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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.
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ECG : Normal Canine Parameters
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ECG : Normal Feline Parameters
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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.
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ECG : MEA
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ECG : MEA
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ECG : MEA
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ECG : MEA
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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.
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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
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Students MUST KNOW thefollowing ECG signatures
-Atrial enlargements
-Ventricular enlargements
-AV Blocks (1st , 2nd and 3rd degree)
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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)
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Right Atrial Enlargement
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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)
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Left Atrial Enlargement
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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
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Biatrial Enlargement
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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)
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Right Ventricular Enlargement
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Right Ventricular Enlargement
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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
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Left Ventricular Enlargement
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Left Ventricular Enlargement
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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
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Bi-Ventricular Enlargement
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Bi-Ventricular Enlargement
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The following ECG findings areimportant, but I will leave it to the
students to determine theirusefulness in routine clinical
analysis.
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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!
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Low Voltage QRS complexes
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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
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Intervals and segments
S-T segment represents the early phase of ventricular
repolarisation
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Intervals and segments
Q-T interval is the summation of ventricular depolarization andrepolarization, and represents ventricular systole
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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
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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.
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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
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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.
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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.
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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)
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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.
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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.
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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.
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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.
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Atrial Premature Complexes
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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.
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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.
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Atrial Fibrillation
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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)
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Ventricular Premature Complexes (VPC)
V i l P C l (VPC)
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Ventricular Premature Complexes (VPC)
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
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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
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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
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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).
Ventricular Fibrillation
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Ventricular Fibrillation
Sinus Block
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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)
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Atrial standstill (associated primarily with Hyperkalemia)
Absence of P waves (in all leads) associated with supraventricular-type QRS.
Low heart rate (
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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).
Wolff-Parkinson-White Syndrome (WPW)
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Wolff-Parkinson-White Syndrome (WPW)
Medical intervention is not required in cases with ventricular pre-excitation
only without tachycardia.
AV blocks
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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
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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)
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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)
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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)
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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
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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)
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( )
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)
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( )
Right Bundle Branch Block (RBBB)
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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 !
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