Arrythmias Flashcards

1
Q

Treatment options for vasovagal?

A

Non medication:
Lifestyle
- reassurance
- Hydration
-RCT

Medication
Midodrine
Fludrocortisone
SSRI

normally no indication for pacemaker but may be considered in:
more than 40
prolonged pauses in loop recorder
nil BP response at tilt table

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2
Q

Duration for non-driving after a vasovagal

A

i.Vasovagal- 24hrs commercial 24hrs
ii.Cardiac syncope(identified and treated)- 4 weeks commercial 3 months
iii.Unexplained blackouts(single)- 6 months commercial 5 years
iv.Unexplained blackouts 2 or more - 12 months/ commercial is 10 years

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3
Q

What is the duration of a short R-P pattern when assessing AVNRT and AVRT

A

AVNRT R-P less than 90ms
AVRT R-P longer than 90ms but may also represent Atypical AVNRT or Atrial Tachycardia

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4
Q

Contraindications for adminstration of Adenosine

A

Severe Asthma(Theophylline will need higher dose)

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5
Q

What is Wolf-Parkinson White Syndrome features in an ECG

A

Presence of a delta wave and tachycardia

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6
Q

What is the utility of EP studies for incidental finding of delta wave in ECG

A

very low but may be considered in high risk jobs
may consider treadmill studies

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7
Q

What location is the most common initiation of local focal atrial triggers

A

i.Pulmonary veins

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8
Q

What is non-valvular AF

A

i. AF with metallic stents
ii. AF with moderate to severe mitral stenosis

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9
Q

Indications for AF ablations

A

i. Symptomatic paroxysmal or persistent AF refractory or intolerant to at least one Class I or Ill antiarrhythmic medication
ii.Catheter ablation can be considered for symptomatic paroxysmal or persistent AF in selected patients with heart failure with reduced ejection fraction

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10
Q

(long question) what are the indications for Digoxin, and it’s mechanism of action.

A

1.For the treatment of mild to moderate heart failure in adult patients.
2.To maintain control ventricular rate in adult patients diagnosed with chronic atrial fibrillation.

MOA:
1.AV node inhibition: Digoxin exerts vagomimetic effects on the atrioventricular (AV) node by stimulating the parasympathetic nervous system. This action slows electrical conduction through the AV node, reducing heart rate. The increase in intracellular calcium levels prolongs phases 4 and 0 of the cardiac action potential, extending the AV node’s refractory period. As a result, conduction through the AV node slows, leading to a decreased ventricular response.
2.

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11
Q

Explain the mechanism of action of adenosine and it’s indications

A

indications: Class IIa
Management of bradycardia
Reversal of organophosphates

Mechanism of Action:
Antimuscarinic that works through competitive inhibition of postganglionic acetylcholine receptors and direct vagolytic action, leading to parasympathetic inhibition of the acetylcholine receptors in smooth muscle. The end effect of allows for preexisting sympathetic stimulation to predominate, creating increased cardiac output and other associated antimuscarinic adverse effects, as described herein

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12
Q

during reversal of Dabigatran, what agent can be used and it’s mechanism of action?

A

Idarucizumab- MOA
specifically and reversibly binding to dabigatran, the oral anticoagulant, and its active metabolites, thereby neutralizing their anticoagulant effect. It’s a humanized monoclonal antibody fragment (Fab) that binds with high affinity, effectively preventing dabigatran from inhibiting thrombin. This binding is so strong that it rapidly and effectively reverses the anticoagulant effect of dabigatran.

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13
Q
A
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