Arrhythmias

Question 1

True or false: Sinus bradycardia from increased vagal tone is often associated with a wandering pacemaker

Answer 1

True (higher amplitude during inspiration when heart rate is faster)

Question 2

Which side of bundle branch block indicates more severe cardiac disease

Answer 2

Left (indicates extensive disruption of myocardium vs right bundle branch can be more easily damaged)

Question 3

What is the Bezold-Jarish reflex

Answer 3

Bradycardia, vasodilation and hypotension secondary to the stimulation of intraventricular receptors (vagal fibers) during tachyc ardia and hyper-contractile ventricle (-> vasovagal syncope = neurocardiogenic = neurally-mediated = reflex syncope)

Question 4

What breeds are predisposed to sick sinus syndrome?

Answer 4

Miniature Schnauzers and Terriers

Question 5

What PR interval defines first degree AV block?

Answer 5

PR > 130 msec in dogs, PR > 90 msec in cats

Question 6

What is the frequency of the ventricular escape rhythm in dogs and cats

Answer 6

Dogs: 20-60 bpm
Cats: 60-140 bpm

Question 7

What type of AV block can be commonly associated with a bundle branch block

Answer 7

Mobitz type II second degree AV block (can result in large QRS when conducted)

Question 8

What drug can be used to differentiate between 2nd degree AV block, type I and II?

Answer 8

Atropine (0.04 mg/kg IV). Type 1 usually improves with atropine and type 2 is unchanged or worsens.

Question 9

What is the difference between atrial standstill and sino-ventricular rhythm? What causes sino-ventricular rhythm?

Answer 9

• Atrial standstill = the sinus impulse does not leave the sinus node -> no conduction of signal to atria and ventricles
• Sino-ventricular rhythm = sinus impulse propagates to AV node via normal pathways but does not propagate to the other atrial myocytes

Sino-ventricular rhythm caused by hyperkalemia

Question 10

What are medical therapeutic options for treatment of bradyarrhythmias

Answer 10

• Parasympatholytics (atropine, glycopyrrolate): decrease vagal tone
• Mixed beta- and alpha-agonists: dobutamine, dopamine
• Pure beta-agonists: isoproterenol (/!\ hypotension due to vasodilation), terbutaline
• Phosphodiesterase inhibitor (aminophylline)

Question 11

What is considered an appropriate response to atropine when confirming vaguely induced bradyarrhythmias?

Answer 11

50%-100% increase in heart rate from baseline

Question 12

What are the 3 temporary cardiac pacing options and associated complications

Answer 12

1. Transvenous:
   - Lead dislodgement (main one)
   - Thrombosis
   - Bleeding
   - Infection
   - Ventricular arrhythmias
   - Cardiac perforation
2. Transcutaneous:
   - Discomfort due to musculoskeletal stimulation
   - Patient movement
   - Ventricular arrhythmias
3. Transesophageal:
   - Only paces atria -> does not work in case of AV block (only sinus nodal dysfunction)
   - Mild esophagitis

Question 13

What are the initial settings for a transvenous temporary pacemaker?

Answer 13

• HR 60-100 bpm
• Energy output 3 mA (can be decreased until finding threshold at which ventricular capture is lost and then set at twice this threshold)
• Sensitivity 3 mV

Question 14

How to set a transcutaneous pacemaker?

Answer 14

• Place ECG
• Apply pacing patch electrodes on each hemithorax (after shaving to ensure good contact)
• Make sure QRS complexes are identified properly by the monitor
• Start pacing and increase energy output until ventricular capture is identified (on ECG or by pulse palpation), keep output 10-20 mA higher than capture threshold (usually 30-160 mA required)

Question 15

Where should the lead of a transvenous temporary pacemaker end

Answer 15

Apex of the right ventricle

Question 16

In transoesophageal pacing, what is AAI mode?

Answer 16

The pacing stimulus paces the atria (A), senses atrial activity (A), and when intrinsic atrial activity is sensed, it inhibits (I) the pacemaker output.

Question 17

What are the mechanisms of tachycardia-induced cardiomyopathy

Answer 17

• Myocardial energy depletion and impaired energy utilization
• Myocardial ischemia due to impaired coronary blood flow
• Abnormal calcium handling

Question 18

What is the QRS width in cases of supraventricular tachyarrhythmias? What is an exception to this?

Answer 18

Usually thin / normal (<70 ms in dogs, < 40 ms in cats).
Will be wide in case of bundle branch block

Question 19

How to differentiate a right bundle branch block from a left bundle branch block

Answer 19

A LBBB has a positive diffusely wide QRS in lead I, II, and III while the QRS is negative in lead II with mostly a large S wave in a RBBB

Question 20

What are indicators of SVT vs VT

Answer 20

• Presence of atrioventricular dissociation (P without QRS) -> VT
• Presence of a fusion beat -> VT
• Presence of capture beat -> VT
• QRS more often “negative” (upside down) with VT
• SVT often > 240/min
• T wave usually negative with VT
• SVT can have positive response to vagal maneuvers

Question 21

What are the different types of supra ventricular tachycardias? Indicate which respond to vagal maneuvers

Answer 21

1. Atrial tachyarrhythmias:
   - sinus tachycardia / gradual response to vagal maneuver
   - sinus nodal reentrant tachycardia
   - atrial tachycardia / abrupt transient response
   - multifocal atrial tachycardia / transient decrease in ventricular rate
   - atrial flutter / transient decrease in ventricular rate
   - atrial fibrillation / no response
2. AV nodal tachyarrhythmias:
   - AV nodal reentrant tachycardia
   - AV reentrant tachycardia (accessory pathway) / abrupt transient response
   - junctional tachycardias

Question 22

Describe vagal maneuvers

Answer 22

• Carotid body massage: apply firm manual pressure medially in the area of the neck (below the angle of the mandible ventral to the wing of the atlas), maintain pressure for 10 sec
• Ocular maneuver: put firm pressure on both eyes directed mediodorsally
• Nasal planum massage (cat): massage firmly the non-haired portion of the nose

Question 23

What is the target ventricular response rate for dogs with Afib in hospital

Answer 23

160-180 bpm
(at home mean HR over 24h Holter should be < 125 bpm)

Question 24

What are the 3 arrhythmogenic mechanisms that can result in VT

Answer 24

• Enhanced automaticity
• Triggered activity
• Reentry

Question 25

What is the definition of ventricular tachycardia and how is it classified

Answer 25

- Definition: 3 or more consecutive ventricular beats occurring at a rate >160-180 bpm - Classification based on duration: Sustained if > 30 sec vs. nonsustained if < 30 sec (VT storm = recurrent sustained Vtach over 24h) - Classification based on morphology: monomorphic (single QRS morphology) vs. pleomorphic (2 or more morphologies in same episode of Vtach) vs. polymorphic (variable morphology beat-to-beat)

Question 26

What are the 3 most reliable diagnostic criteria for VT on ECG ?

Answer 26

Atrioventricular dissociation, fusion beats and capture beats

Question 27

Define fusion beat and capture beat

Answer 27

Fusion beat: summation of a ventricular impulse and simultaneous supra ventricular impulse --> QRS of intermediate morphology and preceded by a P wave Capture beat: supra ventricular impulse conducting through normal conduction pathways to the ventricles during an episode of VT or AIVR

Question 28

What electrolyte abnormalities can contribute to ventricular tachyarrhythmias

Answer 28

- Hypokalemia (increases phase 4 depolarization and prolongs action potential duration -> triggered activity) - Hypomagnesemia (similar to hypoK since Mg is required for Na-K ATPase function to maintain intracellular K) - Hypocalcemia - Hypercalcemia

Question 29

Name medications prolonging the QT segment and a possible consequence

Answer 29

Procainamide, sotalol, domperidone, cisapride, chlorpromazine, erythromycin Can lead to triggered activity and ventricular tachyarrhythmias

Question 30

What is the most common ECG morphology of arrhythmogenic right ventricular cardiomyopathy (ARVC)

Answer 30

- Positive QRS since ventricular complex originates from right side (but can occasionally come from left) - Monomorphic since caused by reentry (single focus)

Question 31

What are the six leads of an ECG?

Answer 31

Bipolar limb leads: I: R arm (-) to L arm (+) II: R arm (-) to L foot (+) III: L arm (-) to L foot (+) Augmented unipolar limb leads: aVR: R arm (+) to common terminal (-) aVL: L arm (+) to common terminal (-) aVF: L foot (+) to common terminal (-)

Question 32

Where is the PR interval measured

Answer 32

Between the beginning of the P-wave and the beginning of the Q-wave

Question 33

What is a normal mean electrical axis for dogs and cats

Answer 33

Dogs: +40 - +100 degrees Cats: 0 - +160 degrees

Question 34

Name causes of mean electrical axis shifts

Answer 34

Right axis deviation: - Right ventricular hypertrophy (pulmonic stenosis, pulmonary hypertension) - Right bundle branch block - Tricuspid valve dysplasia - Tetralogy of Fallot Left axis deviation: - Cardiomyopathy - HyperT4 - HyperK - Left anterior fascicular block

Question 35

What is the effect of hyperkalemia / hypokalemia on the resting membrane potential

Answer 35

Hyperkalemia decreases the resting membrane potential (moves it closer to threshold potential, "less negative") Hypokalemia makes the resting membrane potential more negative

Question 36

How does hypokalemia / hyperkalemia contribute to ECG changes

Answer 36

Hyperkalemia decreases the resting membrane potential which places more Na channels in inactivated state where they cannot be opened -> less depolarization of cells (but if Na channels become open depolarization happens more easily since resting membrane potential is closer to threshold potential) => peaked T wave, prolonged QRS, decreased P wave amplitude, ST elevation or depression Hypokalemia makes the membrane potential more negative -> more Na channels are at a rest state and available for opening and depolarization (prone to tachyarrhythmias), however with severe hypoK the resting membrane potential is so far from the threshold potential that depolarization is impossible => prolonged QT interval, reduced T wave amplitude, ST segment depression

Question 37

How does hypocalcemia / hypercalcemia affect the ECG

Answer 37

- Hypercalcemia: shortened QT interval - Hypocalcemia: prolonged QT interval

Question 38

What are possible indications for cardioversion

Answer 38

Atrial fibrillation, accessory pathway mediated supraventricular tachycardia, atrial flutter, monomorphic ventricular tachycardia (Only if refractory to medical management) When prompt termination of an arrhythmia causing hemodynamic instability is needed Termination of lone afib

Question 39

What is the mechanism of cardio version?

Answer 39

A shock is delivered to a critical mass of the myocardium --> coordinated depolarization of most of the myocytes -->refractory state that interrupts further propagation of electrical impulses allowing SA node to regain control of the cardiac rhythm

Question 40

What mode of defibrillator should be used for cardioversion and why

Answer 40

The synchronous mode should be used to deliver the shock on the R-wave, which is the refractory period of cells. If the shock is delivered on the T-wave there is a risk of inducing ventricular fibrillation.