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
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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.
Clinical significance
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
Clinical significance
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
Clinical significance
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.