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CRRAB 1 Week 3 > K+ and Ca2+ Blockers > Flashcards

K+ and Ca2+ Blockers Flashcards

1
Q

specifically what channels are blocked by class III drugs?

A

class III drugs are the K blockers and they specifically boock the inward rectifier K+ channels

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2
Q

what phase of the actionpotential is altered by K blockers? How?

A

phase 3 - repolarization

slows repolarization down, thus increasing AP duration and effective refractory period

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3
Q

If the AP is prolonged by K blockers, what’s a side effect common to all of them?

A

prolonged QT

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4
Q

If K blockers prolong the time that the cell is unexcitable, what are they apricularly useful for/

A

useful in suppressing reentry arrhythmias

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5
Q

What are the three K blockers we know/

A

Amiodarone
Dofetilide
Ilbutilide

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6
Q

What are the cardiac effects of amiodarone?

A

blocks a lot…

prolongs AP as a K blocker, but also a potent Na blocker, weak beta blocker and weak Ca blockers, so you also get slowed heart rate and slowed AV node conduction

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7
Q

What are the extracardiac effects of amiodarone/

A

peripheral vasodilation

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8
Q

What are the main toxicities of amiodarone?

A

the most important is dose related pulmonary toxicity
others include
1. abnormal liver functions, hypersensitivity hepatitis
2. skin deposits leading to photodermatitis
3. corneal microdeposits in nearly ALL patients - halos develop in peripheral visual fields, rarely leads to blindness
4. hypo and hyperthyroidism

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9
Q

How is amiodarone metabolized?

A

mainly hepatic metabolism to a bioactive metabolite

note - effects will last 1-3 months past cessation!

Substrate for CYP3A4 - so will be influenced by inducers!

inhibits several p450s and can increase concentrations of other drugs

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10
Q

what is amiodarone used for?

A

ventricular tachycardia including v fib! also atrial fibrillation and flutter

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11
Q

What are the cardiac effects of dofetilide?

A

it’s a VERY selective K blocker, so you get prolonged AP and increase QT interval.

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12
Q

What is the main toxicity of dofetilide?

A

life-threatening ventricular arrhythmias because of the long QT

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13
Q

What are the pharmacokinetics of dofetilide?

A

100% bioavailable! hepatic metabolism via CYP3A4

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14
Q

What is the main therapeutic use of dofetilide?

A

maintenance and restoration of normal sinus rhythm in atrial fibrillation

DON”T USE in people with long QT, bradycardia or hypokalemia

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15
Q

What are the cardiac effects of ibutilide?

A

prolong AP as K blocker. Also slows inward Na activator , so delayed repolarization further.

also inhibits Na channel inactivation, which increases the ERP?

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16
Q

What is the main toxicity for ibutilide?

A

excessive QT prolongation and torsades de pointes. can cause life threatening ventricular arrhythmias

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17
Q

How is ibutilide metabolized?

A

hepatic metabolism

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18
Q

What’s the main therapeutic use of ibutilide?

A

acute conversion of a flutter and a fib to normal sinus. more effective in flutter - 20 minutes mean time to termination

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19
Q

What type of Ca2+ channels are specifically blocked by Class IV drugs? WHere are the channels located?

A

L type - located on vascular smooth muscle, cardiac myocytes and SA/AV nodes

20
Q

What are the effects of Class IV drugs on smooth muscle?

A

the channels are responsible for regulating the influx of calcium into the muscle cells, which in turn stimualtes smooth muscle contraction and cardiac myocyte contraction, so blockin gCa entry causes vascular smooth muscle vasodilation

21
Q

What are the effects of Class IV drugs on cardiac myocytes?

A

Ca2+ influx is responsible for the slow repolarization (plateau) of the action potential, so blocking Ca2+ entry shortens phase 2 of the AP and reduces the force of contraction because there’s less Ca2+ available to bind troponin

22
Q

What are the effects of Class IV drugs on nodal cells?

A

the L-type Ca channels play an important role in pacemaker current and in phase 0 of the action potential

blocking Ca entry causes a decreased HR and decreased conduction velocity in the AV node

23
Q

Why can Class IV drugs be used for HTN?

A

because of their smooth muscle vasodilatory effects

decreases systemic vascular resistance and thus lowers arterial blood pressure

24
Q

Why can class IV drugs be used in angina?

A

because they cause vasodilation and decrease HR, the systemic vasodilation reduces arterial pressure which reduces ventricular afterload, thus decreasing oxygen demand

decreased HR and contractility also lead to decreased oxygen demand

can also dilate coronary arteries and prevent vasospams, thereby increasing O2 supply to the myocardium

25
Q

What are the two sublcasses of class IV drugs?

A

dihydropyridines and non-dihydropyridines

26
Q

How do the dihydropyridines and non-dihydropyridines differ?

A

in their selectivity for catrdiac vs. vascular L type Ca 2+ channels
dihydropyridines = vascular type
Non-dihydropyridines = cardiac type (and some vascular)

27
Q

What are the two non-dihydropyridines we need to know?

A

Verapamil and Diltiazem

28
Q

How do Verapamil and Diltiazem’s mechanisms of action differ?

A

verapamil is relatively selective for myocardium and less effective as a systemic vasodilator drugs - treat angina and arrhythmias

Diltiazem has selectivity for both myocardium and vascular Ca2+ channels. So it’s used to treat angina, arrhythmias and HTN (without causing the same degree of reflexive cardiac stimulation as dihydropyridines)

29
Q

What are the main side effects of dihydropyridines?

A

related to vasodilation = flushing, headache, excessive hypotension, edema, and reflexive tachycardia

30
Q

What are the side effects of non-dihydropyridines?

A

excessive bradycardia, impaired electrical conduction and depressed contractility

31
Q

Who should NOT be given non-dihydropyridines?

A

those with preexisting bradycardia, conduction defects or heart failure caused by systolic dysfunciton

32
Q

What other type of antiarrhythmic should the Class IV drugs NOT be given with?

A

beta blockers - the calcium blockade will augment the effects of the beta blockade

33
Q

What is the mechanism of action for adenosine?

A

It activates inward rectifier K channels and inhibits L-type Ca2+ channels, resultin gin hyperpolarization and suppression of Ca2+ dependent action potentials in nodal tissue

this suppresses AV conduction and increases AV rereactory period

34
Q

What is adenosine used for?

A

it’s the drug of choice for prompt ocnversion of paroxysmal supraventricular tachy cardia

note - doesn’t work for a fib or a flut

35
Q

What are the side effects of adenosine?

A

flushing and headache
can produce arterial hypotentsion
Ab block

36
Q

What does caffein do to adenosine?

A

xanthines like caffein will competitively antagonize the binding of adenosine to its receptor, so it will be less effective

37
Q

Adenosine is contraindicated in what patients?

A

paitents with 2 or 3 degree AV block.

38
Q

What is the primary use for digitalis (digoxin)?

A

heart failure

39
Q

What arrhythmias is digoxin also helpful for?

A

atrial fibrillation and flutter - it will reduce the ventricular rate being driven by these two.

40
Q

What is the mechanism for Digitalis to improve cardiac contractility?

A

It inhibits the Na/K/ATPase pump such that intracellular Na concentration increases.

This then reverses the action of the Na/Ca exchanger such that you have more Ca in the cell and thus higher contractility, increasing stroke volume and cardiac output

41
Q

What is the mechanism digitlis uses to the rate of conduction in SA and AV node?

A

activation of vagal efferent nerves

42
Q

What are the side effects of digitalis?

A

extreme AV block (because of the vagal effects on the AV)

drug interactions with all the other antiarrhythmics, NSAIDS and diuretics

43
Q

Who shouldn’t you give digoxin to?

A

people with AV block already
people with wolf parkinson white
people with impaired renal function

44
Q

What does digitalis toxicity look like clinically?

A

GI distress, hyperkalemia, life-threatening arrhythmias (increased automaticity and AV nodal blockade)

45
Q

What does digitalis toxicity look like on EKG?

A

an increased PR interval, plattened T waves and decreased QT interval - like a mustache or checkmark after the R wave

46
Q

What are the 4 questions you should always find an answer for before starting an anriarrhythmic drug?

A
  1. eliminate the cause if possible
  2. make a firm diagnosis
  3. determine the baseline conduction
  4. questions th need for therapy.e

CRRAB 1 Week 3 (7 decks)

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