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Internal Medicine/ Ettinger > Cardiac Arrhythmia > Flashcards

Cardiac Arrhythmia Flashcards

1
Q

What does a atropine response test assess?

A

For bradycardia,
- there is a a response (ie. an increase in heart rate), then the bradycardia is vagal mediated
- if there is no change, then there is an intrinsic disturbance of impulse formation or conduction

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2
Q

How does the respiration cycle change heart rate?

A

heart slow down on expiration and speeds up on inhalation
seen in dogs mostly

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3
Q

What’s ventriculophasic sinus arrhythmia?

A

it’s when the P-P interval that flanks the QRS is shorter than the P-P interval during a block
- seen in high grade 2 or grade 3 AV block
- no clinical significance
- just need to know it’s not an atrial arrhythmia

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4
Q

How does a “wandering pacemaker” appear on ECG?

A
  • variation in the height of the P wave
  • constant P-R interval, constant QRS
  • normal QRS
  • slight variation in R-R interval
  • if in conjunction is respiration sinus arrhythmia, the P wave is taller on inspiration, and shorter an expiration
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5
Q

What are some ECG differentials for wandering pacemaker?

A
  • P pulmonale
  • premature arterial complexes (PACs) –> but the P wave in a wandering pacemaker should not be so premature that it goes into the previous T wave, and the P wave will be taller (not shorter) with an increased heart rate (wandering pacemaker and resp sinus arrhythmia don’t occur at HR >150/min
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6
Q

How high is the high rate to constitute a tacycardia?

A

160/min

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7
Q

How is the ECG for a sinus tachycardia?

A

HR > 160/min
- normal P-QRS-T
- this indicates SA in origin
- may need vagal maneuver to detect the P/T waves

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8
Q

What are the 5 ECG changes that can be seen with a APC?

A
  1. premature sequence of P-QRS-T
  2. QRS = narrow, tall; comparable to sinus rhythm
  3. P wave has a different amplitude compared to sinus rhythm
  4. P-R interval is not the same as a sinus rhythm (shorter or longer)
  5. postextrasystolic pause
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9
Q

What are some differentials for atrial premature contractions?

A

structural abnormalities in the atria
- atrial distension
- atrial tumours, ex. hemangiosarcoma
- cats with hyperthyroidism
- digitalis toxicity and other toxicities

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10
Q

What’s the clinical implication of APC?

A

minor
- increases awareness of atrial abnormalities

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11
Q

How does atrial tachycardia looks like on ECG?

A

looks like a bunch of APC, with increased heart rate

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12
Q

How is atrial tachycardia treated?

A
  • diltiazam
  • propanolol
  • phenylephrine

Long-term oral therapy:
- atenolol
diltiazem

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13
Q

What’s the clinical significance of atrial tachycardia?

A

depends on the underlying cause (similar to atrial premature contraction)
- more commonly seen in older dogs
- can lead to atrial fibrillation

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14
Q

What are the ECG characteristics of atrial flutter?

A
  1. rapid, rhythmic waves (flutter)
  2. doesn’t return to baseline
  3. normal, supraventricular QRS
  4. variable, irregularly irregular R-R interval
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15
Q

How is atrial flutter treated?

A

digoxin and diltiazem

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16
Q

What’s the clinical significance of atrial fibrillation?

A
  • it’s a common arrhythmia
  • 50% of dogs with DCM
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17
Q

What are the ECG features of atrial fibrillation?

A
  1. QRS = supraventricular
  2. irregularly irregularly R-R interval
  3. no visible P waves, replaced by f waves
18
Q

What are some differentials for chaotic irregular rhythm on auscultation, coupled with pulse deficits?

A
  • atrial fibrillation
  • polymorphic ventricular tachycardia
  • frequent VPCs or APCs
19
Q

How can one make sure it’s afib + BBB and not vTach?

A

With vTach, there will be P waves
- a vagal maneuver will reduce the heart rate but won’t have an effect if it’s vTach

20
Q

What’s the most likely cause of atrial fibrillation?

A

enlarged atria

21
Q

What are some ddx for structurally normal atrial fibrillation (aka lone atrial fibrillation)?

A
  • general anesthesia
  • hypothyroidism
  • pericardiocentesis (large, rapid volume)
  • Gi disease
  • volume overload
  • commonly seen in giant breeds
22
Q

How common is atrial fibrillation in cats?

A

less common than in dogs
- mostly with underlying structural defect –> atrial enlargement
- not any worse in outcome vs lone atrial fibrillation (as noted in dogs)
- can be normal in 20-25% of cats

23
Q

How is atrial fibrillation treated?

A

digoxin and diltiazem
goal is so accept the atrial fibrillation, but slow down the ventricular/heart rate

24
Q

How does atrial dissociation look like on ECG?

A

Appears to have 2 rhythms: normal P-QRS-T, with (smaller) P waves that do not result in QRS

25
Q

How is atrial dissociation treated?

A

No treatment required
- incidental, benign

26
Q

What’s the most common arrhythmia?

A

VPC!

27
Q

What are the hallmarks of premature ventricular contractions on ECG?

A
  1. shortened R-R interval
  2. wide bizarre QRS, no associated P wave
  3. different (often very large) T wave
28
Q

What are 2 specific heart diseases in dogs that are almost exclusively arrhythmogenic and causes VPCs?

A
  1. Boxer cardiomyopathy (right ventricular cardiopathy)
  2. German Shepherd inherited sudden cardiac death –> most likely seen in young puppies. If they survive puppyhood, they will be ok
29
Q

What’s the ECG characteristic of accelerated idioventricular rhythm?

A

Looks like ventricular tachycardia but slower
- same causes as VPCs
- Tx = correct underlying cause if possible
- antiarrhythmic meds only if tx for underlying cause is ineffective

30
Q

What’s the clinical implication of ventricular fibrillation?

A

terminal/ fatal
- needs immediate treatment –> defibrillator, CPR

31
Q

Ventricular escape rhythm is common in 3rd degree AV block. How should it be treated?

A

do NOT treat – it actually is life saving

32
Q

What are some ECG characteristics of 3rd degree AV block?

A

complete dissociation
- P-P interval = consistent, but is not always followed by a QRS
- wide bizarre QRS

33
Q

How severe in 3rd AV block in cats?

A

they can also have ventricular escape beats that makes the HR just a bit lower than a regular sinus rhythm - incidental finding

34
Q

What’s the cause of AV blocks?

A

1st degree, and type I 2nd degree:
- most likely functional: high vagal tone, toxicosis, antiarrhythmics, alpha-2 agonist sedatives

type II 2nd degree and 3rd degree:
- can be functional, but often structural –> inflammatory or degenerativeW

35
Q

What’s the treatment for AV blocks?

A

1st degree, and type I 2nd degree: none

type II 2nd degree and 3rd degree: pacemaker BUT may not be needed in cats with sufficient escape ventricular rhythm. Also doesn’t work if there is underlying structural cardiomyopathy (often seen in cats)

36
Q

Which side is the bundle branch block benign?

A

Right bundle branch block = benign
left bundle branch block = L ventricular enlargement

37
Q

What’s the ECG feature for atrial standstill?

A

lack of P wave, but constant R-R interval
- QRS = supraventricular
- low to normal rate

38
Q

What are the top 3 ddx for atrial standstill?

A
  1. moderate to marked hyperkalemia
  2. atrial myopathy
  3. artifact
39
Q

What’s electrical mechanical dissociation?

A

The electrical impulses are not translating into mechanical systole or diastole
- patient typically unconscious and hemodynamically unstable
- pre-terminal
- grave prognosis

40
Q

How does extracellular potassium level effect the cardiac muscle action potential?

A

Potassium level influences the resting membrane potential.
1. Hypokalemia
- hyperpolarizes due to a greater difference between intracellular and extracellular K+ level
- prolongs repolarization –> increases risk of extrasystole

  1. Hyperkalemia
    - faster repolarization = shorter Q-T interval, tented T wave
    - sinus bradycardia. but this is often masked by concurrent conditions that often occur along side with hyperkalemia, so tachycardia might be noted –> heart rate therefore is not a reliable indication of potassium concentration
    - bradycardia due to excitation suppression, atrial > ventricle
41
Q

How does extracellular calcium level affect action potential?

A

it effects the threshold –> effects more profound in skeletal muscles/ other organs than the heart

Decreased calcium = decreased threshold –> easier to depolarize –> muscle fasciculation
- can prolong Q-T interval

Increased calcium = increased threshold –> harder to depolarize
- decreases Q-T interval

42
Q

Describe ECG for sick sinus syndrome

A

simultaneous defect in SA node and AV conduction
- first or 2nd degree AV block
- prolonged sinus pauses
- bursts of supraventricular tachycardia or VPCs at variable rates

Internal Medicine/ Ettinger (93 decks)

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