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Pharmacology & Drugs > Cardio- Antiarrhythmic Drugs > Flashcards

Cardio- Antiarrhythmic Drugs Flashcards

1
Q

How are the forces different between the influx of sodium and the efflux of potassium, and what is the effect on the action potential

A
  • Sodium is going with the electrical and chemical gradient (faster depolarization)
  • Potassium is going with the chemical and against he electrical gradient (slower repolarization)
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2
Q

What is the target for esmolol

A

Short acting Beta-1 blocker

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3
Q

What is the mechanism of action for ibutilide

A

Slows the cardiac repolarization by blocking the rapid component fo the delayed potassium current

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4
Q

What are the effects of class 1A drugs on the action potentials

A
  • Prolonged action potential duration

- Prolonged QRS and QT intervals of the EKG

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5
Q

What class of drug is amiodarone

A

Potassium channel blocker

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6
Q

Which patients populations are more likely to have an adverse reaction to flecainide

A
  • Preexisting ventricular tachyarrhythias
  • Previous MI
  • Ventricular ectopic rhythms
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7
Q

Where does adenosine work in the heart

A

A1 adenosine receptor

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8
Q

Procainamide is used to treat which condition

A

Sustained ventricular tachycardia

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9
Q

What is the method of administration for esmolol

A

Continuous IV, with a rapid onset and termination

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10
Q

What are the pharmacokinetics for lidocaine

A

-Extensive first pass, so can only be administered IV

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11
Q

What are the clinal uses for sotalol

A
  • Life threatening ventricular arrhythmias

- Maintaining sinus rhythm in pts with Afib

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12
Q

What are the clinical situations that mexiletine is used

A
  • Ventricular arrhythmias

- Chronic pains due to diabetic neuropathy and nerve injury

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13
Q

IN the inactivated state of sodium channels, which gates are acting

A

H gates close, starting the refractory period

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14
Q

What are the cardiac adverse effects of lidocaine

A

May cause hypotension in patients with heart failure due to inhibition of the cardiac contractility

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15
Q

What class of drug is esmolol

A

Beta blocker

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16
Q

What class of drug is flecainide

A

Class 1C drug

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17
Q

What are the adverse cardiac effects of Procainamide

A
  • QT interval elongation
  • Induction of torsade de pointes
  • Excessive inhibition of conduction
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18
Q

What is the mechanism that sympthetic effects are seen in the pacemaker cells of the heart

A

All resultsin the increases the levels of cAMP and PKA activity

  • Epi/norepi binds to the B1 adrenergic receptors, increases the adenylate cyclase activity, which increases the cAMP levels and PKA
  • T/L type calcium channels conductance increases from PKA activity
  • Funny channels conductance increases with increased PKA
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19
Q

What is the drug class of ibutilide

A

Class 3 potassium channel blocker

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20
Q

Which class of drug is verapamil

A

Class 4 calcium channel blocker

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21
Q

What is the mechanism of action for adenosine

A

Activates the potassium curing and inhibits the calcium in funny channels, leading to hyperpolarization and suppression of action potentials

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22
Q

What are the effects of potassium blockers on Action potentials

A
  • Prolonged action potential duration
  • Prolonged QT interval
  • Prolonged refractory period
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23
Q

What is the half life of esmolol and what is the metabolism

A

10 minutes due to hydrolysis by blood esterases

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24
Q

Class 1A sodium channel blockers preferentially affect which cells

A

Ectopic pacemaker cells with faster rhythms

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25
Q

What are the mechanims of action for class 4 drugs

A
  • aka Cardioactive calcium channel blockers
  • Decreases the slope of phase 0
  • Increased L type Calcium channel threshold potential
  • Prolonged refractory period in AV node
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26
Q

What receptors are affected by amiodarone

A
  • Blocks potassium channels
  • Blocks inactivated sodium channels
  • Some calcium blocking activity
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27
Q

What are the clinical uses of esmolol

A
  • Supraventricular arrhythmias
  • arrhythmias due to thyrotoxicosis
  • MI ischemia or acute MI with arrhythmias
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28
Q

What are the clinical uses for adenosine

A

-Conversion of paroxysmal SVT into normal sinus rhythm

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29
Q

What drug is given to patients that overdose on class 1 drugs and what is the reasoning

A
  • Bicarbonate, which will try to raise the pH of the blood
  • THis increase in pH will decrease the rate of protonation of the drugs and decrease their effect (because the activated form in protonated)
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30
Q

Most sodium blockers are acting during which state of sodium channels

A

Block the activated or inactivated sodium channels

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31
Q

What is the clinical uses for ibutilide

A

Convert atrial flutter and Afib to sinus

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32
Q

Which clinical situations is lidocaine used

A

Mono or polymorphic ventricular tachycardias, being very efficient in acute MI

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33
Q

What are the effects of beta blockers on the SA node

A

Decreased HR (Increased RR interval)

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34
Q

Class 1A drugs bind to which stare of sodium channels

A

Open (activated) sodium channels

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35
Q

What are the adverse effects of dofetilide

A

QT interval is Prolonged, with increased risk of ventricular arrhythmias

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36
Q

What are the pharmacokinetics of mexiletine

A

Oral drug

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37
Q

Class 1 drugs act in which location

A

Sodium channel blockers

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38
Q

What is the noncardiac effect of verapamil

A

Constipation

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39
Q

Which class of drug is Procainamide

A

Class 1A sodium blocker

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40
Q

What is the mechanism of action for dofetilide

A

Blocks rapid component of the delayed potassium current, so there is a slower HR

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41
Q

What class of drug is mexiletine

A

Class 1B drug

42
Q

Which class of drug is disopyramide

A

Class 1A drug

43
Q

What are the noncardiac adverse effects of quinidine

A
  • Headache, dizziness, tinnitus
  • GI side effects
  • Thrombocytopenia, hepatitis, fever
44
Q

What are the kinetics of class 1B drugs

A

Fast kinetics

45
Q

What class of drug is propranolol

A

Beta blocker

46
Q

What are the noncardiac adverse effects of disopyramide

A

Atropine like symptoms ( dry mouth, urinary retention, blurred vision, continuation)
-Exacerbation of glaucoma

47
Q

What are the channels/affects of sotalol

A
  • Class 2 (beta blocker)

- Class 3 (prolongs AP duration)

48
Q

What is the clinical use of disopyramide

A

Recurrent ventricular arrhythmias

49
Q

What are the adverse affects of propafenone

A
  • Exacerbation of ventricular arrhythmias
  • Metallic tase
  • Constipation
50
Q

Class 1C drugs prefer to bind to which channels

A

Open (activated) sodium channels

-Some potassium channels

51
Q

Class 1B drugs bind to which channels and in which state

A

Bind to inactivated sodium channels, so therefore they prefer the depolarized cells

52
Q

What is the clinical use for dofetilide

A

Converts atrial fib to sinus rhythm and then maintaining it after

53
Q

What are the effects of beta blockers on AV node

A

-Decreased AV conductance (increased PR interval)

54
Q

What class of drug is diltiazem

A

Class 4 calcium channel blocker

55
Q

Which rate of dissociation leads to more sodium channel blockage

A

Slow dissociation rates

56
Q

What is unique about the cells lidocaine targets and its effect

A

Binds to damaged tissue cells and makes them electrically silent , with no effect on normal tissue due to the fast kinetics

57
Q

What are the adverse cardiac effects of amiodarone

A
  • AV block and bradycardia

- Induction of torsade de pointes (low compared to other Class 3)

58
Q

What is the metabolism of dofetilide and how does this affect therapeutic window

A

Eliminated by the kidneys, so the levels have to be very closely monitored

59
Q

Which drugs need to be monitored with amiodarone

A

Inhibitor of CYP, so effects metabolism of many drugs

-Metabolized by CYP3A4, so cimetidine (inhibitor) or refaptin (activator)

60
Q

Why will a sodium channel blocker not affect the slow action potential cells

A

Aka the pacemaker cells in the SA and AV node

-Because there are not sodium channel present there

61
Q

What is the drug class of sotalol

A
  • class 2 Beta blocker

- Class 3 Potassium blocker

62
Q

What are the contraindications for propranolol

A
  • Stress induced arrhythmias
  • Reentrant arrhythmias that involved AV node
  • Afib and flutter
  • Arrhythmias associated with MI
63
Q

What are the clinical uses of amiodarone

A
  • Treatment of ventricular arrhythmias

- Atrial fibrillation

64
Q

What is the class of drug for propafenone

A

Class 1C drug

65
Q

What are the clinical uses for class 4 drugs

A
  • Prevention of paroxysmal SVT

- Rate control for Atrial flutter and fibrillation

66
Q

What are the effects of class 4 drugs

A

Slows the SA node depolarization, leading to bradycardia

Prolonged AP duration and conduction time in the AV node

67
Q

Which form of sodium channel blockers binds to channels

A

Cationic form

68
Q

What are the contraindications for beta blockers

A
  • Asthma
  • Peripheral vascular disease
  • Raynaud’s syndrome
  • Type 1 DM
  • Depressed CO
69
Q

What are the clinical uses for propafenone

A
  • Prevents paroxysmal atrial flutter and SVT without structural diseases
  • Sustained ventricular arrhythmias
70
Q

In the activated state of sodium channels, which set of gates are open

A

-M gates open in depolarization

71
Q

What are the adverse cardiac effects of class 4 drugs

A
  • Negative inotropy
  • AV block
  • SA arrest
  • Hypotension
72
Q

Class 1A sodium channel blockers interact with with channel s

A

Sodium and potassium are both blocked

73
Q

What are the kinetics of Class 1C

A

Slow

74
Q

Class 4 drugs block which channels

A

Activated and inactivated L type Calcium channels

75
Q

Which class of drug is lidocaine

A

Class 1B drugs

76
Q

What are the adverse effects of sotalol

A
  • Depression of cardiac function

- Torsade de pointes

77
Q

What are the effects of class 1C on AP, and the ECG

A
  • No change in the AP duration or QT interval

- Prolonged QRS

78
Q

What are the numbers of normal sinus rhythm and risk of death while on Quinidine

A

2x as likely to have normal rhythm

2-3x likely to have risk of death

79
Q

Which potassium channels are responsible for the regulation of action potentials

A

Voltage gated determine the refractory period

80
Q

What are the extracardiac adverse effects of Procainamide

A
  • Ganglion blocking properties and reduces peripheral vascular resistance leading to hypotension
  • SLE
  • Nausea
81
Q

What are the noncardiac adverse effects of lidocaine

A

Paresthesias, tremors, slurred speech, convulsions

82
Q

What is the clinical uses for Quinidine

A

Restoring rhythm in atrial flutter/fibrillation with normal hearts

83
Q

Which potassium channels are open in the resting state

A

Inward rectifying K+ channels but no current due to equilibrium with the electric and concentration gradients

84
Q

What is the effect on action potentials with regards to class 1B drugs

A
  • Shortens action protentials (because does not affect potassium channels)
  • Does not prolong the action potential or the QT duration
85
Q

What are the cardiac adverse effects of disopyramide

A
  • QT interval prolongation
  • Induction of torsade de pointes
  • Syncope and heart failure due to excessive depression of cardiac condition
86
Q

What are the adverse cardiac effects of quinidine

A
  • QT interval prolongation
  • Induction of torsade de pointes
  • Excessive slowing of conduction
87
Q

How does esmolol and sotalol differ

A

Esmolol (beta blocker)
Sotalol (potassium blocker with some beta blocker)
-Because sotalol is a potassium blocker, it will effect the length of the action potential, therefore the QT is prolonged

88
Q

What are the targets for flecainide

A

Sodium and potassium channels

89
Q

Which drugs uses are contraindicated with propafenone

A

-CYP2D6 or CYP 34A inhibitors (risk of proarrhythmias)

90
Q

What are the clinical uses for flecainide

A

Patients with normal hearts who have:

  • Supraventricular arrhythmias (aka atrial flutter, paroxysmal SVT)
  • Sustained ventricular tachycardia
91
Q

Which class of drug is quinidine

A

Class 1A drug

92
Q

What is the effect of sympathetic activity

A
  • Increased slope due to activity on funny channel and T type Calcium channels
  • Reduced threshold for L type Calcium channels
93
Q

What are the noncardiac effects of amiodarone

A
  • Fatal pulmonary fibrosis
  • Hepatitis
  • photodermatitis (blue grey skin on sun exposed areas)
  • Optical neuritis
  • may cause thyroid issues
94
Q

What are the adverse effects of adenosine

A
  • Shortness of breath
  • Bronchoconstriction
  • Chest burning
  • AV block
  • Hypotension
95
Q

What is the metabolism aspect of ibutilide

A

Administered IV, and is rapidly cleared by hepatic metabolism

96
Q

What are the pharmacokinetics of amiodarone

A

Metabolized by CYP3A4

-Long half life (effects seen 1-3 months after discontinuing)

97
Q

What are the adverse effects of beta blockers

A

Decreased CO
Impaired liver glucose metabolization
Increased VLDL and decreased HDL
Sedation, depression

98
Q

What is a contraindication for Procainamide

A

-accumulates in renal dysfunction, need to measure both drug and active metabolite

99
Q

What are the adverse effects of ibutilide

A
  • QT prolongation and increased risk of ventricular arrhythmias
  • Require continuous EKG monitoring until the QT returns to baseline
100
Q

What is the dissociation kinetics of class 1A

A

Intermediate kinetics

Pharmacology & Drugs (43 decks)

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