lab 6-7 ecg 2014
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Transcript of lab 6-7 ecg 2014
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ECG
ECG Basics
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Objectives
To recognize the normal rhythm of theheart - Normal Sinus Rhythm.
To recognize the 13 most commonrhythm disturbances.
To recognize an acute myocardialinfarction on a 12-lead ECG.
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Normal Impulse ConductionSinoatrial 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 forthe atria to contractbefore the ventricles
contract)
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Pacemakers of the Heart
SA Node - Dominant pacemaker with anintrinsic rate of 60 - 100 beats/minute.
AV Node - Back-up pacemaker with anintrinsic rate of 40 - 60 beats/minute.
Ventricular cells - Back-up pacemakerwith 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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Every 3 seconds (15 large boxes) ismarked by a vertical line.
This helps when calculating the heart
rate.NOTE: the following strips are not marked
but all are 6 seconds long.
3 sec 3 sec
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Reading 12-Lead ECGs
The best way to read 12-lead ECGs is to develop a step-by-step approach (just as we did for analyzing a rhythmstrip). In these modules we present a 6-step approach:
1. Calculate RATE2. Determine RHYTHM3. Determine QRS AXIS
4. Calculate INTERVALS5. Assess for HYPERTROPHY6. Look for evidence of INFARCTION
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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 large boxaway the rate is 300, 2 boxes - 150, 3boxes - 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 ormarkings 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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Normal Sinus Rhythm (NSR)
Etiology: the electrical impulse is formedin the SA node and conducted normally.
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 sinus
tachycardia, sinus bradycardia or an
arrhythmia
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Intervals
Intervals refers to the length of the PR and QT intervalsand the width of the QRS complexes. You should havealready determined the PR and QRS during the rhythmstep, but if not, do so in this step.
In the following few slides well review what is a normaland abnormal PR, QRS and QT interval. Also listed are a
few common causes of abnormal intervals.
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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
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QRS complex
< 0.10 s 0.10-0.12 s > 0.12 s
Normal Incomplete bundlebranch block
Bundle branch blockPVC
Ventricular rhythm
3 rd degree AV block withventricular escape rhythm
Incomplete bundle branch block
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Axis Axis refers to the mean QRS axis (or vector) during ventriculardepolarization. As you recall when the ventricles depolarize (in anormal heart) the direction of current flows leftward and downwardbecause most of the ventricular mass is in the left ventricle. We liketo know the QRS axis because an abnormal axis can suggestdisease such as pulmonary hypertension from a pulmonaryembolism.
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FRONTAL
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The QRS axis is determined by overlying a circle, in the frontalplane. 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 120 o
150 o
180o
-150 o
A QRS axis that falls between -30 o and -90 o is
abnormal and called leftaxis deviation .
A QRS axis that fallsbetween +90 o and +150 o
is abnormal and calledright axis deviation . A QRS axis that fallsbetween +150 o and -90 o isabnormal and calledsuperior right axis deviation .
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We can quickly determine whether the QRS axis isnormal by looking 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)
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How do we know the axis is normal when the QRS
complexes are positive in leads I and II?
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The answer lies in the fact that each frontal leadcorresponds to a location on the circle.
0o
30 o
-30 o
60 o
-60 o-90 o
-120 o
90 o 120 o
150 o
180o
-150 o
I
IIav
avL
avR
Limb leads
I = +0 o
II = +60 o
III = +120 o
Augmented leadsavL = -30 o
avF = +90 o
avR = -150 o
I
IIIII
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0o
30 o
-30 o
60 o
-60 o-90o
-120 o
90 o 120 o
150 o
180 o
-150 o
Since lead I is orientated at 0 o a wave of depolarization directed towardsit will result in a positive QRS axis. Therefore any mean QRS vectorbetween -90 o and +90 o will be positive.
I
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0o
30 o
-30 o
60 o
-60 o-90o
-120 o
90 o 120 o
150 o
180 o
-150 o
Since lead I is orientated at 0 o a wave of depolarization directed towardsit will result in a positive QRS axis. Therefore any mean QRS vectorbetween -90 o and +90 o will be positive.
Similarly, since lead II isorientated at 60 o a wave ofdepolarization directed towardsit will result in a positive QRS
axis. Therefore any mean QRSvector between -30 o and +150 o will be positive.
I
II
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0o
30 o
-30 o
60 o
-60 o-90o
-120 o
90 o 120 o
150 o
180 o
-150 o
Since lead I is orientated at 0 o a wave of depolarization directed towardsit will result in a positive QRS axis. Therefore any mean QRS vectorbetween -90 o and +90 o will be positive.
Similarly, since lead II isorientated at 60 o a wave ofdepolarization directed towardsit will result in a positive QRS
axis. Therefore any mean QRSvector between -30 o and +150 o will be positive.
Therefore, if the QRS complex
is positive in both leads I andII the QRS axis must bebetween -30 o and 90 o (whereleads I and II overlap) and, as
a result, the axis must benormal.
I
II
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0o
30 o
-30 o
60 o
-60 o-90o
-120 o
90 o 120 o
150 o
180 o
-150 o
0o
30 o
-30 o
60 o
-60 o-90o
-120 o
90 o 120 o
150 o
180 o
-150 o
Now using what you just learned fill in the following table. For example, ifthe QRS is positive 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 deviation
II
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0o
30 o
-30 o
60 o
-60 o-90o
-120 o
90 o 120 o
150 o
180 o
-150 o
0o
30 o
-30 o
60 o
-60 o-90o
-120 o
90 o 120 o
150 o
180 o
-150 o
if the QRS is negative in lead I and positive in lead II what is the QRSaxis? (normal, left, right or right superior axis deviation)
QRS Complexes
I
AxisI II+ ++ -
- +
normalleft axis deviation
right axis deviation
II
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0o
30 o
-30 o
60 o
-60 o-90o
-120 o
90 o 120 o
150 o
180 o
-150 o
if the QRS is negative in lead I and negative in lead II what is the QRSaxis? (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-90o
-120 o
90 o 120 o
150 o
180 o
-150 o
II
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Is the QRS axis normal in this ECG? No, there is left axisdeviation.
The QRS is positive in Iand negative
in II.
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To summarize:
The normal QRS axis falls between -30o
and +90o
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 +150 o. Right superior axis deviation occurs when the axis falls between between
+150 o and -90 o.
QRS Complexes
AxisI II
+ +
+ -
- +
- -
normal
left axis deviation
right axis deviation
right superioraxis deviation
A quick way todeterminethe QRS axis is to
look at the QRScomplexes in leads Iand II.
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Hypertrophy
In this step of the 12-lead ECG analysis, we use the ECGto determine if any of the 4 chambers of the heart areenlarged or hypertrophied. We want to determine if thereare any of the following:
Right atrial enlargement (RAE) Left atrial enlargement (LAE) Right ventricular hypertrophy (RVH)
Left ventricular hypertrophy (LVH)
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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
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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 smallbox in height = 1 mm
A cause of RAE is RVH from pulmonary hypertension.
> 2 boxes (in height)
> 1 boxes (in height)
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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
Notched
Negative deflection
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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.
ventricular hypertrophy
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ventricular hypertrophy
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Right ventricular hypertrophy
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RVH
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Right Ventricular Hypertrophy(RVH) & Right AtrialEnlargement (RAE)-KH
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Right ventricular hypertrophy Take a look at this ECG. What do you notice about the axis and QRS
complexes over the right ventricle (V1, V2)?
There is right axis deviation (negative in I,
positive in II) and there are tall R waves in
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Right ventricular hypertrophy Compare the R waves in V1, V2 from a normal ECG and one from
a person with RVH. Notice the R wave is normally small in V1, V2 because the right
ventricle does not have a lot of muscle mass. But in the hypertrophied right ventricle the R wave is tall in V1, V2.
Normal RVH
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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.
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Left Ventricular
Hypertrophy
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Left Ventricular HypertrophyCompare 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)
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Left Ventricular HypertrophyWhy 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 resultingin increased QRS voltage.
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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 or V2
exceeds 35 mm.
However, for now, allyou need to know isthat the QRS voltage
increases with LVH.
Left ventricular hypertrophy
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Left ventricular hypertrophy Take a look at this ECG. What do you notice about the axis and QRS
complexes over the left ventricle (V5, V6) and right ventricle (V1, V2)?
There is left axis deviation (positive in I, negativein 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).
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Left ventricular hypertrophy To diagnose LVH you can use the following criteria *:
R in V5 (or V6) + S in V1 (or V2) > 35 mm , or
avL R > 13 mm
A common cause of LVHis hypertension.
* There are severalother criteria for thediagnosis of LVH.
S = 13 mm
R = 25 mm
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A 63 yo man has longstanding, uncontrolled hypertension. Is there evidenceof 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).
ALTERED IMPULSE
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ALTERED IMPULSECONDUCTION
1. Conduction blocks
(bradyarrhythmias)
2. Process of reentry(tachyarrhythmias )
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Bundle Branch Blocks
Turning our attention to bundle branch blocks
Remember normalimpulse conduction is
SA node AV node Bundle of His Bundle Branches Purkinje fibers
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Normal Impulse ConductionSinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
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Bundle Branch BlocksSo, depolarization ofthe Bundle Branchesand Purkinje fibers are
seen as the QRScomplex on the ECG.
Therefore, a conductionblock of the BundleBranches would bereflected as a change inthe QRS complex.
RightBBB
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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) .
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Bundle Branch BlocksWhy does the QRS complex widen?
When the conduction
pathway is blocked itwill take longer forthe electrical signalto pass throughout
the ventricles.
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Right
BundleBranchBlocks
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Right Bundle Branch BlocksWhat 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
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Left BundleBranch
Blocks
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Left Bundle Branch BlocksWhat 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
3. Axis deviations:
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Right axis
Right axis
Left axis
Right axis
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Right axis
Left axis in frontal leads,and right axis in precordialleads
Asistol
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Arrhythmia Formation
Arrhythmias can arise from problems inthe:
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 BradycardiaSinus Tachycardia
Sinus Tachycardia may be an appropriateresponse 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 AtrialContractions (PACs)
Atrial Flutter
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A re-entrantpathway occurs
when an impulseloops and resultsin self-
perpetuatingimpulseformation.
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Atrial Cell Problems
Atrial cells can also: fire continuously
from multiple fociorfire continuouslydue to multiplemicro re-entrantwavelets
Atrial Fibrillation
Atrial Fibrillation
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Multiple micro re-entrant waveletsrefers to wanderingsmall areas of
activation whichgenerate fine chaoticimpulses. Colliding
wavelets can, in turn,generate new foci ofactivation.
Atrial tissue
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AV Junctional Problems
The AV junction can: fire continuously
due to a loopingre-entrant circuit
block impulses
coming from theSA Node
Paroxysmal
SupraventricularTachycardia
AV Junctional Blocks
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Ventricular Cell Problems
Ventricular cells can: fire occasionally
from 1 or more foci fire continuously
from multiple foci
fire continuouslydue to a loopingre-entrant circuit
Premature Ventricular
Contractions (PVCs)Ventricular Fibrillation
Ventricular Tachycardia
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Arrhythmias
Sinus Rhythms Premature Beats Supraventricular Arrhythmias Ventricular Arrhythmias
AV Junctional Blocks
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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
Etiology: SA node is depolarizing slower
than normal, impulse is conductednormally (i.e. normal PR and QRSinterval).
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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 depolarizing faster
than normal, impulse is conductednormally.
Remember: sinus tachycardia is a
response to physical or psychologicalstress, not a primary arrhythmia.
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Premature Beats
Premature Atrial Contractions (PACs)
Premature Ventricular Contractions (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 the timing aredifferent than a normally generatedpulse from the SA node.
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Premature Atrial Contractions
Etiology: Excitation of an atrial cell
forms an impulse that is then conductednormally through the AV node andventricles.
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When an impulse originates anywhere inthe atria (SA node, atrial cells, AV node,
Bundle of His) and then is conductednormally through the ventricles, the QRSwill be narrow (0.04 - 0.12 s).
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Rhythm #4
60 bpm Rate? Regularity? occasionally irreg.
none for 7 th 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 prematurebeats and look alike, they are calleduniform. When they look different, they arecalled multiform.
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PVCs
Etiology: One or more ventricular cellsare depolarizing and the impulses areabnormally conducting through theventricles.
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When an impulse originates in aventricle, conduction through the
ventricles will be inefficient and the QRSwill be wide and bizarre.
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Ventricular Conduction
Normal Signal moves rapidlythrough the ventricles
Abnormal Signal moves slowlythrough the ventricles
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Supraventricular Arrhythmias
Atrial Fibrillation
Atrial Flutter Paroxysmal Supraventricular
Tachycardia
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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
Atrial Fibrillation
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Atrial Fibrillation
Deviation from NSR No organized atrial depolarization, so
no normal 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
> 80 years old
Atrial Fibrillation
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Etiology: Recent theories suggest that itis due to multiple re-entrant wavelets
conducted between the R & L atria.Either way, impulses are formed in atotally unpredictable fashion. The AVnode allows some of the impulses topass through at variable intervals (sorhythm is irregularly irregular).
h h
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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
l l
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Atrial Flutter
Deviation from NSR No P waves. Instead flutter waves (note
sawtooth pattern) are formed at a rateof 250 - 350 bpm.
Only some impulses conduct throughthe AV node (usually every otherimpulse).
A i l Fl
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Atrial Flutter
Etiology: Reentrant pathway in the right
atrium with every 2nd, 3rd or 4thimpulse generating a QRS (others areblocked in the AV node as the node
repolarizes).
Rh h #7
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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)
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.
PSVT
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PSVT
Etiology: There are several types of
PSVT but all originate above theventricles (therefore the QRS is narrow).
Most common: abnormal conduction inthe AV node (reentrant circuit looping inthe AV node).
V i l A h h i
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Ventricular Arrhythmias
Ventricular Tachycardia
Ventricular Fibrillation
Rh h #8
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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
V t i l T h di
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Ventricular Tachycardia
Deviation from NSR Impulse is originating in the ventricles
(no P waves, wide QRS).
V t i l T h di
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Ventricular Tachycardia
Etiology: There is a re-entrant pathway
looping in a ventricle (most commoncause).
Ventricular tachycardia can sometimes
generate enough cardiac output toproduce a pulse; at other times no pulsecan be felt.
Rh th #9
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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
V t i l Fib ill ti
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Ventricular Fibrillation
Deviation from NSR Completely abnormal.
V t i l Fib ill ti
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Ventricular Fibrillation
Etiology: The ventricular cells are
excitable and depolarizing randomly.
Rapid drop in cardiac output and death
occurs if not quickly reversed
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AV Nodal Blocks
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AV 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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BAV Gr. II, Mobitz II
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Rhythm #10
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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
Rhythm #11
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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
Rhythm #12
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Rhythm #12
40 bpm Rate? Regularity? regular
nl, 2 of 3 no QRS
0.08 s
P waves? PR interval? 0.14 s QRS duration?
Interpretation? 2nd Degree AV Block, Type II
Rhythm #13
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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
Remember
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Remember When an impulse originates in a ventricle,
conduction through the ventricles will beinefficient and the QRS will be wide and
bizarre.
IHD
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IHD
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ST Elevation Infarction
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ST Elevation InfarctionHeres 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
Non-ST Elevation Infarction
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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-waveinversion persists
Ischemia
Infarction
Fibrosis
Diagnosing a MI
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Diagnosing a MITo diagnose a myocardial infarction youneed to go beyond looking at a rhythmstrip and obtain a 12-Lead ECG.
RhythmStrip
12-LeadECG
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Anterior MI
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Anterior MI
Remember the anterior portion of the heart isbest viewed using leads V 1- V4.
Limb Leads Augmented Leads Precordial Leads
Lateral MI
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Lateral MISo what leads do you thinkthe lateral portion of theheart is best viewed?
Limb Leads Augmented Leads Precordial Leads
Leads I, aVL, and V 5- V6
Inferior MI
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Inferior MINow how about theinferior portion of theheart?
Limb Leads Augmented Leads Precordial Leads
Leads II, III and aVF
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What is the rate? Approx. 132 bpm (22 R waves x 6)
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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.
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What is the rhythm? Sinus tachycardia
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What is the QRS axis? Right axis deviation (- in I, + in II)
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Is there evidence ofatrial enlargement?
No (no peaked, notched or negativelydeflected P waves)
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Is there evidence ofventricular hypertrophy?
No (no tall R waves in V1/V2 or V5/V6)
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Infarct: Are there abnormalQ waves?
Yes! In leads V1-V6 and I, avL
Any
Any
Any
20
30
30
30
3030
30
R40
R50
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Infarct: Is the ST elevationor depression?
Yes! Elevation in V2-V6, I and avL.Depression in II, III and avF.
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Infarct: Are there T wavechanges?
No
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