstonefor ma$ing the diagnosis of cardiac ischemia and is used for ma$ing decisions a%out eligi%ility for throm%olytic

therapy

To avoid misinterpreting the ECG& the clinician must have a systematic approach This module is designed toguide the learner through a step#ise approach to ECG interpretation 'pecific e"amples of a variety of

a%normal ECGs are included at the end along #ith a %rief ui*

O!ecti"es

+y the end of this learning module you should have a systematic approach to interpreting the ECG and %e a%le

to identify common ECG a%normalities

The #$ lead E%&
http://meds.queensu.ca/simlab/undergraduate_medicine/technical_skills_programhttp://queensu.ca/http://meds.queensu.ca/medicine/emergency/http://meds.queensu.ca/medicine/emergency/http://queensu.ca/http://meds.queensu.ca/medicine/emergency/http://meds.queensu.ca/simlab/undergraduate_medicine/technical_skills_program


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The ,- lead ECG is made up of the three standard lim% leads (!& !! and !!!)& the augmented lim% leads (a./&

a.0 and a.1) and the si" precordial leads (.,& .-& .2& .3& .4 and .5)

'a"es and comple(es

Inter"als and segments

P) Inter"al* 1rom the start of the 6 #ave to the start of the Q/' comple"


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P) Segment* 1rom the end of the 6 #ave to the start of the Q/' comple"

+ Point* The 7unction %et#een the Q/' comple" and the 'T segment

,T Inter"al* 1rom the start of the Q/' comple" to the end of the T #ave

,)S Inter"al* 1rom the start to the end of the Q/' comple"

ST Segment* 1rom the end of the Q/' comple" (8 point) to the start of the T #ave

ormal "alues

9eart rate 5: ; ,:: %pm

6/ interval :,- ; :-: s

Q/' interval < :,- s

QT interval = half // interval (males = :3: s> females = :33 s)

6 #ave amplitude (in lead !!) < 2 m. (mm)6 #ave terminal negative deflection (in lead

.,)< , m. (mm)

Q #ave= ::3 s (, mm) and = ,?2 of / #ave amplitude in the samelead

Approach to the E%&

Developing a systematic approach to the interpretation of the ECG is a critical s$ill for all clinicians The

follo#ing outlines one such approach

Step #* Determine the heart rate


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There are a num%er of strategies for determining the heart rate @ simple& uic$ techniue is to find a Q/'

comple" that falls on a ma7or vertical grid;line (,)& then count the num%er of large suares to the ne"t Q/'comple" (-) Dividing this num%er into 2:: gives you the heart rate !n the ECG %elo#& there are - large suares

%et#een Q/' comple"es 2::?- gives a heart rate of ,4: %eats per minute

Step $* Measure important inter"als

The measurement of important electrocardiographic intervals usually includes the 6/ interval& the Q/' interval

and the QT interval @t a standard paper speed of -4 mm?second& the #idth of each small suare (,mm)

represents ::3 seconds Ane large suare (4mm) represents :- seconds


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Step .a* %alculate the electrical a(is

The mean Q/' a"is refers to the average orientation of the hearts electrical activity !n most cases& an

appro"imation of the a"is #ill %e sufficient for the ECG interpretation There are many different approaches toa"is determination& %ut this discussion #ill %e limited to a simple techniue #hich uses the leads ! and a.1 tocalculate an appro"imate a"is


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Lead # Lead a/0 Description Interpretation A(is

GB,

0eads ! and a.1eually positive The

a"is #ill %e mid#ay

%et#een : and :

ormal a"is F

3:;4:

GB-

0eads ! and a.1 %oth

positive 0ead ! more

positive than a.1The a"is #ill

therefore %e oriented

more to#ard :

ormal a"is F-: ; 3:

GB2

0ead ! positive 0eada.1 almost

euiphasic

Therefore& the a"is

#ill %e approaching: (Note: when a

lead is equiphasic,

the axis will be 90 tothat lead.)

ormal a"is F:

GB3

0ead ! positive 0ead

a.1 negativeThe

a"is #ill %e orientednegatively past :

0eft a"is

deviation F

;2:

GB4

0ead ! negative 0ead

a.1 positive Thea"is #ill %e oriented

positively past :

/ight a"is

deviation F;,-:

GB5

+oth leads ! and a.1

negative The a"is

#ill %e oriented%et#een ;: and

;,:

!ndeterminatea"is F ;,24


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that the a"is can %e considered in terms of four uadrants& #ith lead ! oriented at :& and a.1 oriented at

H: @n ECG #ith the Q/' a"is oriented to the uadrant %et#een : and : is said to %e normal

@n ECG #ith the Q/' a"is oriented to the uadrant %et#een ;, and ;: is said to have left a(is

de"iation

@n ECG #ith the Q/' oriented to the uadrant %et#een H, and ,: is said to have right a(is

de"iation

@n ECG #ith the Q/' oriented to the uadrant %et#een ;, and ;,: is said to have anindeterminate a(is%ecause one cannot tell if it represents right or left a"is deviation

Step .* %alculate the electrical a(is

The mean Q/' a"is is oriented to#ards the lead #ith the greatest net Q/' deflection To calculate the net Q/'

deflection& add up the num%er of small suares that correspond to the height of the / #ave (positive deflection)&and su%tract the num%er of small suares that correspond to the height of the Q and ' #aves (negative

deflection)

!n actual fact& the net Q/' deflection can %e

appro"imated #ithout resorting to counting suares

!n the e"ample sho#n here& one can easily see thatthe net deflection is slightly more positive than

negative

Step .c* %alculate the electrical a(is

@ppro"imate the net Q/' deflection for leads ! and a.1 /emem%er that the mean Q/' a"is #ill %e oriented

to#ards the lead #ith the greatest positive net Q/' deflection !f the net deflection is positive for %oth& the a"islies %et#een leads ! and a.1 (:;:) and is therefore normal

Step 1* E"aluate the cardiac rhythm


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!f the rhythm is regular& the // interval should %e constant throughout the ECG This can %e chec$ed using

calipers& or more simply %y mar$ing on a piece of paper the distance %et#een t#o / #aves& and comparing thisdistance %et#een pairs of Q/' comple"es on the ECG e"t& chec$ to see if a 6 #ave is present %efore each of

the Q/' comple"es

Step 2* Inspect P 3a"es for atrial enlargement

The 6 #aves in leads !& !!& !!! and ., should %e inspected for evidence of right or left atrial enlargement

Usually& lead !! #ill have the clearest 6 #ave

6 #ave amplitude should not e"ceed 2 small suares (2 mm or :2m.) !f it does& this represents right

atrial enlargement

!n lead .,& the terminal negative deflection of the 6 #ave represents left atrial depolari*ation and should

not e"ceed , mm (:,m.) !f it does& this is indicative of left atrial enlargement

Step 4* Inspect ,)S comple(es for "entricular hypertrophy or lo3 "oltage


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!n the setting of 0eft .entricular 9ypertrophy (0.9)& the left ventricle enlarges

and so the leads oriented to the left ventricle (.4& .5& a.0) #ill IseeI more

electrical activity moving towards them @s #ell& the leads oriented a#ay fromthe left ventricle (.,& .-) #ill IseeI more activity moving away from them !n

0.9 therefore& leads .4& .5 and a.0 #ill have tall / #aves& #hile leads ., and

.- #ill have deep ' #aves (The arro# in the diagram on the right sho#s thedirection of the net electrical activity in 0.9)

., or .- .4& .5 or a.0 The voltage criteria for 0.9are satisfied if the sum of the

amplitude of the deepest '

#ave in ., or .-& and theamplitude of the tallest / #ave

in .4 or .5& is eual to or

greater than 24 mm (24 m.)The voltage criteria are also

satisfied if the amplitude of the

/ #ave in lead a.0 is eual toor greater than ,- mm(,-m.)

Step 5a* Inspect ,)S comple(es for undle ranch lock or fascicular lock

The normal Q/' interval is :,- seconds (2 mm or 2 small suares) on the ECG To correctly determine the

Q/' interval& use the lead #ith the #idest Q/' comple" !f the Q/' comple" is less than or eual to :,-seconds& then no further analysis is necessary !f it is greater than :,- seconds& then you should try to determine

the reason for the a%normally long Q/' interval

@ simple approach is to consider the follo#ing three possi%le causes for Q/' #ideningJ

The type of %undle %ranch %loc$ can usually %e determined from the e"amination of three $ey leadsJ !& ., and

.5


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Step 5* Inspect ,)S comple(es for undle ranch lock or fascicular lock

!n the normal heart& at the %eginning of ventricular depolari*ation& the Q/' a"is is oriented to the right %ecause

of left;to;right depolari*ation of the septum This produces a small / #ave in lead ., !mmediately follo#ing

septal depolari*ation& the left and right ventricles depolari*e The si*e of the left ventricle results in a

predominantly left#ard a"is for the remainder of the Q/' comple"

Step 5c* Inspect ,)S comple(es for undle ranch lock or fascicular lock

!n the setting of /+++& the initial part of the ECG is unchanged %ecause septal depolari*ation and

depolari*ation of the left ventricle are unaffected 9o#ever& the right ventricle depolari*es in a delayed and slo#fashion This results in a #idening of the terminal part of the Q/' comple" and orientation of the a"is of theterminal part of the Q/' comple" to the right


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Step 5d* Inspect ,)S comple(es for undle ranch lock or fascicular lock

!n the setting of 0+++& the septum is activated in a right to left direction& and then there is depolari*ation of theright and left ventricles through the right %undle The result is that the Q/' a"is has a predominantly left

orientation throughout and is #ide secondary to the slo# activation of the left ventricle

Step 5e* Inspect ,)S comple(es for undle ranch lock or fascicular lock

!f the ECG cannot %e characteri*ed as a typical /+++ or a typical 0+++& then it can %e categori*ed as anintraventricular conduction delay This #ill not %e addressed in any more detail at this time

Step 6* Assess , 3a"es and determine significance

The Q #aves should %e assessed and their significance determined& particularly in regard to the diagnosis ofmyocardial infarction 'mall Q #aves are commonly a normal finding in the inferior leads !!! and a.1& and in

the anterolateral leads a.0& !& .4 and .5 Q #aves of ::3 seconds (, mm) duration and greater than one third

the / #aves amplitude in the same lead may %e pathological


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The pathological Q #aves seen in ., ; .5 indicate that this patient has had an anterior M! in the past This

patient also has evidence of an acute inferior M! as sho#n %y the 'T segment elevation in leads !!! and a.1

Step 7* Assess ST segments and T 3a"es

@ssess the 'T segment for the presence of elevations or depressions& together #ith T #ave a%normalities 'T

elevation can indicate the presence of conditions such as acute myocardial in7ury& 6rin*metals (variant) angina&

pericarditis& ventricular aneurysm or myocardial ischemia

This ECG is from a patient #ith an acute inferior M! ote the 'T elevation in the inferior leads (!!& !!! and

a.1) The ECG also sho#s 'T depression in leads .,& .- and .2 ; li$ely a result of reciprocal changesassociated #ith the M!

Step #8* Measure ,T inter"al for specific diagnoses


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The QT interval can %e prolonged secondary to meta%olic disorders and drug effects !t must %e corrected for

heart rate since it is rate dependent The corrected QT interval is calculated using the follo#ing formulaJ

QT! corrected K (QT! o%served) ? (suare root of // interval)

The QT! corrected is often reported #ith computeri*ed ECG interpretation

This ECG is from a male patient #ith familial prolonged QT syndrome The QT! corrected is appro"imately

:4- secondsNormal QTI corrected: 0.0 seconds !or males" 0. seconds !or !emales.

E%& inde(

The follo#ing represent common ECG findings that the clinician should %e familiar #ith

ormal E%&


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@ normal ECG is illustrated a%ove ote that the heart is %eating in a regular sinus rhythm %et#een 5: ; ,::

%eats per minute (specifically - %pm) @ll the important intervals on this recording are #ithin normal ranges

, 6 #aveJ

upright in leads !& a.1 and .2 ; .5

normal duration of less than or eual to :,, seconds

polarity is positive in leads !& !!& a.1 and .3 ; .5> diphasic in leads ., and .2> negative in a./

shape is generally smooth& not notched or pea$ed

- 6/ intervalJ

ormally %et#een :,- and :-: seconds

2 Q/' comple"J

Duration less than or eual to :,- seconds& amplitude greater than :4 m. in at least one standard lead&

and greater than ,: m. in at least one precordial lead Upper limit of normal amplitude is -4 ; 2: m. small septal Q #aves in !& a.0& .4 and .5 (duration less than or eual to ::3 seconds> amplitude less

than ,?2 of the amplitude of the / #ave in the same lead)

represented %y a positive deflection #ith a large& upright / in leads !& !!& .3 ; .5 and a negative

deflection #ith a large& deep ' in a./& ., and .-

in general& proceeding from ., to .5& the / #aves get taller #hile the ' #aves get smaller @t .2 or .3

these #aves are usually eual This is called the transitional *one

3 'T segmentJ

isoelectric& slanting up#ards to the T #ave in the normal ECG can %e slightly elevated (up to -: mm in some precordial leads)

never normally depressed greater than :4 mm in any lead

4 T #aveJ

T #ave deflection should %e in the same direction as the Q/' comple" in at least 4 of the 5 lim% leads

normally rounded and asymmetrical& #ith a more gradual ascent than descent

should %e upright in leads .- ; .5& inverted in a./

amplitude of at least :- m. in leads .2 and .3 and at least :, m. in leads .4 and .5

isolated T #ave inversion in an asymptomatic adult is generally a normal variant

5 QT intervalJ

Durations normally less than or eual to :3: seconds for males and :33 seconds for females

Acute anterolateral MI


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@cute anterolateral M! is recongni*ed %y 'T segment elevation in leads !& a.0 and the precordial leads

overlying the anterior and lateral surfaces of the heart (.2 ; .5) Generally spea$ing& the more significant the'T elevation & the more severe the infarction There is also a loss of general / #ave progression across the

precordial leads and there may %e symmetric T #ave inversion as #ell @nterolateral myocardial infarctions

freuently are caused %y occlusion of the pro"imal left anterior descending coronary artery& or com%inedocclusions of the 0@D together #ith the right coronary artery or left circumfle" artery @rrythmias #hich

commonly preclude the diagnosis of anterolateral M! on ECG and therefore possi%ly identify high ris$ patients

include right and left %undle %ranch %loc$s& hemi%loc$s and type !! second degree atrioventricular conduction

%loc$s

Acute inferior MI

0eads !!& !!! and a.1 reflect electrocardiogram changes associated #ith acute infarction of the inferior aspect ofthe heart 'T elevation& developing Q #aves and T #ave inversion may all %e present depending on the timing

of the ECG relative to the onset of myocardial infarction Most freuently& inferior M! results from occlusion of

the right coronary artery Conduction a%normalities #hich may alert the physician to patients at ris$ include

second degree @. %loc$ and complete heart %loc$ together #ith 7unctional escape %eats ote that the patient%elo# is also suffering from a concurrent posterior #all infarction as eveidenced %y 'T depression in leads .,

and .-


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Acute posterior MI

Lhen e"amining the ECG from a patient #ith a suspected posterior M!& it is important to remem%er that%ecause the endocardial surface of the posterior #all faces the precordial leads& changes resulting from theinfarction #ill %e reversed on the ECG Therefore& 'T segments in leads overlying the posterior region of the

heart (., and .-) are initially hori*ontally depressed @s the infarction evolves& lead ., demonstrates an /

#ave (#hich in fact represents a Q #ave in reverse) ote that the patient %elo# is also suffering from aninferior #all myocardial infarction as evidenced %y 'T elevation in leads !!& !!! and a.1

Acute right "entricular MI

!n patients presenting #ith acute right ventricular M!& a%normalities in the standard ,- lead ECG are restricted

to 'T elevation greater than or eual to , mm in lead a./ @lthough isolated right ventricular M! is usuallyseen in patients suffering from chronic lung disease together #ith right ventricular hypertrophy& it can occur in

patients suffering a transmural infarction of the inferior;posterior #all #hich e"tends to involve the right

ventricular #all as #ell /ight ventricular M! is most commonly caused %y o%struction of the pro"imal right


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coronary artery and is freuently associated #ith right %undle %ranch %loc$ 1urthermore& only 4 ; ,: of

patients suffer from hemodynamic symptoms

Acute septal MI

@cute septal M! is associated #ith 'T elevation& Q #ave formation and T #ave inversion in the leads overlying

the septal region of the heart (.- and .2)

Atrial firillation


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@trial fi%rillation represents disorgani*ed atrial activity #ithout contraction or e7ection The electrocardiogram

demonstrates an irregular %aseline #here the normal 6 #aves are replaced #ith rapidly uivering smalldeflection of varia%le amplitude (f #aves ; outlined %elo#) @n irregularly irregular ventricular rate

demonstrating narro# Q/' comple"es is esta%lished %et#een ,:: ; ,5: %pm @trial fi%rillation is common in

patients #ith rheumatic heart disease& pulmonary em%oli& cardiomyopathy& pericarditis& ischemic heart diseaseand thyroto"icosis !t causes minimal hemodynamic compromise and often the patient presents complaining of

palpitations as the only symptom @lthough hemodynamic compromise is minimal& atrial fi%rillation is an

important ris$ factor for the development of throm%oem%olic complications& such as stro$es and transient

ischemic attac$s

Atrial flutter

The electrocardiogram in atrial flutter is typically characteri*ed %y its Isa#toothI flutter #aves (1 #aves ;arro#s %elo#) %est demonstrated in the inferior leads (!!& !!!& a.1 and .,) @ rapid regular atrial rhythm is

generally demonstrated %et#een -4: and 24: %pm& and the /' rate is determined %y the ratio of

atrioventricular conduction @lthough the usual ratio of @. conduction is -J, (as illustrated %elo#)& ,J,& 2J,& 3J,5J, and other varia%le ratios are also demonstrated& al%eit less freuently Typically& this results in a ventricular

heart rate %et#een ,4: and ,N: %pm @trial flutter is relatively uncommon and is most often seen in patients

presenting #ith acute ischemic heart disease or pulmonary em%olism evertheless& it can present as a chroniccondition in patients #ho suffer from organic heart disease


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%omplete heart lock

Complete heart %loc$ refers to a form of atrioventricular dissociation #here no 6 #ave produces a Q/'

comple" @ sinus or ectopic atrial rhythm develops that fires independently of the ventricles This rhythm may

%e 7unctional (as illustrated %elo#) or ventricular in origin The rhythm is usually regular& %ut may presentirregularly as a result of intermittent premature ventricular %eats 6atients presenting #ith complete heart %loc$

complain of symptoms resem%ling profound %radycardia (loss of atrial $ic$) and reduced cardiac output

(syncope& angina& presyncope)

Digitalis effect


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These glycosides can cause 'T sagging and shortening& %est seen in leads .3& .4 and .5 (see %elo#)

Dual chamer pacemaker

This electrocardiogram demonstrates an artificial cardiac pacema$er #hich is responsi%le for initiatingcontractions #ithin the atria as #ell as the ventricles ote the dou%le pacema$er spi$es associated #ith each

complete cycle of contraction The first spi$e indicates stimuli to the atria& #hile the second pacema$er spi$e

indicates initiation of ventricular contraction


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9yperkalemia

6otassium overdose is freuently seen in patients #ith renal failure or those on O sparing diuretics !n mildhyper$alemia (serum levels less than 54 mE?l)& leads !!& .- and .3 demonstrate tall& tented& symmetrical T

#aves #ith a narro# %ase The 6 #ave remains normal& as does the Q/' comple" Lith moderate O overdose

(54 mE?l ; : mE?l) the Q/' comple" %roadens and the ' #ave is #idened in leads .2 ; .5 This ' #ave

%ecome continuous #ith the tented T #aves and eventually the 'T segment disappears 1urthermore theduration of the 6 #ave is increased& #hile the amplitude is decreased @t O levels greater than : mE?l (see

%elo#)& the 6 #ave duration and 6/ interval duration %oth increase& until the 6 #ave eventually disappears

entirely The Q/' comple" is diffusely %roadened and continuous #ith the tall& tented T #ave in all leads

9ypokalemia

9ypo$alemia is associated #ith progressive 'T depression& progressive flattening or inversion of the T #aves&

the development of U #aves& increased amplitude and duration of the 6 #aves and Q/' comple"es as #ell as a

slight increase in the duration of the 6/ interval 1urthermore& hypo$alemia affects automaticity of the

pacema$er cells and leads to multiple arrhythmias such as sinus %radycardia& atrioventricular %loc$& atrial flutterand Torsades de 6ointes Most commonly& hypo$alemia results from thia*ide diuretic misuse& diarrhea& renal or

adrenal disease Ather causes include infusion of large amounts of glucose or al$ali su%stances& liver cirrhosis

and dia%etic coma


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Left atrial enlargement

0eft atrial enlargement is typically characteri*ed %y an increase in the terminal portion of the 6 #ave +est seen

in lead !!& this terminal deflection is often demonstrated as a distinct second pea$ #ithin the 6 #ave (arro#%elo#) !n some leads& this second pea$ gives the 6 #ave an Im;li$eI shape This deflection does not usually

affect the amplitude of the 6 #ave& %ut may increase its duration to greater than :,- seconds !n addition to this

increased 6 #ave deflection in lead !!& 0@E results in a terminal negative deflection #ithin the 6 #ave %est seen

in lead ., (see %elo#) Lith e"treme 0@E& the amplitude of the 6 #ave may %e increased& and terminalnegativity may %e demonstrated in leads !!& !!! and a.1 (see %elo#) 0eft atrial enlargement may result from left

atrial dilatation& pressure overload (ie from mitral valve disease) or a%normal intra;atrial conduction Ather

terms freuently used to descri%e 0@E include left atrial hypertrophy& left atrial overload and left atriala%normality


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Left "entricular hypertrophy

Electrocardiograms from patients presenting #ith 0.9 demonstrate varia%ly increased / #ave voltage and

duration in leads over the right ventricle (.4 and .5 ; circled %elo#) !n 24 ; : of the cases& there is a

delay %et#een the onset of the Q/' comple" and the / #ave This intrinsicoid deflection may e"tend to greaterthan ::4 seconds 1urthermore& delayed repolari*ation as a result of ventricular hypertrophy generally produces

'T depression and T #ave inversion in the same leads Enlargement of the left ventricle is commonly associated

#ith left atrial enlargement as #ell as incomplete 0+++ 0eads .- and .2 commonly demonstrate increased '#ave amplitude (arro# %elo#)& #hile leads .4 and .5 sho# increased / #ave amplitude 0eft ventricular

hypertrophy may %e associated #ith conditions giving rise to pressure or volume overload of the left ventricle

such as aortic stenosis or systemic hypertension 1urthermore& 0.9 increases patient ris$ of othercardiovascular diseases including myocardial infarction& congestive heart failure& stro$e& arrhythmia and suddendeath


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Left undle ranch lock

!n left %undle %ranch %loc$& activation of the intraventricular septum is reversed and electrical impulses to theleft ventricle are delayed These altered electrical forces produce a #ide Q/' comple" (greater than :,-

seconds in duration) #ith an a%normal morphology !n leads ! and .5& a%normal initial forces fail to produce

any Q #ave or ' #ave& and the resultant / #ave is steep and often notched (circled %elo#) 1urthermore& a deeprapid ' #ave is generated in lead ., (arro# %elo#) The 'T segment is slightly elevated in multiple leads and

the T #ave polarity is diffusely opposite to the ventricular comple"


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Pericarditis

6atients presenting #ith acute pericarditis demonstrate diffuse 'T segment elevation in all leads e"cept a./ and

., (see %elo#) These 'T changes are sometimes associated #ith concurrent 6/ segment depression in thesame leads and an increased sinus heart rate (a%ove ,2 %pm) @t -;4 days after the acute presentation& the 'T

segments return to %aseline 1ollo#ing this return to %aseline& the T #aves in all leads e"cept a./ %ecome

inverted& eventually returning to their previously normal polarity and amplitude over the follo#ing couple of

#ee$s

Premature atrial comple(

6remature atrial comple"es (circled %elo#) are recogni*ed %y three distinct featuresJ

, a premature and unusually shaped 6 #ave (designated 6)- a Q/' comple" resem%ling a normal sinus %eat

2 a follo#ing cardiac cycle that is less than compensatory in duration

6@Cs originate from a focus outside the '@ node 9ence the irregular shape of the 6 #ave& irregular durationof the 66 interval and e"tended duration of the 6/ interval to greater than :,- seconds !t is important to

remem%er that if this 6@C fires very early in the cycle& ventricular activation may not occur& or a reentrant atrial

tachycardia may develop !n normal individuals& 6@Cs may arise from various stimuli including to%acco&

caffeine and alcohol as #ell as strong emotions Ather situations #hich may lead to the development of 6@Csinclude myocardial infarction& various drugs& infections& hypo$alemia and hypomagnesemia


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Premature "entricular comple(

6remature ventricular comple"es (circled %elo#) may arise in normal individuals as #ell as patients suffering

from nearly every form of structural heart disease 6remature ventricular comple"es are recogni*ed as single or

paired unifocal %eats& #ith no preceding 6 #ave& a #ide Q/' comple" of increased amplitude characteristicallylasting greater than :,3 seconds& and a T #ave demonstrating polarity opposite to that of the 6.C They arise

early in the cardiac cycle and are more li$ely to occur during periods of %radyarrhythmia @lthough no 6 #aves

precede the #ide Q/' comple"& retrograde activation of the atria may produce 6 #aves #hich occur after the

6.C or are %uried in their T #aves 6remature ventricular %eats may arise from e"cessive catecholamines&myocardial ischemia or in7ury& electrolyte im%alances& certain medications including digitalis and class !@ and

!C antiarrhythmic agents


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Prolonged ,T inter"al

The QT interval represents the time %et#een the %eginning of the Q #ave until the end of the T #ave Thisinterval is %est measured in lead !! and represents %oth the depolari*ation and repolari*ation phases of the

ventricles !t is significantly influenced %y many factors including heart rate& various medications (especially

uinidine& procainaminde and disopyramide)& hypo$alemia& hypomagnesemia and athletic training Therefore&

ta%les or formulas are often needed to calculate the corrected QT interval (@Tc) to determine if the QT intervalon a particular electrocardiogram is appropriate for its demonstrated heart rate Ane accepted calculation in

determining this QTc is a modified version of +a*etts formula This formula states that the QTc K QT H,N4(ventricular rate ; 5:) ormal values for this corrected QT interval are found to appro"imate :3, seconds&although this value is slightly longer in females and in patients of increasing age !f this calculation is applied to

the ECG demonstrated %elo#& the QTc is measured as :4- seconds PQTc K :4- H ,N4 (5: ;5:)

Pulmonary emolism

Electrocardiogram a%normalities can %e o%served in a minority of patients presenting #ith pulmonary

em%olism These changes are rarely diagnostic unless greater than 4: of the pulmonary vascular compartmentis occluded 6ulmonary em%olism increases resistance to %lood flo# to the right side of the heart& commonly

resulting in cor pulmonale involving right atrial enlargement and right ventricular dilation or hypertrophy 0ead

!!! demonstrates ECG changes #hich mimic acute inferior myocardial infarction (circled %elo#) These changesinclude an increase in the normal Q #ave amplitude& minimal 'T segment elevation& and often shallo# T #ave

inversion 6ulmonary em%olism is differentiated from acute inferior M! %y the a%sence of these changes in theother inferior leads (!! and a.1) Elevated 'T segments& increased ' #ave amplitude and inverted T #ave

polarity may sometimes %e seen in the precordial leads


28/37

)ight atrial enlargement

6atients presenting #ith /@E demonstrate an ECG pattern in #hich the 6 #ave duration is unaffected& %ut its

shape is pea$ed and its amplitude is increased to greater than -4 mm in leads !!& !!!& a.1 (arro#s %elo#) and

sometimes ., Lith e"treme enlargement of the right atrium& the 6 #ave may demonstrate terminal negativityin lead .,& resem%ling 0@E /ight atrial enlargement is commonly associated #ith congenital heart disease&

tricuspid valve disease& pulmonary hypertension and diffuse lung disease 1urthermore& patients presenting #ith

/@E often demonstrate ECG changes associated #ith right ventricular hypertrophy as #ell

)ight undle ranch lock


29/37

@s illustrated in the electrocardiogram %elo#& right %undle %ranch %loc$ presents #ith delayed activation of the

right ventricle& leading to a #ide Q/' comple" lasting greater than :,- seconds @ltered terminal Q/' forcesproduce a terminal / #ave in lead a./ and terminal ' #aves in leads !& a.0& .4 and .5 Triphasic comple"es

are identified as the late intrinsicoid Im;shapedI /'/ comple" in lead .,& and the early intrinsicoid /'

comple" in lead .5

Single chamer pacemaker

@rtificial cardiac pacema$ers are most commonly used in the management of symptomatic %radycardias These

pacema$ers provide electrical stimuli to the atria or ventricles or %oth at a desired rate to cause them to contractregularly at that rate An the electrocardiogram& these electrical impulses are seen as Ipacema$er spi$esI

identified %y their a%rupt vertical spi$e (arro#s %elo#)& preceding the atrial or ventricular comple"& dependingon #hich cham%ers the pacema$er is responsi%le for !n this e"ample& a pacema$er has %een inserted #hich isresponsi%le for providing a regular ventricular rhythm (#ide& %i*arre Q/' comple" ; circled %elo#) o atrial

contractions are present


30/37

Supra"entricular tachycardia - A/ reentry

'upraventricular tachycardia commonly presents in t#o forms ; @. reentry and @. nodal reentry !n @. reentry(%elo#)& the '.T presents as a regular tachycardia originating outside the ventricular myocardium !n this type

of '.T& the @. node is used for impulse conduction to the ventricles& #hile an accessory path#ay is used to

return electrical conduction %ac$ to the atria The heart rate is usually regular& at a rate of ,N: to -4: %pm

(%elo# K , %pm) !n this type of '.T& 6 #aves are al#ays present outside of the Q/' comple"& #hile theirpolarity depends on the atrial insertion of the accessory path#ay The Q/' comple" is narro# #ith a duration

less that :- seconds and an atrioventricular conduction ratio of ,J, !n -4 ; 2: of patients demonstrating @.

reentry& Q/' alternans is present (varying amplitudes of the Q/' comple" in all leads e"cept .3) @. reentry isnot usually associated #ith structural heart disease and commonly presents as a variety of symptoms including

palpitations& nervousness& an"iety& syncope or heart failure


31/37

Supra"entricular tachycardia - A/ nodal reentry

@. nodal reentry is a form of '.T that esta%lishes its atrioventricular circuit entirely #ithin the @. node The

heart rate is usually regular& %et#een ,4: to -4: %pm (%elo# K ,5 %pm) The Q/' comple" is narro# #ith a

duration less than :- seconds and a conduction ratio of ,J, 6 #aves are %uried #ithin the Q/' compel" (as

illustrated %elo#)& although they may %e visi%le at the end of the comple" as a distortion of the terminal forcesDue to the fact that atrial activation originates from the inferior aspect of the right atrium& 6 #ave polarity is

negative in leads !!& !!! and a.1 This form of '.T is usually %enign and is easily converted to sinus rhythm %yvagal maneuvers

/#:/. interchanged

@ccurate electrocardiogram interpretation can only %e achieved if all ,- leads are placed in their appropriate

positions Ane of the more common errors involving lead placement involves reversal of the positioning of

leads ., and .2 (demonstrated %elo#) This mista$e produces an ECG pattern in #hich the normal / and '#ave progressions in the precordial leads ., to .2 is lost


32/37

/entricular tachycardia

.entricular tachycardia is defined as three or more ventricular comple"es in succession at a rate greater than

,:: %pm 6atients presenting #ith ventricular tachycardia often present #ith a regular heart rate %et#een ,::

and -4: %pm (9/ %elo# K ,35 %pm)& in #hich the Q/' morphology is constant and a%normally #ide (greaterthan :,- seconds) 1reuently& these ECGs demonstrate @. dissociation in #hich the ventricular rate is greater

than the atrial rate 6 #aves are freuently hidden #ithin the %road ventricular comple"es& although they can

sometimes %e identified as %umps or notches in the ventricular cycles @lthough patients #ithout heart diseasemay develop paro"ysmal non;sustained ventricular tachycardia& chronic sustained .T is most commonly

associated #ith coronary artery disease& dilated cardiomyopathy and prior myocardial infarction or severe heart

disease


33/37

'olff-Parkinson-'hite syndrome

Electrocardiograms from patients presenting #ith L6L demonstrate a group of characteristic findings

freuently associated #ith paro"ysmal tachycardias and atrial fi%rillation !n L6L& accessory path#ays of

accelerated ventricular impulse formation lead to the development of delta #aves These #aves resem%le

pathological Q #aves and represent initial slurring of the Q/' comple" as a result of early ventriculardepolari*ation through this accessory path#ay (see lead !!& ., and .5 ; arro# %elo#) @s a result& the 6/

interval is shortened to less than :,- seconds and the Q/' direction is altered (lead !!!)& #hile its duration ise"tended to greater than :,: seconds 'econdary T #ave anomalies resulting from a%normal ventricularrepolari*ation are often demonstrated (leads !!& !!!& .-& .2 and .3)

%ase #

This - year old male comes to the E/ complaining of general illness @ resident notices that he has an irregularpulse and performs an ECGJ


34/37

Lhat is the diagnosisR

@trial flutter

Complete heart %loc$

.entricular fi%rillation

@trial fi%rillation

!ncorrect

!ncorrect

!ncorrectCorrect

%ase $

This N- year old female presents in the E/ complaining of su%sternal chest pain radiating into her left arm 'heis diaphoretic and is also complaining of nausea @n ECG is performedJ

Lhat is the most li$ely diagnosisR

@cute anterolateral M!

6osterior M!

Complete heart %loc$

'eptal M!

Correct

!ncorrect!ncorrect

!ncorrect


35/37

%ase .

This 54 year old female presents to the E/ complaining of #ea$ness @ history reveals that she has a history of

congestive heart failure for #hich she ta$es furosemide @n ECG is performedJ


9ypo$alemia

@cute posterior M!

@trial fi%rillation

9yper$alemia

Correct

!ncorrect!ncorrect

!ncorrect


36/37

%ase 1

This - year old male presents in the E/ complaining of severe pleuritic chest pain over the left precordium6hysical e"amination reveals a friction ru% over the left precordium @n ECG is performedJ


9ypo$alemia

6ulmonary em%olism

9yper$alemia

6ericarditis

!ncorrect!ncorrect

!ncorrect

Correct

%ase 2


37/37

This 4 year old male is %rought into the E/ %y paramedics #ho he called %ecause he felt his heart pounding

@n ECG is performedJ


.entricular tachycardia

6ulmonary em%olism

6.C

'.T ; @. reentry

!ncorrect

!ncorrectCorrect

!ncorrect

CongratulationsS

ou have no# completed the @nalysis and !nterpretation of the ECG module

Credits

This #e%;%ased module #as developed and edited %y @dam '*ule#s$i %ased on content #ritten %y Dr

+o% McGra#& Dr 8ason 0ord& Matthe# Lestendorp& 0isa Evans and 8ordan Chen$in for the Queens

University Technical '$ills 6rogram and Department of Emergency Medicine

The module #as created using e"e J e0earning 9TM0 editor #ith support from @my @llcoc$ and the

Queens University 'chool of MedicineMedTech Unit

0icenseJThis module is licensed under the Creative Commons @ttri%ution on;Commercial o Derivatives

license The module may %e redistri%uted and used provided that credit is given to the author and it is used for

non;commercial purposes only The contents of this presentation cannot %e changed or used individually 1ormore information on the Creative Commons license model and the specific terms of this license& please visit

creativecommonsca
http://meds.queensu.ca/undergrad/http://meds.queensu.ca/medtech/http://meds.queensu.ca/medtech/http://meds.queensu.ca/undergrad/http://meds.queensu.ca/medtech/

ecg module basic

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