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Cardiology > Small animal cardiology arrhythmias > Flashcards

Small animal cardiology arrhythmias Flashcards

1
Q

How does the cardiac conduction system work

A

SAN is primary pacemaker, get impulse spreading via atrial myocardial cells to the AV node

AV slows down conduction, allowing atria time to contract fully, then get conduction down bundle of His to purkinje fibres

Purkinje fibres send impulses to large areas of ventircular myocardium at same time to get coordinated ventricular contraction

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2
Q

What do the parts of the ECG trace represent

A

P wave = atrial depolarisation
P-R interval = delay as impulse is at AV node
QRS complex = depolarisation of ventricles
T wave = ventricular repolarisation

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3
Q

What can T wave look like

A

positive, negative or biphasic

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4
Q

Which lead gives the biggest complexes and best mimics electrical activity

A

Lead 2 since most parallel to heart

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5
Q

What does it mean if there is no QRS for a P

A

Conduction pathway is being blocked

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6
Q

What does it mean if there is no P for a QRS

A

Either the P wave is hidden within the QRS
Or the stimulation for the ventricular activation is coming from below the atrium

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7
Q

What does a tall and narrow vs wide and bizzare QRS complex mean

A

Tall and narrow = normal as has used his-purkinje system to get rapid ventricular depolarisation; supraventricular rhythm

If it is wide and bizarre means didn’t use his-purkinje i.e impulse being generated from ventricle

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8
Q

What is sinus arrhythmia

A

Related to vagal tone
Cyclic variation in heart rate associated with respiration; so increased HR on inspiration

Rhythmic irregularity

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9
Q

Is sinus arrhythmia more common in dogs or cats and why

A

Dogs because it is due to vagal tone and cats are usually more stressed

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10
Q

What does wandering pacemaker mean

A

Where P wave morphology varies
Related to which part of the SAN the impulse came from
Also related to vagal tone and is normal in dogs

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11
Q

What are supraventricular premature complexes

A

P waves come in early i.e somewhere within atria is generating an impulse where it shouldn;t be i.e NOT SAN

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12
Q

What are supraventricular tachycardia and what is the main question to ask

A

Narrow QRS complex tachycardia
Ask whether irregular or not

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13
Q

If supraventricular tachycardia is irregular what is it

A

Atrial fbrillation

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14
Q

If supraventricular tachycardia is regular what is it most likely to be

A

Most likely focal atrial tachycardia
(but there are some other options)

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15
Q

What is focal atrial tachycardia

A

A fast regular rhythm with narrow QRS complexes but P wave morphology is different from normal sinus P wave due to ectopic focus in atria generating it

P wave may be before, within or after QRS

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16
Q

What is the main differential for focal atrial tachycardia and how can we tell them apart

A

Sinus tachycardia
If very fast i.e >300 must be FAT since SAN cannot go that fast

Ocular pressure or gag reflex to stimulate vagus will slow rate which can allow you to see P waves and work out whether sinus tachycardia or FAT

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17
Q

What is atrial fibrillation

A

Fast irregular rhythm where there is no organised activity in the atria just some small circuits
Some of these reach the AVN and cause depolrasiation

Associated with severe structural heart disease where atrial size reaches a large enough size to develop these wavelets of activity

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18
Q

What does a atrial fibrillation ECG look like

A

No P waves
Narrow QRS (since coming down his-purkinje)

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19
Q

Which breeds can get lone AF i.e atrial fibrillation without structural heart disease and what is it a risk for

A

Giant breeds
= risk for DCM

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20
Q

What are the 4 types of ventricular tachycardias

A

ventricular premature complexes
Ventricular tachycardia
Ventricular fibrillation
Accelerated idioventricular rhythm (slow vtac)

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21
Q

What are ventricular premature complexes assocaited with and what does the ECG look like

A

Associated with structural heart disease or systemic disease

See wide and bizarre QRS
T wave amplitude large and opposite direction to QRS
May or may not see P waves; but won’t be associated with the ectopic QRS beats

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22
Q

What is bigemini VPC

A

Alternating pattern of sinus and ventricular beats

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23
Q

What is trigemini VPC pattern

A

Sinus beat, sinus beat, venitrcular beat
Pattern

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24
Q

What is monomorphic vs polymorphic VPCs

A

Monomorphic = ventricular beats always look similar i.e in same direction

Polymorphic = ventricular beets look different i.e some +ve some -ve

25
Q

What do polymorphic ventricular beats me

A

There is more than one area of damaged ventricle generating a beat; this is dangerous

26
Q

What is ventricular tachycardia associated with and what does it look like

A

Wide QRS complexes, fast regular rhythm
Associated with structural heart disease or systemic disease
- dangerous

27
Q

What is ventricular fibrillation and what does it look like

A

Terminal irregular rhythm with undulations of different shapes and sizes and no discernable P / QRS / T

Needs CPR and defibrillatino

28
Q

What are the criteria of malignancy with ventricular arrhythmias

A

Complexity: bigemini > couplets> triplets> vtac
Burden i.e no. abnormal beats
R on T phenomenon
Rate (R-R interval)

29
Q

What criteria of malignancy are associated with risk of sudden cardiac death

A

Frequent couplets/triplets
Coupling interval >260 beats/min

30
Q

What is R on T phenomenon and what is it a risk for

A

Where there are two ventricular beats so close together that it is hard to tell where one ends and other starts
= dangerous due to risk of entering ventricular fibrillation

31
Q

What is accelerated idioventricular rhythm and what is it associated with

A

= ventricular rhythm at a slower rate than vtac ~150-180bpm
Nor haemodynamically significant and often benign and self limiting

= Assocaited with extra-cardiac disease; treat THIS not the rhythm

32
Q

Some key differences between pacemaker action potential and ventricular myocyte action potential

A

Ventricular myocte; depolarised by Na+ entry; then has plateau phase where calcium comes in and K+ leaves; then repolarisation down to rest by K+ exit

In pacemaker: there is spontaneous depolarisation to threshold, then depolarisation by calcium entry, repolarisation by K+ exit with NO plateau phase; hyperpolarisation which is corrected by sodium and calcium entry

33
Q

What can we do to treat focal atrial tachycardia and what route can we give drugs

A

Can give drugs oral since they are stable

Acute management:
- Calcium channel blockers: diltiazem
- K+ channel blockers: sotalol, amiodarone
Vagal maneouvres
- Beta blockers; esmolol

Chronic = similar, can do radiofreq ablation of accessory pathway?

34
Q

What are the two broad ways to treat atrial fibrillation and which is more usually done

A

Rate control or rhythm control
- Generally no point doing rhythm control because where there is severe structural heart disease, would just go striaght back

35
Q

How to do rate control for atrial fibrillation

A

Calcium channel blockers to slow conduction through AV node; diltiazem (+/- digoxin)

36
Q

What is the only time we might use digoxin and why don’t we use it more often

A

Has a narrow therapeutic window so not commonly used
Can be used in atrial fibrillation to control the rate

37
Q

What is the aim for atrial fibrillation control with medication

A

Bring heart rate down to <125bpm on home holter ECG
Or <160bpm in the clinic

38
Q

Emergency mangement of sustained Vtac

A

IV lidocaine (sodium channel blocker to stop venitrcular arrhythmia)
Then if not responding add amiodarone
+ can add in sotalol (K+ blocker)

39
Q

Chronic oral management of ventricular arrhtyhmias once converted to sinus rhythm

A

Sotalol; K+ channel blocker
Amiodarone;k+ blocker
Mexiletine (Na+ channel blocker)

40
Q

What is AV block

A

Abnormal atrioventricular conduction with delay/failure of conduction of a sinus impulse through AV node

41
Q

What are some possible causes of bradyarrhythmias

A

Increased vagal tone
Intrinsic AV node disease e.g degenerative fibrosis
Drugs e.g beta-blockers, digoxin, Ca2+ channel blocker

42
Q

What is 1st degree AV block and what is it associated with

A

Delayed conduction through AV node assocaited with high vagal tone
So see prolonged PR interval with normal QRS

43
Q

What is type 1 second degree AV block

A

Where there are intermittent single non-conducted P waves (PR interval lengthens prior to the block)

= assocaited with high vagal tone

44
Q

What is type 2 second degree AV block

A

Where there are single or multiple non-conducted P waves but with constant PR itnerval
= assocaited with pathology

45
Q

How can we subdivide two 2 second degree AV block

A

Into high or low grade depending on how many P waves in a row have not been conducted
higher grade means that ventricles have longer period without contracting so more likely to see syncope etc

46
Q

What is third degree AV block

A

Persistent failure of AV conduction
There is no relationship between P waves and QRS complexes

47
Q

What may ventricles be depolarised by in third degree AV block

A

BY junctional beats from the AV node/his bundle –> generates narrow QRS complex

Or ventricular escape rhythm from ventricle which generates wide and bizarre complex at slower rate than sinus rhythmW

48
Q

What is the cause of third degree AV block

A

Myocardial damage/AV node degeneration
typically irreversible

49
Q

What is the difference betwen premature and escape beats and how would we treat them differently

A

Premature means come early from ventricle so wide and bizarre

Escape beats = coming from ventricle but after long pause in ventricular rhtyhm; also wide and bizarre

Would treat premature beats with lidocaine but NOT escape beats because these are what is keeping the animal alive

50
Q

What rate is ventricular escape rhythm in dogs/cats

A

Dogs <60bpm
Cats 80-140bpm

51
Q

What is atrial standstill

A

Where impulses not conducted through the atrial myocardium so there are no P waves

INstead have a slow ventricular rhythm
QRS complexes may be normal or wide/bizarre

52
Q

What are two possible causes of atrial standstill

A

Secondary to hyperkalaemia
Due to primary atrial myocardial disease = persistent i.e not reversible

53
Q

What would we classify as sinus arrest and what are some possible causes

A

Pause of >3 times normal R-R interval

e.g as part of SSS, due to drugs like amiodarone/digoxin, electrolyte imbalances, myocarditis, idiopathic

54
Q

What is sick sinus syndrome and what are the clincial signs and signalment

A

Abnormal sinus node function
Signs = weakness, lethargy, ataxia, collapse
Commonly seen in small breed dogs e.g terries, westies

55
Q

ECG findings with sick sinus syndrome and treatment

A

Sinus bradycardia
Low mean HR
Intermittent sinus arrest
Intermitten 1st/2nd degree AV block
May see supraventricular tachycardia

Need a pacemaker to fix

56
Q

What is the atropine response test for bradyarrhytmias

A

Used to assess the degree to which AV block or SSS is vagally mediated

Give IM or SC atropine and repeat ECG at 20, 30 and 40 mins
A positive response will be increase in HR >150bpm, abolition of sinus arrest, significant improvement in AV vlock

57
Q

Treatment of bradyarrhythmias

A

Treat underlying disease e.g hyperkalaemia if present
Use pacemaker if indicated
Chronitropic drugs e.g terbutaline, theophylline

58
Q

WHen is a pacemaker indicated

A

Unstable high grade 2nd/3rd grade AV block
Sick sinus syndrome

59
Q
A

Cardiology (6 decks)

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