ecg basic محاضرة الدكتور الكبسي

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Dr Mohammed Alkebsi ([email protected])

BASIC ELECTROCARDIOGRAMBASIC ELECTROCARDIOGRAM

INTERPRETATIONINTERPRETATION

Mohammed Al-Kebsi, MSc, PhD, FGHAAs. Prof of Cardiology

Al-Thawra Cardiac CenterSanaa University

[email protected]

[email protected] Mohammed Alkebsi ([email protected])

Learning Modules

ECG Basics

How to Analyze a Rhythm

Normal Sinus Rhythm

Heart Arrhythmias

Diagnosing a Myocardial Infarction

Advanced 12-Lead Interpretation

Dr Mohammed Alkebsi ([email protected]) Dr Mohammed Alkebsi ([email protected])

Phases of the EKG

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ECG Paper:ECG Paper: Dimensions

5 mm

1 mm

0.1 mV

0.04 sec

0.2 sec

Speed = rate

Voltage~Mass



ECG BasicsECG Basics

ECG graphs:

1 mm squares

5 mm squares

Paper Speed:

25 mm/sec standard

Voltage Calibration:

10 mm/mV standard


Frontal Plane Leads:Frontal Plane Leads: Standard (bipolar) Leads:

I: RA- to LA+

II: RA- to LL+

III: LA- to LL+

Augmented Vector (Unipolar) LeadsaVR: to RA+

aVL: to LA+

aVF: to LL+

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V1 : 4V1 : 4thth ICS &ICS &RtRt sternalsternal borderborder

V2 : 4V2 : 4thth ICS & LtICS & Lt sternalsternal borderborder

V3 : midway, between V2 & V4V3 : midway, between V2 & V4

V4 : 5V4 : 5thth ICS, midICS, mid clavicularclavicular lineline

V5 : 5V5 : 5thth ICS, anteriorICS, anterior axillaryaxillary lineline

V6 : 5V6 : 5thth ICS, midICS, mid axillaryaxillary lineline


Inferior

II, III, AVF

Antero-Septal

V1,V2, V3,V4

Lateral

I, AVL, V5,

V6

Posterior

V1, V2, V3

RIGHT LEFT


Step approach to analyze ECGStep approach to analyze ECG

Rate

Rhythm

P wave morphology

PR interval

QRS interval,

QRS complex morphology

ST segment

T wave

Electrical axis

U wave

QT duration

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Cardiac Cycle Basics:Cardiac Cycle Basics:

Begins with SA Node depolarization

P P = 1 Cycle

Heart rate (pulse) is determined by ventricledepolarization/contraction

R R = 1 heart beat

P PR R


Calculating Heart Rates

Sinus Rhythm: Each QRS complex is precededby P wave

NSR: Within the intrinsic rate of the SA Node: 60-100 bpm

Tachycardia: >100 bpm

Bradycardia: < 60 bpm


Method 1Method 1 Count the number of small squares between R R waves (X):

Divide 1500 by X:

Rate = 1500 / X Example: X = 201500 / 20 =75Rate = 75 bpm

Paper Speed: 25 mm/ sec

60 seconds / minute

60 X 25 = 1500 mm / minute


Method 2Method 2 Count the number of big squares between R R waves (X):

Divide 300 by X:

Rate = 300 / X Example: X = 4300 / 4 =75Rate = 75 bpm

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Dr Mohammed Alkebsi ([email protected]) 100

10101010

RR

30303030

R

Method 3Method 3

R

150300 Dr Mohammed Alkebsi ([email protected])

Take 6 sec strip (30 large boxes)

Count the R/R waves X 10

When there is irregularity in ECG.

1 2 3 4 5 6

1 2 3 4 5 6 7

Method 4Method 4


Blue Segment: -30to +90Is normal QRSaxis Dr Mohammed Alkebsi ([email protected])

Interpreting AxisInterpreting Axis

Deviation:Deviation:

Normal ElectricalAxis:(Lead I + / aVF +)

Left Axis Deviation:Lead I + / aVF

Right Axis Deviation:Lead I - / aVF +

No ManNo Mans Lands Land

- Both I and aVF are

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How do we Determine Axis???

Normal ax is Right axis dev iat ion Lef t axis dev iat ion

Lead I Positive Negative Positive

Lead II Positive Positive or negative Negative

Lead III Positive or negative Positive Negative

Method 1Method 1


Method 2Method 2 using theusing the hexaxialhexaxial diagramdiagram


Method 3Method 3 Simplest methodSimplest method

Shaking handsShaking hands

Check Leads:I and aVF


Rhythm ID: AlgorithmRhythm ID: Algorithm

P-Wave: What is the atrial rhythm? < 0.12 sec (3 mm)

QRS: What is the ventricular rhythm?

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PP--wavewave

It is important to remember that the P waverepresents the sequentialactivation of the RAand LA, and it is common to see notched orbiphasic P waves of RA and LA activation.

P duration < 0.12 sec

P amplitude < 2-3 mm


Normal PNormal P--WaveWave

Sinus: Normal, Tachy, Brady


Irregular P waveIrregular P wave

Premature Beats: Narrow P waves: PACs


Abnormal shape of PAbnormal shape of P--WaveWave

P Pulmonale Tall Peaked

RA enlargement secondary to

PH (COPD)

P-Mitrale Broad notched

LA enlargement secondary to

MVD

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Abnormal shape of PAbnormal shape of P--WaveWave


Absent PAbsent P--WaveWave

Absent P: V-tach, A-fib, Junctional Rhythm

Rate: 4060 bpm Rhythm: Regular

P Waves: Absent, inverted, buried, or retrograde retrogradePR Interval: None, short. QRS: Normal (0.060.10 sec)


Irregular PIrregular P--WaveWave

Irregular P: A-Flutter


Fibrillation vs. Flutter?Fibrillation vs. Flutter?

Multi-focal origins -chaotic

Rate: >400 bpm

IRREGULAR-R

One focus - organized

Rate: 200-400 bpm

REGULAR - R

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Ventricles: QRS RhythmsVentricles: QRS Rhythms

Regular rhythms?

R-R intervals equivalent

Regular irregular rhythms?

R-R intervals equivalent with occasionalirregularities

Irregular rhythms?

R-R intervals irregular


RegularRegular IrregularIrregular

Premature Beats: PVC

Widened QRS, not preceded P wave

Usually does not disrupt P-wave regularity

T wave is inverted after PVC

Followed by compensatory ventricular pause


PVC Patterns:PVC Patterns:

PVC: 1 Isolated beat

Couplet: 2 consecutive PVCs

Bigeminy: PVC every other beat

Non-Sustained VT: >3 beats for less than 1 minute

Sustained VT: > 1 minute of ventricular tachycardia


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TT--wavewave

The T wave is the most labile wave in theECG.

T wave changes including low-amplitude Twaves and abnormally inverted T waves maybe the result of many cardiac and non-cardiacconditions.

The normal T wave is usually in the samedirection as the QRS except in the rightprecordial leads (V1,V2).

Normally; T wave is always upright in leads I,

II, V3-6, and always inverted in lead aVR. Theother leads are variable depending on thedirection of the QRS and the age of thepatient.


TT--wavewave

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DD of T Wave InversionDD of T Wave Inversion

Q wave and non-Q wave MI (e.g., evolvinganteroseptal MI).

Myocardial ischemia

Subacute or old pericarditis

Myocarditis

Myocardial contusion (from trauma)

CNS disease causing long QT interval(subarrachnoid hemorrhage).



Idiopathic apical hypertrophy (a rare form ofhypertrophic cardiomyopathy)

Mitral valve prolapse

Digoxin effect

RVH and LVH with "strain" (see below: Twave inversion in leads aVL, V4-6 in LVH)




Nice Seeing "U" AgainNice Seeing "U" Again

The normal U wave has the same polarity asthe T wave and is usually less than one-thirdthe amplitude of the T wave.

Best seen in the right precordial leadsespecially V2 and V3.

U wave is asymmetric with the ascending limbmoving more rapidly than the descending limb

(just the opposite of the normal T wave).

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ECG IntervalsECG Intervals

PR Interval: 0.12 - 0.20 sec QRS Duration: 0.06 - 0.10 sec QTc Men < 0.43

borderline o.43-0.45 prolonged >0.45

Women < 0.43 borderline o.43-0.47 prolonged >0.47


QT intervalQT interval

Bazett'sBazett's FormulaFormula:: QTQTcc = (QT)/= (QT)/SqRootSqRoot RR (inRR (inseconds)seconds)

Poor Man's GuidePoor Man's Guideto upper limits of QT:to upper limits of QT:For HR = 70For HR = 70 bpmbpm, QT, QT

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Conduction Disturbance?Conduction Disturbance?

Ectopic Beats:

wide QRS complexes

AV Blocks:

Prolonged P-R intervals

Ventricular: Bundle Branch Blocks

Wide QRS / Normal P-R


HEART BLOCKHEART BLOCK

S-A block occurs in the conduction between theSA node and atria.

A-V Blocks occur in the conduction between theatria and ventricles

Ventricular Blocks: Occur in the Bundle Branches


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S-A block occurs inthe conductionbetween the SAnode and atria.


A-V Blocks occurin the conductionbetween the atriaand ventricles


VentricularBlocks: Occur inthe BundleBranches


Sinus arrestSinus arrest

The SA node fails to d ischarge and then resumes.

Electrical activity resumes either when the SA node resets itself or when a

lower latent pacemaker begins todischarge.

The pause (arrest) time interval is not a multiple of the normal P-P interval.

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SA blockSA block


AtrioAtrio--Ventricular Blocks:Ventricular Blocks:

SA Node fires, but conduction is impaired:

Degrees of Block:

1: Conduction delayed, but QRS captured

2: Partial Block: Occasional ventricularcapture

3: Complete: Atria and ventricles completelydissociated


First Degree Block:First Degree Block:

Prolonged P- R interval


Second Degree Block:Second Degree Block:

Type I: Wenckebach

P-R Interval gets progressively longer untilthe AV conduction is completely blocked:

When AV conduction blocked, there is notQRS complex

QRS is normal

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Second Degree Block:Second Degree Block: Type II:

Regular ventricular rate slow

2:1, 3:1 or 4:1 P:R waves

Only occassional but regular ventricularcapture

QRS is normal


Third Degree (Complete) AV BlockThird Degree (Complete) AV Block

AV conduction is completely dissociated

Ventricles contract at intrinsic rate (30-40 bpm)

Normal P waves, but more than QRS waves

QRS complexes may be normal or widened


Identifying AV Blocks:Identifying AV Blocks:

1: P = R > .20 Regular

2:Mobitz I P > R Progressive

Irregular

2:Mobitz II P > R Constant Regular

3: P > R GrosslyIrregular

Regular(20-40 bpm)

Name Conduction PR-Int R-R Rhythm


Bundle Branch Blocks

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Turning our attention to bundle branch blocks

Remember normalimpulse conduction is

SA node

AV node

Bundle of HisBundle BranchesPurkinje fibers


Normal Impulse ConductionSinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers



So, depolarization of theBundle Branches andPurkinje fibers are seenas the QRS complex onthe ECG.

Therefore, a conductionblock of the BundleBranches would bereflected as a change inthe QRS complex.

RightBBB


Bundle Branch BlocksWith Bundle Branch Blocks you will see two changeson the ECG.

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).

Look at the Vleads to recognize

Bundle Branch

Blocks

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Why does the QRS complex widen?


RBBBWhat QRS morphology is characteristic?

V1

QRS durationQRS duration 110ms110ms

rSRrSR pattern or notched R wave in V1pattern or notched R wave in V1

Wide S wave in I and V6Wide S wave in I and V6

Rabbit Ears


LBBB

What QRS morphology is characteristic?

QRS durationQRS duration 120ms120ms

Broad R wave in I and V6Broad R wave in I and V6

Prominent QS wave in V1Prominent QS wave in V1

Absence of q waves (includingAbsence of q waves (including

physiologic q waves) in I and V6physiologic q waves) in I and V6


LBBB

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RBBB


Guess: RBBB or LBBB?

Wide QRSRabbit Ears inV1 and V2

= RBBB!


Guess: RBBB or LBBB?

Wide QRSMostly downin V1 and V2Mostly up inlead V6

= LBBB!

Recall that in either RBBB or LBBB,

the QRS must be wide (> .12 sec)Dr Mohammed Alkebsi ([email protected])

ST Segment Analysis:ST Segment Analysis:

Ischemia DiagnosisIschemia Diagnosis

Key Reference Points:

Isoelectric line: Use the PR segment asreference

J-Point: Point at which QRS complex ends andST segment begins

ST Slope: Downsloping > Horizontal > Upsloping(questionable/angina)

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STST--DepressionDepression

>1.0 mm depression:

Downsloping: Very predictive

Horizontal: Very predictive

Upsloping: Predictive if angina present

>2.0 mm depression

Usually indicative of ischemia


Determining Regions of infarctionDetermining Regions of infarction

RCA: Inferior myocardium

II, III, aVF

LCA: Lateral myocardium

I, aVL, V5, V6

LAD: Anterior/Septal myocardium

V1-V4


ECG Changes

Ways the ECG can change include:

Appearanceof pathologicQ-waves

T-waves

peaked flattened inverted

ST elevation &

depression


ECG Changes & the Evolving MI

There are twodistinct patternsof ECG changedepending if theinfarction is:

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

Non-ST Elevation

ST Elevation

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ST Elevation Infarction

ST depression, 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-waves

ST segments and T-waves return to

normal, but Q-waves persist

Ischemia

Infarction

Fibrosis



Heres a diagram depicting an evolving infarction:

A. Normal ECG prior to MI

B. Ischemia from coronary artery occlusionresults in ST depression (not shown) andpeaked T-waves

C. Infarction from ongoing ischemia results inmarked ST elevation

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

F. Fibrosis (months later) with persistent Q-

waves, but normal ST segment and T-waves



Heres an ECG of an acute MI:

Question:What ECG

changes doyou see?

Extra credit:What is therhythm? Atrial fibrillation (irregularly irregular with narrow QRS)!


Heres an ECG of an inferior wall MI later in time:

Now what doyou see in the

inferior leads?

ST elevation,Q-waves and

T-waveinversion

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Non-ST Elevation Infarction

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-wave

inversion persists

Ischemia

Infarction

Fibrosis


Non-ST Elevation Infarction

Heres an ECG of an evolving non-ST elevation MI:

Note the STdepressionand T-waveinversion inleads V2-V6.

Question:What area ofthe heart isinfarcting?

Anterolateral


Left Ventricular

Hypertrophy


Left Ventricular Hypertrophy

Many sets of criteria for diagnosing LVH havebeen proposed:

Sensitivity Specificity

The sum of the S wave in V1and the R wave in either V5 orV6 > 35 mm

43% 95%

Sum of the largest precordial R

wave and the largest precordialS wave > 45 mm 45% 93%

Romhilt-Estes Point System 50-54% 95-97%

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Romhilt-Estes Point System for LVH

Criterion Points

Amplitude (any of the following:

Largest R or S wave in any limb lead 20mm

S in V1 or V2 30mm

R in V5 or V6 30mm

3

ST depressions or T wave inversions in lateral

precordial leads, I, and/or aVL

3

Left atrial enlargement 3

Left axis deviation 2

QRS duration 90 ms 1

Intrinsicoid deflection in V5 or V6 50 ms 1

4 points Probable LVH 5 points Definite LVH Dr Mohammed Alkebsi ([email protected])


Compare these two 12-lead ECGs. What standsout as different with the second one?

Normal Left Ventricular Hypertrophy

Answer: The QRS complexes are very tall

(increased voltage)


Right Ventricular Hypertrophy

Right axis deviation

Right atrial enlargement

Downsloping ST depressions in V1-V3 (RV strain

pattern) Tall R wave in V1

Although there is no widely accepted criteria fordetecting the presence of RVH, any combination ofthe following EKG features is suggestive of itspresence:


Everything is clear?

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Summary

Dont worry too much right now about

trying to remember all the details. Youll

focus more on advanced ECG

interpretation in your clinical years!


Summary

TAILORED ECG


Frontal Plane QRS Axis = +75 degrees-KH Frontal Plane QRS Axis = +15 degrees-KH

QRS Axis QRS Axis


Frontal Plane QRS Axis = -45 degrees-KH Right Axis Deviation

QRS Axis QRS Axis

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Frontal Plane QRS Axis = +150 degrees (RAD)-KH

QRS Axis


Sinus Pause or

Arrest


Long QT Interval-KH

The QT interval duration is greater than 50% of the RR interval, a good indication

that it is prolonged in this patient. Although there are many causes for the longQT, patients with this are at risk for malignant ventricular arrhythmias, syncope,

and sudden death.


Hyperkalemia and Old Inferior MI

The T waves are tall, peaked and have a narrow base, making them very

uncomfortable to sit on ! These changes are characteristic of hyperkalemia. TheQRS is also slightl y widened, another feature of hyperkalemia. Q waves in III and

aVF indicate an old inferior MI.

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Left Atrial Abnormality & 1st degree AV Block-KH






The rhythm is sinus rhythm with a rate of about 75/minute. There is first degree atrioventricular

block demonstrated by a PR interval of 300 milliseconds.

An inferolaterali nfarction is indicated by the Q waves in leads II, III, aVF (inferior) and there

are Q waves as well as I, aVL, V5 and V6 . The poor R wave progression in the precordial

leads and the marked posterior rotation of the QRS axis suggests an anterior infarction as well.

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The rhythm is sinus rhythm with at 50/minute. The PR interval is 180 ms. The

QRS axis is normal

Q waves are seen in lead II, III and aVF as well as V2 V4. There is ST-

segment elevation in the inferior leads and precordial leads V1-V4. This

suggests an anterior myocardial infarction of undetermined age and a possibly

inferior infarction (the q wave in AVF is boarder-line). The T waves are also

inverted in the lateral leads.Dr Mohammed Alkebsi ([email protected])



Right Bundle Branch Block


Right Atrial Enlargement

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Left Bundle Branch Block

Dr Mohammed Alkebsi ([email protected])Left Atrial Enlargement





(with frequent PVCs)

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Everything is clear?


The rhythm is sinus tachycardia at approximately 120/minute. The P waves arebiphasic in V1. The PR interval is 140 ms. There is an M shaped QRS complex(rSR' variant) in leads V1 to V3. In addition there are deep and slurred S waves inleads I, aVL, V5 and V6. There are also prominent S waves proceeded by small rwaves in II, III and aVF as well as left axis deviation of the first part of the QRS.Together, these phenomena indicate the presence of a bifascicular block: rightbundle branch block and left anterior hemiblock..The ST elevation seen in leads II, III and aVF and ST depression in leads I andaVL suggest acute inferior injury/infarction. There is also slight ST elevation inV1. The ST elevation in V1 suggests acute anterior i schemia/injury/infarction.


Four days later, the sinus rhythm has slowed down(approximately 80/minute) and the degree of ST

changes have diminished. This indicates that theacute process of infarction/ischemia is evolving.

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The rhythm is sinus rhythm at approximately 70/min. The deep S waves in the inferior

leads and a left axis deviation i ndicates left anterior hemiblock.

There is poor R wave progression in the anterior precordial leads with a QS complex

in V4. There is ST segment elevation in leads V1 to V4. T here are very small or R

waves leads II, III and aVF. All of these phenomena point towards the presence of an

anterior wall and possible inferior wall infarction.Dr Mohammed Alkebsi ([email protected])

This tracing shows sinus rhythm at 70 /minute andsupraventricular trigeminy (ie., every third beat is premature).The mean ventricular rate is about 80. There are Q waves inleads II, III and aVF indicating the presence of an inferiorinfarction. There is no significant ST deviation so the infarction isprobably old.


Six weeks later, the premature atrial beats have resolved. Thereis sinus rhythm with a rate of about 75/minute. The PR interval

has widened to 232ms which indicates a first degreeatrioventricular block. There is a new right bundle branch blockas demonstrated by the rSR' complex in V1 and V2 as well asthe wide, slurred S waves in I and V6.


This tracing shows sinus rhythm at 82/minute. The PR interval is 180 ms. TheQRS interval duration of 260 ms indicates a conduction defect. There is an Mshaped QRS complex (rSR' variant) in leads V1 to V3. In addition there are Swaves in leads I, aVL, V5 and V6. There are also prominent S waves proceeded

and small r waves in II, III and aVF . The QRS has as a left axis deviation. Thesefindings indicate the presence of a bifascicular block, right bundle branch and leftanterior hemiblock..

The inverted T waves in V1 and V2 are probably due to the conductiondisturbance and not ischemia.

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This tracing shows sinus tachycardia at 112/minute. The PR interval is 140 ms. Right atrialenlargement is suggested by the tall P waves in lead II and left artrial abnormality by thenegative P wave deflection in V1. There is a slight rSR' morphology in V1 and V2 but nodeep S waves in I or V6. This could indicate the presence of a partial right bundle branchblock.

Narrow but large Q waves are present without ST segment deviation in leads II, III and aVFsuggesting an old inferior infarction. The deep QS wave in V3 suggest an anterior infaction.The peaked T waves in V3-V6 suggest the presence of acute anterior ischemia.Q waves usually evolve later in a Q wave infarction. Here, the Q waves and peaked T wavescoexist. An explanation for this is that the Q waves represent an old or remote infarction

while the peaked T waves represent an active ischemic process, or that the Q waves haveappeared more radilythan expected.


This tracing shows sinus tachycardia a t a rate of 120/minute.The PR interval is 175 ms. The third beat of the tracing isprobably a ventricular premature beat. There is significant STelevation in the inferior leads III and aVF showing an acuteinferior infarction. The ST depression in the lateral leads may bereciprocal to this inferior infarction. Deep Q waves are seen inV1-V4 along with a poor R wave progression suggest a an oldanterior infarction.


The rhythm is complete (3rd degree) atrioventricular block with anodal escape and a ventricular rate o f 50/minute. There is asmall but significant ST elevation inferior leads II, III and avF

indicating an acute inferior injury. Deep Q waves in V1-V3 showan anterior infarction which is probably old. The ST elevation inleads V5 and V6 suggest latteral wall acute injury.


This tracing shows sinus tachycardia at a rate of 115/minute. The PRinterval is120ms. There are large R waves in the anterior leads V1-V3.This could be the reciprocal equivalent of Q waves posteriorly. Theseleads also show slight anterior ST segment depression and peaked,inverted T waves which can be interpreted as posterior injury and

ischemia (i.e., reciprocal ST segment elevation and peaked T waves).Although true posterior wall infarctions are usually associated with aninferior infarction (not seen in this tracing), this tracing does suggest apossible acute true posterior Q wave infarction. The use of posteriorEKG electrodes can be helpful cases of suspected true posterior Qwave infarction.

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This tracing shows sinus rhythm at a rate of87/minute. The PR interval is 175 ms. The small rwaves or QS deflections in III and aVF suggest a

possible old inferior infarction.. Dr Mohammed Alkebsi ([email protected])

This tracing shows sinus bradycardia. The rate is 45/minute. ThePR interval is 200ms. There is high voltage R waves in V2 andV5 which could suggest biventricular hypertrophy.

The peaked T waves in V2 and V3 along with slight ST segmentelevation in those leads suggest the early stages of an acuteanterior infarction although similar findings can be found withwhat is called "early replarization". There a re deep but narrow Qwaves in II, II and aVF suggesting a remote inferior infarction.


This tracing shows sinus rhythm. The rate is 60/minute. There isan M shaped QRS complex (rSR' variant) in leads V1 to V3. Inaddition there are deep and slurred S waves in V6. There arealso prominent S waves proceeded by very small r waves in II,III and aVF as well as a left axis deviation of -60. Together,these findings suggest bifascicular block: right bundle branchand left anterior hemiblock (The left axis deviation could alsorepresent an old inferior infarction with regenerated R waves inthe inferior leads).

There is ST segment depression in leads V1 to V3. Thisprobably indicates reciprocal changes due to the conductiondisturbance and is not subendocardial ischemia of the anteriorwall or an acute transmural injury of the posterior wall


This tracing shows sinus tachycardia.The rate is 123/min. The PR interval isnormal at 120ms. The Q waves in II, IIIand aVF suggest an inferior infarction.The slight ST elevation in the inferiorleads and more pronounced elevation inleads V2-V3 suggest acute injury or

infarction.

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This tracing shows sinus rhythm. The rate is80/minute. Beat #11 and #14 are prematureventricular beats (as suggested by the wide QRScomplex, the compensatory pause {first beat} and theabsence of a preceding P wave). An inferior infarction(possibly acute) is suggested by the presence ofslight ST segment elevation and Q waves in leads II,III and aVF. Q waves are also seen in precordialleads V1-V4 suggestive of an old anterior infarction.The tracing would have to be compared to an old oneto determine if the infarctions are new or old.


The recording shows sinus tachycardia with a rate of110/minute, the eight beat is an atrial premature beat.The PR interval is 180 ms. There is a left axisdeviation of -70 degrees. There is a left anteriorhemiblock.

There is ST segment elevation in V2-V5 whichindicates acute anterior injury/infarction. This is mostlikely an acute anterior infarction.

There is also poor R wave progression which isprobably related to the left anterior hemiblock.


I. The recording shows sinus rhythmwith a rate of 80/minute. The PR intervalis 160 ms. There are relatively tall T

waves in the anterior leads suggesting

the presence of early anterior wall

ischemia/injury. The Q waves in III are

not significant as there are no significantQ waves in the other inferior leads.


II. This recording taken 1 hour and 15minutes later, now shows ST segmentelevation, signifying the evolution of an

acute anterior infarction.

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A 55 year old man with 4 hours of "crushing" chest pain


This patient has a very ominous ECG. There is widespread STelevation and evolving Q waves in multiple leads including the inferiorleads (II, III, and aVF) and the precordial leads (V1 to V6). This patientis having an extensive myocardial infarction. It is possible that she hashad a previous inferior MI and is now having an anterior MI (or, theopposite is also possible). Another explanation is that the LAD (leftanterior descending artery) was serving as a collateral vessel to a totallyoccluded right coronary artery. In any case, there is extensivemyocardial damage, there must be severe systolic left ventricular

dysfunction, and the cardiogenic shock is probably due to pump failure.


The ECG shows "pre-excitation" and is consistentwith the Wolff-Parkinson-White syndrome. The pre-excitation of the ventricles occurs due to a bypasstract which bypasses the delay inherent in the AVnode. The PR interval is short due to ventricular pre-excitation, which also causes a Delta wave to bepresent. This ECG shows a Type B bypass tractresulting from a right-sided accessory pathway.Bypass tracts may be associated with AVreciprocating tachycardias, rapid conduction duringatrial fibrillation, and sudden cardiac death.


This patient has ECG criteria for left ventricular hypertrophy "with strain." He meets voltagecriteria for LVH. The "sagging" ST depression respresents the "strain" pattern which istypical of severe left ventricular hypertrophy. About 80% of patients with aortic stenosiswillhave ECG criteria for left ventricular hypertrophy. Multiple criteria have been proposed forthe ECG diagnosis of LVH.

The Estes Criteria include:

1. Amplitude: 3 pointsAny one of the following:

Largest R or S wave in the limb leads >20 mm S wave in V1 or V2 greater than or equal to 30 mm R wave on V5 or V6 greater than or equal to 30 mm 2. ST-T wave changes of LVH Without digoxin: 3 points With digoxin: 1 point 3. Left atrial enlargement: 3 points

4. Left axis deviation of 30 degrees or more: 2 points5. QRS duration longer than 0.09 seconds6. Intrinsicoid deflection in V5 or V6 greater than or equal to 0.05 seconds: 1point

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This patient with mitral stenosis has marked left atrialenlargement as reflected in the P wave in lead V1. The "Pterminal force" (the state negative portion of the P wave) isgreater than one box by one box. There is marked right axisdeviation from right ventricular hypertrophy - probably resultingfrom secondary pulmonary hypertension. The elevated left atrialpressure resulting from the mitral valve obstruction has led topulmonary artery hypertension. The right ventricular hypertrophyresults as a response to the pulmonary hypertension.Atrial fibrillation typically occurs in such patients, but this patientremarkably is still in sinus rhythm. Shortness of breath,orthopnea, and exercise intolerance are typical. Patients maydevelop thrombo-embolic strokes from mitral stenosis and thesepatients require warfarin anticoagulation - particularly if they arein atrial fibrillation.


This patient has a narrow complex tachycardia. Narrow complextachycardias are essentially always supra-ventricular in origin.Conversely, wide complex tachycardias can be either supra-ventricular or ventricular in origin.In general, the differential diagnosis of narrow complextachycardia includes:

Sinus tachycardia

Atrial fibrillation Atrial flutter Multifocal atrial tachycardia AV nodal re-entry tachycardia AV reciprocating tachycardia

SA nodal re-entry tachycardia Atrial tachycardia


The patient has developed very rapid ventricular tachycardiaand the cardiovascular collapse is related to the rapid rate. Herequires immediate cardioversion. Ventricular tachycardia canoccur during the first several days of acute myocardial infarctionand is the most common cause of out-of-hospital, sudden deathcomplications of acute myocardial infarctions. Coronary careunits (CCUs) were originally developed to treat ventriculartachycardia and ventricular fibrillation in such patients - theoriginal CCUs had little else to offer. VT occurring during the first24 hours of myocardial infarction does not require specific, long-

term evaluation.


Sinus rhythm

Normal axis

Small Q waves in leads II, III, VF

Biphasic T waves in leads II, V6;inverted T

waves in leads III, VF

Markedly peaked T waves in leadsV1V2

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Complete heart block

Ventricular rate 45/min Dr Mohammed Alkebsi ([email protected])

Narrow-complex tachycardia, rate about 200/min

No P waves visible

Normal axis

Regular QRS complexes

Normal QRS complexes, ST segments and T

waves

Clinical interpretation

This is a supraventricular tachycardia, and since

no P waves are visible this is a junctional, or

atrioventricular nodal, tachycardia.


Sinus rhythm

Peaked P waves, best seen in lead II

Right axis deviation

Dominant R waves in lead V1

Deep S waves in lead V6

Inverted T waves in leads II, III, VF, V1V3

Severe right ventricular hypertrophy.


Atrial fibrillation with a ventricular rate of

about

40/min

Left axis

Left bundle branch block

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The heart rate is 120/min and the QRS complex durations is 150ms. There is a conspicuous lack of clearly seen P waves.Ventricular tachycardia is possible with the QRS complexduration of 150 ms but is unlikely as the r in V1 is small, the R/Sratio in lead V6 is less than one and there is no sign of AVdissociation or of capture beats. The rhythm is probably a sinustachycardia with first degree heart block (P waves falling on theT waves) or a junctional tachycardia.

Right bundle branch block is indicated by rSR' variantmorphology in V1-V3 and wide, slurred S waves in I and V6.There is a left axis deviation. Inferior infarction is indicated bythe qs complexes in III and aVF. It is probably old.


ECG Quiz 6


82 year old man with respiratory distress. Cath emergently?

Sinus tachycardia and LVH

with secondary repolarizationabnormality

Emergent cath revealed no

significant CAD.Dr Mohammed Alkebsi ([email protected])

78 year old man, baseline ECG.

ECG 6 months later, with chest pain.

A-Fib, PVC, LBBB

The new ECG shows LBBB with inferolateral ST elevations. Nocath was performed. (The patient was DNR/DNI with severedementia and his HCPOA did not want invasive procedures.)

Peak CK 1242, CK-MB 171.5, Troponin T 6.560.

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66 year old woman with chest pressure and abnormal troponin.

Sinus rhythm with SI, QIII, TIII, and anterior T waveinversions.

Cardiac cath revealed no significant CAD.

CT revealed massive PE.


59 year old woman h/o CABG with N/V and diaphoresis. Cath emergently?

Sinus tachycardia and LVH with

secondary repolarization abnormality.

Emergent cath was deferred. Serialcardiac biomarkers were negative.

Elective cath revealed no culprit CAD.


66 year old man with sudden CP followed by syncope. What is the diagnosis?

Sinus tachycardia with P pulmonale and

inferior injury pattern.However, with the widespread STdepressions (> 7 leads), LM or 3-vessel

disease is possible.

Cath revealed severe 3-vessel disease.Dr Mohammed Alkebsi ([email protected])

18 year old man with palpitations. What is the rhythm? His subsequent ECG:

The first ECG shows ectopic atrial tachycardia. Note the inverted P waves in leads II,III, and AVF and compare to the second ECG, when the patient is in sinus rhythm.

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