Antiarrhythmia Flashcards

1
Q

What is the Sinoatrial node pacemaker potential

A

the rate of firing of the SA node set the heart - initiates the cardiac cycle

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2
Q

what do pacemaker cell membrane contain

A

HCN gated channels which are hyperpolarisation activation

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3
Q

what are the three phases of the myocardial heart potential

A

Phase 4 (prepotential), Phase 0, Phase 3

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4
Q

what happens in phase 4

A
  • pacemaker Na+ influx, Ca2+ channels recover from inactivation
    -pumps restore ion gradients
    -activated by hyperpolarisation (phase 3)
    -HCN mediates a ‘funny current’, stimulates K+ efflux, Na+ influx
    -Na+ influx dominates causes slow depolarisation of membrane
    -Reaches threshold, upstroke inactivates HCN
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5
Q

what happens during Phase 0

A

Ca2+ influx, upstroke of the slow pacemaker action potential
triggers at the threshold potential (~55mV)
Increase in movement of Ca2+ into cell

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6
Q

what happen during Phase 3

A

Ca2+ channels inactivated
delayed K+ efflux, increase in K+ efflux
causes hyperpolarisation

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7
Q

give the five steps of ventricular myocyte action potential

A

0) Na+ channel open
1) Na+ channel close, Fast K+ channel open
2) Ca2+ channel open, Fast K+ channel shut
3) Ca2+ channel close, slow K channels open
4) resting potential

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8
Q

how does the sympathetic nerves affect the heart rate

A

-Activation cause release of noradrenaline (binds to B1 adrenoreceptors on cardiac pacemakers and myocyte cell membrane
- increases opening of HCN channels in pacemaker cells
- increase Na+ influx and and Ca2+ influx increases
-increase slope of pre potential (phase 4)
=heart rate increases

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9
Q

How does the parasympathetic nerves affect the heart rate

A

-Activates the release of ACh (binds to muscarinc receptor)
-decrease opening HCN channels which decrease Na influx, and slows the opening of Ca2+ channel which decreases influx
-opens additional K+ channels (ligand-gated) which increases K+ efflux
-Hyperpolarises membrane and reduce slope of pre-potential
=heart rate decrease

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10
Q

How does vagal tone affect heart

A

-decrease heart rate

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11
Q

what two things affect heart rate

A

-vagal tone
-sympathetic tone
-intrinsic rate of firing of SAN cell = 100-110 APs

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12
Q

What is early after depolarisation

A

occurs when normal HR is low, suppressed by high heart rate
Occurs when AP is prolonged
-some Ca2+ channels inactivated during shoulder
-reactivates to give EAD

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13
Q

what is delayed after-depolarisation

A

seen at increased HR, associated with elevated calcium concentration
- Ca2+ activation of Na/K channel (depolarising)
-NaCa exchanger 3:1 electrogenic
- can cause toxic doses of cardiac glycosides

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14
Q

what is used to treat bradycardias

A

Atropine
Isoproterenol
Artifical pacemaker

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15
Q

what does atropine do

A

switch off vagal nerve, blocks vagal inhibition of sinuous and AV node

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16
Q

what does isoproterenol

A

activates B receptors (beta agonists)

17
Q

what is adenosine used to treat

A

tachycardia

18
Q

what is the mechanism of action for adenosine

A

dilates coronary vessels
reduces B adrenergic receptor mediated increase in myocardial contractility
depresses both sinoatrial and atrioventricular node activities

19
Q

what is used to treat a-systole (heart electrical system fails entirely)

A

adrenaline + epinephrine

20
Q

What is used to treat ventricular fibrillation

A

amiodarone + lignocaine

21
Q

what are the adverse effects of atropine

A

anticholinergic = dry mouth, mydriasis
postural hypotension

22
Q

how many class of antiarrhthymiac drugs are there which treats tachycardia

A

4

23
Q

what is Class I drugs

A

Na channel blockers (2 classes)

24
Q

what is an example of Class Ia drug and what is the mechanism of action

A

= quinidine, propatenone
lengthens action potential duration and refractory period

25
Q

what is an example of Class Ib drug and what is the mechanism of action

A

=lidocaine
shorts action potential duration and refractory period
-blocks fast Na channels and slows phase 0 depolaristion
specifci effect on rapidly depolarising tissue (use dependent effects)

26
Q

what are lidocaine adverse effects

A

hypotension, heart block, neurotoxicity, fits

27
Q

what are the contra-indications of lidocaine

A

-Hepatic clearance decreased in elderly, people with heart failure and liver disease
Not absorbed via oral route and have a short half life

28
Q

what are the two types of Beta-blocker

A

-Non cardioselective = also blocks B2 receptors = Propranolol
-Cardioselective= less potent blocks of B2 receptor =
Atenolol (B1 selective)

29
Q

how do beta blockers treat tachycardia

A

-reduce intrinsic rate in sinus and AV node
-decreases Heart rate, blood pressure and cardiac work
-reduce renin secretion

30
Q

what are the adverse effects of beta blockers

A

B1 effects = bradycardia + heart failure
B2 effects = excerbation of asthma, cool peripheries, muscular aches, worsening intermittent claudication
Others= Fatigue, Nightmare/sleep disturbances, withdrawal effects (angina & MI), Unawareness of hypoglycaemia

31
Q

what is example of class III AntiArrhythmic and how do they work?

A

Amioderone = K+ channel blockers
prolongs action potential and refractory period, lengths QT interval

32
Q

what is the indication for using a class III AA drugs

A

effective for ventricular and supra ventricular tachycardia
1st line treatment for ventricular fibrillation
improves survival in patients with recurrent ventricular tachycardia

33
Q

what are the adverse effects of amioderone

A

-Thyroid disturbance
-Pulmonary fibrosis
-Pro-arrhythmias and torsade de points
-peripheral neuropathy
-hepatitis
-blue-grey skin discolouration

34
Q

There are three subtypes for calcium channel blockers (Class IV)

A
  • Dihydropyridines = predominately vascular effects
  • Benzothiapines = mixed vascular + cardiac effects
  • Phenylalkylamine = predominantly cardiac effects
35
Q

what is the most prescribed Ca2+ channel blocker to treat arrhtythmias

A

verapamil (a Phenylalkylamine)

36
Q

how does verapamil work

A

Slows phase 1/2 which slows calcium entry
reduce rate and conduction velocity in sinus and AV nodes

37
Q

What are the adverse effects of verapamil

A

heart failure, hypotension, constipation, vasodilation, oedema and flushing

38
Q

what is the contraindication for verapamil

A

myasthenia gravis