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CRRAB 1 week 2 > Na+ Channels Blockers and Beta Blockers > Flashcards

Na+ Channels Blockers and Beta Blockers Flashcards

1
Q

What two classes of the antiarrhythmics can be used to deal with a reentry issue and why?

A
  1. Na+ channel blockers - because they can slow AP duration and thus slow ocnduction, making it a bidirectional block
  2. K+ channel blockers - because they prolong the effective refractory period, slowing conduction
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2
Q

How do the Na+ channel blockers slow conduction specifically?

A

they block Na+ entry into the cell, thus prolonging phase 0 and slowing conduction

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3
Q

How do the K+ channel blockers promote the refractory time of the cell specifically?

A

It slows the efflux of K+ during phase 3 so the cell doesn’t repolarize as quickly and sodium channels stay inactivated for longer - prolonging the refractory time of the cell

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4
Q

What is accommodation?

A

when heart tissue is damaged and can’t generate ATP, the Na/Ca and Na/K exchangers don’t work and you get depolarization of the RPM - hence the Na+ are inactivated and can’t take part in the depolarization

The depolarization then falls on Ca2+, which makes is resemble a slow-response AP - and develop automaticity

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5
Q

In general, how do you deal with accomodation?

A

you need to convert the permeability profile back to fast-response and allow Na+ permeability to dominate the depolarization
hence, you need to alter the Ca2+ permeability

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6
Q

Specifically what calcium channels are blocked by Ca2+ channel blockers?

A

They block the T-type channels, which are depolarized at relatively low membrane potentials - this slows the influx of Ca2+ and allows for Na+ channels to fully repolarize and excite the cell in a fast-response manner

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7
Q

Do the Na+ channel blockers bind to and block slow or fast Na+ channels

A

the fast ones - the ones responsible for the rapid depolarization

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8
Q

What do Na+ channel blockers do to alter the shape of the action potential curve?

A

if decreases the slop of phase 0, so depolarizaiton is slowed

the amplitude of the action potential is also decreased

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9
Q

Na+ channel blockers will decrease conduction velocity in what type of heart tissue, then? Why?

A

Na+ channel blockers will decrease conduction velocity in non-nodal tissue

they won’t have an effect on nodal tissue because the nodal APs are dependent on Ca2+

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10
Q

How are the Na+ channel blockers divided into subdivisions?

A

based on their differing effects on action potential duration and effective refractory period.

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11
Q

What are the Na+ channel blocker’s effects on effective refractory period actually due to?

A

not due to the Na+ blockade, but rather the non-specific secondary activity on efflux of K+ in phase 3

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12
Q

Rank the subclasses of Na+ channel blockers in terms of effectivness of Na+ blockade?

A

1c better than 1a better than 1b

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13
Q

Rank the Na+ channel blocker subclasses based on which increases the effective refractory period the most

A

1A more than 1C (actually not much at all) more than 1B (which actually decreases it!)

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14
Q

What are three class 1B drugs?

A

What are three class 1B drugs?

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15
Q

What are three class 1B drugs?

A

lidocaine
tocainide
mexiletine

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16
Q

lidocaine
tocainide
mexiletine

A

lidocaine
tocainide
mexiletine

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17
Q

lidocaine
tocainide
mexiletine

A

afib
atrial flutter
supraventriculae and ventricular tachyarrhythmias

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18
Q

What are the class 1Bs typically used to treat?

A

ventricular tachyarrhythmias

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19
Q

What are the class 1Cs typically used to treat?

A

surpaventricular tachyarrhythmias and ventricular tachyararhythmias

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20
Q

What are the effects of Beta-blockers?

A

They inhibit sympathetic activation of cardiac automaticity and conduction, so they slow the heart rate, decrease AV node conduction velocity,and increase AV node refractory period

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21
Q

What are the beta blockers used to treat?

A

supraventricular arrhythmias and to reduce ventricular ectopic depolarizations (as seen in MI)

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22
Q

What are the cardiac effects of procainamide?

A

class 1A antiarrhythmic - slows upstroke of AP, slows conduction, prolongs QRS on EKG and prolongs ERP by non-specific blockade of K+ channels

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23
Q

WHat are the extracardiac effect sof procainamide?

A

ganglion blocking properties leading to reduced peripheral vascular resistance and causing hypotention

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24
Q

What are the two important toxicities of procainamide?

A

Because of the excessive AP prolongation, you have QT interval prolongation with potential induction or torsades de pointes

Long term use can cause a syndrome resemble lupus erythematosus

25
Q

How is procainamide metabolized?

A

the drug is metabolized to NAPA (has class 3 activity) in the liver.

NAPA excreted by kidneys

15-20% plasma protein binding

26
Q

What are the cardiac effects of quinidine?

A

class 1A antiarrhythmic - slows upstroke of AP, slows conduction, prolongs QRS on EKG, prolongs effective refractory period by non-specific blockade of K+ channels, antimuscarinic effects

27
Q

What are the extracardiac effects?

A

antimuscarinic effects = adverse GI with diarrhea, nausea, and vomiting

conchonism - headache, dizziness, tinnitus at toxic concentrations

28
Q

What’s the major toxicity of quinidine?

A

excessive QT prolongation with induction of torsades de pointes, arrhtymia and syncope

29
Q

Describe the pharmacokinetics of quinidine?

A

readily absorbed from GI tract, eliminated by hepatic metabolism and excreted via kidneys

30
Q

Why is quinidine rarely used for arrhythmias?

A

because of the extracardiac adverse effects - other drugs are much better tolerated

31
Q

What are the cardiac effects of disopyramide?

A 
slows upstroke of AP
slows conduciton
prolongs QRS
prolongs ERP
antimuscarinic effects
32
Q

What are the extracardiac effects of disopyramide?

A

atorpine-like activity, so urinary retention, dry mouth, blurred vision, constipation

33
Q

What’s the main toxicity for disopyramide?

A

excessive QT prolongation and torsades depoints

may precipitate heart failure de novo or in patients with preexisting left ventricular dysfunction - so don’t use in patients with heart failure

34
Q

What are the pharmacokinetics for disopyramide?

A

loading dose is NOT recommended because of risk of precipitating heart failure. hepatic metabolism, renal excretion. protein binding 50-60%

35
Q

What is disopyramide used for in the US?

A

ventricular arrythmias only

36
Q

WHat are the cardiac effects of lidocaine?

A

selective depression of conduction in depolarized cells. Little effect seen on EKG in normal sinus rhythm.

37
Q

What are the toxicities of lidocaine?

A

it’s one of the least cardiotoxic class 1 antiarrhytmics! Most common effects are paresthesias, tremor, nausea of central origin, lightheadedness, hearing disturbances, slurred speech, convulsions. Most common in elderly.

38
Q

What are the pharmacokinetics of lidocaine?

A

extensive first-pass hepatic metabolism, so only 3% of oral dose apears in plasma, thus you have to give parenterally

half life of only 1-2 hours

39
Q

What are the main therapeutic uses for lidocaine?

A

it’s the agent of choice for termination of ventricular tachycardia and prevention of v fib after cardioversion in the setting of acute ischemia.

However, it’s NOT used prophylactically because it increases total mortality for some unknown reason

40
Q

What are the cardiac effects of mexiletine? WHat is it actually?

A

It’s an orally active congener of lidocaine!!!

Selective depression of conduction in depolarized cells. Little effects seen on EKG in normal rhythm.

41
Q

What are the extracardiac effects of mexiletine?

A

there’s significant efficacy in relieving chronic pain due to diabetic neuropathy and nerve injury!!!!

42
Q

What are the common adverse effects of mexiletine?

A

tremor, blurred vision, lethargy, nausea

43
Q

How is mexiletine metabolized/

A

hepatic metabolism
renal excretion
protein binding 50-60%
half life 8-20 hours (longer than lido)

44
Q

What is tocainide?

A

another lidocaine analog

45
Q

What are the pharmacokinetics of tocainide?

A

glucuronidation metabolism!
renal excretion
protien binding 10-20%

46
Q

What is tocainide used for?

A

nothing - not sold in US anymore

47
Q

What are the cardiac effects of flecainide?

A

slows upstroke of AP
slows conduction
potent blocker of Na+ and K+ channels with slow unblocking kinetics
Does NOT prolong the AP or QT interval

48
Q

What are the toxicities of flecainide?

A

severe exacerbation of arrhythmia if given to someone with a preexisting ventricular tachyarrhythmias and those with previous MI and ventricular ectopy

49
Q

What are the pharmacokinetics of flecainide?

A

metabolism and elimination both hepatic and renal. protein binding 40%

50
Q

What are the cardiac effects of propafenone?

A

slows upstroke of AP
slows conduciton
!!Weak beta-blocking activity!!
spectrum of action similar to quinidine, but doesn’t prolong AP

51
Q

What are the toxicities of propafenone?

A

metallic taste and constipation

arrhytmia exacerbations can also occur

52
Q

What is the therapeutic use for propafenone?

A

supraventricular arrhythmias

53
Q

What are the cardiac effects of moricizine?

A

slows upstroke of AP
slows conduction
does not prolong AP duration

54
Q

What are the pharmacokinetics of moricizine?

A

extensive first pass hepatic metabolism

protein binding 95%!

55
Q

What is moricizine used for?

A

nothing anymore - not sold in the US. Was used for ventricular arrhytmias

56
Q

Who should you NOT give the 1Cs to?

A

people with pre-existing structural damage like an MI - they will make the arrhythmias way worse

57
Q

What are 4 examples of beta blockers?

A

proporanalol
acebutolol
esmolol
sotalol

58
Q

What are the major general toxicities of the beta blockers

A

can precipitate CHF, so don’t use in patients with CHF

can also inhibit bronchodilation and exacerbate asthma, so use with caution

59
Q

What is the extra toxicity of sotalol among the beta blockers?

A

It can cause QT prolongation and torsades de pointes, so we only use it for severe arrhythmias

CRRAB 1 week 2 (15 decks)

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