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Pharm > Cardio II > Flashcards

Cardio II Flashcards

1
Q

What is the consequence of arrhythmias in terms of mechanical performance?

A

Ventricular stroke volume may be directly affected, leading to a decrease in cardiac output

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2
Q

What is the consequence of arrhythmias in terms of proarrhythmic/arrhythmogenic?

A

If not corrected, may lead to more severe forms of arrhythmias

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3
Q

What is the consequence of arrhythmias in terms of thrombogenesis?

A

Chronic arrhythmias may lead to the generation of thrombin in heart chambers

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4
Q

What are the four ways of decreasing spontaneous activity?

A
  1. Decreased phase 4 slope
  2. Increased threshold
  3. Increased maximum diastolic potential
  4. Increased AP duration
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5
Q

What are the two ways of increasing refractoriness?

A

Na channel blocker or AP prolonging

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6
Q

What is the MOA of Na channel blockers to increase refractoriness?

A

Shifts the voltage dependence of recovery

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7
Q

What is the MOA of AP prolonging drugs?

A

Blocks K channels, to slow the rate of K efflux

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8
Q

What is the general MOA of class I agents?

A

Block fast Na channels in the conductive tissues of the heart

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9
Q

What is the effect of class I drugs on the maximum depolarization rate?

A

Decreases

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10
Q

What is the effect of class I drugs on the automaticity and conduction?

A

Reduce automaticity

Delay conduction

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11
Q

What is the effect of class I drugs on ERP?

A

prolonged, leading to increased ERP/APD

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12
Q

What are the two major diseases that class I drugs are used in?

A

MI induce arrhythmias

Ventricular dysrhythmias

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13
Q

What type of drug is quinidine?

A

Class Ia

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14
Q

What type of drug is procainamide?

A

Class Ia

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15
Q

What type of drug is disopyramide?

A

Class Ia

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16
Q

What are the three class Ia drugs?

A

Quinidine
Procainamide
Disopyramide

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17
Q

What type of drug is lidocaine?

A

Class Ib

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18
Q

What type of drug is mexiletine?

A

Class Ib

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19
Q

What type of drug is propafenone?

A

Class Ic

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20
Q

What type of drug is flecainide?

A

Class Ic

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21
Q

What is the MOA of class Ia drugs? How does this affect the depolarization curve? (3)

A

Blocks both Na and K channels, and blocks Ca channels at high doses

Na block = prolonged phase 0
K blocked = delayed phase 3 repolarization
Ca blocked = depressed phase 2 and nodal phase 0

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22
Q

What is the primary MOA of quinidine?

A

Blocks rapid Na channel, lowering Vmax of phase 0

Causes slowed conduction

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23
Q

What are the three dose- dependent effects of quinidine?

A
  1. Blocks K channels (Increased APD)
  2. Blocks alpha receptors (lower BP)
  3. Blocks M receptors (higher HR)
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24
Q

What are the applications of quinidine?

A

only used in refractory cases of AF/ atrial flutter

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25
Q

What are the adverse effects of Quinidine? (4)

A

n/v/d
Cinchonism
Hypotension
Proarrhythmic

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26
Q

What is cinchonism, and what drug may cause it?

A

Tinnitus, hearing loss, blurred vision

Quinidine

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27
Q

How can Quinidine decrease Bp?

A

blocking alpha receptors

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28
Q

How can Quinidine cause torsades de pointes?

A

Block K channels can lead to an increased QT via prolonged plateau

29
Q

What is the MOA of Procainamide? (2)

A

Blocks rapid inward Na channel to slow conduction

Blocks K channels to prolong APD and refractoriness

30
Q

What are the clinical application of Procainamide? (4)

A

Suppress life threatening ventricular arrhythmias

Reentrant SVT
A-fib
A-flutter d/t WPW

31
Q

What is the effect of Procainamide on M and alpha receptors? Consequence of this?

A

None, thus no hypotension or tachycardia

32
Q

What is wolf-parkinson white syndrome (WPW)?

A

two pathways of ventricular conduction (slow and fast)

33
Q

What are the adverse cardiac effects of Procainamide?

A

Arrhythmia aggrevation

Torsades de pointes

34
Q

What are the adverse extracardiac effects of Procainamide?

A

SLE like syndrome

N/v

35
Q

What are the drugs that should never be given to a pt with a h/o torsades de pointes?

A

Procainamide

Quinidine

36
Q

What is the MOA of Lidocaine?

A

Blocks open and inactivated Na channels, causing a shortened repolarization, reduced Vmax, and lowered phase 4

37
Q

What is the effect of Lidocaine on the cardiac AP?

38
Q

What are the two effects of lidocaine in abnormal conduction systems?

A

Slows ventricular rate

potentiates infranodal block

39
Q

What is the clinical application of lidocaine?

A

treat ventricular arrhythmias (second choice after amiodarone)

40
Q

Is lidocaine effective for prophylaxis of arrhythmias after an MI? How about in atrial tissue

41
Q

Why must lidocaine be given IV, with multiple loading doses?

A

Has an extensive first pass effect

42
Q

What are the adverse reactions of lidocaine?

A

tinnitus/Szs in rapid bolus

43
Q

What is the MOA of class Ic drugs?

A

Strong binding to Na channels, causing strong effects on phase 0 depolarization

44
Q

What is the effects of class Ic drugs on Qt interval? QRS complex? PR?

A

QT unchanged
Longer QRS
Longer PR

45
Q

What type of drug is propafenone? MOA?

A

Class Ic

Strongly inhibits Na channels

46
Q

What is the adverse effect of propafenone?

A

beta adrenergic inhibition =

47
Q

Propafenone looks similar structurally to what drug? What is the consequence of this?

A

Propranolol

Lowers HR and ventricular output

48
Q

Why should you avoid giving pts with heart failure propafenone?

A

beta blocking effects will decrease CO

49
Q

What type of drug is Flecainide? MOA?

A

Class Ic

Blocks Na and prolonger 0, widens QRS, and markedly slows intraventricular conduction

50
Q

What are the clinical application for Flecainide?

A

Refractory life-threatening ectopic ventricular arrhythmias

51
Q

Why isn’t Flecainide used as a first line treatment against ventricular arrhythmias?

A

Propensity for fatal proarrhythmic effects

52
Q

What type of drugs are class II drugs? MOA?

A

beta blockers

Slow SA node automaticity
Lower AV node conduction
Decrease ventricular contractility

53
Q

When are class 2 drugs used?

A

Supraventricular arrhythmias due to excessive sympathetic activity

54
Q

What is the only type of antiarrhythmic drugs found to be clearly effective in preventing sudden cardiac death in pts with prior MI?

A

Class ii (beta blockers)

55
Q

What is the MOA of class III drugs?

A

Work on everything, except adenosine (Ca, Na, K, alpha, beta, ACh)

56
Q

What is the main effect of class III drugs?

A

Prolong phase 3 repolarization (prolonged QT)

57
Q

What is the clinical use of class III drugs?

A

Arrhythmias

58
Q

What are the 5 class 3 drugs?

A 
Dronedarone
Amiodarone
Sotalol
Ibutilide
Dofetilide
59
Q

What class of drug is Amiodarone?

60
Q

What is the effect and consequence of Amiodarone on K channels?

A

Blocks, prolongs refractoriness and APD

61
Q

What is the effect and consequence of Amiodarone on Na channels?

A

Blocks Na channels that are in the inactivated state

62
Q

What is the effect and consequence of Amiodarone on Ca channels?

A

Blocks to slow SA node phase 4

63
Q

Does amiodarone have a competitive or noncompetitive block on alpha, beta, and M receptor?

A

Noncompetitive

64
Q

What are the clinical applications of Amiodarone? (3)

A

Convert AF
AV node tachycardia
Acute termination of VT or VF

65
Q

What are the main adverse effects of amiodarone?

A

DEA (metabolic product) has very high antiarrhythmic potency

rapid redistribution out of heart may lead to early recurrence of arrhythmias

66
Q

Why is the fact that amiodarone is lipid soluble problematic?

A

Difficult to determine the [plasma]

67
Q

What are the side effects of using Amiodarone Iv?

A

Decreases cardiac contractility and PVR, causing hypotension

68
Q

What is the most serious side effect of amiodarone?

A

Lethal interstitial pneumonitis

69
Q

What are the effect of amiodarone on hyperthyroidism or hypothyroidism?

A

can cause either via destruction

Inhibit Iodine conversion

Pharm (73 decks)

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