ecg fgy final
TRANSCRIPT
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ELECTROCARDIOGRAMCC Ybaez, Fiel G.
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ECG Diagnostic tool which measures the
electrical activity of the heart providing arecord of cardiac electrical activity, as wellas information about the hearts function and structure
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CONDUCTING SYSTEM OF THE HEARTSinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
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USES OF ECG1. to determine cardiac rate2. to define cardiac rhythm3. to detect signs of chamber hypertrophy4. to diagnose old or new myocardial
infarction5. to identify intracardiac conduction
disturbances6. to aid in the diagnosis of ischemic heart
disease, pericarditis, myocarditis, electrolyteabnormalities, and pacemaker malfunction
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Resting state : myocytes are POLARIZED Negatively charged
Stimulated to contract : DEPOLARIZED Positively charged Depolarization moves as a WAVE throughout
the myocardium causing contraction Recovery phase : REPOLARIZED
Myocytes return to resting state
BASICS
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REMEMBER: as the positive wave within the heart cells moves
AWAY from a positive (skin) electrode, there is aNEGATIVE (DOWNWARD) DEFLECTION recorded on ECG.
as the positive wave within the heart cellsmoves TOWARD a positive (skin) electrode,there is a POSITIVE(UPWARD) DEFLECTION recorded on ECG.
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Pacemakers of the Heart SA Node - Dominant pacemaker with an
intrinsic rate of 60 - 100 beats/minute . Atrial foci - Back-up pacemaker with an
intrinsic rate of 60-80 beats/min . AV Node - Back-up pacemaker with an
intrinsic rate of 40 - 60 beats/minute . Ventricular cells - Back-up pacemaker
with an intrinsic rate of 20 - 45 bpm .
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ECG Tracing
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WAVEFORMS
Movement away from the baseline,either in a (+) or (-) direction
1) P wave Atrial depolarization
2) QRS complex
Ventricular depolarization(N:0.04 0.12 seconds)
3) T wave
Ventricular repolarization
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SEGMENTS
Lines between waveforms1) PR segment conduction delay
through the AV node2) ST segment isoelectric; ventricles
still depolarized
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INTERVALS Combination of waveforms and segments
1) PR interval - atrial depolarization +conduction delay through the AV node
(N: 0.12 0.20 secs) 2) QT interval - ventricular depolarization +
ventricular repolarization
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LIMB LEADSA. Standard Bipolar Leads (frontal axis)
Lead I: Right arm-left armLead II: Right arm-left legLead III: Left arm-left leg
B. Augmented Unipolar Leads
aVR: Right armaVL: Left armaVF: Left foot
Figure 3. Heference system
Limb Leads
Right arm : RA ( red )Left arm : LA ( yellow )Right Foot : ground ( black )Left foot : L F ( green )
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CHEST LEADSV1 = 4 th ICS RSBV2 = 4 th ICS LSBV3 = between V2 & V4
V4 = 5 th ICS LMCLV5 = 5 th ICS LAALV6 = 5 th ICS LMAL
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The ECG PaperAMPLITUDE Measurement
Vertical, measured in mVOne large box - 0.5 mV
TIME measurementHorizontal, in secsRecording speed of ECG paper = 25mm/secTherefore:
1mm = 0.04sec (1 small square) 5mm = 0.20sec (1 big square) 25mm = 1.0sec (5 big squares) 30mm = 1.2sec (6 big squares)
75mm = 3.0sec (15 big squares)
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COMPONENTS OF ECG
INTERPRETATION1) RATE
2) RHYTHM3) AXIS4) HYPERTROPHY5) INFARCTION
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1. Calculate the heart rate .
Heart rate assessment by rule of 300
Steps in ECG Interpretation
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HEART RATE1500 method Divide 1500 by the number of small
squares between 2 consecutive QRScomplexes
6-second method
- count the number of QRS complexesin a 6 second strip and multiply by 10
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2. Rhythm Analysis Determine regularity
Assess the P waves Determine PR interval Determine QRS duration
Steps in ECG Interpretation
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Normal Sinus Rhythm (NSR)
Etiology: the electrical impulse is formed in the SAnode and conducted normally.
This is the normal rhythm of the heart; other rhythms that
do not conduct via the typical pathway are calledarrhythmias.
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2. Rhythm: Determine regularity
Look at the R-R distances Regular (are they equidistant apart)?
Occasionally irregular ? Regularly irregular ?
Irregularly irregular ?
R R
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2. Rhythm: 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 ?
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P wave normal: Upright in ALL leads except aVR;
height < 2.5 mm in lead II width < 0.12 s in lead II
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2. Rhythm: Determine PR intervalDetermine whether the rhythm is regular or irregular. Measure the PR interval . Normal is0.12 0.20 secs .
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2. Rhythm: QRS duration
Normal: 0.04 - 0.12 seconds.
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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, sinusbradycardia or an arrhythmia
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II. RHYTHM ABNORMALITIES
1. Irregular Rhythms2. Escape3. Premature Beats
4. Tachyarrhythmias5. Flutter 6. Fibrillation7. Heart Blocks
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IRREGULAR RHYTHMS: Wanderingpacemaker
Pacemaker activity wandering from the SA node tonearby atrial automaticity foci
P wave shape varies Atrial rate less than 100 Irregular ventricular rhythm
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IRREGULAR RHYTHMS: Multifocal AtrialTachycardia
P wave shape varies Atrial rate exceeds 100 Irregular ventricular rhythm
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IRREGULAR RHYTHMS: Atrial Fibrillation
Deviation from NSR No organized atrial depolarization, so no
normal P waves Atrial activity is chaotic (resulting in an
irregularly irregular rate), rapid-firing of multiple atrial automaticity foci
Occ. Atrial depolarization gets through the AV Nodeto stimulate the ventricles thus an irregularventricular rhythm .
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ESCAPE (Check for P waves and rate) ESCAPE RHYTHM : an automaticity focus escapes
overdrive suppression to pace at its inherent rate Atrial escape rhythm Junctional escape rhythm Ventricular escape rhythm
ESCAPE BEAT : an automaticity focus transiently escapes overdrive suppression to emit one beat
Atrial escape beat
Junctional escape beat Ventricular escape beat
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PREMATURE BEATS: Premature AtrialBeat
Originates suddenly from an irritable atrial automaticityfocus and produces an abnormal P wave earlier thanexpected
Due to: adrenaline, increased sympathetic stimulation,
caffeine, amphetamines, cocaine or other B1 receptor stimulants, excess digitalis, hyperthyroidism
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PREMATURE BEATS: PrematureJunctional Beat
Occurs when an irritable automaticity focus in the AVJunction suddenly fires a premature stimulus that isconducted to and depolarizes the ventricles (andsometimes the atria inverted p wave)
Due to: adrenaline, increased sympathetic stimulation,caffeine, amphetamines, cocaine or other B1 receptor stimulants, excess digitalis, hyperthyroidism
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PREMATURE BEATS: PrematureVentricular Contraction
Originates suddenly in an irritable automaticity focus in aventricle and produces a giant ventricular complex onECG
6 or more PVCs per minute is considered pathological Due to: low oxygen or hypokalemia
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TACHYARRHYTHMIASSupraventricular tachycardia (SVT)
-This is a term which include both nodal and atrial tachycardia
Paroxysmal AtrialTachycardia
Sudden, rapid firing of a veryirritable atrial automaticity focusRate: 150-250/min
P waves that do not look like thesinus generated p waves.
Paroxysmal JunctionalTachycardia
AV junction focus produces a rapidsequence of QRS-T cycles at 150-250/minQRS may be slightly widened
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TACHYARRHYTHMIASParoxysmal Ventricular Tachycardia (PVT or VT) Very irritable ventricular automaticity focus that suddenly
paces at 150-250/min Enormous, consecutive, PVC-like complexes Independent pacing of the atria and the ventricles Signify cardiac hypoxia
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FLUTTER
Atrial flutter Rate of 250 to 350 bpm Flutter waves or saw tooth
Ventricular FlutterSingle ventricular automaticity focus firing at 250-350/minSmooth sine-wave appearance with no jagged waves
Almost invariable deteriorates into ventricular fibrillation
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FIBRILLATIONAtrial fibrillation
Many irritable atrial fociRapid, erratic atrial rhythm 350-450 bpmIrregular ventricular response
Ventricular fibrillationMultiple ventricular foci rapidly discharge producing a totally erraticventricular rhythm without identifiable wavesbag of worms Rate 350-450bpm
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HEART BLOCKS
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P-R interval is prolonged (i.e. >0.20 sec .)
FIRST-DEGREE AV BLOCK
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Progressive prolongation of P-R interval with eachsucceeding beat until there is a dropped beat
Longest P-R interval is the one immediately beforethe dropped beat
Shortest P-R interval is the one associated with thefirst conducted beat after the dropped beat
SECOND DEGREE AV BLOCKTYPE I (WENCKEBACH)
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P-R interval of conducted beats may be normal or longbut fixed , then there is a dropped beat
P-R interval must be constant for all conducted beats
MOBITZ TYPE II SECOND DEGREE AV BLOCK
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Any form of atrial activity may be seen or there may be no
atrial activity
no consistent or meaningful relationship between atrialand ventricular activity. Variable PR and RP intervals.
QRS may be normal in shape, duration and axis but moreoften are abnormal and are of constant morphology
QRS rate is usually constant and lies within the range of 20-40 beats/min.
THIRD DEGREE (COMPLETE) AV BLOCK
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RIGHT BUNDLE BRANCH BLOCK
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LEFT BUNDLE BRANCH BLOCK
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3. Determine the QRS axis Axis refers to the direction of
depolarization as it passes through theheart The mean QRS vector points downward
and toward the patients left side
Steps in ECG Interpretation
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The QRS axis is determined by overlying a circle, in the frontal plane.
By convention, the degrees of the circle are as shown. The normal QRS axis lies between -30 o and +90 o .
0o
30 o
-30 o
60 o
-60 o-90 o
-120 o
90 o 120o
150 o
180 o
-150 o
A QRS axis that falls between -30 o and -90 o is
abnormal and called left axis deviation . A QRS axis that falls between +90 o and +150 o is abnormal andcalled right axis deviation .
A QRS axis that falls between +150 o and -90 o is abnormal andcalled extreme right axisdeviation .
3. AXIS
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QUADRANT METHOD
Lead I aVF
Normal axis positive Positive
Left axis deviation positive Negative
Right axis
deviation
negative Positive
Extreme right axisdeviation
Negative negative
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TO LOCATE THE AXIS IN DEGREES
1. Locate the axis quadrant2. Look for QRS complex with the
smallest or most biphasic (equally
positive and negative) deflection in thelimb leads
3. Identify the lead axis that runs
perpendicular to that lead
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Identify the lead axis that runs perpendicularto that lead
LAD NORMAL ERAD RADMost
isoelec
tric
Axis Mostisoele
ctric
Axis Mostisoele
ctric
Axis Mostisoele
ctric
Axis
I -90 AVF 0 I -90 AVF +180AVR -60 III +30 AVL -120 II +150
II -30 AVL +60 III -150 AVR +120AVF 0 I +90 AVF -180 I +90
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4. Hypertrophy or enlargementEnsure that the QRS complex follows everyP wave , measuring between 0.08 0.12seconds.
Steps in ECG Interpretation
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4. Hypertrophy or enlargement- Check for signs of hypertrophy orenlargement (atrial) .
ATRIAL : Examine height and width of P wave in leads II and V1 for abnormalities.
Steps in ECG Interpretation
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ATRIAL ENLARGEMENT
Initial component of diphasic P wave in V1 is larger
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II V1
B
V1
ATRIAL ENLARGEMENT
Terminal portion of diphasic P
wave in V1 is large and wide
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>0.08
>0.08
>3mm
RAE - peaked P wave >2.5mm in any leadLAE - biphasic, notched, widened (>3 small
boxes)- late inversion of P wave in V1 of >1mm
ATRIAL ENLARGEMENT
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SIGNIFICANCE Cause: COPD or pulmonary embolus Look for atrial arrhythmias with atrialabnormalities Treatment is to treat the underlyingcause Mnemonic: P pulmonale for peaked
p wave and pulmonary cause
ATRIAL ENLARGEMENT
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SIGNIFICANCE OF LEFT ATRIALENLARGEMENT
commonly seen in mitral valve diseaseand systemic hypertension
treatment is directed to underlying cause Mnemonic: P mitrale or M-shaped p
wave and mitral problems
ATRIAL ENLARGEMENT
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VENTRICULAR HYPERTROPHY
A. Sokolow-Lyon Criteria :R in V1 + S in V5-V6 > 11 mmR in V1 > 7mmR : S in V1 > 1RAD > +90 degrees
B. Additional Criteria:
QR in V1S1 Q3 patternS1 S2 S3 patternp pulmonale
RIGHT VENTRICULAR HYPERTROPHY
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1. S wave in V1 + R wave in V5 or V6> 35mm
2. R in AVL > 11mm3. Romhilt and Estes Criteria
VENTRICULAR HYPERTROPHYLEFT VENTRICULAR HYPERTROPHY
VENTRICULAR HYPERTROPHY
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VENTRICULAR HYPERTROPHYLEFT VENTRICULAR HYPERTROPHY
B. Romhilt- Estes Criteriaa. Amplitude (any of the ff.)
a. Largest R or S wave in the limb leads > 20mmb. S wave in V1 or V2 > 30mmc. R wave in V5 or V6 > 30mm
b. ST-T segment changes typical of LV strainpatternwithout digitaliswith digitalis
c. LAE: terminal negativity of the P wave in V1 is 1mm ormore in depth with a duration of 0.04 seconds or more
d. LAD: 30 degress or moree. QRS duration > 0.09 seconds (but 0.05 sec
3 points
3 points1 point
3 points2 points1 point1 point
TotalPossible LVH=3; probable LVH=4; Definite LVH>5
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VENTRICULAR HYPERTROPHY
Common causes: hypertension andaortic stenosis/insufficiency & CAD
A compensatory mechanism initially
LVH worsens prognosis in the long run
SIGNIFICANCE OFLEFT VENTRICULAR HYPERTROPHY
VENTRICULAR HYPERTROPHY
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VENTRICULAR HYPERTROPHYCOMBINED VENTRICULAR HYPERTROPHY
1. The ECG meets one or more of thediagnostic criteria for isolated left and rightventricular hypertrophy
2. The precordial leads show signs of leftventricular hypertrophy, but the QRS axis isgreater than +90 degrees (RAD)
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5. Check for signs of ischemia,injury and infarction.
Classic Triad of MIIschemiaInjuryInfarction
Steps in ECG Interpretation
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5. Check for signs of ischemia,injury and infarction.
12-Lead ECG sees the heart from 12different views.
Therefore, the 12-Lead ECG helps you seewhat is happening in different portions of theheart.
The rhythm strip is only 1 of these 12 views.
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The 12-Leads ECG
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
Anterior portion ofthe heart
Lateral portionof the heart
Inferior portion of theheart
best viewed usingleads V1- V4 .
Leads II, III and aVF
Leads I, aVL, and V5- V6
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5. Check for signs of ischemia,injury and infarction. - Check for the ST segment and Twaves .
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ECG ChangesWays the ECG can change include:
AppearanceofpathologicQ-waves
T-waves
peaked flattened inverted
ST elevation &depression
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ST segment elevation or depression:
determined by measuring at 0.04 sec. (1 smallbox) after the end of the QRS complex (J point)
ST elevation : >1mm
ST depression :
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INFARCTION
Results from the complete occlusion of acoronary artery . The area suppliedbecomes non-viable and cannot contract.
The resulting cardiac hypoxia alsocauses irritability in one or moreventricular foci, producing deadlyarrhythmia.
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ISCHEMIA
Characterized by inverted T-waves Since the chest leads are nearest the ventricles
always run down V1-V6 for T-wave inversion
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ECG findings in Myocardial Ischemia
1. At least 1mm ST-segment depression2. Symmetrically or deeply inverted T waves3. Abnormally tall T waves
4. Normalization of abnormal T waves5. Prolongation of the QT interval in addition to
the above
6. Others: arrhythmias, bundle branch blocks,AV blocks, or electrical alternans
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INJURY
May be acute or recent Elevation of the ST segment earliest sign of
infarction to record on ECG
If the ST segment is elevated withoutassociated Q waves , this may represent a non-Q wave infarction that may herald animpending larger infarct
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INFARCTION
The Q wave makes the diagnosis of infarction
A significant Q wave is at least one smallsquare wide (0.04 sec) or one-third of the entireQRS amplitude
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ECG Criteria for Myocardial Infarction
Any of the following :1. ST elevation > 2mm in 2 or more chest
leads or > 1 mm in 2 or more limbleads
2. Q waves > 0.04 sec
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Anterior MI
the anterior portion of the heart is best viewed using leads V 1- V4.
Limb Leads Augmented Leads Precordial Leads
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Lateral MI
the lateral portion of the heart isbest viewed
Limb Leads Augmented Leads Precordial Leads
Leads I, aVL, and V 5- V6
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Inferior MI
Now how about the inferior portionof the heart?
Limb Leads Augmented Leads Precordial Leads
Leads II, III and aVF
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LOCATING MILeads involved LV Areas
V1-V4 anterior infarctionV1-V2 antero-septal
V3-V4 antero-lateralI, AVL lateralII, III, AVF inferior
Large R, ST depression V1, V2 acute post.infarction
Locating MI
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Locating MILeads involved LV Areas
II, III and AVF Inferior wallI & AVL High lateral wallV1, V2 Septal wallV3, V4 Anterior wallV5, V6 Lateral wallV1-V3 Anteroseptal wallV3-V6, I, AVL Anterolateral wallV5, V6, II, III, and AVF Inferolateral wallAlmost all leads Diffuse/global/massiveMirror image of V1, V2 Posterior LV wall
V3R and V4R RV wall
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Inferior Wall MI
This is an inferior MI. Note the ST elevation in leads II, IIIand aVF.
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Anterolateral MI
This persons MI involves both the anterior wall (V 2-V4) and the lateralwall (V 5-V6, I, and aVL)!
Myocardial Ischemia/Infarction
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.
Hyperacute phase (few hours) ST segment elevation;deep and wide Q wave
Early evolving phase (few days) deep and wide Q
wave, elevated ST segment, diphasic T waveLate evolving phase (2-3 wks) deep and wide Q wave,sharply inverted T wave
Resolving phase (years) deep and wide Q wave;almost normal T wave
Myocardial Ischemia/Infarction
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ECG Changes & the Evolving MI
There are two distinctpatterns of ECGchange depending ifthe infarction is:
ST Elevation (Transmural or Q-wave), or Non-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 tonormal, but Q-waves persist
Ischemia
Infarction
Fibrosis
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ST Elevation Infarction
Diagram depicting an evolving infarction:A. Normal ECG prior to MI
B. Ischemia from coronary arteryocclusion results in ST depression (notshown) and peaked T-waves
C. Infarction from ongoing ischemiaresults in marked ST elevation
D/E. Ongoing infarction with appearance of
pathologic Q-waves and T-waveinversion
F. Fibrosis (months later) with persistentQ- waves, but normal ST segment and T-waves
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ST Elevation Infarction
Heres an ECG of an inferior MI:
Look at the inferior leads (II, III, aVF).
Question: What ECGchanges doyou see?
ST elevationand Q-waves
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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
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Non-ST Elevation Infarction
Heres an ECG of an evolving non -ST elevation MI:
Note the STdepression and T-wave inversion in
leads V 2-V6.
Question: What area of the heart isinfarcting?
Anterolateral
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MISCELLANEOUS
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PULMONARY EMBOLUS Large S wave in Lead I , and a Q wave and an
inverted T wave in Lead III (S1Q3T3) Characterizes acute cor pulmonale
Often there is RBBB
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.
Hypocalcemia prolonged QTcHypercalcemia shortened QTc
Metabolic
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POTASSIUMHYPERKALEMIA- P wave flattens down, the QRS complex wides, and the
T wave becomes peaked
HYPOKALEMIA- The T wave becomes flat (or inverted) and a U wave
appears
Hypokalemia and Hyperkalemia
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yp yp
END
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-END-