Ecg Fgy Final

7/31/2019 Ecg Fgy Final

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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



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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



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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.



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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.



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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



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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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Common causes: hypertension andaortic stenosis/insufficiency & CAD

A compensatory mechanism initially

LVH worsens prognosis in the long run

SIGNIFICANCE OFLEFT 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



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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


Leads I, aVL, and V 5- V6


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Inferior MI

Now how about the inferior portionof the heart?


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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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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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-

Ecg Fgy Final

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