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ESA 4 Rev > Anti-Arrythmic agents > Flashcards

Anti-Arrythmic agents Flashcards

1
Q

What ECG changes do you see in WPW?

A

Shortened PR

Lengthened QRS

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2
Q

Which class 1 agent is only used for ventricular arrhythmia?

A

Lidocaine

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3
Q

What are the side effects of 1a agents?

A

Pro-arrythmia
Hypotension
Dizziness, confusion
GI

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4
Q

What ECG changes does flecainide cause?

A

Increase QRS, QT and PR (also decreases automaticity)

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5
Q

What ECG changes do 1a agents cause?

A

Increase QRS and QT

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6
Q

What ECG changes do 1b agents cause?

A

Increase QRS in ischaemic tissue only

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7
Q

What are the side effects of flecainide?

A

Pro-arrythmia
Sudden death with chronic use
CNS
GI

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8
Q

What effects do beta blockers have?

A

Decrease phase 4 - automaticity

Prolong AV repolarisation - increased RP

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9
Q

What effects do beta blockers have on ECG?

A

Decrease HR

Increase PR

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10
Q

What arrhythmia are beta-blockers used to treat?

A

Converting re-entry at AV node
SVT - protect ventricles from high atrial rates
Sinus tachycardia

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11
Q

Why are beta-blockers used post-MI?

A

Decrease oxygen demand of heart - negative isotropy and chronotropy
Inhibit sympathetic activity following MI - ventricular arrhythmias.

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12
Q

What are the side effects of beta blockers?

A 
Bronchospasm - asthmatic
Hypotension 
Tremor
Fatigue 
Insomnia
Cold hands
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13
Q

When are beta blockers inappropriate?

A

Partial AV block or heart failure - decrease CO

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14
Q

What are the side effects of Amiodarone?

A 
Pulmonary fibrosis
Raised LDL
Hypothyroidism
Optic neuritis 
Hepatic injury
Photosensitivity
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15
Q

What effect does Sotalol have on ECG?

A

Lengthened QT

Decreased HR

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16
Q

What are side effects of sotalol?

A

Pro-arrythmia
Fatigue
Insomnia

17
Q

What type of CCB are used to treat arrhythmias?

A

Phenylalkylamine - verapamil

18
Q

What are the effects of CCB?

A

Decrease automaticity - Phase 0 pacemaker
Decrease AV conduction
Increase AV refectory period

19
Q

What ECG changes with CCB?

A

Increased PR

HR altered - baroreflex

20
Q

What are SE of CCB?

A

Hypotension

GI

21
Q

What is the mechanism of adenosine?

A

Endogenous - given IV, short t1/2

A1 receptors - Gi coupled - opens K+ channels -> hyperpolarisation

22
Q

What are the effects of adenosine?

A

Slows AV conduction

Decrease automaticity - phase 4

23
Q

What is adenosine used for?

A

CAD diagnosis

Re-entrant supra ventricular arrhythmias

24
Q

What is vernakalent mechanism?

A

Atrial specific K+ channel blocker.
Decrease atrial conduction
Potency increases as HR increases

25
Q

What is vernakalent used for?

A

Convert recent onset AF to sinus rhythm

26
Q

What is Ivabradine MOA?

A

Inhibits If in SA node - decrease automaticity and HR.

27
Q

What is a SE of Ivabradine?

A

Flashing lights

28
Q

What is Ivabradine used for?

A

Sinus tachycardia

Decrease HR in HF or angina as NO effect on BP

29
Q

What is digoxin MOA?

A

Increase vagal activity, RP
Decrease AV conduction and slow HR
Inhibit Na+/K+ ATPase - increase inotropy

30
Q

What is digoxin used for?

A

Not used alone

Slow HR in permanent AF patients

31
Q

How does atropine work?

A

Muscarinic antagonist - block vagal activity

32
Q

What is atropine used for?

A

Vagal bradycardia - increase AV conduction and HR

33
Q

What AF rate control drugs are there?

A

Beta blocker -bisprolol
CCB - verapamil, diltiazem
+/- Digoxin

34
Q

What AF rhythm control drugs are there?

A

Sotalol
Flecainide + bisoprolol
Amiodarone

35
Q

When must flecainide never be used?

A

If structural abnormality or IHD

Alone to treat AF - need AV node blocking drug, either BB or CCB.

36
Q

What is used to treat ventricular tachycardia?

A

Beta blocker
Lidocaine - if ischaemia
Amiodarone

37
Q

What is used to treat WPW?

A

Flecainide

Amiodarone

ESA 4 Rev (16 decks)

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