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CRRAB 1 week 2 > Intro to Antiarrhythmic Drugs > Flashcards

Intro to Antiarrhythmic Drugs Flashcards

1
Q

Arrhythmias consist of cardiac depolarizations that deviate from normal in what three potential ways?

A

rate of impulse
impulse site of origin
conduction of impulse

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2
Q

In the atrial, purkinje and ventricular cells, what ion current leads to depolarization?

A

NA+

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3
Q

In the SA and AV ndoal cells, depolarizaion depends on what ion current/

A

Ca2+

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4
Q

What are the three potential states for the Na+ channel?

A

resting = no Na passes thorugh
activated = Na enters the cell
Inactivated - inactivation gate is closed, no Na passes thorugh

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5
Q

Although most Ca2+ channels become activated and inactivated in the same manner as Na+ channels, how do they differ?

A

the transition between activated and inactivated occurs more slowly and at more positive membrane potentials

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6
Q

For both cell types, final repolarization (phase 3) results from permeability to what ion?

A

K+

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7
Q

What two currents are collectively called the Ik?

A

rapidly activating potassium current

slowly activating potassium current

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8
Q

Why does the resting potential of a cell affect the number of action potentials that can be evoked?

A

Membrane potential determines how many channels are open - via activation/inactivation gates

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9
Q

So…If Na+ channels inactivate between 75 and -55mV, will more Na+ channels be available for diffusion at -60 mV or -80 mV.

A

-80 mV - fewer channels will be in the inactivated state

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10
Q

During the positive membrane potential during plateau (phase 2), are any Na+ channels available?

A

none

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11
Q

What happens to the Na+ channels during repolarization?

A

they recover from inactivation and become available

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12
Q

What period spans the time when all Na+ channels are inactivated to when enough are open again?

A

the refractory period

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13
Q

What happens if you add a drug that blocks Na+ channels?

A

the total number of Na+ channels available at optimal conditions will be decreased
at suboptimal conditions, the Na+ channels will be uanvailable dur to both inactivation gate closure AND drug blockade

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14
Q

Na+ channel recovery time increases with depolarization or hyperpolarization of the membrane potnetial?

A

depolarization - they stay inactivated longer

this means depolarized cells recover more slowly and the refractory period increases

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15
Q

Depolarization to what membrane potential will abolish Na+ currents

A

-55 mV - they’re all inactivated

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16
Q

What are the potential factors that lead to arrhythmia?

A 
Ischemia
Drug Toxicity
Hypoxia
Acidosis / Alkalosis
Electrolyte Abnormalities
Overstretching of Cardiac Fibers
Excessive Catecholamine Exposure
Autonomic Influences
Scarred or Diseased Tissue
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17
Q

Pacemaker cell impulse formation is split into the diastolic interval and the action potential. Which is more important for increasing heart rate?

A

the diastolic - increase Na+ permeability

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18
Q

What are the two ways you can slow the diastolic interval?

A

flatten the slope of the diastolic interval - make it take more time

hyperpolarize the diastolic interval, make it need to go further

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19
Q

Drugs blocking what receptor will act to slow the pacemaker?

A

beta-adrenoceptor (inhibits NE sympathetics)

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20
Q

What are some things - conditions or drugs that will increase the slope of diastolic interval speeding up the pacemaker?

A 
hypokalemia
beta adrenoceptor stimulants
positive chronotropic drugs
fiber stretch
acidosis
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21
Q

What are afterdepolarizations?

A

they’re membrane voltage oscillations that result in transient, abnormal depolarizations of cardiac myocytes during phase 2, 3, or 4 of the cardiac AP (either early afterdepolarization or delayed afterdepolarization)

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22
Q

When do early afterdepolarizations occur?

A

DURING the action potential and interrupt orderly repolarization of the myocyte

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23
Q

What causes early afterdepolarizations during late phase 2?

A

opening more Ca2+ channels

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24
Q

What causes early afterdepolarizations in early pase 3?

A

opening of Na+ channels

25
Q

Inhibition of K+ channels will cause early afterdepolarizations in what phase?

A

both phase2 and 3

26
Q

Are early afterdepolarizations exacerbated at slow or rapid heart rates?

A

slow

27
Q

When do delayed afterdeplarizations occur?

A

occur after the AP when the membrane is nearly or fully repolarized, but before another AP would normally occur

28
Q

What are DADs caused by>

A

elevated cytosolic Ca2+ levels - overload of the SR causes spotnaneous release of Ca2+ and leads to depolarizing current

29
Q

Are delayed afterdepolarizations exacerbated at slow or fast heart rates?

A

fast

30
Q

Afterdepolarizations can lead to arrhythmias more likely when the AP duration is abnormally short or long?

A

long

31
Q

What are the two general types of heart blocks?

A

partial or complete

32
Q

Where can blocks occur?

A

SA node, AB node, bundle of his (infra-hisian block), bundle branch block, fascicles (hemiblocks)

33
Q

What is reentry?

A

when the impulse reenters and excites areas of the heart more than once - also called “circus movement”

34
Q

What are the required conditions for reentry to occur?

A
  1. there must be an obstacle to homogenous conduction
  2. there must be a unidirectional block at some point
  3. conduction time must exceed the effective refractory period
35
Q

What is an example of reentry that is strictly anatomical?

A

Wolff-Parkinson-White syndrome, where you get the bundle of kent - an abnormal electrical accessory connection between atria and ventricle, allowing the impulse to conduct

36
Q

Why is timing everything for reentry to occur?

A

If conduction is too slow, you end up with a bidirectional block and you can’t get reentry

If conduction is too fast (which would be close to normal, 1. you end up with a bidirectional block and 2. the impulse travels around the unidirectional block too quicky, reaching tissue that is still refractory

37
Q

What are the Class I antiarrhythmics?

A

Na+ channel blockers - alter AP duration and kinetics of Na+ channel blockage

38
Q

What are the Class II antiarrhytmics?

A

beta-adrenoceptor blockade - block sympathetic nervous system effects on the heart

39
Q

What are the Class III antiarrhtymics?

A

K+ channel blockers - prolongation of the effective refractory period

40
Q

What are class IV antitarhytmics?

A

Ca2+ channel blockade

slows conduction where depolarization is Ca2+ dependent

41
Q

What do all the antiarrhythmics have in common?

A

They are all “use” or “state dependent” drugs, meaning they bind readily to activated or inactivated channels so they only work in areas where depolarization is abnormal

42
Q

Antiarhyrthmics block electrical activity during what situations?

A

fast tachycardia (when there are many channel activation and inactivations per unit time)

significant loss of resting potential (many inactivated channel during rest)

43
Q

What is the goal for an antiarrhythmic in a reentry arrhythmia that depends on depressed conduction? (hint - it’s counterintuitive)

A

you want to slow conduction speed which will change the block from unidirectional to bidirectional – no more reentry

44
Q

Is channel specificity directly or inversely related to dose of antiarrhytmic drugs?

A

inversely - higher dose, more spillover to secondary channels

especially with the Class I Na+ blockers affected K+ channels

45
Q

How do we classify cardiac arrhythmias based on heart rate? heart rhythm? site of origin?

A

tachycardia vs bradycardia
regular v sirregular
supraventircular vs ventricular

46
Q

What would you see on EKG with premature atrial contractions?

A

early extra beats that originate in the atria, so you’ll see a p wave riding right on the tail of a T wave - everything is otherwise normal, it’s just the timing

47
Q

What would you see on EKG with paroxysmal supraventricular tachycardia?

A

It’s a rapid, usually regular rhythm originating from above the ventricles - begins and ends suddenly.

48
Q

What would you see on EKG with accessory pathway tachycardias? (bypass tract tachycardias)

A

It’s a rapid heart rhythm due to an extra abnormal pathway or connection between the atria and ventricles (Like WPS syndrome) - you get a delta wave or “slurred” upstroke in the QRS somplex

49
Q

What are the three variants of AV nodal reentrant tachydardia? What is the general cause?

A

it’s a rapid heart rate due to more than one pathway thorugh the AV ndoe

atrial tachycardia, atrial fibrilllation, atrial flutter

50
Q

What is atrial fibrillation?

A

irregular heart rhythm where many impulses begin and spread in the atria competing for a chance to travel through the AV node. the result is a disorganized, rapid, irregular rhythm. You get less coordinated atrial contraction as well.

51
Q

What is atrial flutter and how doe it differ from fibrillation?

A

There are many impulses that are vying to travel to the AV node, but they occur in a mroe organized loop. This means it’s different from fibrillation because it’s more regular.

52
Q

What will you see on EKG with PVCs?

A

they’re extra early beats beginning in the ventricles. You see a big QRS spike that’s occuring right after a T wave without the usual P wave in between

53
Q

What is ventricular tachycardia?

A

It’s a rapid rhythm originating form the ventricles - this prevents the heart from filling with blood and less is pumped thorugh the body.

54
Q

What is ventricular fibrillation and why is it an emergency?

A

It’s erratic, disorganized firing impulses from the ventricles - like a quiver. the ventricles can’t contract or pump any blood. On EKG you’ll be unable to discern where any of the waves are.

55
Q

What’s the treatment for v-fib?

A

CPR and defibrillation

56
Q

What will long QT syndrome look like on EKG?

A

If the time between the Q wave and the end of the T wave is over 450 ms, that’s long QT

57
Q

Long QT syndrome increases the risk for what life-threatening form of V-tach?

A

torsade de pointes

58
Q

What will sinus node dusfunction look like on EKG?

A

a slow hear rhythm where you get nothing for 3+ seconds with no SA node activity

59
Q

What will a heart block look like on EKG? How can you see the difference between partial and complete blocks?

A

If there’s a blockage in the AV node for example…

The SA will trigger a P wave, but then you don’t get the associated QRST…just more P waves. IF the AV node is working otherwise fine, the AV node will fire it’s own ventricular contractions, so you may get QRST still, just not associated with a P wave - they’re independent.

Complete = none of the QRST will be associated with a P wave
Partial = some of the QRST will be associated with a P wave

CRRAB 1 week 2 (15 decks)

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