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ECG INTERPRETATION MANUAL (PDF)

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					                              Lancashire & South Cumbria
                                                Cardiac Network




            ECG INTERPRETATION MANUAL

                      THE ABNORMAL ECG




                 Lancashire And South Cumbria
             Cardiac Physiologist Training Manual




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Butler L, Pearce,K           07/10/2005
                             AV NODAL BLOCKS
                              (HEART BLOCKS)


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




                                     Causes: -

       Increased vagal tone in digitalis therapy
       IHD
       Rheumatic 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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Butler L, Pearce,K           07/10/2005
                FIRST DEGREE HEART BLOCK (1º)

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 2º or 3º heart block.




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Butler L, Pearce,K           07/10/2005
              SECOND DEGREE HEART BLOCK (2º)

                           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 perfusion
       Confusion
       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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Butler L, Pearce,K           07/10/2005
                               Mobitz Type II (2º)


Conduction times through the AV node are constant but there is a variability of the
number of impulses which are conducted through the ventricles.




ECG criteria

       Rate – Normal or slow
       Rhythm – Regular P waves
                 Regular QRS complexes
       P Wave – Normal
       PR interval – Normal and constant

    But may be 2/3 P waves preceding QRS complexes

       NB Clinical significance and treatment is higher than Mobitz Type I.
          Permanent pacing is recommended



2 : 1 AV Block

There may be 2/3 P waves preceding QRS complexes as a constant pattern

               Ratio 2 : 1
                     3:1


          NB Clinical significance and treatment is the same as for Mobitz I




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Butler L, Pearce,K           07/10/2005
       THIRD DEGREE / COMPLETE HEART BLOCK (3º)




         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 do’s” 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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Butler L, Pearce,K           07/10/2005
                         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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Butler L, Pearce,K           07/10/2005
                                    (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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Butler L, Pearce,K           07/10/2005
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 Ι, 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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Butler L, Pearce,K           07/10/2005
                          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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Butler L, Pearce,K           07/10/2005
                                                 (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) Ι, 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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Butler L, Pearce,K           07/10/2005
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 but
the duration of the QRS does not exceed 0.1 seconds.




LJR/KAP..BBB001.




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Butler L, Pearce,K           07/10/2005
    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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Butler L, Pearce,K           07/10/2005
                               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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Butler L, Pearce,K           07/10/2005
                              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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Butler L, Pearce,K           07/10/2005
                                  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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                           VENTICULAR ECTOPICS



E.C.G Criteria: -

                    Premature

                    Bizzare shaped QRS

                    Wide Complex

                    compensatory pause

                    A run of 3 or more can be classified as VT.




                                VE




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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 is
described 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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Butler L, Pearce,K           07/10/2005
                               VENTRICULAR FIBRILLATION

                    Chaotic, uncontrolled, multiple depolarisation’s resulting in non- –
                    uniformed ventricular contractions.
                    No clearly identified QRS
                    No cardiac output
                    Loss of Consciousness



Treatment: -

                           DC Defibrillation




VF




LJR/KAP..AVA.001.




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Butler L, Pearce,K           07/10/2005
      ATRIAL ENLARGEMENT / HYPERTROPHY

The P wave reflects atrial depolarisation and is recorded as soon as the impulse leaves
the 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 in
workload.

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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Butler L, Pearce,K           07/10/2005
                                      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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Butler L, Pearce,K           07/10/2005
                        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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Butler L, Pearce,K           07/10/2005
                                                        II




                                  V1




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Butler L, Pearce,K           07/10/2005
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 (75º +) ]




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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                           LEFT ATRIAL HYPERTROPHY


In LAH the la component of the p wave is increased in voltage and duration.



Since the terminal part of the p wave is produced by left atrial depolarisation it
follows that the total duration of the p wave is increased.



Also since the La component increases in amplitude the p wave in lead II becomes
bifid (notched) and in V1 the negative component becomes dominant.




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Butler L, Pearce,K           07/10/2005
                                          II




 V1




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Butler L, Pearce,K           07/10/2005
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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Butler L, Pearce,K           07/10/2005
                            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 hypertrophy
are 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 disease
    HOCM
    pulmonary hypertension together with aortic valve disease or mitral
    incompetence.




LJR..AE001.




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Butler L, Pearce,K           07/10/2005
                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 an
increase in muscle mass.



                                      ECG criteria

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

(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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Butler L, Pearce,K           07/10/2005
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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Butler L, Pearce,K           07/10/2005
LEFT VENTRICULAR HYPERTROPHY




RIGHT VENTRICULAR HYPERTROPHY




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Butler L, Pearce,K           07/10/2005
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 giving
rise 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 (not
diagnostic) 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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Butler L, Pearce,K           07/10/2005
             CORONARY VASCULAR DISEASE


The heart is a muscle whose function is to pump blood and Oxygen around the body,
this muscle receives its own blood supply and Oxygen from vessels known as the
CORONARY ARTERIES.

Atheroma:-           Is the build up of Plaque/Fat which cause
                     narrowing in the CORONARY ARTERIES.

Risk Factors:- Include Smoking, Hypercholesterolemia, Hypertension,
                      Obesity, Diabetes and Family History.



There are three main Stages of FIBRINOLYSIS


              NORMAL                                        STAGE 1




              STAGE 2                                       STAGE 3




STAGE 1       Moderate Atherosclerosis    ANGINA
STAGE 2       Severe Atherosclerosis      CHRONIC ISCHAEMIA
STAGE 3       Complete Occlusion          MYOCARDIAL INFARCT




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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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Butler L, Pearce,K           07/10/2005
INFARCTED MYOCARDIUM - myocardium electrically dead.

The electrode lying over the area of infarction has the effect of looking through the
infarcted area as a window. This therefore will detect and record potentials from the
myocardium directly opposite.


INJURED MYOCARDIUM - myocardium is never completely polarized

The electrode lying over the area of injury will record ST Segment elevation on the
ECG because of the myocardium retaining its polarity.


ISCHAEMIC MYOCARDIUM - myocardium exhibits impaired repolarisation

The electrode lying over the area of ischaemia will record T wave changes on the
ECG.




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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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Butler L, Pearce,K           07/10/2005
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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Butler L, Pearce,K           07/10/2005
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 arrhythmia’s.
                 (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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LEFT

       The left coronary artery originates from just above the left coronary cusp of
       the aortic valve and supplies the following.

                      Anterior wall of the left ventricle (LAD)

                      Posterior wall of the left ventricle (LCX)

                      SA Node in 45% of patients (LCX)

                      AV Node in 10% of patients (LCX)

                      The inferior two thirds of the Right Bundle Branch

                      The anterior superior division of the Left Bundle Branch

                      A portion of the postero inferior division of the Left
                      Bundle Branch


Possible Complications

                      Heart Failure

                      Conduction defects

                             RBBB

                             Left Anterior Hemi-Block

                             Left Posterior Hemi-Block

                             1st, 2nd, 3rd Degree heart blocks

                             Tachyarrhythmias




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                            LOCATION OF INFARCTION




                                        -
       Anterior                                                          Posterior


               +                                                             -




I, AVL, V LEADS




                                              Inferior

                                       +




                                      II, III, AVF



Leads I, AVL and the V1 chest 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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Butler L, Pearce,K           07/10/2005
                     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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If after exercise an inverted U wave is seen, it is indicative of myocardial ischaemia.



                        SUBENDOCARDIAL INFARCTION




                                                     LV
                        RV




ECG evidence ;

Primary ST segment depression
T wave inversion
Reciprocal ST segment elevation in the cavity lead



               Early                               Late


CAVITY
LEAD




LEFT PRE
CORDIAL
LEAD


The pattern simulates myocardial ischaemia. However the ischaemia will be transitory
whereas the infarct will persist.
If the PRIMARY change is ST segment depression it will be seen in all leads except
AVR.




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Butler L, Pearce,K           07/10/2005
                              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.




LJB.002.03


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