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Cardiology > Lectures 8-9: Mechanisms of Antiarrhythmics > Flashcards

Lectures 8-9: Mechanisms of Antiarrhythmics Flashcards

1
Q

Summarize ion movements during ventricular AP

A

0: Na+ in; 1: Na+ in vs K+ out; 2: Ca2+ in vs K+ out; 3: K+ out; 4: K+ out vs NCX in

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2
Q

Three currents relevant for drugs

A

INa, ICa, IKr (rapid delayed rectifyer)

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3
Q

Na+ current is the main determination of…

A

Conduction velocity = speed of upstroke proportional to speed of conduction

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4
Q

Impaired Na+ current would lead to…(2)

A

Slower upstrokes and longer delays between APs

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5
Q

Na+ channel has three states. Describe.

A
  1. Resting (closed at negative voltage) –> 2. Open (“m” gates open due to depolarization) –> 3. Inactivated (“h” ball and chain blocking, despite “m” gates being open due to time)
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6
Q

If a cell is at -85 mV for a long time, about…(% in states)

A

85% channels will be closed, 0% open, and 15% will be inactivated

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7
Q

If a cell is at 0mV for a long time, about…(% in states)

A

0% channels will be closed, 0.5% will be open, 99.5% inactivated

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8
Q

Summarize channel states related to diastole and how this is related to time in diastole

A
  1. Diastole: ~85% channels closed but available; 2. Upstroke/Plateau: transition to open, then inactive; 3. Diastole: return to ~85% closed bu available IF THERE’S ENOUGH TIME
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9
Q

Most antiarrhythmic drugs bind how to different states…

A

Bind open, inactivated and UNBIND when CLOSED

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10
Q

Sinus bradychardia and tachycardia indicate a dysfunctional ________. How do you know it’s sinus?

A

SA node; normal P wave

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11
Q

Describe Paroxysmal Supraventricular Tachycardia. What does it indicate?

A

Tachycardia w/ narrow QRS complexes which indicate ventricular excitation through conduction system. Generally reflects reentry through two pathways in the AV node.

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12
Q

What does Paroxysmal mean?

A

Comes and goes

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13
Q

Describe Atrial Flutter/Fibrillation. What is of note here and what does it mean?

A

P waves are random/indistinct. Note that R-R intervals are irregular as well, which means that only SOME atrial excitations are propagating into ventricles.

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14
Q

Describe Premature Ventricular Contractions (PVCs)

A

Wide QRS complexes, which means that ventricles are exciting themselves

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15
Q

If two PVCs have different shapes this indicates?

A

Multiple ectopic foci

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16
Q

Describe Ventricular Tachycardia. If each one is similar, what do we call it?

A

Wide QRS complexes and tachycardic rate; monomorphic

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17
Q

What are three mechanisms that could initiate arrhythmia

A
  1. EADs, 2. DADs, 3. Reentry
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18
Q

Describe what is associated with Early Afterdepolarizations (EADs). What channel is involved? What can this cause?

A

Occur with a long AP and slow HRs; second upstroke due to reactivation of ICa; second upstroke can propagate and cause PVC

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19
Q

So, one of the first arrhythmic manifestations of EADs is a…

A

PVC (but other arrhythmias can manifest later on)

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20
Q

Describe the ion involvement in Delayed Afterdepolarizations (DADs).

A

Result from spontaneous release of intracellular Ca2+ from SR and occur when cells are overloaded with Ca2+

21
Q

What can cause a cell to be overloaded w/ Ca2+

A

Fast HRs, beta-adrenergic stimulation

22
Q

A smaller, slow depolarization is related to what current in DADs? Why?

A

Na+-Ca2+ exchange current (INCX); increaed intracellular Ca2+ leads to increased extrusion via NCX, and more intraceullar cations –> membrane depolarization

23
Q

How could you get a full AP in in a DAD?

A

If Na+ current is activated

24
Q

What is the textbook explanation for reentry

A

You have a region of heart tissue that cannot be excited by impulse in one direction (unidirectional block) but the impulse can travel through this region in the other direction, creating a loop

25
Q

What is Dr. Sobie’s explanation for reentry?

A

Requires fibers w/ different AP lengths and an intervening blood island. If a premature stimulus occurs, AP will propagate on short AP side of the blood island but be blocked on the other. By the time it gets around the island, it can propagate up the long AP side –> loop

26
Q

What is the “blood island”?

A

Can either be anatomical (AV node) OR functional (due to tissue damage OR to temporary differences in refractoriness)

27
Q

What could the premature stimulus be?

A

EAD or DAD

28
Q

Arrythmia mechanisms…

A

The important arrhythmias are initiated by EADs or DADs, maintained by reentry

29
Q

Prevent EADs…

A

Since EADs result from reactivation of Ca2+ current, blocking Ca2+ current should inhibit EAD formation

30
Q

Prevent DADs…

A

DADs require two steps: (1) spontaneous release of Ca2+ (2) triggering of a second action potential; Step (1) can be inhibited by blocking β-adrenergic signaling; Step (2) can be inhibited by blocking Na+ channels

31
Q

How long is a cardiac AP?

A

300 ms

32
Q

How do wavelengths relate to treating arrhythmias?

A

If you increase AP wavelength (via increase in duration) to larger than the path length, you won’t be able to generate a reentry loop

33
Q

Class I blocks…

A

Na+ currents, to stop secondary AP, preventing DADs

34
Q

Class II blocks…

A

Beta-blockers to lower heart rate, prevent Ca2+ overload and DADs

35
Q

Class III blocks…

A

K+ currents to prolong APD to prevent reentry loops

36
Q

Class IV blocks…

A

Ca2+ currents to reduce Ca2+ overload –> prevent EADs

37
Q

Why are beta-blockers (Class II) antiarrhythmic?

A

Beta stimulation causes more Ca2+ into cell and into SR via phosphorylation by PKA; beta-blockers block this, decreasing spontaneous SR Ca2+ release and DADs

38
Q

Why are Ca2+ channel blockers (Class IV) antiarrhythmic?

A

Blocking Ca2+ current allows for slower AP propagation in AV node (because AP upstrokes in AV node are ICa dependent); F

39
Q

Class IA

A

Unblock: medium; IKR: strong block –> medium reduction in upstroke velocity, prolonged AP

40
Q

Class IB

A

Unblock: fast; IKR: weak block –> small reduction in upstroke velocity, small decrease in APD (due to Na+ channel block)

41
Q

Class IC

A

Unblock: slow; IKR: weak block –> large reduction in upstroke velocity, small decrease in APD (due to Na+ channel block)

42
Q

If the cardiac cell is slight depolarized (~-70 mV), what will happen w/ Class I drugs?

A

All Class I bind more strongly to O and I states, so there will be more drug binding (ischemic cells)

43
Q

Class I: Pharmacokinetics

A

Lidocaine (IB) is metabolized quickly so admin is IV

44
Q

Class I: Non-cardiac SEs (2)

A
  1. Long-term procainimide (IA) treatment leads to anti-nuclear Abs and can cause lupus-like symptoms; 2. All Class IA drugs have some antimuscarinic activity and can cause fluid retention, dry mouth, constipation
45
Q

Class I: Cardiac SEs

A

Because they unbind slowly, Class IC are the most dangerous and are used infrequently

46
Q

What is the negative effect of Na+ channel blockers?

A

Reduce Na+ current, reduce CV, reduce wavelength, so if you get a reentry, it will “stick” –> arrhythmia

47
Q

What is the negative effect of K+ blockers?

A

APD prolongation encourages EADs

48
Q

What does reverse rate dependence mean?

A

Class III drugs prolong APs more at slow rates where the negative effect is more detrimental

Cardiology (22 decks)

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