Anti-Arrythmic agents Flashcards

(37 cards)

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
What is vernakalent used for?
Convert recent onset AF to sinus rhythm
26
What is Ivabradine MOA?
Inhibits If in SA node - decrease automaticity and HR.
27
What is a SE of Ivabradine?
Flashing lights
28
What is Ivabradine used for?
Sinus tachycardia | Decrease HR in HF or angina as NO effect on BP
29
What is digoxin MOA?
Increase vagal activity, RP Decrease AV conduction and slow HR Inhibit Na+/K+ ATPase - increase inotropy
30
What is digoxin used for?
Not used alone | Slow HR in permanent AF patients
31
How does atropine work?
Muscarinic antagonist - block vagal activity
32
What is atropine used for?
Vagal bradycardia - increase AV conduction and HR
33
What AF rate control drugs are there?
Beta blocker -bisprolol CCB - verapamil, diltiazem +/- Digoxin
34
What AF rhythm control drugs are there?
Sotalol Flecainide + bisoprolol Amiodarone
35
When must flecainide never be used?
If structural abnormality or IHD | Alone to treat AF - need AV node blocking drug, either BB or CCB.
36
What is used to treat ventricular tachycardia?
Beta blocker Lidocaine - if ischaemia Amiodarone
37
What is used to treat WPW?
Flecainide | Amiodarone