BSU CON Basic-Advance ECG Interpretation 2012

8/2/2019 BSU CON Basic-Advance ECG Interpretation 2012

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ECG RhythmInterpretation

LEVI ADRIANO SANTANA, RN

Bulacan State UniversityCollege of Nursing

Philippine Heart Association/ Philippine College of Cardioloy

Certified BLS/ ACLS Provider


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ECG Basics


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Normal Impulse Conduction

Sinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers


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Impulse Conduction & the ECG

Sinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers


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The PQRST

P wave - Atrial

depolarization

T wave - Ventricularrepolarization

QRS - Ventriculardepolarization


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The PR Interval

Atrial depolarization

+

delay in AV junction(AV node/Bundle of His)

(delay allows time

for the atria tocontract before theventricles contract)


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Pacemakers of the Heart

SA Node - Dominant pacemaker withan intrinsic rate of 60 - 100beats/minute.

AV Node - Back-up pacemaker withan intrinsic rate of 40 - 60

beats/minute. Ventricular cells - Back-up pacemaker

with an intrinsic rate of 20 - 45 bpm.


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The ECG Paper

Horizontally

One small box - 0.04 s

One large box - 0.20 s

Vertically

One large box - 0.5 mV


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The ECG Paper (cont)

Every 3 seconds (15 large boxes) ismarked by a vertical line.

This helps when calculating the heartrate.

3 sec 3 sec

l


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How to Analyze aRhythm


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Rhythm Analysis

Step 1: Calculate rate. Step 2: Determine regularity.

Step 3: Assess the P waves.

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


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Step 1: Calculate Rate

Option 1 Count 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


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Option 2

Find a R wave that lands on a bold line.

Count the # of large boxes to the next Rwave. If the second R wave is 1 largebox away the rate is 300, 2 boxes - 150,3 boxes - 100, 4 boxes - 75, etc. (cont)

R wave


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Option 2 (cont)

Memorize the sequence:

300 - 150 - 100 - 75 - 60 - 50

Interpretation?

300

150

100

75

60

50

Approx. 1 box less than

100 = 95 bpm


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Step 2: Determine regularity

Look at the R-R distances (using a caliper

or markings on a pen or paper).

Regular (are they equidistant apart)?Occasionally irregular? Regularly irregular?Irregularly irregular?

Interpretation?Regular

R R


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Step 3: 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


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Step 4: Determine PR interval

Normal: 0.12 - 0.20 seconds.(3 - 5 boxes)

Interpretation?0.12 seconds


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Step 5: QRS duration

Normal: 0.04 - 0.12 seconds.(1 - 3 boxes)

Interpretation?

0.08 seconds


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Rhythm Summary

Rate 90-95 bpm

Regularity regular

P waves normal

PR interval 0.12 s

QRS duration 0.08 s

Interpretation?

Normal Sinus Rhythm


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Normal Sinus Rhythm


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Normal Sinus Rhythm (NSR)

Etiology: the electrical impulse isformed in the SA node and conductednormally.

This is the normal rhythm of the heart;other rhythms that do not conduct viathe typical pathway are calledarrhythmias.


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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 sinustachycardia, sinus bradycardia or anarrhythmia


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Arrhythmia Formation

Arrhythmias can arise from problemsin the:

Sinus node Atrial cells

AV junction

Ventricular cells


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SA Node Problems

The SA Node can:

fire too slow

fire too fast

Sinus Bradycardia

Sinus Tachycardia

Sinus Tachycardia may be an appropriate

response to stress.


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Atrial Cell Problems

Atrial cells can:

fire occasionally

from a focus

fire continuouslydue to a loopingre-entrant circuit

Premature Atrial

Contractions (PACs)

Atrial Flutter


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Teaching Moment

A re-entrantpathway occurswhen animpulse loopsand results inself-

perpetuatingimpulseformation.


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Atrial Cell Problems

Atrial cells can also: fire continuously

from multiple fociorfire continuously

due to multiplemicro re-entrantwavelets

Atrial Fibrillation

Atrial Fibrillation


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Teaching Moment

Multiple micro re-entrant wavelets

refers to wandering

small areas ofactivation whichgenerate fine chaotic

impulses. Collidingwavelets can, in turn,generate new foci of

activation.

Atrial tissue


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AV Junctional Problems

The AV junctioncan:

fire continuouslydue to a loopingre-entrant circuit

block impulsescoming from theSA Node

Paroxysmal

SupraventricularTachycardia

AV Junctional

Blocks


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Ventricular Cell Problems

Ventricular cells can:

fire occasionallyfrom 1 or more

foci fire continuously

from multiple foci

fire continuouslydue to a looping

re-entrant circuit

Premature Ventricular

Contractions (PVCs)

Ventricular Fibrillation

VentricularTachycardia


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Arrhythmias

Sinus Rhythms

Premature Beats


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Rhythm #1

30 bpm Rate?

Regularity? regular

normal

0.10 s

P waves?

PR interval? 0.12 s

QRS duration?

Interpretation? Sinus Bradycardia


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Sinus Bradycardia

Deviation from NSR- Rate < 60 bpm


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Sinus Bradycardia

Etiology: SA node is depolarizingslower than normal, impulse isconducted normally (i.e. normal PRand QRS interval).


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Rhythm #2

130 bpm Rate?

Regularity? regular

normal

0.08 s

P waves?

PR interval? 0.16 s

QRS duration?

Interpretation? Sinus Tachycardia


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Sinus Tachycardia

Deviation from NSR

- Rate > 100 bpm


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Sinus Tachycardia

Etiology: SA node is depolarizingfaster than normal, impulse isconducted normally.

Remember: sinus tachycardia is aresponse to physical or psychologicalstress, not a primary arrhythmia.


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Premature Beats

Premature Atrial Contractions(PACs)

Premature VentricularContractions (PVCs)


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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


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Premature Atrial Contractions

Deviation from NSR These ectopic beats originate in the

atria (but not in the SA node),therefore the contour of the P

wave, the PR interval, and thetiming are different than a normallygenerated pulse from the SA node.


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Premature Atrial Contractions

Etiology: Excitation of an atrial cellforms an impulse that is thenconducted normally through the AVnode and ventricles.


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Teaching Moment

When an impulse originatesanywhere in the atria (SA node, atrial

cells, AV node, Bundle of His) andthen is conducted normally throughthe ventricles, the QRS will be narrow(0.04 - 0.12 s).


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Rhythm #4

60 bpm Rate?

Regularity? occasionally irreg.

none for 7th QRS

0.08 s (7th wide)

P waves?

PR interval? 0.14 s

QRS duration?

Interpretation? Sinus Rhythm with 1 PVC


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PVCs

Deviation from NSR Ectopic beats originate in the ventricles

resulting in wide and bizarre QRScomplexes.

When there are more than 1 premature

beats and look alike, they are calleduniform. When they look different, theyare called multiform.


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PVCs

Etiology: One or more ventricularcells are depolarizing and theimpulses are abnormally conducting

through the ventricles.


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Teaching Moment

When an impulse originates in aventricle, conduction through theventricles will be inefficient and the

QRS will be wide and bizarre.


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Ventricular Conduction

NormalSignal moves rapidlythrough the ventricles

AbnormalSignal moves slowlythrough the ventricles


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Arrhythmias

Supraventricular Arrhythmias

Ventricular Arrhythmias


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Rhythm #5

100 bpm Rate? Regularity? irregularly irregular

none

0.06 s

P waves?

PR interval? none

QRS duration?

Interpretation? Atrial Fibrillation


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Atrial Fibrillation

Deviation from NSR

No organized atrial depolarization,

so no normal P waves (impulses arenot originating from the sinusnode).

Atrial activity is chaotic (resulting inan irregularly irregular rate).

Common, affects 2-4%, up to 5-

10% if > 80 years old


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Atrial Fibrillation

Etiology: Recent theories suggestthat it is due to multiple re-entrant

wavelets conducted between the R &L atria. Either way, impulses areformed in a totally unpredictablefashion. The AV node allows some ofthe impulses to pass through atvariable intervals (so rhythm isirregularly irregular).


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Rhythm #6

70 bpm Rate? Regularity? regular

flutter waves

0.06 s

P waves?

PR interval? none

QRS duration?

Interpretation? Atrial Flutter


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Atrial Flutter

Deviation from NSR No P waves. Instead flutter waves

(note sawtooth pattern) areformed at a rate of 250 - 350 bpm.

Only some impulses conductthrough the AV node (usually everyother impulse).


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Atrial Flutter

Etiology: Reentrantpathway in the rightatrium with every2nd, 3rd or 4thimpulse generating a

QRS (others areblocked in the AVnode as the noderepolarizes).


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Rhythm #7

74148 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)


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PSVT

Deviation from NSR

The heart rate suddenly speeds up,often triggered by a PAC (not seenhere) and the P waves are lost.


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PSVT

Etiology: There are several types of

PSVT but all originate above theventricles (therefore the QRS isnarrow).

Most common: abnormal conductionin the AV node (reentrant circuitlooping in the AV node).


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Ventricular Arrhythmias

Ventricular Tachycardia



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Rhythm #8

160 bpm Rate?

Regularity? regular

none

wide (> 0.12 sec)

P waves?

PR interval? none QRS duration?

Interpretation? Ventricular Tachycardia


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Deviation from NSR

Impulse is originating in theventricles (no P waves, wide QRS).


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Etiology: There is a re-entrant

pathway looping in a ventricle (mostcommon cause).

Ventricular tachycardia cansometimes generate enough cardiacoutput to produce a pulse; at othertimes no pulse can be felt.


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Rhythm #9

none Rate?

Regularity? irregularly irreg.

none

wide, if recognizable

P waves?


Interpretation? Ventricular Fibrillation


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Deviation from NSR

Completely abnormal.


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Etiology: The ventricular cells areexcitable and depolarizing randomly.

Rapid drop in cardiac output anddeath occurs if not quickly reversed


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Atrioventricular Nodal Blocks

1st Degree AV Block

2nd Degree AV Block, Type I

2nd Degree AV Block, Type II

3rd Degree AV Block


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Rhythm #10

60 bpm Rate?

Regularity? regular

normal

0.08 s

P waves?

PR interval? 0.36 s QRS duration?

Interpretation? 1st Degree AV Block


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1st Degree AV Block

Deviation from NSR

PR Interval > 0.20 s


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1st Degree AV Block

Etiology: Prolonged conduction delayin the AV node or Bundle of His.


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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

a.k.a. Weckebach or Mobitz I


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Deviation from NSR

PR interval progressively lengthens,then the impulse is completelyblocked (P wave not followed by

QRS).


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Etiology: Each successive atrialimpulse encounters a longer andlonger delay in the AV node until oneimpulse (usually the 3rd or 4th) fails

to make it through the AV node.


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Deviation from NSR

Occasional P waves are completelyblocked (P wave not followed byQRS).


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Etiology: Conduction is all or nothing

(no prolongation of PR interval);typically block occurs in the Bundle ofHis.


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Rhythm #13

40 bpm Rate?

Regularity? regular

no relation to QRS

wide (> 0.12 s)

P waves?


Interpretation?3rd Degree AV Block

a.k.a. Complete Heart Block


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3rd Degree AV Block

Deviation from NSR

The P waves are completely blockedin the AV junction; QRS complexesoriginate independently from below

the junction.


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3rd Degree AV Block

Etiology: There is complete block of

conduction in the AV junction, so theatria and ventricles form impulsesindependently of each other. Without

impulses from the atria, the ventriclesown intrinsic pacemaker kicks in ataround 30 - 45 beats/minute.


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Remember

When an impulse originates in aventricle, conduction through theventricles will be inefficient and the

QRS will be wide and bizarre.

Diagnosing a Myocardial


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Diagnosing a MyocardialInfarction


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Diagnosing a MI

To diagnose a myocardial infarction youneed to go beyond looking at a rhythmstrip and obtain a 12-Lead ECG.

Rhythm

Strip

12-Lead

ECG


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RhythmStrip

12-Lead

ECG


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The 12-Lead ECG

The 12-Lead ECG sees the heartfrom 12 different views.

Therefore, the 12-Lead ECG helpsyou see what is happening indifferent portions of the heart.

The rhythm strip is only 1 ofthese 12 views.


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The 12-Leads

The 12-leads include:

3 Limb leads

(I, II, III)

3 Augmented leads(aVR, aVL, aVF)

6 Precordial leads(V1- V6)


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Views of the Heart

Some leads geta good view ofthe:

Anterior portion

of the heart

Lateral portion

of the heart

Inferior portion

of the heart


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ST Elevation

One way todiagnose anacute MI is to

look forelevation ofthe ST

segment.


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ST Elevation (cont)

Elevation of theST segment

(greater than 1small box) in 2leads isconsistent with

a myocardialinfarction.


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Anterior View of the Heart

The anterior portion of the heart isbest viewed using leads V1- V4.


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Anterior Myocardial Infarction

If you see changes in leads V1 - V4that are consistent with amyocardial infarction, you canconclude that it is an anterior wallmyocardial infarction.


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Putting it all Together

Do you think this person is having amyocardial infarction. If so, where?


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InterpretationY thi i h i t


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Yes, this person is having an acuteanterior wall myocardial infarction.


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Other MI Locations

Now that you know where to look for ananterior wall myocardial infarction letslook at how you would determine if the

MI involves the lateral wall or theinferior wall of the heart.


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Other MI Locations

First, take a lookagain at thispicture of theheart.

Anterior portion

of the heart

Lateral portionof the heart

Inferior portion

of the heart


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Other MI Locations

Second, remember that the 12-leads of the ECG lookat different portions of the heart. The limb andaugmented leads see electrical activity movinginferiorly (II, III and aVF), to the left (I, aVL) and tothe right (aVR). Whereas, the precordial leads see

electrical activity in the posterior to anteriordirection.

Limb Leads Augmented Leads Precordial Leads


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Other MI Locations

Now, using these 3 diagrams lets figurewhere to look for a lateral wall and inferiorwall MI.



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Anterior MI

Remember the anterior portion of the heartis best viewed using leads V1- V4.



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Lateral MI

So what leads do youthink the lateral portionof the heart is bestviewed?


Leads I, aVL, and V5- V6


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Inferior MI

Now how about theinferior portion of theheart?


Leads II, III and aVF


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Now, where do you think this person ishaving a myocardial infarction?


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Inferior Wall MIThis is an inferior MI Note the ST


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This is an inferior MI. Note the STelevation in leads II, III and aVF.


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How about now?


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Anterolateral MIThis persons MI involves both the anterior wall


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This persons MI involves both the anterior wall(V2-V4) and the lateral wall (V5-V6, I, and aVL)!


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ST Elevation and

Non-ST Elevation MIs


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ST Elevation and non-ST Elevation MIs

When myocardial blood supply is abruptlyreduced or cut off to a region of the heart,a sequence of injurious events occurbeginning with ischemia (inadequate

tissue perfusion), followed by necrosis(infarction), and eventual fibrosis(scarring) if the blood supply isn'trestored in an appropriate period of time.

The ECG changes over time with each ofthese events


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ECG Changes

Ways the ECG can change include:

Appearanceof pathologicQ-waves

T-waves

peaked flattened inverted

ST elevation &depression


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ECG Changes & the Evolving MI

There are twodistinct patternsof ECG change

depending if theinfarction is:

ST Elevation(Transmural orQ-wave), or

Non-ST Elevation (Subendocardialor 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 of

Q-waves

ST segments and T-waves return tonormal, but Q-waves persist

Ischemia

Infarction

Fibrosis


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Heres a diagram depicting an evolving infarction:

A. Normal ECG prior to MI

B. Ischemia from coronary artery

occlusion results in ST depression (notshown) and peaked T-waves

C. Infarction from ongoing ischemiaresults in marked ST elevation

D/E. Ongoing infarction with appearanceof pathologic Q-waves and T-waveinversion

F. Fibrosis (months later) with persistentQ- waves, but normal ST segment andT- waves


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Heres an ECG of an inferior MI:

Look at theinferior leads

(II, III, aVF).

Question:What ECGchanges doyou see?

ST elevationand Q-waves

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


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Non-ST Elevation Infarction

Heres an ECG of an inferior MI later in time:

Now what do you see in the inferior leads?

ST elevation, Q-waves and T-wave inversion


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ST depression & T-waveinversion

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


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

Note the STdepressionand T-wave

inversion inleads V2-V6.

Question:What area of

the heart isinfarcting?

Anterolateral


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Left Ventricular Hypertrophy


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Compare these two 12-lead ECGs. Whatstands out as different with the second one?

Normal Left Ventricular Hypertrophy

Answer: The QRS complexes are very tall(increased voltage)

f l h


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Why is left ventricular hypertrophy characterized by tallQRS complexes?

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase inelectrical forces moving through the myocardium resulting

in increased QRS voltage.

f l h


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Criteria exists to diagnose LVH using a 12-lead ECG. For example:

The R wave in V5 or V6 plus the S wave in V1 orV2 exceeds 35 mm.

However, for now, allyou need to know isthat the QRS voltageincreases with LVH.


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Bundle Branch Blocks

B dl B h Bl k


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Turning our attention to bundle branchblocks

Remember normal

impulse conduction is

SA node

AV node

Bundle of His Bundle BranchesPurkinje fibers

N l I l C d ti


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Normal Impulse Conduction

Sinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers

B dl B h Bl k


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So, depolarization ofthe Bundle Branchesand Purkinje fibersare seen as the QRS

complex on the ECG.

Therefore, a conductionblock of the Bundle

Branches would bereflected as a change inthe QRS complex.

Right BBB

B dl B h Bl k


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With 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 branchblock).

B dl B h Bl k


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Why does the QRS complex widen?

When the conduction

pathway is blocked itwill take longer forthe electrical signalto pass throughout

the ventricles.

Ri ht B dl B h Bl k


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Right Bundle Branch Blocks

What QRS morphology is characteristic?

V1

For RBBB the wide QRS complex assumes aunique, virtually diagnostic shape in those

leads overlying the right ventricle (V1 and V2).

Rabbit Ears

L ft B dl B h Bl k


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Left Bundle Branch Blocks

What QRS morphology is characteristic?

For LBBB the wide QRS complex assumes acharacteristic change in shape in those leads

opposite the left ventricle (right ventricularleads - V1 and V2).

Broad,

deep Swaves

Normal


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END

Documents

BSU CON Basic-Advance ECG Interpretation 2012