2011-06-17_Belajar EKG (dr.Ika SpJP)

8/3/2019 2011-06-17_Belajar EKG (dr.Ika SpJP)

1/129

ECG RHYTHM INTERPRETATIONECG Basics


2/129

Reading 12-Lead ECGs

The best way to read 12-lead ECGs is to develop a step-by-stepapproach (just as we did for analyzing a rhythm strip). In thesemodules we present a 6-step approach:

1. Determine RHYTHM2. Calculate RATE3. Determine QRS AXIS

4. Calculate INTERVALS5. Assess for HYPERTROPHY6. Look for evidence of INFARCTION


3/129

Rhythm Rate Axis Intervals HypertrophyInfarct

how to systematically analyze a rhythm bylooking at the rate , regularity, P waves, PR

interval and QRS complexes.


4/129

Rhythm Analysis

Step 1: Determine regularity.Step 2: Calculate rateStep 3: Assess the P waves.

Step 4: Determine PR interval.Step 5: Determine QRS duration.


5/129


Tip: the rhythm strip portion of the 12-lead ECG is a goodplace to look at when trying to determine the rhythm becausethe 12 leads only capture a few beats.

Lead II

Rhythm?

Atrial fibrillation

Rhythm strip

1 of 12 leads


6/129

Determine regularity

Look at the R-R distances (using a caliper ormarkings on a pen or paper).Regular (are they equidistant apart)?Occasionally irregular? Regularly irregular?Irregularly irregular?

Interpretation? Regular

R R


7/129

Assess the P waves

Are there P waves?Do the P waves all look alike?Do the P waves occur at a regular rate?Is there one P wave before each QRS?

Interpretation? Normal P waves with 1 P wave for every QRS


8/129

Arrhythmia Formation

Arrhythmias can arise from problems in the: Sinus node Atrial cells AV junction

Ventricular cells


9/129

SA Node Problems

The SA Node can:fire too slow

fire too fast

Sinus Bradycardia

Sinus Tachycardia

Sinus Tachycardia may be an appropriateresponse to stress.


10/129

Atrial Cell Problems

Atrial cells can:fire occasionally

from a focus

fire continuously

due to a looping re-entrant circuit

Premature Atrial

Contractions (PACs)

Atrial Flutter


11/129

Teaching Moment

A re-entrantpathway occurswhen an impulseloops and results inself-perpetuating

impulse formation.


12/129

Atrial Cell Problems

Atrial cells can also: fire continuously

from multiple fociorfire continuously

due to multiplemicro re-entrantwavelets

Atrial Fibrillation

Atrial Fibrillation


13/129

Teaching Moment

Multiple micro re-entrant waveletsrefers to wanderingsmall areas ofactivation whichgenerate fine chaoticimpulses. Collidingwavelets can, in turn,generate new foci ofactivation.

Atrial tissue


14/129

AV Junctional Problems

The AV junction can:fire continuouslydue to a looping re-entrant circuitblock impulsescoming from the SANode

Paroxysmal Supraventricular Tachycardia

AV Junctional Blocks


15/129

Ventricular Cell Problems

Ventricular cells can:fire occasionallyfrom 1 or more focifire continuouslyfrom multiple foci

fire continuouslydue to a looping re-entrant circuit

Premature Ventricular Contractions (PVCs)

Ventricular Fibrillation

Ventricular Tachycardia


16/129

Arrhythmias

Sinus Rhythms Premature Beats Supraventricular ArrhythmiasVentricular Arrhythmias



17/129

Sinus Rhythms

Sinus Bradycardia

Sinus Tachycardia


18/129

Rhythm #1

30 bpm Rate? Regularity? regular normal

0.10 s

P waves?

PR interval? 0.12 s QRS duration?

Interpretation? Sinus Bradycardia


19/129

Sinus Bradycardia

Deviation from NSR

- Rate < 60 bpm


20/129

Sinus Bradycardia

Etiology: SA node is depolarizing slower than

normal, impulse is conducted normally (i.e.normal PR and QRS interval).


21/129

Rhythm #2

130 bpm Rate? Regularity? regular normal

0.08 s

P waves?


Interpretation? Sinus Tachycardia


22/129

Sinus Tachycardia

Deviation from NSR

- Rate > 100 bpm


23/129

Sinus Tachycardia

Etiology: SA node is depolarizing faster thannormal, impulse is conducted normally.Remember: sinus tachycardia is a response tophysical or psychological stress, not a primary

arrhythmia.


24/129

Premature Beats

Premature Atrial Contractions (PACs)

Premature Ventricular Contractions (PVCs)


25/129

Rhythm #3

70 bpm Rate? Regularity? occasionally irreg. 2/7 different contour

0.08 s

P waves?

PR interval? 0.14 s (except 2/7) QRS duration?

Interpretation? NSR with Premature Atrial

Contractions


26/129

Premature AtrialContractions

Deviation from NSRThese ectopic beats originate in the atria(but not in the SA node), therefore thecontour of the P wave, the PR interval,and the timing are different than anormally generated pulse from the SAnode.


27/129

Premature Atrial

Contractions

Etiology: Excitation of an atrial cell forms animpulse that is then conducted normallythrough the AV node and ventricles.


28/129

Teaching Moment

When an impulse originates anywhere in theatria (SA node, atrial cells, AV node, Bundle of

His) and then is conducted normally throughthe ventricles, the QRS will be narrow (0.04 -0.12 s).


29/129

Rhythm #4

60 bpm

Rate? Regularity? occasionally irreg.

none for 7 th QRS

0.08 s (7th wide)

P waves?


Interpretation? Sinus Rhythm with 1 PVC


30/129

PVCs

Deviation from NSR Ectopic beats originate in the ventricles resulting inwide and bizarre QRS complexes.When there are more than 1 premature beats andlook alike, they are called uniform. When theylook different, they are called multiform.


31/129

PVCs

Etiology: One or more ventricular cells aredepolarizing and the impulses are abnormallyconducting through the ventricles.


32/129

Teaching Moment

When an impulse originates in a ventricle,conduction through the ventricles will beinefficient and the QRS will be wide andbizarre.


33/129

Ventricular Conduction

Normal Signal moves rapidlythrough the ventricles

Abnormal Signal moves slowlythrough the ventricles


34/129

Arrhythmias

Sinus RhythmsPremature Beats

Supraventricular ArrhythmiasVentricular Arrhythmias



35/129

Supraventricular Arrhythmias

Atrial Fibrillation

Atrial Flutter

Paroxysmal Supraventricular Tachycardia


36/129


37/129

Atrial Fibrillation

Deviation from NSR No organized atrial depolarization, so nonormal P waves (impulses are notoriginating from the sinus node).Atrial activity is chaotic (resulting in an

irregularly irregular rate).Common, affects 2-4%, up to 5-10% if > 80years old


38/129

Atrial Fibrillation

Etiology: Recent theories suggest that it isdue to multiple re-entrant waveletsconducted between the R & L atria. Eitherway, impulses are formed in a totallyunpredictable fashion. The AV node allows

some of the impulses to pass through atvariable intervals (so rhythm is irregularlyirregular).


39/129

Rhythm #6

70 bpm Rate? Regularity? regular

flutter waves

0.06 s

P waves?

PR interval? none QRS duration?

Interpretation? Atrial Flutter


40/129

Atrial Flutter

Deviation from NSRNo P waves. Instead flutter waves (notesawtooth pattern) are formed at a rateof 250 - 350 bpm.

Only some impulses conduct through theAV node (usually every other impulse).


41/129

Atrial Flutter

Etiology: Reentrant pathway in the rightatrium with every 2nd, 3rd or 4th impulsegenerating a QRS (others are blocked in theAV node as the node repolarizes).


42/129

Rhythm #7

74 148 bpm Rate? Regularity? Regular regular

Normal none

0.08 s

P waves?

PR interval? 0.16 s none QRS duration?

Interpretation? Paroxysmal Supraventricular

Tachycardia (PSVT)


43/129

PSVT

Deviation from NSRThe heart rate suddenly speeds up, oftentriggered by a PAC (not seen here) and theP waves are lost.


44/129

PSVT

Etiology: There are several types of PSVT butall originate above the ventricles (therefore theQRS is narrow).

Most common: abnormal conduction in the AVnode (reentrant circuit looping in the AV node).


45/129

Ventricular Arrhythmias




46/129

Rhythm #8


none

wide (> 0.12 sec)

P waves?


Interpretation? Ventricular Tachycardia


47/129


Deviation from NSR Impulse is originating in the ventricles (noP waves, wide QRS).


48/129


Etiology: There is a re-entrant pathwaylooping in a ventricle (most common cause).

Ventricular tachycardia can sometimes

generate enough cardiac output to produce apulse; at other times no pulse can be felt.


49/129

Rhythm #9

none Rate? Regularity? irregularly irreg.

none

wide, if recognizable

P waves?


Interpretation? Ventricular Fibrillation


50/129


Deviation from NSR Completely abnormal.


51/129


Etiology: The ventricular cells are excitableand depolarizing randomly.

Rapid drop in cardiac output and deathoccurs if not quickly reversed


52/129

Arrhythmias

Sinus RhythmsPremature Beats

Supraventricular ArrhythmiasVentricular ArrhythmiasAV Junctional Blocks


53/129

AV Nodal Blocks

1st Degree AV Block

2nd Degree AV Block, Type I

2nd Degree AV Block, Type II

3rd Degree AV Block


54/129

Rhythm #10


normal

0.08 s

P waves?


Interpretation? 1st Degree AV Block


55/129

1st Degree AV Block

Deviation from NSR PR Interval > 0.20 s


56/129

1st Degree AV Block

Etiology: Prolonged conduction delay in theAV node or Bundle of His.


57/129

Rhythm #11

50 bpm Rate? Regularity? regularly irregular

nl, but 4th no QRS

0.08 s

P waves?

PR interval? lengthens QRS duration?

Interpretation? 2nd Degree AV Block, Type I


58/129


Deviation from NSRPR interval progressively lengthens, thenthe impulse is completely blocked (P wavenot followed by QRS).


59/129


Etiology: Each successive atrial impulseencounters a longer and longer delay in theAV node until one impulse (usually the 3rd or4th) fails to make it through the AV node.


60/129

Rhythm #12


nl, 2 of 3 no QRS

0.08 s

P waves?


Interpretation? 2nd Degree AV Block, Type II


61/129


Deviation from NSR Occasional P waves are completelyblocked (P wave not followed by QRS).


62/129


Etiology: Conduction is all or nothing (noprolongation of PR interval); typically blockoccurs in the Bundle of His.


63/129

Rhythm #13


no relation to QRS

wide (> 0.12 s)

P waves?


Interpretation? 3rd Degree AV Block


64/129

3rd Degree AV Block

Deviation from NSR The P waves are completely blocked in theAV junction; QRS complexes originateindependently from below the junction.


65/129

3rd Degree AV Block

Etiology: There is complete block of conduction in the AV junction, so the atriaand ventricles form impulses independentlyof each other. Without impulses from the

atria, the ventricles own intrinsic pacemakerkicks in at around 30 - 45 beats/minute.


66/129

Remember

When an impulse originates in a ventricle,conduction through the ventricles will beinefficient and the QRS will be wide and bizarre.


67/129


If you use the rhythmstrip portion of the 12-lead ECG the total

length of it is always 10seconds long. So youcan count the numberof R waves in therhythm strip and

multiply by 6 todetermine the beatsper minute. Rate? 12 (R waves) x 6 = 72 bpm


68/129

Calculate Rate

Option 1Count the # of R waves in a 6 second rhythm strip,then multiply by 10.Reminder: all rhythm strips in the Modules are 6

seconds in length.Interpretation?

9 x 10 = 90 bpm

3 sec 3 sec


69/129

Calculate Rate

Option 2Find a R wave that lands on a bold line.Count the # of large boxes to the next R wave. If the second R wave is 1 large box away the rate is300, 2 boxes - 150, 3 boxes - 100, 4 boxes - 75, etc.(cont)

R wave


70/129

Calculate Rate

Option 2 (cont)1500 : ( small boxes R-R )300 : ( medium boxes R-R )

Interpretation?

3

00

1

50

1

00 75 60 50

1500 : 15 = 100 300 : 3 = 100


71/129

Normal Sinus Rhythm (NSR)

Etiology: the electrical impulse is formed inthe SA node and conducted normally.

This is the normal rhythm of the heart; otherrhythms that do not conduct via the typical

pathway are called arrhythmias.


72/129

NSR Parameters

Rate 60 - 100 bpm Regularity regular P waves normal PR interval 0.12 - 0.20 s QRS duration 0.04 - 0.12 s

Any deviation from above is sinus tachycardia,sinus bradycardia or an arrhythmia


73/129


Axisrefers to the mean QRS axis (or vector) during ventriculardepolarization. As you recall when the ventricles depolarize (in a normalheart) the direction of current flows leftward and downward because mostof the ventricular mass is in the left ventricle. We like to know the QRS axis

because an abnormal axis can suggest disease such as pulmonaryhypertension from a pulmonary embolism.


74/129


The QRS axis is determined by overlying a circle, in the frontal plane.By convention, the degrees of the circle are as shown.

The normal QRS axis lies between -30 o and +90 o.

0o

30 o

-30 o

60 o

-60 o-90 o

-120 o

90 o 120o

150 o

180 o

-150 o

A QRS axis that falls between -30 o and -90 o is abnormal and called leftaxis deviation.

A QRS axis that falls between +90 o and +150 o is abnormal and calledright axis deviation .

A QRS axis that falls between +150 o and -90 o is abnormal and calledsuperior right axis deviation .

A i


75/129


We can quickly determine whether the QRS axis is normal bylooking at leads I and II.

If the QRS complex isoverall positive (R > Q+S) in leads I and II, the QRSaxis is normal .

QRS negative (R < Q+S)

In this ECG what leadshave QRS complexesthat are negative?equivocal?

QRS equivocal (R = Q+S)

A i


76/129

0o

30 o

-30 o

60 o

-60 o-90 o

-120 o

90 o 120o

150 o

180 o

-150 o


if the QRS is negative in lead I and negative in lead II what is the QRS axis?(normal, left, right or right superior axis deviation)

QRS Complexes

I

AxisI II+ ++ -

- +

- -

normalleft axis deviationright axis deviation

right superioraxis deviation

0o

30 o

-30 o

60 o

-60 o-90 o

-120 o

90 o 120o

150 o

180 o

-150 o

II

A i


77/129

Rate Rhythm Axis Intervals HypertrophyInfarct

Is the QRS axis normal in this ECG? No, there is left axis deviation.

The QRS is positive in I and negative in II.

A i


78/129


To summarize:The normal QRS axis falls between -30 o and +90 o because ventriculardepolarization is leftward and downward.Left axis deviation occurs when the axis falls between -30 o and -90 o.Right axis deviation occurs when the axis falls between +90 o and +150o.Right superior axis deviation occurs when the axis falls between between +150 o and -90 o.

QRS Complexes

AxisI II

+ ++ -

- +

- -

normalleft axis deviationright axis deviation

right superioraxis deviation

A quick way to determinethe QRS axis is to look at theQRS complexes in leads Iand II.

I l


79/129

PR interval

< 0.12 s 0.12-0.20 s > 0.20 s

High catecholaminestates

Wolff-Parkinson-WhiteNormal AV nodal blocks

Wolff-Parkinson-White 1st Degree AV Block


I t l


80/129

QRS complex

< 0.10 s 0.10-0.12 s > 0.12 s

Normal Incomplete bundlebranch block

Bundle branch blockPVC

Ventricular rhythm

Remember: If you have a BBB determine if it is a right or left BBB. If you need a refresher see Module VI .

3 rd degree AV block withventricular escape rhythm

Incomplete bundle branch block



81/129

QT interval

The duration of the QT interval isproportionate to the heart rate. The fasterthe heart beats, the faster the ventriclesrepolarize so the shorter the QT interval.Therefore what is a normal QT varieswith the heart rate. For each heart rate youneed to calculate an adjusted QT interval,called the corrected QT (QTc):

QTc = QT / square root of RR interval


I t l


82/129


QTc interval

< 0.44 s > 0.44 s

Normal Long QT

A prolonged QT can be very dangerous. It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes. Causes include drugs, electrolyte abnormalities, CNS disease, post-MI, and congenital heart disease.

Torsades de Pointes

Long QT


83/129


PR interval? QRS width? QTc interval?0.08 seconds 0.16 seconds 0.49 seconds

QT = 0.40 s

RR = 0.68 s

Square root of

RR = 0.82 QTc = 0.40/0.82 = 0.49 s

Interpretation of intervals? Normal PR and QRS, long QT

I t l


84/129

Tip: Instead of calculating the QTc, a quick way to estimate if theQT interval long is to use the following rule:

A QT > half of the RR interval is probably long.

Normal QT Long QT

QT

RR

10 boxes

23 boxes 17 boxes

13 boxes



85/129

Right atrial enlargement Take a look at this ECG. What do you notice about the P waves?

The P waves are tall, especially in leads II, III and avF.Ouch! They would hurt to sit on!!

Rhythm Rate Axis Intervals Hypertrophy Infarct


86/129

Right atrial enlargement To diagnose RAE you can use the following criteria:

II P > 2.5 mm, or

V1 or V2 P > 1.5 mm

Remember 1 small box in height = 1 mm

A cause of RAE is RVH from pulmonary hypertension.

> 2 boxes (in height)

> 1 boxes (in height)



87/129

Left atrial enlargement Take a look at this ECG. What do you notice about the P waves?

The P waves in lead II are notched and in lead V1 they have a deep and wide negative component.

Notched

Negative deflection



88/129

Left atrial enlargement To diagnose LAE you can use the following criteria:

II > 0.04 s (1 box) between notched peaks , or

V1 Neg. deflection > 1 box wide x 1 box deep

Normal LAE

A common cause of LAE is LVH from hypertension.



89/129

Right ventricular hypertrophy Take a look at this ECG. What do you notice about the axis and QRScomplexes over the right ventricle (V1, V2)?

There is right axis deviation (negative in I, positive in II) and there are tall R waves in V1, V2.


h


90/129

Right ventricular hypertrophy Compare the R waves in V1, V2 from a normal ECG and one from aperson with RVH.Notice the R wave is normally small in V1, V2 because the right ventricledoes not have a lot of muscle mass.But in the hypertrophied right ventricle the R wave is tall in V1, V2.

Normal RVH


h


91/129

Right ventricular hypertrophy To diagnose RVH you can use the following criteria:

Right axis deviation , and

V1 R wave > 7mm tall

A commoncause of RVHis left heart

failure.


h


92/129

Left ventricular hypertrophy Take a look at this ECG. What do you notice about the axis and QRScomplexes over the left ventricle (V5, V6) and right ventricle (V1, V2)?

There is left axis deviation (positive in I, negative in II) and there are tall R waves in V5, V6 and deep S waves in V1, V2.

The deep S wavesseen in the leads overthe right ventricle arecreated because theheart is depolarizingleft, superior andposterior (away fromleads V1, V2).


H h


93/129

Left ventricular hypertrophy To diagnose LVH you can use the following criteria*:

R in V5 (or V6) + S in V1 (or V2) > 35 mm, oravL R > 13 mm

A common cause of LVHis hypertension.

* There are several other criteria for the diagnosis of LVH.

S = 13 mm

R = 25 mm


H h


94/129

A 63 yo man has longstanding, uncontrolled hypertension. Is there evidence of heart disease from his hypertension? (Hint: There a 3 abnormalities.)

Yes, there is left axis deviation (positive in I, negative in II), left atrial enlargement (> 1 x 1 boxes in V1) and LVH (R in V5 = 27 + S in V2 = 10 > 35 mm).


B dl B h Bl k


95/129

Bundle Branch Blocks

With Bundle Branch Blocks you will see two changes on theECG.

1. QRS complex widens (> 0.12 sec).2. QRS morphology changes (varies depending on ECG lead, and if

it is a right vs. left bundle branch block).

Ri ht B dl B h Bl k


96/129

Right Bundle Branch Blocks

What QRS morphology is characteristic?

V1

For RBBB the wide QRS complex assumes aunique, virtually diagnostic shape in thoseleads overlying the right ventricle (V 1 and V 2).

Rabbit Ears

L ft B dl B h Bl k


97/129

Left Bundle Branch Blocks

What QRS morphology is characteristic?

For LBBB the wide QRS complex assumes acharacteristic change in shape in those leadsopposite the left ventricle (right ventricularleads - V 1 and V 2).

Broad,deep Swaves

Normal

Rhythm Rate Axis Intervals Hypertrophy


98/129

To diagnose a myocardial infarction you need togo beyond looking at a rhythm strip and obtaina 12-Lead ECG.

RhythmStrip

12-LeadECG


ST El ti


99/129

ST Elevation

One way todiagnose an

acute MI is tolook forelevation of theST segment.

ST Ele ation (cont)


100/129

ST Elevation (cont)

Elevation of the STsegment (greater

than 1 small box) in2 leads is consistentwith a myocardialinfarction.

Anterior View of the Heart


101/129

Anterior View of the Heart

The anterior portion of the heart is best viewedusing leads V 1- V4.

Putting it all Together


102/129


Do you think this person is having a myocardialinfarction. If so, where?

Other MI Locations


103/129

Other MI Locations

Second, remember that the 12-leads of the ECG look at differentportions of the heart. The limb and augmented leads seeelectrical activity moving inferiorly (II, III and aVF), to the left (I,aVL) and to the right (aVR). Whereas, the precordial leads seeelectrical activity in the posterior to anterior direction.

Limb Leads Augmented Leads Precordial Leads

Other MI Locations


104/129

Other MI Locations

Now, using these 3 diagrams lets figure where tolook for a lateral wall and inferior wall MI.


Anterior MI


105/129

Anterior MI

Remember the anterior portion of the heart is bestviewed using leads V 1- V4.


Lateral MI


106/129

Lateral MI

So what leads do you thinkthe lateral portion of theheart is best viewed?


Leads I, aVL, and V 5- V6

Inferior MI


107/129

Inferior MI

Now how about the inferiorportion of the heart?


Leads II, III and aVF



108/129


Now, where do you think this person is having amyocardial infarction?

Inferior Wall MI


109/129

Inferior Wall MI

This is an inferior MI. Note the ST elevation inleads II, III and aVF.



110/129


How about now?

Anterolateral MI


111/129

Anterolateral MI

This persons MI involves both the anterior wall (V 2-V4) and the lateral wall (V 5-V6, I, and aVL)!

ECG Changes


112/129

ECG Changes

Ways the ECG can change include:

Appearanceof pathologicQ-waves

T-waves

peaked flattened inverted

ST elevation &depression

ECG Changes & the Evolving


113/129

ECG Changes & the EvolvingMI

There are twodistinct patterns

of ECG changedepending if theinfarction is:

ST Elevation (Transmural or Q-wave), or Non-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

ST Elevation Infarction


114/129


ST elevation, peaked T-waves, then T-wave inversion

The ECG changes seen with a ST elevation infarction are:

Before injury Normal ECG

ST elevation & appearance ofQ-wavesST segments and T-waves return tonormal, but Q-waves persist

injury

Infarction

Fibrosis



115/129

Heres a diagram depicting an evolving infarction: A. Normal ECG prior to MI

B.Injury from coronary artery occlusion results inST depression (not shown) and peaked T-waves

C. Infarction from ongoing ischemia results inmarked ST elevation

D/E. Ongoing infarction with appearance of pathologic Q-waves and T-wave inversion

F. Fibrosis (months later) with persistent Q-waves, but normal ST segment and T- waves



116/129

Heres an ECG of an inferior MI:

Look at theinferior leads (II,III, aVF).

Question: What ECGchanges doyou see?

ST elevationand Q-wavesExtra credit: What is therhythm? Atrial fibrillation (irregularly irregular with narrow QRS)!

Non-ST Elevation Infarction


117/129

Heres an ECG of an inferior MI later in time:

Now what doyou see in theinferior leads?

ST elevation,Q-waves andT-waveinversion

Non-ST Elevation Infarction


118/129

ST depression & T-wave inversion

The ECG changes seen with a non-ST elevation infarction are:

Before injury Normal ECG

ST depression & T-wave inversion

ST returns to baseline, but T-waveinversion persists

Ischemia

Infarction

Fibrosis

SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct


119/129

A 16 yo young man ran into a guardrail while riding a motorcycle.In the ED he is comatose and dyspneic. This is his ECG.



120/129

What is the rate? Approx. 132 bpm (22 R waves x 6)



121/129

What is the rhythm? Sinus tachycardia



122/129

What is the QRS axis? Right axis deviation (- in I, + in II)



123/129

What are the PR, QRSand QT intervals?

PR = 0.12 s, QRS = 0.08 s, QTc = 0.482 s



124/129

Is there evidence ofatrial enlargement?

No (no peaked, notched or negatively deflected P waves)



125/129

Is there evidence ofventricular hypertrophy?

No (no tall R waves in V1/V2 or V5/V6)



126/129

Infarct: Are there abnormalQ waves?

Yes! In leads V1-V6 and I, avL

Any

Any

Any

20

30

30

30

3030

30

R40

R50



127/129

Infarct: Is the ST elevationor depression?

Yes! Elevation in V2-V6, I and avL.Depression in II, III and avF.



128/129

Infarct: Are there T wavechanges?

No



129/129

ECG analysis: Sinus tachycardia at 132 bpm, right axis deviation,long QT, and evidence of ST elevation infarction in the anterolateral leads (V1-V6, I, avL) with reciprocal changes (the ST depression) in the inferior leads (II, III, avF).

This young man suffered anacute myocardial infarction afterblunt trauma. Anechocardiogram showedanteroseptal akinesia in the leftventricle with severely

depressed LV function(EF=28%). An angiogramshowed total occlusion in the

2011-06-17_Belajar EKG (dr.Ika SpJP)

Documents