ECGs Flashcards
What is the pacemaker of the heart and why?
Most of the cells within the heart have the ability to
generate their own electrical activity, but the sinoatrial
node is the fastest to do so and is, therefore, the ‘rate
controller’ or pacemaker of the heart.
The rate of the sinoatrial node is influenced by the balance in autonomic tone, involving the sympathetic (which increases the rate) and parasympathetic (which decreases the rate) systems.
How does conduction in the heart occur?
The sinoatrial node normally initiates the electrical
discharge for each cardiac cycle. Depolarisation spreads through the atrial muscle cells. The depolarisation wave then spreads through the atrioventricular node, but it does so more slowly, thereby creating a time delay.
Conduction passes through the atrioventricular ring
(from the atria into the ventricles) through a narrow
pathway called the bundle of His. This then divides in
the ventricular septum into left and right bundle branches (going to the left and right ventricles). The left bundle branch divides further into anterior and posterior fascicles. The conduction tissue spreads into the myocardium as very fine branches called Purkinje fibres.
What is the T wave?
Repolarisation of the ventricles
Outline a normal sinus rhythm
In normal sinus rhythm, the stimulus originates regularly
at a constant rate from the sinoatrial node (dominant pacemaker), depolarising the atria and ventricles normally and producing a coordinated atrioventricular contraction.
The ECG shows a normal P wave followed by normal
QRS and T waves. The rhythm is regular (constant) and
the rate is normal for age, breed and species. The size
of the ECG complexes are typically small in cats and, therefore, obtaining an artefact-free tracing is important
in order to clearly identify the ECG complexes.
What is a wandering pacemaker?
slight variation in P wave amplitude, can be positive/ negative/ isoelectric and v hard to see
Occurs as a result of the dominant pacemaker shifting from the SA node to other pacemaker cells with a high intrinsic rate within the atria
What is sinus arrhythmia
In the case of sinus arrhythmia, the stimulus originates
from the sinoatrial node, but the rate varies (increases
and decreases) regularly. This is usually associated with the variation in autonomic tone which is often synchronous with respiration and is therefore sometimes called respiratory sinus arrhythmia.
CLINICAL FINDINGS
The heart rhythm varies with some regularity, increasing and decreasing in rate, and there is a pulse for every heartbeat.
ECG FEATURES
The ECG shows a normal P wave followed by normal
QRS and T waves. The rhythm varies in rate, often associated with respiration. The rhythm is sometimes described as being regularly irregular (ie, the variation in rate is fairly regular). The rate is normal for age, breed and species
What is sinus tachycardia?
In the case of sinus tachycardia, the sinoatrial node generates an impulse and depolarisation which occurs faster than normal.
Rhythm is still normal, as is ECG and PE findings (pulses may be weak if really fast)
What is sinus brady cardia?
In the case of sinus bradycardia, the sinoatrial node generates an impulse and depolarisation which occurs more slowly than normal. This can be a normal feature in some giant-breed dogs and in athletically fit animals.
How do you describe the number of ectopic beats in an ECG?
Premature ectopic complexes may occur singly, in pairs or in runs of three or more; the last is referred to as tachycardia.
Tachycardia may be continuous, in which case it is known as persistent or sustained, or may be intermittent, which is termed paroxysmal
How do you describe the timing of ectopic beats?
Ectopic complexes that occur before the next normal complex would have been due are termed premature; those that occur following a pause, such as a period of sinus arrest or in the case of complete heart block, are termed escape complexes
How do you describe the frequency of ectopic beats?
The number of premature ectopic complexes in a tracing may vary from occasional to very frequent. When there is a set ratio, such as one sinus complex to one ectopic complex, this is known as bigeminy; when there is one ectopic to two sinus complexes, this is termed trigeminy
How may the T wave appear after a VPC?
Often opposite to the QRS and large
What happens in a ventricular premature complex
From an ectopic focus/ foci within the ventricular myocardium
Conduction occurs cell to cell rather than through conduction tissue
What would you find on exam with VPCs?
N.B this would be the same for supraventricular premature complexes
May sound like a trip in the rhtyhm, may be silent with a gap in the rhtyhm, depends on when it occurs
Pulse deficit
If they are frequent, will sound like an irregular rhythm
If premature beats are very frequent, the heart will sound v chaotic, with a much slower pulse rate than heart rate
Sustained ventricular tachycardia will sound relatively normal, pulses palpable but reduced in strength, becoming weaker with faster heart rates
What are the ECG features of VPCs?
Wide and bizarre
T wave large and opposite
What would you call a short burst of ventricular premature complexes which are of different shapes?
multiform paroxysmal ventricular tachycardia
What is R-on-T phenomenom?
a ventricular premature complex occurs so early that it is superimposed on the T wave of the preceding ventricular premature complex
What is ventricular tachycardia?
run of three or more ventricular premature complexes
How do you divide supraventricular complexes?
Those which occur in the atrial muscle mass (atrial
ectopics); and
* Those which arise from within the atrioventricular
node or bundle of His (junctional or nodal ectopics).
How can you identify a supraventricular complex?
occurs as a premature beat, which means that it is
primarily recognised by its premature timing
Looks like a normal QRS as has had to go through the bundle of his to get to the ventricles
P wave morphology is often different
What are the ECG features of supraventricular tachycardia
QRS-T complexes, which have a normal morphology,
are seen to occur prematurely. The ECG features are:
Normal QRS morphology (except with bundle branch
block);
The QRS complex is seen to occur prematurely;
P waves may or may not be identified;
If P waves are seen, they are usually of an abnormal
morphology (ie, non-sinus) and the P-R interval may
differ from that seen in a normal sinus complex.
What would you find clinically with atrioventricular dissocaition?
The heart rhythm will sound fairly normal and the pulse should match the heart rate.
What are the ECG features of atrioventricular dissociation?
The ECG shows a ventricular rate that is usually very
slightly faster than the atrial rate. The P waves may
occur before, during or after the QRS complex. The
P waves and QRS complexes are independent of each
other, with the QRS complexes appearing to ‘catch up’
on the P waves. Atrioventricular dissociation should be
differentiated from complete heart block. In the case of
heart block, the ventricular rate is slow and much lower than the atrial rate; in atrioventricular dissociation, the atrial and ventricular rates are not dissimilar (and usually at a normal or faster rate).
What occurs in atrial fibrillation?
Fibrillation means rapid irregular small movements of
fibres. In atrial fibrillation, one of the most common
arrhythmias seen in small animals, depolarisation waves occur randomly throughout the atria. As atrial fibrillation originates above the ventricles, it can also be classified as a supraventricular arrhythmia.
What are the clinical findings of atrial fibrillation?
The heart rhythm sounds chaotic and the pulse rate is
often half the heart rate, especially with fast atrial fibrillation. This is a very common arrhythmia in dogs and can be strongly suspected on auscultation by its chaotic rhythm and 50 per cent pulse deficit. Very frequent premature beats (ventricular or supraventricular) can mimic it.
What are the ECG findings of atrial fibrillation?
Normal QRS morphology (except when there is
bundle branch block);
* The R-R interval is irregular and chaotic (note this is
easier to hear on auscultation!);
* The QRS complexes often vary in amplitude;
* There are no recognisable P waves preceding the
QRS complex;
* Sometimes, fine irregular movements of the baseline known as ‘f waves’ - are seen as a result of the atrial
fibrillation waves. However, frequently these f waves are indistinguishable from baseline artefact (eg, muscle
tremor) in small animals.
What occurs in ventricular fibrillation?
Ventricular fibrillation is nearly always a terminal event
associated with cardiac arrest. The depolarisation waves occur randomly throughout the ventricles. There is therefore no significant coordinated contraction to produce any cardiac output. If the heart is visualised or palpated, fine irregular movements of the ventricles are evident and likened to a ‘can of worms’. Ventricular fibrillation can follow ventricular tachycardia.
CLINICAL FINDINGS
No heart sounds are heard. No pulse is palpable.
ECG FEATURES
The ECG shows coarse (larger) or fine (smaller) rapid,
irregular and bizarre movement with no normal waves or complexes.
What is sinus block?
When the impulse from the SA node fails to be conducted to the atrial muscle
On C/E, will note a small gap in the rhythm, this may not be distinguishable from a normal rhtyhm such as sinus arrhythmia
On ECG, a beat is skipped (ie a P wave or QRS is not produced, so you get a flat line equivalent to twice to RR interval
What is sinus arrest?
When the SA node fails to generate an impulse (has temporarily stopped)
Will hear a pause in the rhythm, no pulse
On ECG, there will be a flat line, greater than 2 RR intervals, often followed by a ventricular escape complex
What is sick sinus syndrome?
Sick sinus syndrome refers to an abnormally functioning sino atrial node and is probably better termed sinus node dysfunction.
This umbrella term refers to any abnormality of sinus node function ,including severe sinus bradycardia and sinus arrest.
In some situations, the profound bradycardia alternates with supraventricular tachycardia and this is known as the ‘bradycardia-tachycardia syndrome’.
Reported to occur most commonly in female miniature schnauzers of six years of age or more, also common in westies
Not reported in cats
Degeneration of the conducting system
What can you hear on auscultation with sick sinus syndrome
Variable Can be short followed by fast Bradycardia variable rhythm with long pauses May be pulse deficits during tachycardias May be no pulse during periods of arrest
What are the ECG findings of sick sinus syndrome
Can vary a lot
may get bradycardia
may get sinus arrest without escape beats
In bradycardia-tachycardia syndrome, may get sinus arrest followed by supraventricular tachycardia
What is atrial standstill?
Absence of atrial activity
Due to a failure of atrial muscle depolarisation - SA node is still releasing an impulse
Hyperkalaemia is the most common cause in dogs
What are the clinical findings
Often a bradycardia < 60
What are the ECG findings of atrial standstill
Absence of P waves
Needs to be an excellent ECG with no movement to dx this confidently!
What is heart block?
Failure of normal conduction through the AV node
First degree - delay in conduction
Second degree - conduction through the AV node intermittently fails
Third (complete) - complete failure of conduction through the AV node. A second pacemaker below the AV node takes over
What are the clinical/ ECG findings of first degree AV block?
Cannot hear anything abnormal
Prolonged P-R interval
What will you hear on auscultation/ ECG with second degree block?
hear occasional pauses in rhythm
Sometimes a very faint artrial contraction (s4) can be heard
Sometimes lack of QRS for the P
When the P-R interval increases prior to the block, this is Mobitz type 1 - often associated with high vagal tone, a physiological response
When the P-R interval is the same before the block, this is Mobitz type 2, and the ratio or normal to skipped is often constant
Where may the new pacemaker arise from in third degree AV block?
- Lower atrioventricular node or bundle branches producing a normal QRS (ie, junctional escape complex) ,usually at a rate of around 60 to 70/ minute
- Purkinje cells producing an abnormal QRS-T complex (ie, ventricular escape complex), usually at a rate of 30 to 40/minute.
What are the findings with third degree AV block?
Often a slow bradycardia, good pulses
P waves regular and fast
QRS complexes much slower
the two are not associated with each other
Usually QRS complexes are wide and bizarre
Is an escape rhythm
What is left or right bundle branch block?
Due to a failure or delay in the conduction through the mentioned bundle branch block
the other ventricle depolarisation is normal, the mentioned one is through myocardial cell tissue, leading to a very prolonged complex
What are the findings associated with right bundle branch block?
Heart sounds normal, normal pulses
In some dogs, a split second sound may be heart due to delayed closure of the pulmonic valve
ECG - QRS complex prolonged (>0.07 sec)
QRS complex is deep and slurred
Mean electrical axis is to the right
What are the findings associated with left bundle branch block?
Heart sounds normal, normal pulses
ECG - QRS complex prolonged (>0.07 sec)
Positive complexes are seen in leads I, II, III, and aVF and negative ones occur in a VR and aVL
Left bundle branch block needs to be differentiated from a left ventricular enlargement pattern
What is left anterior fascicular block?
Failure of conduction through the anterior fascicle of the left bundle branch
Common in cats, rare in dogs
normal heart sounds and pulses
What are the ECG features of left anterior fascicular block?
Normal QRS complex
Tall R waves in Leads 1 and aVF
Deep S waves > R in leads II, III and aVF
Can occur with atrial fibrillation
How do you measure HR in an ECG?
Normally count per 6 sec then x 10
If P and QRS are not associated/ regular, then mark the rates down seperately
How can you measure boxes on an ECG?
At 50mm/ sec, a 1mm box =0.02 sec
How do you measure the complexes?
P wave amplitude and duration R wave amplitude and QRS duration P-R interval QT interval T wave morphology S=T segment elevation or depression
Why may a QRS complex be small in a dog
Smaller the further away from the heart the leads are
Can be smaller in obese animals
What is electrical alternans?
Alteration in the size of the QRS complexes nearly every other beat
Can be seen in severe pericardial effusion
What can notching in the R wave mean?
Seen commonly in small animals with heart disease, the significance of the notches is debatable -
occur with microscopic intramural myocardial infarction or may be associated with areas of myocardial fibrosis.
Intraventricular conduction defects and as light notch is sometimes also seen with ventricular prexcitation in the upstroke of the R wave (deltawave).
artefactually in tracings in which there is excessive muscle tremor or electrical interference
When may you see S-T abnormalities?
Pericarditis
Severe myocardia infarction/ ischaemia (full wall thickness)
Depression - endomyocardial ischaemia 9e.g. infarction/ cardiomyopathy
- K imbalance
- Digitalis toxicity
How may LA enlargement appear on an ECG?
Prolonged P wave
May be notched
if both, is termed P mitrale
How may RA enlargement appear on an ECG?
Increased amplitude of P wave
P-pulmonale
P-pulmonale commonly seen in breeds which are pre disposed to common airway dz
What may suggest left ventricular enlargement?
tall R waves
Prolonged QRS duration
S-T segment sagging
What suggests right ventricular enlargement?
Deep S waves
prolonged QRS
When may you see large t waves?
Myocardial hypoxia
hyperkalaemia
What are the signs of hyperkalaemia on an ECG?
Progressive bradycardia
Tented T waves
Atrial standstill with a sinoventricular rhtyhm
ventricular fibrillation or asystole
What do the different leads represent on an ecg?
Lead 1 - RF to LF
Lead II - RH to LH
Lead III - LF to LH
What are the augmented leads?
Compares 1 electrode to the other 2
What is +ve and -ve in lead II?
LH +ve
RF -ve
Why is the QRS normally positive on a lead 2 ECG?
The left ventricle is dominant
conduction going from the right atrium to the left ventricle
LH is + lead to +ve deflection in ECG
What are the rough ways of assessing the mean electrica axis?
Lead with the tallest QRS
Lead perpendicular to the lead with the closest to isoleclectric lead
What would you see on an ECG of bundle branch block?
conduction disorder
Wide and bizarre QRS Normal P waves In lead II, the QRS is positive in left block, and negative in right PR interval is normal QRS for every P P for every QRS
What are the ddx for bradycardia?
Sinus bradycardia Sinus arrhythmia AV block 1st degree 2nd degree 3rd degree Sinus arrest Atrial standstill Sick sinus syndrome
What are the ddx for tachyarrhythmia?
Sinus tachycardia
Supraventricular tachycardia (SVT)
SV premature complexes
Atrial fibrillation/flutter
Ventricular tachycardia
VPCs
Sick sinus syndromeWhat are the questions to ask in a logical approach in an ECG?
Is there a P for every QRS? (if not, then the depolarisation is not originating from the SA node)
Is there a QRS for every P? (No suggests a block)
Is the rhythm regular or irregular?
Irregularly or regularly irregular?
Does the QRS look normal?
What are some pathological things to remember with sinus arrythmia
May be seen in brachycephalics
In severe resp disease
Is regularly irregular
Outline first degree AV block
P-R interval over 0.13 sec (below this is normal)
May suggest high vagal tone
Not really an issue for the patient
Where do ectopic beats originate from?
Abnormal areas of myocardium
What is ventricular bigeminy
when each normal QRS is followed by a premature complex
When is tachycardia likely to be pathological
No P waves
>160bpm likely
>200 v likely
What can ventricular tachycardia look similar to?
Bundle branch block with SVT
What is an accelerated idioventricular rhythm?
<180 bpm
frequently seen as a complication of severe systemic illness and are usually not associated with evidence of impaired cardiac performance
ventricular rhythm that alternates with the normal sinus rhythm
interval between the last sinus complex and first ventricular complex is often longer than the normal sinus R-R interval, indicating that the two rhythms are competing with each other for control of the heart. In doing so, the practitioner will note that when the sinus rate slows below the rate of the AIR, the ventricular beats appear
What heart rate would be considered an emergency
<60 - watch
<40 real concern
With tachycardia, base on
Haemodynamic status
Demeanour
Pulse quality
BP - although normal BP does not mean you don’t need to do anything
The higher the heart rate the more urgent the treatment
What are the main treatments for bradyarrhythmias?
Atropine - hard to give at home
Terbutaline (Bricanyl) B2 agonist
Propantheline - parasympatholytic - hard to get hold of
Theophylline (Corvental)
pacemaker
Outline the Vaughn - Williams classification for anti-dysrhthmics
Class 1 - Na channel blockers
- 1a quinidine, procainamide
- 1b - mexilitine, lidocaine
- 1c not really used
Class 2 - B blockers
Atenolol, esmolol, propanolol
Class III - K channel blockers
Sotalol, amiodarone
Class IV - calcium channel blockers
Diltiazem, verapamil
Digoxin - centrally acting
What is the mechanism of action of amiodarone/ its monitoring needs
all 4 classes
Needs liver and thyroid monitoring
What are the phases of the action potential?
0 - Na floods into the cell, depolarisation
1 - K slow efflux, then Ca influx
2 - K fast influx
3 - repolarisation, K extruded
Where do the different classes of anti-arrythmics work on the action potential
Class I - phase 0, Na blockers
Class III - K channel blokcers, prevent repolarisation
IV - Ca channel blockers so 1-2
How do calcium channel blockers and digoxin act on the SA and AV nodes
CCBs slow transmission through the node
Digoxin increases vagal tone
How do you treat ventricular tachycardia?
IV lidocaine, 2mg/kg up to 4 times
If not working, check lytes as low Mg or low K make it less effective
If lidocaine ineffective, B blocker
If lidocaine is working but there are blips, CRI lidocaine whilt starting oral meds
How do you investigate ventricular arrhythmias?
Abdo u/s
echo
troponin
Assess severity by holter before deciding if needs long term tx
How do you treat arrythmias?
Sotalol or mexilitine
How do you treat atrial fibrillation?
Can consider cardioversion, but not always successfful, only in a few referral centres, needs to have structurally normal heart, and have only recently gone into A fib
otherwise digoxin (aim for a trough of between 0.5-0.9 on bloods) Best in combination with diltiazam
Outline the use of digoxin
For A fib
Slows conduction through the AV node as a centrally acting vagomimetic
S/E - GI signs, brady and tachydysrhythmias
Weak positive inotrope
Acts on Na K pump (therefore affects Na Ca exchanger)
What are the mechanisms of SVT?
Focal atrial tachycardia Junctional tachycardia AV nodal re‐entrant tachycardia Accessory pathway Atrial flutter
What is wolf parkinson white syndrome?
Rapid paroxymal SVT associated with accessory pathway
Seen in labs
Can consider catheter ablation as a cure in referral settings
How can holters help to diagnose DCM in Dobermans and ARVC in boxers in the pre clinical stage?
Measure VPCs in 24 hours < 4 definitely normal <50 probably ignored Suspicious - >50 in doberman, 100-300 in boxer Affected >1000
How do you treat ventricular tachycardias?
Acute
Lidocaine
Esmolol
Amiodarone? - avoid, can cause anaphylaxis
Chronic
Sotalol
Mexilitine
Amiodarone - if others don’t work
How can you treat supraventricular tachycardias?
Acute
Vagal manoeuvres (e.g. pressing on eyes, carotid sinus)
Esmolol
Verapamil?
Chronic Diltiazem Digoxin Beta blockers? Amiodarone?
What are the most common causes of ventricular tachycardia?
DCM GDV splenic or liver masses Sepsis Hypoxia
