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CRRAB 1 > K+ and Ca++ Blockers > Flashcards

K+ and Ca++ Blockers Flashcards

0
Q

Amiodarone site of action

A

Primarily: K+ channel blocker
Also: potent Na+ channel blocker, weak beta blocker, weak Ca channel blocker

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1
Q

Class III drugs have what activity (be specific)? What is the effect?

A

Inward rectifier K+ channel blocker

Slowed Repolarization

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2
Q

What are the effects of amiodarone (cardiac and extracardiac)?

A

Prolongs the action potential

Extracardiac: peripheral vasodilation

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3
Q

Basic toxicity of Amiodarone (4)

A

Bradycardia & heart block in pts with preexisting SA or AV node dis.
Accumulates in tissues (heart, lung, liver, skin, tears)
Effects up to 3 months post discontinuation.
Blocks peripheral T4 (thyroxine) to T3 (triiodothyronine)

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4
Q

Metabolism of Amiodarone

  • Location
  • Enzyme
  • Drug interactions
A

Hepatic metabolism with CYP3A4
Major metabolite is bioactive
Inhibits several P450s, interfering with statins, digoxin, and warfarin

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5
Q

Therapeutic use of Amiodarone

A

Ventricular tachycardia, including V-fib.

Effective for atrial fibrillation and flutter - off label use

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6
Q

More severe adverse effects of Amiodarone (4)

A
  • abnormal liver function, hypersensitivity hepatitis
  • skin deposits -> photodermatitis (grey-blue skin w/ sun exposure)
  • Corneal microdeposits (in nearly all patients) -> halos in peripherals, rarely optic neuritis -> blindness
  • Hypo and hyperthyroidism
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7
Q

Dofetilide drug class and cardiac effects

A

Class III, a very selective K+ channel blocker (unlike Amiodarone)
- Prolongs refractory period in His-Purkinje and ventricles -> increased QT interval

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8
Q

Dofetilide toxicity

A

Can cause life-threatening ventricular arrhythmias

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9
Q

Dofetilide therapeutic uses

A

Maintenance and restoration of NSR in a-fib

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10
Q

Contraindications for Dofetilide

A

Long QT, bradycardia, hypokalemia

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11
Q

Pharmacokinetics of Dofetilide

A

100% bioavailable

Hepatic metabolism via CYP3A4

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12
Q

Ibutilide Class and Cardiac Effects

A 
Class III (K+ channel inhibitor) -> prolongs repolarization
Also a slow inward Na+ activator -> delays repolarization -> inhibits Na+ channel inactivation -> increased ERP
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13
Q

Ibutilide therapeutic use

A

ACUTE conversion of a-fib or flutter to NSR

More effective in flutter w/ mean time to termination = 20 min

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14
Q

Ibutilide pharmacokinetics

A

Hepatic metabolism

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15
Q

Ibutilide toxicity

A

Excessive QT prolongation -> Torsades de pointes

Life-threatening polymorphic ventricular arrhythmias

16
Q

General effects and side effects of Class III Drugs

A

Proarrhythmic AND antiarrhythmic

Prolonging QT can -> torsades de pointes

17
Q

Class IV drugs binding site

A

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

18
Q

What does the channel that is the target of class IV drugs do normally?

A

L-type Ca channels regulate influx of calcium into smooth muscle cells -> smooth muscle and myocyte contraction

19
Q

Effects of Class IV drugs (4)

A
  • Vascular smooth muscle relaxation (vasodilation)
  • Decreased myocardial contractility
  • In cardiac myocytes: shortens phase 2 (plateau), reduces force of contraction because there is lass Ca available to bind troponin
  • In nodal cells: blocks phase 0 depolarization -> dec HR, dec conduction velocity, especially in AV node
20
Q

Therapeutic indications for class IV drugs and why

A

HTN: decreases TPR via smooth muscle relaxation -> decreased arterial blood pressure, primarily affects arterial vessels
Angina: Vasodilation and dec HR -> dec O2 demand, also dilates coronary arteries -> inc O2 supply to myocardium
Arrhythmias: dec pacemaker depolarization rate=good for ectopic foci, dec conduction velocity, prolonged repolarization -> block reentry

21
Q

How do subclasses of Class IV drugs differ? What are the classes?

A

Differ in specificity for cardiac vs. vascular L-type channels
Dihydropyridines and Non-Dihydropyridines

22
Q

Dihydropyridines are selective for ________. Recognizable by what naming convention?

A

Smooth muscle

Ends in “pine”

23
Q

Dihydropyridine uses and what it doesn’t work for (why?)

A

Used for hypertension: reduces systemic vascular resistance and arterial pressure.
Not used for angina: vasodilation -> compensatory increase in heart rate and contractility -> increased O2 demand (bad reflex loop)

24
Q

Which drugs make up the class IV non-Dihydropyridines? (2)

A

Verapamil and Diltiazem

25
Q

Rank the dihydropyridine subclass vs the two non-dihydropyridines in order of most selective for myocardium to most selective for vascular smooth muscle

A

Verapamil - Diltiazem - Dihydropyridines

26
Q

How does Verapamil work? What are its cardiac effects and indications?

A

Relatively selective for the myocardium
Reverses coronary vasospasm. Decreases contractility, HR, and velocity of conduction -> decreased O2 demand
Indications: angina and arrhythmias

27
Q

What is Diltiazem’s cardiac vs. vascular L-type Ca channel specificity?

A

Intermediate between Verapimil (myocardium) and Dihydropyridines (vascular) –> cardiac depressant and vasodilator actions

28
Q

Diltiazem and the hydropyridines both –> vasodilation. Why can Diltiazem be used with angina when hydropyridines can’t?

A

Diltiazem also acts as a cardiac depressant, not only a vasodilator. Therefore, there is less risk of reflex cardiac stimulation caused by hypotension.

29
Q

Side effects of dihydropyridines

A

Flushing, HA, excessive hypotension, edema, reflex tachycardia

30
Q

Side effects of non-dihydropyridines

A

Excessive bradycardia, impaired electrical conduction e.g. AV block, depressed contractility

31
Q

Contraindications to calcium channel blockers

A

Preexisting bradycardia, conduction defects, heart failure caused by systolic dysfunction - especially for non-dihydropyridines, but also for dihydropyridines.

32
Q

Adenosine MOA

A

Ca channel block -> suppresses nodal APs + inward K+ channel activation -> hyperpolarization

33
Q

Adenosine therapeutic uses

A

SVT. Not effective for a-fib or flutter.

34
Q

Contraindication to adenosine

A

heart block

35
Q

Digitalis (digoxin) MOA

A

Inhibits Na/K ATPase -> inc Na in cell -> reversed action of Na/Ca pump -> inc Ca in cell -> improved contractility. Also activates vagal efferents to heart.

36
Q

Uses for Digoxin

A

Primarily HF. Also for reducing vent rate driven by high atrial rate (a-fib or flutter)

37
Q

Digitalis toxicity: EKG

A

EKG: arrhythmias, “Salvador Dali’s mustache” checkmark in ST segment, flattened T waves.

38
Q

Main causes of Digitalis toxicity

A

Renal impairment, especially in elderly + narrow TI

CRRAB 1 (12 decks)

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