week 8 Flashcards

1
Q

examples of Class 1A antiarrhythmics

A

Disopyranamide
Quinidine
Procainamide

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

mechanism of action of class 1A antiarrhythmics

A

Blocks fast Na channels.
Prolongs phase 0 in non pacemaker cardiac cells.
prolongs action potential and refractory period.
Also has potassium channel blockade

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

example of class 1B antiarrhythmic

A

lignocaine

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

mechanism of action of class 1B antiarrythmic

A

weak blockade of Na channels.
preferentially bind to inactive Na channels of ischaemic tissue.
Prolongs phase 0 and shortens phase 3, decreases the AP.

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

indication of class 1B antiarrhythmics

A

Ventricular arrhythmias

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

example of class 1C antiarrhythmic

A

Flecainide

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

mechanism of action of of flecainide

A

block fast Na channels during phase 0.
Slow dissociation kinetics, binds and unbinds slowly.
Profound suppression of conduction in accessory pathways and ectopic foci.
No effect on AP or QT.

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

what can flecainide interact with?

A

Digoxin
Increases levels by 15%

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

mechanism of action of amiodarone

A

Class 3 anti-arrhythmic - blocks K channel.
Also has Class 1,2 and 4 properties.
Prolongs phase 3 of AP, increase AP,ERP, QTi.
Main effect is delaying repolarization to prevent re-entry arrhythmias.

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

elimination of amiodarone

A

half life has 2 phases, 50% 3-10 days. remainder over several weeks to months.
excreted in bile and faeces.
accumulates in tissues.

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

adverse effects of amiodarone

A

Pulmonary fibrosis, can be fatal.
Hypo/hyper thyroidism.
Photosensitivity, blue grey skin.
Ataxia, peripheral neuropathy.
Hepatotoxicity.
Bradycardia.

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

mechanism of action of Sotalol

A

Class 3 antiarrhythmic - blocks K channels.
Also has Class 2 properties - Beta blocker.
Prolongs phase 3 repolarisation, increases AP and QTi.
Decrease heart rate, AV node conduction.

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

adverse reactions of Sotalol

A

Increases QT interval, high risk of torsades de point.
especially in renal impairment, hypokalaemia, high doses.

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

pharmacokinetics of Sotalol

A

oral or IV.
Not metabolised, renally excreted.
Onset 1-2 hours.
t1/2 12 hours.

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

contraindications of sotalol

A

long QT syndrome.
Bradycardia.
Asthma/COPD.
Renal failure.

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

what are class 4 antiarrhythmics

A

Calcium channel blockers

17
Q

mechanism of action of CCB

A

Block L-type voltage gated Ca channels
Reduce Ca influx in cardiac myocytes, nodal tissues, vascular smooth muscle.

18
Q

subtypes of CCB

A

Dihydropyridines and non dihydropyridines

19
Q

examples of dihydropyridine CCB

A

Amlodipine, nifedipine

20
Q

main effects of dihydropyridine CCB

A

vasodilation, decreasing BP.
used in HTN and angina.
Blocks vascular Ca channels

21
Q

main effects of non dihydropyridines CCB

A

decrease HR and contractility
used in SVT, AF, angina.
Block cardiac Ca channels.

22
Q

mechanism of action of verapamil

A

non dihydropiridine CCB.
blocks L type calcium channels in SA node, AV node, myocardium.
Reduce Ca influx.
Negative inotrope.

23
Q

contraindications of verapamil

A

avoid in HFrEF
Heart block, bradycardia
Beta blocker use

24
Q

pharmacokinetics of verapamil

A

oral or IV.
highly protein bound.
hepatic metabolism.
half life 4-7 hours.
urinary and foecal excretion.

25
mechanism of action of Adenosine
binds to A1 adenosine receptors in AV node. Opens K cahnnels, potassium leaves, hyperpolarising the cell. Decreases CAMP, inhibits Ca influx. Creates a hyperpolarised state
26
what does Adenosine do to K channels and movement
opens K channels K leaves the cell
27
what does Adenosine do to Calcium movement in the cell
Inhibits Ca influx
28
Digoxins effect on Na/K/ATPase
Inhibits Na/K/ATPase. Increases intracellular na. This decreases na/Ca exchanger. Increases intracellular Ca. Increases contractility - positive inotrope
29
Digoxins effect on vagus nerve
Increases vagal tone. increases Ach, stimulating K channel and increasing K efflux. Decreasing AV node conduction. Hyperpolarising cell, slows heart rate down.
30
Clinical uses of magnesium in antiarrhythmics
Torsades de Pointes Digoxin toxicity Hypomagnesaemia arrhythmias VT/VF arrest