abnormal ecg manual

8/8/2019 Abnormal ECG Manual

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Lancashire & South Cumbria

Cardiac Network

ECG INTERPRETATION MANUAL

THE ABNORMAL ECG

Lancashire And South CumbriaCardiac Physiologist Training Manual

Z:\Manuals\ECG Manuals\STUDENT ECG Manuals\abnormal ECG manual.doc

Butler L, Pearce,K 07/10/2005


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AV NODAL BLOCKS

(HEART BLOCKS)

Disturbances of intra cardiac conduction occur principally in the AV node.

Causes: -

Increased vagal tone in digitalis therapy

IHDRheumatic endocarditis

Degeneration of the conducting tissue

Sclerotic disease of the surrounding structures

Cardiac surgery trauma

When the AV node is damaged there is a delay or total block of impulses at the AV

Node and conduction through it is affected.




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FIRST DEGREE HEART BLOCK (1)

The impulse originates, as normal in the SA node but conduction through the AV

node is slower than normal.

This gives a prolonged PR interval. The rest of the complex is normal.

ECG criteria

Rate Normal

Rhythm Regular

P Wave Normal

QRST Normal

But: PR interval more than 0.2 seconds

PR interval is constant

Clinical significance

If the rate is normal there is no affect on the patient.

Treatment

None indicated unless the rate is very slow then treat as bradycardia.

If associated with organic heart disease it may progress to 2 or 3 heart block.




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SECOND DEGREE HEART BLOCK (2)

Mobitz Type I (Wenkebach)

Conduction through AV node becomes progressively delayed until it fails completely.

The beat is dropped. The cycle repeats.

ECG criteria

Rate Normal or slow

Rhythm Regular P waves

Irregular QRS complexes

P Wave Normal

QRST Normal

But: - PR interval increases with each cycle (not constant) - Dropped beat.


If the rate is normal no affect.

If the rate is slow symptoms.

Symptoms

Low cardiac output state

Drop in BP

Peripheral vasoconstriction

Poor tissue perfusionConfusion

LOC

Treatment

If CO is normal no treatment.

Oxygen administration will relieve hypoxia.

Drug therapy can increase SA node rate and therefore increase ventricular rate.

NB: - can deteriorate to complete heart block.




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THIRD DEGREE / COMPLETE HEART BLOCK (3)

The AV node fails completely and none of the sinus impulses are conducted to

the ventricles. There is no ventricular response to normal sinus P waves.

Now pacemaker cells with the next fastest intrinsic discharge rate (or ventricular

ectopic focus must take over to stimulate the ventricles. This is known as an

idioventricular rhythm, but the intrinsic ventricular rate is very slow (30-40 bpm). The

ECG shows complete atrio-ventricular dissociation, the P wave rate being normal

whereas the ventricular rate is slow.

If the idioventricular pacemaker fails it will lead to ventricular standstill which

manifests clinically as Stokes-Adams syncopal attacks.

Cardiac Syncope Stokes-Adams attacks

Caused by

1. Complete heart block with slow ventricular rates and/or failure of pacing focus

2. Sudden onset rapid tachyarrhythmia usually paroxysmal VT or VF.

The attack may last a few seconds to minutes. The patient may become unconscious,

cyanosed and may convulse.

The patients report dizzy dos or faints. Ambulatory monitoring can be used to

confirm diagnosis.

Treatment requires insertion of a permanent pacemaker.

Transient complete heart block usually due to MI involves the insertion of a

temporary pacing wire until normal AV Nodal conduction returns.

KAP/LJR.. AVB001.




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BUNDLE BRANCH BLOCK

A delay of conduction in either of the bundle branches.

Right Bundle Branch Block

In RBBB the right ventricle is stimulated by the impulse from the left ventricle.

Phase of activation:-

BLOCK

(2) (2)

(1)

((

(3)

The septum depolarises from left to right as normal. (1)

The left ventricle is depolarised as normal. (2)

Finally the right ventricle is depolarised late (wide) in an anterior movement. (3)

Resulting QRS is wide due to slow conduction through myocardial cells.




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(1) (2)

V1 V6(3)

Resulting complex in leads orientated towards the right ventricle have RSR1 complex

in V1.

The proximal limb of the complex (R1) is due to the stimulus spreading through the

right ventricle and since it is late it is unopposed by LV depolarisation and it is

therefore of high magnitude.

In leads orientated towards left ventricle (V5, V6) and AVL a broad and slurred S

wave is seen.

This is due to the late depolarisation of the free wall of the RV away from electrode

V6.




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RBBB & MI

If abnormal Q waves are present they will not be masked by the BBB pattern.

This is because there is no alteration of the initial part of the complex RS (in V1) and

abnormal Q waves can still be seen.

Significance of RBBB

RBBB is seen in :-

(1) occasional normal subjects

(2) pulmonary embolus

(3) coronary artery disease

(4) ASD

(5) active carditis

(6) RV diastolic overload

ECG criteria for RBBB

(1) QRS duration exceeds 0.12 seconds

(2) RSR complex in V1

(3) Delayed S wave in , V5, V6

(4) ST/T must be opposite in direction to the terminal QRS

(is secondary to the block and does not predispose primary ST/T changes)

Partial / Incomplete RBBB is diagnosed when the pattern of RBBB is present but

the duration of the QRS does not exceed 0.1 seconds.




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Left Bundle Branch Block

In LBBB the left ventricle is activated from the right bundle.

Phase of activation :-

BLOCK

(1a) (3)

(1b)

(2)

Impulse passes to the left of the septum below the block (1a) at the same time as the

paraseptal region. (1b)

Activation of the RV follows (small magnitude). (2)

Finally delayed activation of the LV which is slow due to conduction through normal

myocardium. (3)




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(1a)

(3)

(2) (1b)

V1 V2 V6

(1)

(1b)

(2) (2)

(1) (1a)

(3)

ECG criteria for LBBB

(1) Prolonged QRS complexes, greater than 0.12 seconds

(2) Wide, notched QRS (M shaped) , AVL, V5, V6

(3) Wide, notched QS complexes are seen in V1 (due to spread of activation away

from the electrode through septum + LV)

(4) In V2, V3 small r wave is seen due to activation of paraseptal region




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LBBB & MI

MI should not be diagnosed in the presence of LBBB Q waves are masked by

LBBB pattern.

Significance of LBBB

LBBB is seen in :-

(1) Always indicative of organic heart disease

(2) Found in ischaemic heart disease

(3) Found in hypertension.

Partial / Incomplete LBBB is diagnosed when the pattern of LBBB is present butthe duration of the QRS does not exceed 0.1 seconds.

LJR/KAP..BBB001.




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ATRIAL AND VENTRICULAR ARRHYTHMIAS

Remember normal sinus rhythm.

Consider four components of the above :

P wave

PR interval

QRS complex

T wave

Providing the process of depolarisation throughout the heart is initiated in the SA

node and the conduction system is normal, then the above mentioned events will

occur sequentially.

- Atrial depolarisation

- Atrial contraction

- AV nodal delay

- Ventricular depolarisation

- Ventricular contraction

- Ventricular relaxation

If for any reason this sequence of events is disturbed then the effects will

consequently be recorded on the ECG.

The sequence can be disturbed for many reasons, one of these is the presence of an

irritable focus or foci in some part of the atrial or ventricular myocardium, which

initiates depolarisation of the atrium or ventricles before the next expected sinus

discharge.




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ATRIAL ECTOPIC BEATS

E.C.G Criteria :-

Premature P wave

Bizzare shaped P wave

Compensatory pause (resets SA NODE)

Following the atrial ectopic beat, conduction through the AV node can be one of the

following :-

Normal

Short

Prolonged

Blocked

NB. The AV node acts as a safety mechanism protecting the ventricles from any atrial

rhythm disturbances.

SVE




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ATRIAL FIBRILLATION

E.C.G Criteria :-

Small, rapid, irregular fibrillation waves (400 600bpm)

QRS morphology is normal

Ventricular rate is irregular (110 160bpm)

Common causes: -

Mitral Valve Disease

Thyrotoxicosis

Cardiomyopathies

Treatment: -

Digoxin (lowers ventricular rate)

Sotalol

DC Cardioversion




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ATRIAL FLUTTER

E.C.G Criteria: -

Rapid regular atrial contraction (220 350bpm)

Broad, Bizarre Flutter waves

No Iso-electric shelf

Usually regular ventricular rate (with ratio P waves: QRS)

Common Causes: -

Rheumatic Heart Disease

Ischaemic Heart Disease

Treatment: -

DC Cardioversion

RF Ablation

Sotalol




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VENTRICULAR UNIFOCAL ECTOPICS

The ventricular ectopics arise from the same focus and therefore are the same

morphology in any given lead.

VENTRICULAR MULTIFOCAL ECTOPICS

The ventricular ectopics arise from more than one focus and therefore have different

morphologies in any given lead.




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VENTRICULAR BIGEMINY

An ECG which shows alternating sinus beats and ventricular premature beats isdescribed as ventricular bigeminy.

There is usually a constant interval between the sinus beat and the ventricular ectopic

beat suggesting the sinus beat controls the discharge of the ventricular ectopic.

VENTRICULAR TRIGEMINY

A ventricular ectopic followed by two sinus beats.

RV ECTOPICS

The ventricular ectopic which arises in the right ventricle will give a Left Bundle

Branch Block pattern.

The main spread of the impulse is away from the electrode at V1 resulting in a

downward V1 deflection.

The spread of the impulse is towards the electrode at V6 resulting in an upward V6

deflection.

V6

V1




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LV ECTOPICS

The ventricular ectopic which arises in the left ventricle will give a Right Bundle

Branch Block pattern.

V6

V1




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VENTRICULAR FIBRILLATION

Chaotic, uncontrolled, multiple depolarisations resulting in non-

uniformed ventricular contractions.

No clearly identified QRSNo cardiac output

Loss of Consciousness

Treatment: -

DC Defibrillation

VF

LJR/KAP..AVA.001.




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ATRIAL ENLARGEMENT / HYPERTROPHY

The P wave reflects atrial depolarisation and is recorded as soon as the impulse leavesthe SA node.

The SA node is situated in the right atrium hence RA activation occurs before LA

activation.

The two processes overlap as LA activation actually begins before RA activation ends.

AVNODE

SA NODE




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Hypertrophy is enlargement / thickening of the muscle in response to an increase inworkload.

When atrial enlargement occurs the P wave is altered with an increase in amplitude or

width of the corresponding atrial component.

Normal P wave

Lead II

pyramid shaped

smooth apex

amplitude not exceeding 2.5 mm

duration not exceeding 0.12 secs

RA COMPONENT LA COMPONENT

RA COMPONENT LA COMPONENT

Both RA and LA components are directed towards lead II positive waveforms.




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Normal P wave

Lead V1

The RA is situated anteriorly and to the right of the ventricles.

The LA is situated more posteriorly, behind the ventricles.

The RA force is directed towards lead V1 hence the 1st

(RA) component is upright in

V1.

The LA force is directed a little away from V1 and hence the 2nd (LA) component is

slightly negative.

LA (2)

(1)

RA (1) (2)

V1

As the two forces overlap the result is a P wave that is mainly upright with a slight

negative terminal (Diphasic).




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RIGHT ATRIAL HYPERTROPHY

In RAH the RA component of the P wave is increased in voltage and duration.

Since the RA component of the P wave is normally seen as a positive deflection in

both II and V1 the P wave height is increased in both of these leads.

NB: Since right atrial depolarisation is normally complete well before LA

depolarisation the delay that occurs in conduction with RAH to the RA component is

not enough to affect overall duration time of the P wave.

Hence only amplitude of the P wave is affected in RAH, not duration.




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II

V1




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ECG CRITERIA FOR RAH

P wave amplitude is more than 2.5mm (some say 3mm) in leads II, III or AVF.

[Occasionally the P wave vector is towards III and AVF (75 +) ]

Associated Findings

1. positive part V1 greater than 1.5mm

2. usually RVH

Clinical Significance

1. usually due to pulmonary disease leading to RVH and hence RAH, hence the term

p pulmonale

2. any other disease that leads to RVH e.g. pulmonary stenosis

3. rarely RA infarction/ischaemia

*p pulmonale peaked p waves*




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II

V1




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ECG CRITERIA FOR LAH

1. m shaped p wave greater than 0.12 seconds in duration in leads II, III and avf

2. p wave in V1 shows a dominant negative component

Associated findings

1. frequently LVH

2. with mitral stenosis only LAH can be found with RVH


1. any condition that gives rise to LVH , e.g. AS, AI, HOCM, hypertension

2. mitral stenosis

3. LA infarction/ischaemia, likely if ischaemic heart disease is present

* p mitrale m shaped p waves *




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BI-ATRIAL HYPERTROPHY

To diagnose bi-atrial hypertrophy is not as difficult as with bi-ventricular

hypertrophy.

Each individual atria affects a different part of the p wave whereas hypertrophy of

each ventricle affects the same part of the QRS.

ECG CRITERIA

Diagnosis can be made whenever the criteria for both right and left atrial hypertrophyare fulfilled.

Limb leads

1. p wave greater than 2.5 mm in height

2. p wave greater than 0.12 seconds in duration

V1

1. positive component greater than 2mm in height

2. negative component greater than 1 mm deep


Found in conditions which give rise to bi-ventricular hypertrophy.

e.g. congenital heart diseaseHOCM

pulmonary hypertension together with aortic valve disease or mitral

incompetence.

LJR..AE001.




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VENTRICULAR HYPERTROPHY

LEFT VENTRICULAR HYPERTROPHY

The left ventricular myocardium will thicken as a reaction to hypertension, aortic

stenosis and mitral regurgitation.

These are conditions ventricle has to perform more work than usual. Results in anincrease in muscle mass.

ECG criteria

Increased forces result in a longer intrinsic deflection time (or ventricular activationtime).

(1) V1 & V2 deep S waves greater than 30mm

(2) V4, V5, V6, I & AVL tall R waves greater than 27mm

(3) * Or sum of S wave V1 + R wave V6 should be greater then 37mm *

(4) Left Axis Deviation

(5) Ventricular activation time greater than 0.12secs

Strain Pattern

Leads facing the LV (V5 & V6) may show a strain pattern.

This is a reflection of the abnormal state of the myocardium.

ECG for strain

(1) In leads facing the LV, usually in V5, V6, I & AVL

(2) depressed, convex ST segment depression

(3) inverted T waves




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RIGHT VENTRICULAR HYPERTROPHY

This usually occurs in cor pulmonale, and in some congenital heart defects when the

RV becomes dominant.

In RVH, the potential force of the RV is greatly increased.

ECG criteria

(1) R wave in leads over right ventricles V1, V2, V3. V4

(2) The S wave in V6 becomes more conspicuous

(3) Right Axis Deviation

moderate RVH R wave dominance V1, V2

severe RVH R wave dominance V1-V4

Strain Pattern

(1) Seen in leads facing the right ventricle (V1, V2,V3)

(2) Depressed convex ST segment

(3) Inverted T wave




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LEFT VENTRICULAR HYPERTROPHY

RIGHT VENTRICULAR HYPERTROPHY




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BI-VENTRICULAR HYPERTROPHY

This is difficult to diagnose from the ECG since the phases of ventricular activation, 2

+ 3 occur together then the forces of activation may cancel each other out givingrise to a normal QRS amplitude.

However, the duration may still be above 0.12 seconds.

If either ventricle is more dominant then that ventricular hypertrophy will more

evident on the ECG.

ECG Criteria

(1) It may exist without ECG changes

(2) QRS duration may be to above 0.12 seconds.

(3) T wave may be present in the precordial leads

(4) ECG criteria met for LVH with an axis of +90 (RAD) is suggestive (notdiagnostic) of biventricular hypertrophy

(5) Occasionally RVH with LAD is seen

Clinical Significance

(1) Aortic valve disease + pulmonary hypertension

(2) Cardiomyopathy

(3) Occasionally congenital heart disease

LJR/KAP..VH001.




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MYOCARDIAL INFARCTION

Cross sectional analysis of an area of infarcted myocardium reveals the three

electrically differentiated zones.

E

E = Electrode

Infarcted Myocardium Injured Myocardium Ischaemic Myocardium




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There are FOUR stages of myocardial infarction (MI) these are described as follows.

STAGE 1 ACUTE STAGE -------- HOURS OLD

Acute stage of injury The myocardium is not yet dead and unless rapid intervention

is possible then death of the affected area of muscle will certainly follow. In the case

of rapid intervention then the area of death may be reduced although even with

treatment some necrosis will take place.

The typical shape of the ECG leads which are positioned directly over the injured area

of myocardium will show significant ST segment elevation of greater than 2 mm,

there may also be a reduction in the size of the R wave.

There will be ST segment depression in the areas of myocardium opposite the injured

area these are known as RECIPROCAL CHANGES.




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STAGE 2 LATER PATTERN --------- DAYS OLD

In stage 2 the injured myocardium is now starting to necrose and this results in Q

waves beginning to appear on the ECG which are representations of depolarization on

the opposite wall of the heart, this is due to the window effect over the area of dead

myocardium.

Q - wave

1

3

2

3




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Depolarisation of the ventricles demonstrates a Q wave appearance due to the

activation of 1 and 2 travelling away from the electrode.

The electrode is looking through the electrical window were no electrical activity

occurs.

The ST segment elevation will lessen as the area of injury either becomes Ischaemic

or dies.

T waves now begin to appear representing the area of ischaemia which is surrounding

the infarcted muscle.

STAGE 3 LATE PATTERN ----------- WEEKS OLD

In stage three, the zone of injury has now evolved into infarcted myocardium.

There is a pathological Q wave seen on the ECG due to the electrical window being

present

The ST segment has now returned to normal/Iso-electric line because the injured area

has now necrosed or become ischaemic.

There is now a symmetrically inverted T wave present on the ECG which represents

persistent ischaemia surrounding the area of infarct.

Q wave




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STAGE 4 OLD INFARCT ---------- MONTHS TO YEARS

In stage 4 the zone of ischaemia has recovered and the ECG returns to almost normal.

However there are changes which allow us to identify a previous infarct on the ECG.

The pathological Q wave is considered the finger print for life of a previous

myocardial infarction.

The R wave height is reduced in the leads positioned directly over the area of infarct.

Q wave

NB in patients who have persistent ST elevation following an infarct this can be an

ECG indication of a ventricular ANEURYSM.




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SYMPTOMS OF MYOCARDIAL INFARCTION

Chest pain usually occurs in 90% of patients, this is not relived by GTN.

There may also be obvious signs of NAUSEA, SOB, and PERSPIRATION.

Clinical Signs

PALLOR, SWEATING, IRREGULAR PULSE, HYPOTENSION, RAISED JVP.

ECG Changes

Although the ECG changes occur relatively quickly in many patients there is a small

percentage these changes may take anything up to 24hrs to occur. A small percentage

of patients may have no E.C.G changes.

Blood Tests

Death to the myocardium causes a release of enzymes into the blood

Stream, the main enzymes which are checked are CK, AST, LDH and Cardiac

Troponin. The level of enzymes may give some indication as to the size of the Infarct.

Prognosis

30% die within 3 hours of onset of pain.

18% mortality in Coronary Care Units.

80% of all cardiogenic shock patients die.

45% of deaths are due to primary arrhythmias.

(these are mostly out of hospital deaths)




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CORONARY ARTERY ANATOMY

LEFT CORONARY ARTERY

Left Main Stem

Left Anterior Descending

Diagonal

Intermediate

Left Circumflex

Marginals

Septals




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RIGHT CORONARY ARTERY

Sino Atrial Branch

Right lateral Intraventricular

Marginal branch

Posterior

Descending

Artery

* In 90% of patients the PDA arises from the RCA indicating a right dominant

system

In the other 10% the PDA arises from the LCX.




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CORONARY ARTERY BLOOD SUPPLY

RIGHT

The right coronary originates from just above the right coronary cusp of the

aortic valve and supplies the following

INFERIOR wall region of the left ventricle

SA Node in 55% of patients

AV Node in 90% of patients

Bundle of His in 90% of patients

The superior third of the Right Bundle Branch

The postero inferior division of the Left Bundle Branch

Vagus nerve fibres.

Possible Complications

Heart Blocks 1st, 2nd ,3rd Degree heart block

Bradycardias

Hypotension

Other complications from MI are reduced LV function which

may lead to cardiac failure and can increase the risk of

tachyarrhythmias.




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LOCATION OF INFARCTION

-

Anterior Posterior

+ -

I, AVL, V LEADS

Inferior

+

II, III, AVF

Leads I, AVL and the V1chest lead are orientated so they look at the anterior surface

of the heart.

Leads II, II and AVF are orientated so they look at the inferior surface of the heart.

NB no leads are orientated towards the posterior surface of the heart.




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INFERIOR INFARCT

The inferior region of the heart is basically the inferior wall of the Left

Ventricle. An inferior infarct is due to occlusion of the RCA, this will also causes

damage to the Right Ventricle.

ANTERIOR INFARCT

An Anterior Infarct may cause damage to a larger area of myocardium dependent on

were the occlusion takes place so an Extensive Anterior Infarct will be cause by

Proximal occlusion of the LCA.

ANTEROSEPTAL

This is caused by an occlusion of the SEPTAL ARTERY of the LAD(proximal to the septal artery)

ANTERO-LATERAL

This is caused by an occlusion of the DIAGONAL BRANCHES of the LAD

APICAL

This is caused by an occlusion of the distal portion of the LAD

An apical infarct may also occur due to occlusion of the RCA being an extension of

an Inferior Infarct




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ECG CHANGES INDICATING REGION OF INFARCT

INFERIOR II, III and AVF---------------RCA

ANTERIOR I, and AVL--------------------LCA

ANTERO-SEPTAL I, AVL, V1, V2, V3

ANTERO-LATERAL I, AVL, V4, V5, V6

EXTENSIVE ANTERIOR I, AVL, V1, V2, V3, V4, V5, V6

APICAL I, AVL, V3, V4




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POSTERIOR WALL MYOCARDIAL INFARCTION

The POSTERIOR wall of the heart involves the Poster-Basal aspect of the left

ventricle.

It is situated between the lateral (superior) and Inferior surfaces.

The posterior region is fed its oxygen/blood supply via the Left Circumflex Artery.

ANTERIOR POSTERIOR

None of the conventional ECG leads are orientated towards the posterior surface of

the heart therefore the diagnosis can only be made from the inverse or mirror image

changes which occur in leads which are orientated to the UNINJURED anterior

surface of the heart.




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LEAD V1

Normal appearance Acute stage of Posterior

Infarct

ECG FEATURES

1) Tall and slightly widened R waves in right precordial leads (V1 V2)

The Anterior forces are more dominant due to the lack of opposing

posterior forces

2) Tall upright symmetrical T waves

3) Depression of the ST Segment which may look concave in leads (V1 V2)

NB This could be ischaemia if points 1 + 2 are not present




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DIFFERENTIAL DIAGNOSIS OF TALL R WAVES V1 + V2

Right ventricular hypertrophy (check for Rightward axis and check T waves)

Right Bundle Branch Block (check the T waves in RBBB they are usually

Inverted)

Type A WPW (check if there is a Delta wave)




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ISCHAEMIA

E J J+60

E POINT baseline between P and QRS

J POINT compared to E point

level of ST depression

J + 60 60 equates to 60 ms, however other values can be chosen.

measures the gradient /slope of the ST segment, from the J point.




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NORMAL BORDERLINE

(probably normal)

Baseline Upsloping

ABNORMAL ABNORMAL

Flat Downsloping




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THE MECHANISM OF ISCHAEMIC CHANGES

Ischaemia is caused by transient subendocardial injury to the ventricular muscle mass.

AVR

V6

V5

In leads orientated towards the injured surface (i.e. AVR) the usual injury pattern of

ST elevation is seen.

In leads orientated away from the injured surface (i.e. V5,V6), ST depression is seen.

In leads where ST depression is seen, the T wave will be inverted.

An ischaemic T wave is symmetrical, taller and pointed.

U WAVE




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PRINZMETAL ANGINA

Sub-epicardial injury, characterized by transient ST elevation in leads orientated

towards the injury.

Thought to be due to coronary artery spasm +/- coronary artery disease.

ECG findings

ST elevation in leads orientated towards the area of injury

R wave amplitude is increased

U wave inversion

Frequently left anterior hemiblock

Complications

Ventricular Ectopics, Ventricular Tachycardia, Transient AV block.

abnormal ecg manual

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