Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which side of bundle branch block indicates more severe cardiac disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the Bezold-Jarish reflex

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What breeds are predisposed to sick sinus syndrome?

A

Miniature Schnauzers and Terriers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What PR interval defines first degree AV block?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are medical therapeutic options for treatment of bradyarrhythmias

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

50%-100% increase in heart rate from baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 3 temporary cardiac pacing options and associated complications

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the initial settings for a transvenous temporary pacemaker?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How to set a transcutaneous pacemaker?

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where should the lead of a transvenous temporary pacemaker end

A

Apex of the right ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

In transoesophageal pacing, what is AAI mode?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the mechanisms of tachycardia-induced cardiomyopathy

A
  • Myocardial energy depletion and impaired energy utilization
  • Myocardial ischemia due to impaired coronary blood flow
  • Abnormal calcium handling
18
Q

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

A

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

19
Q

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

A

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

20
Q

What are indicators of SVT vs VT

A
  • 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
21
Q

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

A
  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
22
Q

Describe vagal maneuvers

A
  • 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
23
Q

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

A

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

24
Q

What are the 3 arrhythmogenic mechanisms that can result in VT

A
  • Enhanced automaticity
  • Triggered activity
  • Reentry
25
Q

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

A
  • 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)
26
Q

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

A

Atrioventricular dissociation, fusion beats and capture beats

27
Q

Define fusion beat and capture beat

A

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

28
Q

What electrolyte abnormalities can contribute to ventricular tachyarrhythmias

A
  • 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
29
Q

Name medications prolonging the QT segment and a possible consequence

A

Procainamide, sotalol, domperidone, cisapride, chlorpromazine, erythromycin

Can lead to triggered activity and ventricular tachyarrhythmias

30
Q

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

A
  • Positive QRS since ventricular complex originates from right side (but can occasionally come from left)
  • Monomorphic since caused by reentry (single focus)
31
Q

What are the six leads of an ECG?

A

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 (-)

32
Q

Where is the PR interval measured

A

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

33
Q

What is a normal mean electrical axis for dogs and cats

A

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

34
Q

Name causes of mean electrical axis shifts

A

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

35
Q

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

A

Hyperkalemia decreases the resting membrane potential (moves it closer to threshold potential, “less negative”)

Hypokalemia makes the resting membrane potential more negative

36
Q

How does hypokalemia / hyperkalemia contribute to ECG changes

A

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

37
Q

How does hypocalcemia / hypercalcemia affect the ECG

A
  • Hypercalcemia: shortened QT interval
  • Hypocalcemia: prolonged QT interval
38
Q

What are possible indications for cardioversion

A

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

39
Q

What is the mechanism of cardio version?

A

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

40
Q

What mode of defibrillator should be used for cardioversion and why

A

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.

Cardiovascular (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions