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IMED3001 > Antiarrhythmic drugs > Flashcards

Antiarrhythmic drugs Flashcards

1
Q

What creates a constant potential difference of -85 in cardiomyocytes?

A

The presence of lots of extracellular potassium

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2
Q

What is required to activate an action potential in a cardiomyocyte?

A

To be at threshold potential.

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3
Q

How is potassium kept inside the cell?

A

Through a sodium potassium pump

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4
Q

How is potential in cardiomyocytes achieved?

A

From adjacent cells upstream in the conduction system

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5
Q

Why does the cardiomyocyte remain positive during the action potential?

A

Due to influx of positive ions in the form of calcium which stimulate SR calcium release.

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6
Q

What happens after calcium cells enter cardiomyocytes during action potentials?

A

Calcium channels turn themselves off and potassium channels reopen to allow potassium back out of the cell.

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7
Q

How is the gradient of sodium outside the cell and potassium inside the cell maintained?

A

Na+/K+ ATPase allows sodium out and potassium in.

It is universally expressed on cells and used for so many reasons

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8
Q

How is the calcium gradient maintained?

A

Export of calcium is done by a sodium calcium exchanger.

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9
Q

Is the Na+ Ca2+ exchanger ATP dependent?

A

No

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10
Q

How is an action potential initiated in the SA node?

A

Their potential increases at a regular rate due to presence of leaky sodium and calcium are being allowed to slowly leak into the cell until threshold where voltage gated channels open up immediately.

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11
Q

What is an effective refractory period?

A

No tetanic contraction is possible because while the plateau is taking place a new AP can’t be triggered.

Amount of time a cell will remain indifferent to a new stimulus that can trigger an action potential.

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12
Q

What is bradyarrhythmia?

A

Heart rate too slow. These are not treated pharmacologically. Instead they are treated by using a pacemaker.

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13
Q

What are tachyarrhythmias and what types are there?

A

Ectopic beats

Tachycardia (several ectopic beats in a row)

Fibrillation (disintegration of electrical activity)

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14
Q

What are supraventricular tachyarrhythmias?

A

Atria or structures between atria and ventricles (they are put together because of how similar they are)

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15
Q

Are ventricular tachycardias safe?

A

Hell no they are an emergency!!

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16
Q

What is the solution to ventricular fibrillation?

A

Electrical defibrillator also an emergency

17
Q

How are tachyarrhythmias generated?

A

Reentry (commonest)

Enhanced automaticity in cells that usually are not pacemaker cells (less common)

Afterpotentials (digoxin: Not discussed here)

18
Q

What are reentrant tachycardias?

A

When a cell enters an effective refractory period that is randomly induced blocking impulse and no conduction takes place in that direction. Conduction arrives from another adjacent impulse. then it triggers an impulse in the opposite direction which causes what is known as a circus rhythm. This will end up taking over the sinoatrial node and result in a new uncoordinated arrhytmic beat.

19
Q

What are the types of antiarrhythmic drugs?

A

Class I: Na+ Channel blockers

Class II: Beta adrenergic blockers

Class III: Prolong effective Refractory Period

Class IV: Ca2+ Channel Blockers: see antihypertensive drugs lecture

Adenosine

Digoxin: see heart failure lecture

20
Q

How can tachyarrhythmias be managed?

A

Suppressing enhanced automaticity (This is done by class II and Calcium channel blockers)

Prolong Effective refractory period (Class III)

Slow conduction in tissue (Class I)
Depress resting membrane potential (adenosine)

Enhance parasympathetic vagus activity

21
Q

How can conduction be slowed in tissues?

A

Blocking sodium channels which means that sodium efflux is slowed down and rate of rise of potential is slowed.

22
Q

How does slowing down conduction in tissues help with arrhythmias?

A

reentry rhythms have to return at exactly the right time to “catch” cells out of their refractory period to trigger an action potential in the wrong direction

23
Q

What are examples of Na+ channel blockers?

A

Lignocaine

Flecainide

24
Q

What is the risk of using a class I drug?

A

It could enhance the risk of arrhythmia if the reentry circuit is slowed down causing timing to fall into the critical range. This is why these drugs can only be prescribed by specialists.

25
Q

What are class II anti arrhythmic drugs?

A

Beta 2 adrenergic blockers

26
Q

How does beta adrenergic blockade help against reentry?

A

It slows heart rate down. I.e the rate of heart beats starting. It does this by slowing down influx of Na and Ca from leaky membrane channels.

27
Q

What does enhanced and reduced automaticity?

A

Enhanced (faster)

Reduced (slowed down)

28
Q

Can enhanced automaticity result in arrhythmias?

A

Yes

29
Q

What other effects can beta adrenergic blockers have on heart rhythm?

A

They can reduce the rate at which the 0 phase of the cardiac potential depolarizes in the same way that sodium blockers do without the same risk.

They can reduce risk of sudden death after a heart attack

They can be good treatment for heart failure, angina, and hypertension

30
Q

What are some examples of beta adrenergic blockers?

A

Metropolol, atenolol, bisoprolol

-olol is often used following the name

31
Q

What do class III drugs do?

A

They prolong action potential duration & effective refractory period

32
Q

What are the side effects of amiodarone?

A

Idiosyncratic toxicity (Causes hypothyroidism, hyperthyroidism, pulmonary fibrosis, corneal deposits, photosensitivity, proarrhythmic in long QT syndrome)

Lipid soluble

Iodine containing

Low hepatic clearance (half life of 1 month in the body)

33
Q

What is a more ideal prolonger of ERP class III drug?

A

Sotalol (also acts as a beta blocker)

34
Q

What does adenosine do?

A

Outside the cell they act as short term transmitters acting like hormones

35
Q

Where on the heart can we find adenosine receptors?

A

Atrial and AV conducting tissue

36
Q

How does adenosine affect the cells?

A

Potassium channels are linked to the receptors. More potassium exits cell and therefore it reduces the resting membrane potential. This results in ectopic impulses not firing. This only works in tissue with abundant adenosine channels.

37
Q

What are some limitations to using adenosine?

A

Can’t be used systemically and only through IV rapidly due to its rapid hydrolysis (it is often paracrine).

Causes transient asystole and bronchospasm (adenosine receptors on the bronchus but it is also short lived)

Adenosine receptor antagonists (eg caffeine) antagonise its arrhythmic effects

IMED3001 (46 decks)

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