ecg analysis and interpretation

7/28/2019 ECG Analysis and Interpretation

1/66

ECG : Analysis & Interpretation

Steps :

1. Heart rate

2. Heart rhythm - check for deviation from normal in terms of origin

(automaticity) or sequence (conductivity) of heart

action.

- check whether it is occasional, frequent, continuous,regular or irregular, repetitive or occurring with

many combinations.

3. Measure complexes and intervals.4. Evaluate the waveform morphology.

5. Determine MEA - vector always point towards hypertrophy but

away from infarcted areas.- more reliable in narrow-chested animals/breeds.


2/66

ECG : Normal Canine Parameters


3/66

ECG : Normal Feline Parameters


4/66

ECG : MEA

MEA indicates average direction of the electrical activation signals in

the heart during a cardiac cycle.

Three methods :

1. Using isoelectric leads.

2. Looking for strongest QRS deflections.

3. Calculating from Lead I and Lead III.

- MEA should be interpreted with evidences from other leads or other

clinical evidences, can be very tricky in broad-chested animals and cats.- MEA depends on muscle mass and not the thickness of the myocardial

wall. A dog with dilated cardiomyopathy may not necessary show

abnormal MEA.


5/66

ECG : MEA


6/66

ECG : MEA


7/66

ECG : MEA


8/66

ECG : MEA


9/66

Waveforms and PQRST deflections

Abnormalities of the atrium, ventricle and their associated conduction

systems will be evident on the ECG.

Atrial abnomalities look at P wave (morphology, amplitude + duration)

Ventricular abnormalities QRS complexes (esp S and Q), precordial

leads, deviation from normal MEA

Conduction abnormalities delayed or oddly defined intervals, abnormalamplitudes, abnormal wave patterns seen in precordial leads, e.g. W

wave (Lead V10) in right bundle branch block is quite diagnostic.


10/66

Waveforms and PQRST deflections

As a general rule (AGAIN).a quick but not absolutely reliable guide !

P relates to atrial problems

QRS ventricular or conduction problems

R left ventricular problems

S right ventricular problems

PR conduction through the AV bundle

ST period during the repolarization of the

ventricles. Typically associated with

electrolytes


11/66

Students MUST KNOW thefollowing ECG signatures

-Atrial enlargements

-Ventricular enlargements

-AV Blocks (1st , 2nd and 3rd degree)


12/66

Right Atrial Enlargement

Characterised by

Tall P waves (>0.4mv dogs / 0.2 mv in cats)

P wave can be very tall, slender and peaked (P pulmonale) especially in

chronic pulmonary disease.

Associated with

Chronic respiratory disease (blockade/collapsed trachea) or congenital

defects (Interatrial SD)


13/66

Right Atrial Enlargement


14/66

Left Atrial Enlargement

Characterised by

Long P duration

Notched and wide P wave. Notching itself is not necessarily abnormal.

Associated with

Mitral valvular disease or congenital defects (aortic stenosis, also seen inVSD and PDA)


15/66

Left Atrial Enlargement


16/66

Biatrial Enlargement

Characterised by

Long P duration and very tall P wave.

Notching is frequent.

Associated with

Chronic Tricuspid or Mitral valvular disease or various congenital heartdefects


17/66

Biatrial Enlargement


18/66

Right Ventricular Enlargement

Characterised by

Right axis deviation

Large S waves in I, II, III and aVF and probably Q waves as well.

Positive T wave in lead V10

Associated with Congestive Heart Failure (as in severe dirofilariasis), mitral or tricuspid

valve insufficiency, acute cor pulmonale due to pulmonary embolism (as a

result of heartworm treatment) and various congenital heart defects

(Tetralogy of Fallot)


19/66



20/66



21/66

Left Ventricular Enlargement

Characterised by

Left axis deviation

Large QRS complexes in lead II and aVF, tall R and T (25 %) waves

Coving or depressed S-T segment (aka endocardial ischaemic change)

Associated with Eccentric hypertrophy secondary to volume overload (mitral

insufficiency, VSD, PDA), Concentric hypertrophy secondary to pressure

overload (aortic stenosis), dilated cardiomyopathy


22/66



23/66



24/66

Bi-Ventricular Enlargement

This condition is more difficult to determine accurately but oftentimes the

diagnosis of left ventricular enlargement is more accurate. This is because

left ventricular forces can easily counteract any increased forces from the

right (remember ECG is dependent on volume and mass)

Characterised by

Large QRS complexes, tall S and R waves Deep Q waves quite characteristic of biventricular enlargements

Evidences of right and left atrial enlargements

Associated with

Mitral and tricuspid valve insufficiency, dilated cardiomyopathy, PDA

and mitral insufficiency


25/66



26/66



27/66

The following ECG findings areimportant, but I will leave it to the

students to determine theirusefulness in routine clinical

analysis.


28/66

Low Voltage QRS complexes

The amplitude and voltage of a normal QRS complex is dependent on

breed, age and size of the dog. Generally low voltage QRS is suggestive of

the following conditions :

artifact (signal/response calibration required ?)

obesity ?

pericardial effusion

severe myocardial damage severe MI, loss of muscle mass

pulmonary disease (pulmonary edema, pneumonia)

pleural effusion

pneumothorax

ALWAYS CONSIDER THEM AS ARTIFACTS FIRST BEFORE

DECIDING ANYTHING FURTHER!


29/66

Low Voltage QRS complexes


30/66

Intervals and segments

S-T segment (depressed or elevated)

Normally the ST segment is isoelectric because the cells are almost equallydepolarised and there is no driving force for current to flow from one region of the

heart to another. An exception is when part of the heart is ischaemic: then there can beST segment depression or elevation.

wandering baseline ? Pseudodepression due to tachycardia (as a result of prominent

Ta wave)

depression with prominent R wave indicates myocardial ischaemia,

hyperkalemia/hypokalemia, subendocardial MI.

elevation with prominent R wave indicates MI of the entire thickness of the left

ventricle, pericarditis

Q-T interval (prolonged or shortened) not so important in vet. med.

Prolonged hypocalcemia (hypoparathyroidism, eclampsia), hypokalemia, ethylene

glycol poisoning, hypothermia

Shortened hyperkalemia, hepercalcemia


31/66


S-T segment represents the early phase of ventricular

repolarisation


32/66


Q-T interval is the summation of ventricular depolarization andrepolarization, and represents ventricular systole


33/66

Students MUST KNOW thefollowing ECG signatures

-Sinus Rhythm

-Important Sinus Arrhythmias

-AV Blocks (1st , 2nd and 3rd degree)

-APCs and VPCs

- and may be WPW syndrome


34/66

Rhythms and Arrhythmias

Rhythms and arrhythmias can be summarised into 4 categories

according to their origin (sinus, junctional and ventricular) and causes

(impulse formation and conduction):

1.Sinus normal sinus rhythm, sinus tachycardia, sinus bradycardia,

wandering sinus pace maker.

2.Abnormalities of impulse formation Sinus arrest, APC, atrial

tachycardia, atrial fibrillation, AV junctional escape rhythm, VPC,

ventricular tachycardia, ventricular escape rhythm.

3.Abnormalities of impulse conduction SA block, atrial standstill, AV

block (first degree, second degree, third degree or complete heart

block).

4.Abnormalities of both impulse conduction and formation.

Escape rhythm happens when the pacemaker with the highest automaticity changes its firing pace and had to

be rescued by the other pacemaker.


35/66

Arrhythmias

Classification of rhythms :

A.Normal sinus impulse formation

- normal sinus rhyhm- sinus arrhythmia

B.Disturbances of sinus impulse formation

- sinus bradycardia- sinus tachycardia

C.Disturbances of ventricular impulse formation

- ventricular premature complexes

- ventricular tachycardia

- ventricular asystole

- ventricular fibrillation


36/66

Arrhythmias

D.Disturbances of impulse conduction :

- sinus arrest or block

- sick sinus syndrome

- atrial standstill

- ventricular pre-excitation

- 1st degree AV block

- 2nddegree AV block- 3rddegree AV block

- Left bundle branch block

- Right bundle branch blockArrhythmias = abnormality in rate, regularity or site of origin of

the cardiac impulse OR a disturbance in conduction of impulse

that the normal sequence of activation of the atria and ventricle isaltered.


37/66

Arrhythmias

There are three different sites of origin for arrythmias, they can be

identified based on the morphology of P wave and QRS

complexes :

a.)Atrial (sinus) P wave is +ve and present, constant P-R

interval and normal duration QRS.

b.)Junctional P wave absent or ve, normal or short durationQRS. May occur with BBB which causes poor morphology and

prolonged duration on the QRS.

c.)Ventricular P waves absent (may even be superimposed onQRS). QRS wide and bizarre and may be +ve (left) of ve (right)

depending on which ventricle is the site of origin.


38/66

Arrhythmias

The automaticity (ability to initiate impulse) of the site further

describe the arrythmia by being :

i.too fast (tachycardia)ii.too slow (bradycardia)

iii.too irritable (premature)

iv.not irritable (block)


39/66

Sinus bradycardia

Defined as heart rate < 120 (cats), < 70 (dogs) or < 60 (large

dogs).

Associated with :

physiologic changes intubation, vomiting, hypothermia,

elevated intracranial pressure, hypothyroidism, good conditioning.

pathological systemic disease with toxicity (renal failure),

hyperkalemia, cardiac arrest.

Physiologic sinus arrthymia arise due to waxing and waning of

vagal tone during normal respiration. During inspiration the

vagal tone of the heart will be suppressed rendering brief s.

tachycardia, this becomes s.bradycardia or normal pace when

the respiratory system relaxes activation of vagal tone.


40/66

Sinus Tachycardia

Defined as heart rate > 240 (cats), > 140 (dogs) or > 120 (large

dogs), > 180 (toy breeds), > 220 (puppies).

Associated with :

physiologic changes exercise, pain or restraint.

pathological fever, hyperthyroidism, shock, anaemia, CHF,

hypoxia.


41/66

Wandering sinus pacemaker

Characterised by changing gradual change in P wave morphology

(gradually appearing or dissapearing), common in dogs. However,

both QRS and P-R durations are not affected.

No specific treatment is required.


42/66

Atrial Premature Complexes

Caused by supraventricular impulses originating from an ectopic

atrial site (not SA node). The ectopic site arise as a result of

increase automaticity of the atrial myocardial fibres / single re-

entrant circuit.

Important feature P waves touches T waves of previous beat

and resets the SA node therefore there should be a brief pause

after the APC.

Associated with atrial enlargement, cardiomyopathy, mitral

insufficiency.APC may be hard to spot, may gives rise to atrial tachycardia or

even atrial fibrillation.


43/66

Atrial Premature Complexes


44/66

Atrial Tachycardia

Rapid regular rhythm arising from atrial sites other than the SA node. 3 or more

APC = Atrial tachycardia

Characteristics :-

Tachycardia, prolonged or normal P-R interval (depending on the origins of

the ectopic site).

QRS = normal, but P wave

have unusual configuration.


45/66

Atrial Fibrillation

Caused by numerous disorganised atrial impulses bombarding the AV node. Af

causes rapid and totally irregular atrial and ventricular rate. Ventricular rate

becomes irregular as few fibrillatory waves managed to be condcuted through

the AV junction to the ventricles.Hallmark of AF = absence of P waves replaced by oscillations of f waves.

A.k.a. saw-tooth waves.

In dogs and cats, the QRS may still be evident albeit differing in amplitudes. Inungulate where the Purkinje fibres penetrate deep into the myocardium, the f

waves and QRS superimposed on each other.

Associated with atrial enlargement, early signs of DCM (dilated

cardiomyopathy) or DCM itself. Toxicity. AF may even occur without anyevident cardiac disease.


46/66

Atrial Fibrillation


47/66

Ventricular Premature Complexes (VPC)

Cause by impulses generated within the ventricles, instead of the

SA Node. VPC is an important condition associated with

weakness, syncope, exercise intolerance and sudden death.

Characterised by wide and bizarre QRS, dissociated P waves.

VPC usually followed by a quiet compensatory pause.

Associated with cardiomyopathies (large dogs / cats),hyperthyroidism (cats), congenital defects (aortic stenosis),

chronic valve disease, traumatic myocarditis, digitalis toxicity,

myocarditis, cardiac neoplasia.

i l C l ( C)


48/66


V i l P C l (VPC)


49/66


This dog hadVentricular Bigeminy a condition where VPCs and

normal PQRST complexes are occuring at a fixed interval.

In this case it is a Uniform VB as the ectopic pacemaker that gave rise to

the VPC is stationary.

VB may be seen in PDAs and rarely during thiopentone anaesthesia

V t i l T h di


50/66

Ventricular Tachycardia

The result of 3 or more VPCs. Characterised by ventricular rate > 150 bpm.

No relation ship between P and QRS. There will be ventricular fusion and

capture complexes (with P waves). Uncommon in cats.

V t i l A t l


51/66

Ventricular Asystole

You see this in dying animals ! A medical emergency because this condition

indicates absence of pacemaker impulses. No pulse can be detected and CO may

be = 0.

Indicated by absence of QRS complex. P waves may be present if the animalhas complete AV block.

V t i l Fib ill ti


52/66

Ventricular Fibrillation

Occurs when cells of the ventricular myocardium depolarise in a chaotic and

uncoordinated manner. No pulse can be felt and Co is 0.

Characterised by rapid, irregular rhythm with bizarre waves and oscillations

(large = coarse fibrillation easier to treat; small = fine fibrillation reqepinephrine to convert them into coarse fibrillation first before attempting any

treatment).

Associated with shock, anoxia, trauma, myocardial infarction, electrolyte andacid imbalances, anaesthetic reactions, digitalis toxicity, electric shock,

myocarditis, hypothermia.

Requires agrresive therapy. Electric cardioversion is often instituted

immediately (remember the defibrillator ?) , alternatively a precordial thumpmay be helpful (although it may not work most of the time).



53/66


Sinus Block


54/66

Sinus Block

Occasional failure of SA node to initiate an impulse, as a result no heart beat

can be detected. No ventricular escape rhythms ! Prolonged pauses usually

results in low CO

An incidental finding in brachycephalic breed dogs, hereditory stenosis of theAV bundle (esp in pure breeds). Associated with elctrolyte imbalance, intense

vagal stimulation, drug toxicity (digitalis, quinidine).Treatment is not really

recommended if animal is asymptomatic.

Atrial standstill (associated primarily with Hyperkalemia)


55/66

Atrial standstill (associated primarily with Hyperkalemia)

Absence of P waves (in all leads) associated with supraventricular-type QRS.

Low heart rate (


56/66

Wolff-Parkinson-White Syndrome (WPW)

WPW syndrome consists of ventricular pre-excitation with paroxysmal

supraventricular tachycardia. Ventricular pre-excitation occurs when

impulses originating from the SA node or atrium activate a portion of ventricle

prematurely through the AV node. The remainder of the ventricle is still

activated normally through the usual conduction system.

Charaterized by normal P waves, normal rhythm, short P-R interval, widened

QRS (often with slurring or notching of the upstroke of the R wave = delta

wave) or even bizarre looking QRS. Heart rate may be very high (dog > 300bpm, cats > 400 bpm).

Associated with congenital defect of the conduction system, ASD, tricuspid

valve dysplasia in dogs, hypertrophic cardiomyopathy in cats.Occular or sinus carotid pressure will slow heart rates down, often treated with

direct current shock or drugs (lidocaine, procainamide dogs or propanolol,

atenolol in cats).



57/66


Medical intervention is not required in cases with ventricular pre-excitation

only without tachycardia.

AV blocks


58/66

AV blocks

AV block referred to a delay or interruption in conduction of a supraventricular

impulse through the AV junction and AV bundle. Three types :

A.)1st degree = delay in conduction.

B.)2nd degree = intermittent disruptions of conduction. Further classified

according to the location of blocks. Normal in horses and young animals.

C.)3rd degree = complete or permanent interruption of conduction.

Since P-R = duration taken by the impulse to travel from atria to ventricles.

Therefore, this parameter will be most affected.

Morphology of QRS will indicate whether the block is at the level of AV node

(i.e. above AV bundle normal QRS) or below the AV bundle (bizarre QRS).Due to the dependence of block regions of the ventricle on the aberrant

electrical signal from the excited ventricle.

1st degree AV block


59/66

1 degree AV block

Caused by delay in conduction of a supraventricular impulse through the AV

junction and AV bundle. P, QRS are usually normal. Only prolongation of P-R

interval (>0.13 s in dogs, >0.09 s in cats).

Caused by aging changes in Cocker spaniel and Dachshunds (due todegenerative changes of the conduction system), associated with drug therapy

(digoxin, propanolol, quinidine infact 50 % of digitalised dogs have

prolonged P-R), potassium imbalance, hypothyroidism or protozoal

myocarditis.

2nddegree AV block (Mobitz type I, usually Type A)


60/66

2 degree AV block (Mobitz type I, usually Type A)

Characterised by intermittent failure or disturbance of Av conduction. One or

more P waves are not followed by QRS-T complexes. Progressive prolongation

of P-R and shortening of R-R until P is blocked. Therefore the ventricular

waves become slower compared to atrial waves. QRS duration is often normal.

Type I AV block is often due to conduction failure above the bifurcation of AV

bundle.

2nddegree AV block (Mobitz type I, usually Type A)


61/66

2 degree AV block (Mobitz type I, usually Type A)

Characterised by intermittent failure ordisturbance of AV conduction. One or

more P waves are not followed by QRS-T complexes. Progressive prolongation

of P-R and shortening of R-R until P is blocked. Therefore the ventricular

waves become slower compared to atrial waves. QRS duration is often normal.

Type I AV block is often due to conduction failure above the bifurcation of AV

bundle.

2nddegree AV block (Mobitz type II, usually Type B)


62/66

deg ee V b oc ( ob t type , usua y ype )

Characterised by normal P

waves and QRS with

abnormal configuration

(similar to bundle bunch

block characteristics).

Frequency and the severity of

the block is unpredictable.

May developed into advanced

2nddegree AV block = when

>2 consecutive P waves are

blocked.

Associated with cardiac

neoplasia, myocarditis (Lyme

disease), hereditary stenosis

of the AV bundle (pugs),hypertophic cardiomyopathy

or hyperthyroidism in cats.

Electrolyte imbalance and

drugs (eg Xylazine, Digoxin).

3rddegree AV block


63/66

g

The cardiac impulse is completely

blocked in the region of the AV

junction and/or all bundle

branches. The atrial rate is normal

but idioventricular escape rhythm

is slow (therefore more P than

QRS syncope). P wave have not

constant relationships with QRS.

QRS may be normal (pacemaker inthe lower AV junction), or bizarre

(if pacemaker is in the ventricle or

bundle branch blocks are present).

Associated with VSD, aorticstenosis, endocarditis,

myocarditis, idiopathic fibrosis

(in older dogs esp Cocker

Spaniels), DCM, cardiacneoplasia.

Left Bundle Branch Block (LBBB)


64/66

( )

Due to the delay of block of the conduction in the LBB, either the main branch

or anterior/posterior fascicles. The supraventricular impulse activates the right

ventricle via the RBB. The left ventricle was activated much later or not at all,

causing bizarre QRS.

Characterized by prolonged QRS (>0.08 s in dogs, >0.06 s in cats). QRS

positive in leads I, II, III, aVF. Rather uncommon in dogs and cats as the LBB

is large and extensive.

Associated with direct cardiac trauma (e.g. MVA or HBC, cardiac needle

puncture), cardiomyopathy, ischaemic cardiomyopathy (ateriosclerosis of the

coronary artery, MI), subvalvular aortic stenosis (when septum and LBB are

affected).

LBB does not cause haemodynamic abnormalities. May give similar features as

to that of LVH, please verify with echocardiography or radiography.

Left Bundle Branch Block (LBBB)


65/66

( )

Right Bundle Branch Block (RBBB)


66/66

g ( )

Causes are similar to

LBBB, but it involved the

RBB. Similar to LBBB,

RBBB is also an incidental

finding that does not cause

any heamodynamic

abnormality. The block

can be complete

(prolonged QRS) or

incomplete (normal or near

normal QRS duration).

Associated with chronicvalvular fibrosis,

heartworm disease,

hyperkalemia,

cardiomyopathy.Note the large S waves !

ecg analysis and interpretation

Documents