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CRAAB 2 > Nordgren: Anti-arrhythmic Drugs > Flashcards

Nordgren: Anti-arrhythmic Drugs Flashcards

1
Q

What is an arrhythmia?

A

A condition of the heart in which the electrical is faster, slower or irregular.

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2
Q

What is tachycardia?

A

Faster heart beat

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3
Q

What is bradycardia?

A

Slower heart beat

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4
Q

What are three ways that arrhythmias can deviate from normal?

A
  1. Rate of impulse
  2. Impulse at the site of origin
  3. Conduction of Impulse
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5
Q

Arrhythmias are also examples of…

A

cardiac depolarizations

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6
Q

The transmembrane potential through cells is determined by the concentrations of what three ions?

A

Na, K, Ca

Water soluble so don’t pass through membrane without specific ion channels

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7
Q

What accounts for the differences in the shape of observed AP for pacemaker and contractile cardiac cells?

A

Differences in ion permeability

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8
Q

What regulates the flow of ions though ion specific channels?

A

Ion channels are controlled by “gates” that are voltage sensitive and can be modulated by ion concentration and metabolic conditions.

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9
Q

What causes the depolarization of atrial, purkinje and ventricular cells?

A

Na current

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10
Q

What causes the depolarization of SA and AV nodal cells?

A

Ca current

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11
Q

What is difference between the depolarization of SA/AV nodal cells and atrial/purkinje/ventricular cells?

A

Ca and Na channels are activated/inactivated in the same way BUT the transitions in Ca channels occur more slowly and at more positive membrane potentials.

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12
Q

What causes the final repolarization of the action potential in all cell types?

A

Na/Ca inactivation and the growth of K permeability

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13
Q

When does the final repolarization of the action potential occur?

A

Phase 3

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14
Q

What are three factors that help to bring the membrane potential back to the K equilibrium potential?

A
  1. Rapidly activating K current
  2. Slowly activating K Current
  3. Ikr + Iks collectively called “Ik”
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15
Q

Why may some drugs that block Ik have little effect on the repolarization of SA nodal cells?

A

SA nodal cells may be controlled by a different K current

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16
Q

What is one of the most important relationships to consider when looking at the pathophysiology of arrhythmias and the drugs used to treat them?

A

The relation between RESTING potential of the cell and the number of APs that can be evoked.

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17
Q

What determines how many ion channels are open?

A

Membrane potential through activation and inactivation gates

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18
Q

Na channel inactivation gates close between -75 and -55. How many Na channels will be available for diffusion of Na at -60? At -80?

A

Fewer Na channels will be available for diffusion of Na than if AP occurred at -80.

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19
Q

At a positive membrane potential (ex. the plateau of phase 2), how many Na channels are available?

A

None!

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20
Q

What happens to Na channels during repolarization?

A

Na channels recover from inactivation and become available.

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21
Q

What is the refractory period?

A

The time phase between Phase 0 and sufficient recovery of Na channels in Phase 3 to allow another AP.

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22
Q

What happens to the AP if you add a drug that BLOCKS Na channels?

A
  1. Total # channels available at optimal conditions will be decreased (phase 4).
  2. At subotimal conditions, channels will be unavailable d/t both inactivation gate closure and drug blockade.
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23
Q

Why does Na channel recovery time increase w/ depolarization of the membrane potential?

A
  1. Depolarized cells recover more slowly!

2. Increases the refractory period of the cell.

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24
Q

What does a Na channel blockade do to recovery time? Where is the recovery time the greatest?

A

It PROLONGS the recovery time at any given membrane potential.

At depolarized potentials

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25
Q

What happens to Na currents if the resting potential depolarizes to -55mV?

A

It abolishes Na current–all Na channels are inactivated.

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26
Q

Depolarization of resting potential to -55 mV usually abolishes Na currents. What is an exception to this rule? What cells are an example of this exception?

A

Severely depolarized cells support special APs under circumstances that INCREASE Ca or DECREASE K permeability.

SA and AV nodal cells because they have a normal RMP in the range of -50 to -70.

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27
Q

What factors 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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28
Q

Factors that cause arrhythmia do so by disturbing what to necessary cardiac processes?

A
  1. Impulse formation

2. Impulse conduction

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29
Q

What are pacemaker cells responsible for?

A

Impulse formation

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30
Q

What are the two phases of impulse formation described as?

A
  1. Diastolic Interval

2. Action Potential Phases

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31
Q

What will shortening of either the diastolic interval or the action potential phase do?

A

Increase pacemaker rate leading to an increase in heart rate.

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32
Q

Out of the two phases of initial impulse formation which is the more important of the two?

A

Diastolic Interval

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33
Q

What are two ways to slow the pacemaker cell?

A
  1. Alter the slope of the diastolic interval (phase 4 of the pacemaker potential)
  2. Hyperpolarize the diastolic interval so it takes longer to reach the threshold
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34
Q

How does vagal discharge of acetylcholine affect impulse formation?

A

It SLOWS the pacemaker.

35
Q

How do beta-adrenoceptor blocking affect impulse formation?

A

They release NE (catecholamines)/sympathetic innervation leading to a reduced slope of diastolic interval, ultimately slowing the pacemaker.

36
Q

How do you increase the speed of the pacemaker?

A

Alter the slop of the diastolic interval (more rapid change)

37
Q

What are examples of physiological processes that speed up the pacemaker?

A
  1. Hypokalemia
  2. Beta-adrenoceptor stimulation
  3. Positive chronotropic drugs
  4. Fiber stretch
  5. Acidosis
38
Q

What are afterdepolarizations?

A

Membrane voltage oscillations that result in transient, abnormal depolarizations of cardiac myocytes during phase 2, 3, or 4 of the cardiac AP.

39
Q

What are the two ways to describe afterdepolarizations?

A
  1. Early afterdepolarization

2. Delayed afterdepolarization

40
Q

When do early afterdepolarizations occur and what do they do?

A

Occur DURING and AP and interrupt orderly repolarization of the myocyte.

41
Q

What causes early afterdepolarization?

A
  1. Late phase 2- opening of more Ca channels
  2. Early phase 3: Opening of Na channels
  3. Both: inhibition of K channels
42
Q

When is early afterdepolarization exacerbated? Why?

A

At SLOW heart rates. There is a better chance another can happen on top of it.

43
Q

When does a delayed afterpolarization occur?

A
  1. AFTER the Ap, when the cell is nearly or fully repolarized, but before another AP would occur.
44
Q

What causes delayed afterdepolarization?

A

Elevated cytosolic Ca levels overloads the SR and causes a spontaneous release of Ca and leads to depolarizing current.

45
Q

What exacerbates delayed afterdepolarization?

A

Fast heart rates

46
Q

Why are afterdepolarizations bad? When are they most likely to occur?

A

They lead to arrythmias!

When AP duration is abnormally long.

47
Q

What is a block?

A

When an electrical signal is slowed or disrupted as it moves through the heart.

48
Q

Where can blocks occur?

A 
SA node
AV node
Bundle of His (Infra-hisian block)
Bundle Branch
Fascicles (hemiblocks)
49
Q

What is a partial block?

A

When electrical impulses are DELAYED or ocassionaly stopped.

50
Q

What is a complete block?

A

Electrical impulses are completely STOPPED.

51
Q

What is re-entry?

A

When an impulse reenters and excites areas of the heart more than once.

*Also called circus movement

52
Q

What are the three things that must happen in order for re-entry to occur?

A
  1. There must be an obstacle to homogenous conduction
  2. There must be a unidirectional block at some point in the circuit
  3. The conduction time (how long it takes for the signal to go through/around) must exceed the effective refractory period
53
Q

What is a unidirectional block?

A

Prevents the passage of an impulse when it approaches from one direction but not from the other.

54
Q

What is a bidirectional block?

A

A block that prevents passage of an impulse in both directions.

55
Q

What is Wolff Parkinson-White syndrome?

A

When a heart has an extra anatomical feature called a BUNDLE OF KENT that leads to an abnormal electrical accessory connection between the atria and ventricle.

56
Q

What does the bundle of kent do?

A
  1. It allows for impulse to be conducted without going through the AV node and causing a ventricle to prematurely contract.
  2. It can also be a conduit for re-entry to the atria.
57
Q

When is the only TIME reentry can occur?

A

When conduction has been depressed for some critical amount of time.

58
Q

What happens when conduction is too slow or twoo fast?

A

Both lead to bidirectional blocks and therefore NO reentry.

59
Q

What happens when an impulse travels around a unidirectional block too quickly?

A

Reaches tissue that are still refractory> no reentry

60
Q

What causes conduction to slow down?

A

Decreased Ca or Na current

61
Q

What causes arrhythmias?

A
  1. Abnormal pacemaker activity

2. Abnormal impulse propagation

62
Q

What do antiarrhythmic drugs aim to do?

A
  1. Reduce pacemaker activity

2. Modify conduction/refractoriness

63
Q

What are the 4 major pharmacologic mechanisms for arrhythmias?

A
  1. Na channel blockade (class I)
  2. β-Adrenoceptor Blockade (class II)
  3. K+ channel blockade (Class III drugs)
  4. Ca channel blockade (Class IV)
64
Q

What is the MOA of a Na channel blockade do? Class?

A

Alters AP duration and kinetics of Na channel blockade.

Class I

65
Q

What is the MOA of a Beta adrenoceptor blockade do? Class?

A

Blockade the SNS effects in the heart.

Class II

66
Q

What is the MOA of a K channel blockade do? Class?

A

Prolongation of the effective refractory period.

Class III

67
Q

What is the MOA of a Ca channel blockade? Class?

A

Slows conduction where depolarization is Ca dependent.

Class IV

68
Q

What drugs are 1A Na channel blockers?

A

Quinidine
Procainamide
Disopyramide

69
Q

What drugs are subgroup 1B Na channel blockers?

A

Lidocaine

Mexilitine

70
Q

What drugs are 1C Na channel blockers?

A

Flecainide

Propafenone

71
Q

What drugs are K channel blockers?

A

Amiodarone
Dofetilide
Ibutilide

72
Q

What drugs are Ca channel blockers?

A

Verapamil

Diltiazem

73
Q

What drugs are Beta adrenergic blockers?

A

Propanolol
Acebutolol
Esmolol
Sotalol.

74
Q

What two drugs are misc arrhythmic?

A

Adenosine

Digitalis

75
Q

When are “use” or “state dependent” drugs useful?

A

They are good channel blocking drugs.

  1. Bind readily to activated (phase 0)/inactivated channels (Phase 2)
  2. Bind poorly or not at all to rested channels (prevent drug from binding in this state/promotes drug dissociation from receptors when channel becomes rested.)
76
Q

When can “state dependent” drugs block electrical activity?

A
  1. Fast tachycardia- many channel activations/inactivations per unit time
  2. Significant loss of resting potential- many inactivated channels during rest (lose RP channels are transformed to inactivated state when they should be in a resting state)
77
Q

What is the goal of antiarrythmic drugs?

A

To suppress ectopic atuomaticity adn abnormal conduction occurring in depolarized cells, while minimally affecting the electrical activity of normally polarized parts of the heart.

78
Q

What is the approach for antiarrhythmic drugs?

A

Identify the specific mechanism of arrhthmia and exploit what makes it different.

79
Q

What does a reentry arrhthmia depend on?

A
  1. Depressed conduction
  2. Unidirectional block

*Slow conduction speed> bidirectional block> no reentry > not a problem

80
Q

What are two ways to address reentry arrhythmias?

A
  1. Na and Ca channel blockade

2. K channel blockade

81
Q

How does a Na and Ca channel blockade address a reentry arrhythmia?

A

It causes a steady state reduction in the number of available unblocked channels, which reduces excitatory currents to a level below that required for propagation.

82
Q

How does a K channel blockade address a reentry arrhythmia?

A

Prolongs recovery time of channels still able to reach the rested and available state, which increases refractory period.

83
Q

What do you have to worry about with many of the antiarrhythmetic drugs, particularly the Na channel blockers?

A

Many of these drugs lack channel specificity, so as you increase the dose, there is a greater spillover to secondary channels. Also, channel specificity is inversely related to dose, so at high doses the drugs can effect all the channels.

CRAAB 2 (9 decks)

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