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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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Step 1: Calculate Rate
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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Step 1: Calculate Rate
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
Ventricular Fibrillation
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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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Ventricular Tachycardia
Deviation from NSR
Impulse is originating in theventricles (no P waves, wide QRS).
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Ventricular Tachycardia
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?
PR interval? none QRS duration?
Interpretation? Ventricular Fibrillation
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Ventricular Fibrillation
Deviation from NSR
Completely abnormal.
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Ventricular Fibrillation
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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2nd Degree AV Block, Type I
Deviation from NSR
PR interval progressively lengthens,then the impulse is completelyblocked (P wave not followed by
QRS).
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2nd Degree AV Block, Type I
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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2nd Degree AV Block, Type II
Deviation from NSR
Occasional P waves are completelyblocked (P wave not followed byQRS).
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2nd Degree AV Block, Type II
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?
PR interval? none QRS duration?
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.
Limb Leads Augmented Leads Precordial Leads
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Anterior MI
Remember the anterior portion of the heartis best viewed using leads V1- V4.
Limb Leads Augmented Leads Precordial Leads
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Lateral MI
So what leads do youthink the lateral portionof the heart is bestviewed?
Limb Leads Augmented Leads Precordial Leads
Leads I, aVL, and V5- V6
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Inferior MI
Now how about theinferior portion of theheart?
Limb Leads Augmented Leads Precordial Leads
Leads II, III and aVF
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Putting it all Together
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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Putting it all Together
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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ST Elevation Infarction
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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ST Elevation Infarction
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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Non-ST Elevation Infarction
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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Non-ST Elevation Infarction
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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Left Ventricular Hypertrophy
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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Left Ventricular Hypertrophy
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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Left Ventricular Hypertrophy
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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Bundle Branch Blocks
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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Bundle Branch Blocks
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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Bundle Branch Blocks
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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Bundle Branch Blocks
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