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CRRAB 1 > Nordgren Week 4 > Flashcards

Nordgren Week 4 Flashcards

1
Q

Cardiac effects of amiodarone

A

blocks K channels, prolongs AP (also a potent Na+ channel blocker, and weak blocker of B-receptors and Ca channels to slow HR and AV node conduction)

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2
Q

Amiodarone extracardiac effects

A

causes peripheral vasodilation

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3
Q

Toxicity of Amiodarone

A

bradycardia and heart block in pts with preexisting SA or AV node ds; drug accumulates in tissues (heart, lung, liver, skin, tears) blocks peripheral conversion of T4 to T3 and source of inorganic iodine

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4
Q

Pharmacokinetics of Amiodarone

A

hepatic metabolism; major metabolite is bioactive; complex elimination T1/2 1-3 months past cessation and measurable in tissue up to year

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5
Q

Where is Amiodarone metabolized?

A

CYP3A4

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6
Q

What other drugs does Amiodarone cause increased levels of via P450?

A

statins, digoxin, warfarin

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7
Q

Therapeutic use of Amiodarone?

A

ventricular tachycardia, including ventricular fibrillation, atrial fibrillation and flutter

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8
Q

Black Box Warning on Amiodarone

A

dose related pulmonary toxicity; abnormal liver function, hypersensitivity hepatitis, skin deposits (photodermatitis, gray-blue skin discoloration in sun-exposed areas), corneal microdeposits (in nearly all patients), halos develope in peripheral visual fields, rarely optic neuritis leading to blindness and hypo or hyperthyroidism

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9
Q

Cardiac effects of Dofetilide (Class III K+ channel blocker)

A

Very selective K+ channel blocker. Prolongs AP. The increase in QT interval observed is a result of prolongation of refractory period in the His-Purkinje system and ventricles.

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10
Q

Toxicity of Dofetilide (Class III K+ channel blocker)

A

Can cause life-threatening ventricular arrhythmias

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11
Q

Pharmacokinetics (Class III K+ channel blocker)

A

100% bioavailable! Hepatic metabolism via CPY3A4.

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12
Q

Therapeutic Use (Class III K+ channel blocker)

A

Maintenance and restoration of normal sinus rhythm in atrial fibrillation. Contraindicated in long QT, bradycardia, hypokalemia.

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13
Q

Cardiac effects of Ibutilide (Class III K+ channel blocker)

A

Prolongs AP. Also slow inward Na+ activator, which delays repolarization inhibits Na+ channel inactivation, which increases ERP

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14
Q

Toxicity of

Ibutilide (Class III K+ channel blocker)

A

Excessive QT-interval prolongation and torsades de pointes. Can cause life-threatening ventricular arrhythmias.

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15
Q

Pharmacokinetics of Ibutilide (Class III K+ channel blocker)

A

hepatic metabolism

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16
Q

Therapeutic Use of Ibutilide (Class III K+ channel blocker)

A

Acute conversion of atrial flutter and fibrillation to normal sinus rhythm. More effective in flutter… mean time to termination = 20 min.

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17
Q

Cardiac effects of Verapamil (Class IV Antiarrhythmic Ca Channel Blocker)

A

Blocks both activated and inactivated L-type Ca2+ channels, so greater affect in tissues that fire frequently, those less polarized, or nodal tissue.

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18
Q

Extracardiac effects of Verapamil (Class IV Antiarrhythmic Ca Channel Blocker)

A

peripheral vasodilation

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19
Q

Toxicity of Verapamil (Class IV Antiarrhythmic Ca Channel Blocker)

A

Large doses can induce AV block, or when used in patients with AV nodal disease. Constipation, lassitude, nervousness, peripheral edema.

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20
Q

Pharmacokinetics Verapamil (Class IV Antiarrhythmic Ca Channel Blocker)

A

hepatic metabolism

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21
Q 
Therapeutic Use
of Verapamil (Class IV Antiarrhythmic Ca Channel Blocker)
A

Supraventricular tachycardia, atrial fibrillation and flutter (reduces ventricular rate, not convert back to sinus rhythm), occasionally ventricular arrhythmias. Contraindicated in Wolff-Parkinson-White.

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22
Q

Cardiac effects of Diltiazem (Class IV Antiarrhythmic Ca Channel Blocker)

A

Similar to verapamil but with more smooth muscle-relaxing effect and produces less bradycardia.

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23
Q

Adenosine (Class V Antiarrhythmic)

A

increase K+ out of cells to hyperpolarizing the cell and decrease I calcium

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24
Q

Effect of Verapamil on QRS

A

increased PR interval

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25
Q

Effect of Ibutilide, Dofetilide (Class III K+ channel blocker)

A

increased QT interval

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26
Q

What is the drug of choice in diagnosing/terminating certain forms of SVT?

A

adenosine

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27
Q

What is the duration of action of adenosine?

A

15 seconds

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28
Q

What blunts the effects of adenosine (adenosine atagonists)?

A

theophylline and caffeine

29
Q

What are the adverse effects of adenosine?

A

flushing, hypotension, chest pain, sense of impending doom, bronchospasm

30
Q

What class of drugs are proarrhythmic as well as antiarrhythmic

A

Class III (K Channel Blockers)

31
Q

What med has mostly class III effects, but some class IV as well?

A

Amiodarone

32
Q

Because of its class IV effects what can Amiodarone lead to?

A

bradycardia and atrioventricular block

33
Q

What are contraindications to Amiodarone (a class III potassium channel blocker)?

A

heart block or sinoatrial node dysfunction

34
Q

What is the action class IV meds?

A

bind to L-type Ca channels on the vascular smooth muscle, cardiac myocytes and SA/AV nodes–>vascular smooth muscle relaxation (vasodilation) and decreased myocardial contractility

35
Q

What is the action of class IV in the smooth muscle?

A

channels are responsible for regulating the influx of calcium into muscle cells, which in turn stimulates smooth muscle contraction and cardiac myocyte contraction

36
Q

What does Ca influx do in the cardiac myocytes?

A

responsible for the slow repolarization (plateau) of the action potential (shorten phase 2), reduced force contraction

37
Q

Why is the contraction force reduced with Class IV drugs?

A

less Ca available to bind to troponin

38
Q

How do Class IV (Ca channel blockers) effect nodal cells?

A

decreased HR and decreased conduction velocity (of AV node) via phase 0

39
Q

How do class IV (Ca channel blockers) effect HTN?

A

decrease systemic vascular resistance (TPR) through smooth muscle relaxation

40
Q

What vessels do class IV (Ca channel blockers) affect? what do they do?

A

arterial vessels; decrease TPR via smooth muscle relaxation

41
Q

What is often the cause of angina?

A

ischemia of the heart muscle

42
Q

What are the therapeutic indications for class IV (Ca channel blockers)?

A

angina, arrhythmias

43
Q

How do Ca channel blockers (Class IV) effect afterload? oxygen demand

A

systemic vasodilation reduces arterial pressure, reduces ventricular afterload, decreases oxygen demand

44
Q

What are the two ways that Ca channel blocker decrease oxygen demand and the one way they increase oxygen supply?

A

1.reduce ventricular afterload 2.decrease HR and contractility 1.dilate coronary arteries and prevent/reverse coronary vasospasm

45
Q

What are the 2 ways that Ca channel blockers work on arrhythmias?

A

decrease pacemaker depolarization rate-> good for ectopic foci that are causing aberrant AP firing; decrease conduction velocity and prolong repolarization at the AV node (helps to block reentry mechanisms, which can cause SVT)

46
Q

What are the 2 subclasses of Class IV Ca channel blockers?

A

Dihydropyridines and Non-dihydropyridines

47
Q

smooth muscle selective class Ca channel blocker

A

Dihydropyridines

48
Q

primarily used to reduce systemic vascular resistance and arterial pressure, reduce HTN

A

Dihydropyridines

49
Q

What Ca channel blocker is generally NOT used to tx angina because the vasodilator and pressure lowering affects can lead to reflex cardiac stimulation (tachycardia and increased contractility) which can dramatically increase myocardial oxygen deman

A

Dihydropyridines

50
Q

What is the ending of name of Dihydropyridines?

A

-pine

51
Q

Name the 2 Non-Dihydropyridines (Ca channel blockers)

A

Verapamil and Diltiazem

52
Q

relatively selective for myocardium, less effective as a systemic vasodilator drug; tx angina and arrythmia by reducing myocardial oxygen demand and reversing coronary vasospasm

A

Verapamil

53
Q

intermediate between verapamil and dihydropyridines in its selectively for vascular Ca channels; both cardiac depressant and vasodilator actions

A

Diltiazem

54
Q

able to reduce arterial pressure without producing the same degree of reflex cardiac stimulation caused by dihydropyridines

A

Diltiazem

55
Q

Side effects of Dihydropyridines

A

flushing, headache, excessive hypotension, edema and reflex tachycardia

56
Q

What is a poor choice for angina because of the activation of sympathetic reflexes and lack of direct cardiac effects?

A

Dihydropyridines

57
Q

What has been shown to be safer anti-hypertensive drugs because of reflex responses?

A

long-acting dihydropyridines

58
Q

What are the AE of non-dihydropyridine?

A

excessive bradycardia, impaired electrical conduction (AV block) and depressed contractility

59
Q

Contraindications of Non-Dihydropyridine?

A

preexisting bradycardia, conduction defects or heart failure caused by systolic dysfunction

60
Q

What drug should Class IV drugs not be administered to patients? why?

A

B-blocker because those also depress cardiac electrical and mechanical activity

61
Q

Cardiac effects of Verapamil (Class IV antiarrhythmic)

A

blocks both activated and inactivated L-type Ca channels so greater affect in tissues that fire frequently, those less polarized or nodal tissue

62
Q

What is contraindicated in Wolff-Parkinson-White?

A

Verapamil

63
Q

What is similar to Verapamil, but has more smooth muscle-relaxing effect and produces less bradycardia?

A

Diltiazem

64
Q

Contraindications for Digitalis?

A

hypokalemic, AV block, Wolff-Parkinson-White

65
Q

What can lead to enhanced plasma levels of digoxin?

A

impaired renal function

66
Q

Common drug interactions with Digoxin?

A

Class IA, II, III, IV, NSAIDs, diuretics

67
Q

Digitalis signs of toxicity?

A

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

68
Q

How can Digitalis cause a multitude of arrhythmias?

A

increased automaticity and decreased AV conduction

69
Q

What does the EKG look like with the digitalis effect?

A

increased PR interval, flattened T waves, decrease QT interval (salvador dali’s mustache)

CRRAB 1 (9 decks)

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