Causes + tx of cardiac arrhythmias

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Last updated 3:06 PM on 9/30/26
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58 Terms

1
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How can arrhythmias be classified?

  • Brady/Tachy

  • Paraxysmal (episodic)/ sustained

  • Tachy can be supraventricular/ Ventricular


2
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How can arrhythmias be monitored?

Standard ECG (2-3 minutes)

Holter monitor (24h-7days)

Implantable device (years)

3
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What is the general cardiac cause of weakness and syncope?

  • Compromised cardiac output


4
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What can cause a compromised cardiac output leading to weakness and syncope?

  • Congenital heart disease

  • DCM

  • HCM

  • Cardiac tamponade

  • Neoplasias

  • Arryhthmias

    • tachy —> too fast not enough time for ventricles to fill for adequate SV

    • brady —> too slow not enough O2


5
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What are the two types of action potentials in the heart? What is their main difference?

  • Pacemaker (nodal) cells action potentials

    • Primary due to influx of Ca

  • Cardiac myocytes

    • Primarily due to influx of Na


6
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Recall the vaughan williams classification of antiarrhythmic drugs?

Class I- Na channel blocker (1° myocardial cells) —> slow upstroke of depolarisation

Class II- Beta blocker (1° nodal cells) —> slow depolarisation

Class III- K channel blocker (1° myocardial) —> lengthen AP duration

Class IV- Ca channel blocker (1° nodal cells) —> slow depolarisation

Misc: Digoxin —> slow conduction across AVN

'Never Buy Kennel Club Dogs'

7
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What is this ecg showing?


Supraventricular tachycardia

  • from above ventricles

  • Fast conduction because only above ventricle affected so narrow complexes

  • regular rhythm (except AFib)

Narrow QRS

8
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What is arrhythmias are classed as SVTs?

  • sinus tachy

  • focal atrial tachy

  • multi-focal atrial tachy

  • orthodromic atrioventricular reciprocating tachy

  • AFib

  • atrial flutter

  • focal junctional tachy

  • junctional ectopic tachy

  • atrioventricular node reentry tachy


9
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When could a SVT look wide not narrow?

If bundle branches are damaged?

10
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What is the most common pathological arrhythmia in animals?

AFib

11
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What is AFib associated with?

  • Most commonly atrial stretch from underlying heart disease (MMVD, DCM)

    • Can occur in abscence of heart disease if mass of atria is large in larger animals (lone AFib)


12
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Explain what happens during AFib?

‘Fibrillating’ atria with chaotic depolarisation

  • No coordinated atrial depolarisation so absence of p wave

    • May see fibrillating baseline

  • Timing of depolarisation reaching AVN is irregular (ventricular rate irreg)

    • Irregular R-R interval

irregularly irregular

13
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What is this ecg showing?


AFib

14
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How is AFib treated?

  • Manage underlying condition

  • don’t try to convert to sinus rhythm (likely AFib with reoccur)

  • AIM control the ventricular response rate to AFib (decr HR) —> <140bpm, but ideally <125bpm

  • Drugs that slow conduction through AV node

    • Class 4s- Ca channel blocker —> Diltiazem

    • Digoxin

Better heart rate control with combination Digoxin + Diltiazem

15
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What are beta blocker typically not use to tx AFib?

would worsen already poor systolic function

(NEVER use in uncontrolled CHF)

16
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What effect does diltiazem have?

  • slow conduction across the AVN

  • Negative inotrope (clinically insignificant)


17
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What effect does digoxin have?

  • Negative chronotrope (slows heart rate)

  • ‘Vagomimetic’ —> enhances vagal tone and slows conduction across the AV node

  • Weak +ve inotrope

    • Blocks Na+/K+ ATPase → Ca2+ accumulation (inprove contract.)


18
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What should you be careful of when using Digoxin?

  • Digoxin toxicity

    • Start with cautious dose and check plasma levels

    • GI signs


19
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<p><span>What is Orthodromic atrioventricular re-entrant tachycardia (OAVRT)?</span></p>

What is Orthodromic atrioventricular re-entrant tachycardia (OAVRT)?

Wolf-Parkinson White syndrome

  • Abnormal connection between atria and ventricles (band of muscle)

  • Conduction from the atria to the ventricles can occur across the pathway

  • ACCESSORY PATHWAY MEDIATED SVT


20
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How does OAVRT present on ECG?

  • Short P-R in sinus rhythm

    • slurred QRS upstroke = delta wave (ventricular pre excitation)

  • Rapid narrow QRS complex tachycardia


<ul><li><p>Short P-R in sinus rhythm</p><ul><li><p>slurred QRS upstroke = delta wave (ventricular pre excitation)</p></li></ul></li><li><p>Rapid narrow QRS complex tachycardia</p></li></ul><p></p>
21
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What is the typical presentation of OAVRT?

  • Labrador retrievers + GR

  • Typically young (1-2 yr/o)

  • Syncope and exercise intolerance

  • Very fast HR

  • Can present in heart failure bc tachycardia induce cardiomyopathy


22
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How can OAVRT be treated?

Radiocatheter ablation (burn accessory pathway)

23
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How is SVT treated in an emergency situation?

  • Vagal manoeuvre

    • Ocular compression

    • Carotid massage

    • Gag reflex

  • IV esmolol (beta blocker)

  • IV diltiazem (IV verapamil if diltiazem unavailable)

  • Oral diltiazem if IV preparation not available

  • Oral sotalol can also be effective

In first opinion try oral options whilst evaluating- probably will work

24
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What does a ventricular arrhythmia look like on an ecg?

Typically, wide QRS complexes

  • not conducted along the specialised conduction fibres therefore slow conduction

ventricular ectopics = VECs + VPCs

25
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What is the difference between ventricular escape complex and ventricular premature complexes?

Look the same on ECG

  • Ventricular escape complexes occur after a long pause (‘escape’ death)

  • Ventricular premature complexes (VPCs) occur before you’d expect them (premature)


26
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<p>What does this ECG show?</p>

What does this ECG show?

ventricular premature complex (triplet + couplet)

27
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What are the different classifications of monomorphic VTACH?

  • Non-sustained <30s

  • Sustained >30s

  • Incessant >12h

(wide QRS all look the same)

<ul><li><p>Non-sustained &lt;30s</p></li><li><p>Sustained &gt;30s</p></li><li><p>Incessant &gt;12h</p></li></ul><p>(wide QRS all look the same)</p>
28
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How does a VTACH present on ecg?

  • wide QRS

  • R-R interval constant (regular rhythm on ausc)

  • ± P wave (not associated with the QRS or hidden within QRS)


<ul><li><p>wide QRS</p></li><li><p>R-R interval constant (regular rhythm on ausc)</p></li><li><p>± P wave (not associated with the QRS or hidden within QRS)</p></li></ul><p></p>
29
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What are the two most likely mechanisms of monomorphic VTACH?

1. Re-entry - a small circuit of electricity racing around and around an area of unhappy myocardium

2. Triggered activity – an unhappy island of ventricular myocardial cells discharging inappropriately at a fast rate

30
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How does polymorphic VTACH differ from monomorphic?

More malignant cause – more than one region of unhappy ventricular myocardium


31
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What signs of malignancy can be seen on ECG along side polymorphic ventricular tachy?

  • Faster rates (the faster the worse)

  • R on T phenomenon – two or more consecutive complexes so close together as to start their R wave on the preceding complex T wave


32
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What can ventricular tachy trigger?

VFib

(tx of ventricular tachy aim to prevent VFib)

33
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<p>What does this ECG show?</p>

What does this ECG show?

VFib

34
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What is the difference between accelerated idioventricular rhythm and ventricular tachy?

  • Same morphology on ECG

  • Only difference is rate

    • >180-200= VTACH

    • <180 = AIVR

  • AIVR typically not haemodynamically compromised

    • Typically don't require treatment

    • Most often extra cardiac cause (eg: severe GI disease, splenic lesion, pancreatitis)


35
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<p>What does this ECG show?</p>

What does this ECG show?

accelerated idioventricular rhythm

(wide QRS, HR<180, BP normal)

36
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List some differentials of causes of ventricular arrhythmias

  • Underlying cardiac disease – CHF, cardiomyopathies, myocarditis, myocardial hypoxia, ischaemia etc.

  • Catecholamines – stress, pain

  • Acidosis

  • Hypokalaemia

  • Abdominal disease – GDV, splenic lesions (not just haemangiosarcoma), sepsis, pancreatitis etc.

  • Thoracic trauma (myocardial trauma)

  • Drug induced - eg: digoxin toxicity


37
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How do you decide whether to treat ventricular arrhythmias?

Only treat if necessary so:

  • Treat if haemodynamically significant (eg: hypotensive, collapsed etc.)

  • Treat if very fast / close coupling intervals / ‘R on T’

  • Treat if multifocal


38
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What do you do before treating ventricular arrhythmias?

Ensure no electrolyte or acid-base disturbances

39
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How do you treat ventricular arrhythmias in an emergency case?

  • Lidocaine (Class IB)

    • Na+ channel blocker —> act on myocardial cells

    • bolus then cardiac resynchronization therapy

  • Esmolol (Class II- not used much)

    • short acting beta blocker

  • Amiodarone CRI (risk of anaphylaxis)

    • class 3 —> K channel blocker

Less common tx

  • Magnesium chloride

  • If completely refractory, electrical DC cardioversion (requires GA and a defibrillator)


40
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What treatment do you use for a non emergency ventricular arrhythmia?

  • Sotalol - Class 3

  • Mexiletine - Class 1B

  • Amiodarone- Class 3 (similar to digoxin)

    • Risks of hepatotoxicity and thyroid dysfunction (long term)

  • Atenolol - Class 2

    • risk if underlying heart dz


41
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List some of the causes of bradyarrythmias

  • Sinus bradycardia (normal)

  • Sinus arrest (no P wave)

  • Sinoventricular rhythm (hyperkalaemia – think urinary obstruction in cats)

  • AV Block


42
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What tends to be the underlying cause of atrial standstill

  • Hyperkalaemia (K+)

    • Urinary obstruction

    • renal failure (oliguric / anuric patients)

    • Hypoadrenocorticism (Addison’s disease)


43
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How does atrial standstill occur and how does it present on ecg?

  • Sinoatrial node is driving the rhythm as normal BUT there is no atrial depolarisation

    • Atria more sensitive to K+ than ventricles

  • Absent P waves, spikey T waves, mild prolongation of the QRS complex

(atrial myocardium are more sensitive to high K+ than ventricular myocardium)

44
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<p>What is this ECG showing?</p>

What is this ECG showing?

atrial standstill

45
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What is this showing?


Atrial standstill with ventricular escape complexes

(no P wave, wide QRS + slow HR)

46
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What are some of the causes of sinus arrest?

  • Sick sinus syndrome (’Brady – Tachy syndrome – think West Highland White Terriers)

  • Sinus node dysfunction

  • Drugs (eg: amiodarone, digoxin, sotalol)

  • Electrolyte changes

  • Atrial myocarditis

(a sinus pause lasting for more than 3 times the normal P-P interval)

47
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<p>What does this ECG show?</p>

What does this ECG show?

sinus arrest

48
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What are the classes of AV block?

First degree

  • P: QRS normal but prolonged P-R interval

    • P for every QRS but elongated gap between P + QRS

Second degree

  • P:QRS normal but some non conducted P wave

    • Mobitz 1- no pattern and tends to physiological

    • Mobitz 2 - pattern and more pathological

Third degree

  • No association between P waves and QRS complexes, often fast sinus rate (freq p waves, wide QRS (ventricular escapes), HR often 20-40 in dogs


49
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<p>What does this ECG show?</p>

What does this ECG show?

Ist degree AV block

  • P:QRS = 1:1 (just like normal sinus rhythm)

  • Prolonged P-R interval (>130ms in a dog)


50
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What are some of the causes and treatment of first degree AVB?

  • High vagal tone

  • Drug effect

  • Breed morphology related (brachy)

  • Tx- typically incidental with no treatment required


51
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<p>What do these ECGs show?</p>

What do these ECGs show?

2nd degree AV block —> non-conducted P waves

top = Mobitz 1 (Wenkebach phenomenon)

bottom = Mobitz 2

52
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How do the 2 types of second degree AV block present on ECG?

Mobitz 1

  • time for the signal to pass through the heart gets longer and longer with each beat until a QRS is completely dropped (P-QRS get progressively longer until QRS dropped)

Mobitz 2

  • not a prolongation of the P-R interval before the complete AV block/P-wave with missing QRS complex

  • often a pattern

    • 2:1 = 2 P waves for every 1 QRS

    • 4:3 = 4 P waves for every 3 QRS


53
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<p>What does this ECG show?</p>

What does this ECG show?

third degree AVB

  • No association between P waves and QRS complexes (electricity cannot get through the AV node)

  • fast sinus rate —> frequent P wave

  • QRS wide (VECs)

  • HR abt 20-30bpm (dog) 100-130 bpm (cats)


54
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How do you treat third degree AVB in dogs vs cats?

  • Dogs- emergency, refer for pacemaker ASAP

  • Cats- cats HR often 100-130 better at compensating so often incidental finding


55
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How do you treat bradyarrhythmia?

  • Treat underlying disorder

  • Test response to anticholinergics (atropine) if vagally mediated

    • If HR increases suggests underlying disease causing high vagal tone

  • If life threatining refer for pacemaker if poss or trial a B agonist (terbutaline)

  • Oral meds


56
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List some possible oral meds used in the treatment of bradyarryhtmias

  • B agonist- terbutaline

  • Anti-cholinergics – propantheline

  • Beta sympathomimetics – terbutaline

  • Xanthin derivatives – theophylline

  • Pimobendan – more blood per heartbeat


57
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Explain what happens in atropine response test

  • Before= Sinus arrhythmia, sinus arrest, and ventricular escapes

  • 30 minutes post atropine = If sinus tachycardia – proves bradycardia was vagally mediated


58
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What are the two approaches to implant a pacemaker?

  • Transvenous- via right jugular pacing lead passed through the right atrium, across the tricuspid valve into the right ventricle

  • Epicardial- transabdominal pacing lead attached to epicardium (usually in cats bc size)

(gold standard tx for 3rd degree AVB or atrial standstill)