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Cardiovascular Med II Final > Drugs used in Cardiac Arrhythmias - Konorev > Flashcards

Drugs used in Cardiac Arrhythmias - Konorev Flashcards

1
Q

What channels allows for the phase 4 of the Pacemaker AP?

A

Funny current, I(f) channels; and slow Ca++ influx T-type channels

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2
Q

what factors determine the firing rate, or automaticity of the pacemaker cells?

A
  1. rate of spontaneous depolarization in phase 4 (i.e. the slope): decreased slope = decreased rate thus need more time to reach threshold
  2. Threshold potential - the potential at which AP is triggered
  3. Resting potential - if potential is less negative, less time is needed to reach the threshold- firing rate increase
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3
Q

Class 1 antiarrhythmic drugs block what channel?

A

Sodium channel

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4
Q

what are the different categories of drugs in Class 1 antiarrhythmic ?

A

1A, 1B and 1C

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5
Q

Quinidine, procainamide and Disopyramide are what class of drugs?

A

Class 1A antiarrhythmia

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6
Q

Lidocaine and mexiletine are what class of drugs?

A

Class 1B antiarrhythia

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7
Q

Flecainide and propafenone are what class of drugs?

A

Class 1C antiarrhythmia

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8
Q 
What class of drugs belong to the following class of antiarrhythmic drugs
A. Class 2
B. Class 3
C. Class 4
D. Miscellaneous / class 5
A

Class 2: Beta blockers (esmolol, propranolol)
Class 3: Potassium channel blocker (amiodarone, dronedarone, sotalol, dofetilide, ibutilide)
Class 4: Cardioactive CCB (verapamil and diltiazem
Miscellaneous agent: adenosine

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9
Q

What is the MOA of class 1A drugs?

A
  • Block Na channels, slow impulse conduction, reduce automatism of latent pacemakers.
  • Use-dependent block - preferentially bind to open (activated) Na channels and so ectopic pacemaker cells with faster rhythms will be preferentially targeted and thus phase 0 slope will be decreased.
  • K channel is also blocked and this causes prolongation of AP duration and prolongs QRS and QT intervals on EKG
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10
Q

What is the MOA of class 1B drugs?

A
  • use dependent block - bind to inactivated Na channels and so preferentially bind to depolarized cells.
  • dissociate from channel with fast kinetics - no effect on conduction in normal tissues.
  • shortens AP
  • More specific action on Na channel - (do NOT block K channel, do not prolong AP or QT duration on EKG)
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11
Q

What is the MOA of class 1C drugs?

A
  • Blocks Na channel, slow impulse conduction
  • preferentially bind to open (activated) Na channel
  • Dissociate from the channel with slow kinetics
  • Block certain K channels
  • Do not prolong action potential duration and QT interval duration of the ECG
  • Prolong QRS interval duration
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12
Q

what is the normal sympathetic effect on the pacemaker action potential?

A
  • Increase slope of phase 4 due to effects on I(f) and T-type Ca channel
  • Reduced threshold due to effect on L type Ca channel
  • AP occurs sooner.
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13
Q

What is the MOA of propranolol and esmolol as a class 2 antiarrhythmic drug?

A
  • Slows action potential (blocks I(f) and T-type Ca channel, and by Increasing threshold due to effect on L-type Ca channel); this effect on SA node thus decreases HR (increases RR interval)
  • Ventricular myocardium: decrease Ca2+ overload, prevent delayed afterdepolarization
  • Increase PR interval
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14
Q

What is the MOA of class 3 antiarrhythmic drug K channel blocker?

A
  • Blocks potassium channels, which prolongs action potential duration and QT interval on ECG. Most effective at slow heart rates
  • Prolongs refractory period
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15
Q

what is the MOA of class 4 antiarrhthmic drugs (CCB: verapamil/diltiazem)?

A
  • Block both activated and inactivated L-type Ca channel
  • active in slow response cells - decrease the slope of phase 0 depolarization
  • slow SA depolarization, cause bradycarida
  • prolong action potential duration and refractory period in AV node
  • Prolong AV node conduction time
  • May suppress delayed afterdepolarizations- amy be effective in DAD-induced ventricular arrythmias.
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16
Q

Which Class 1A drug has antimuscarinic activity is used to treat sustained ventricular tachycardias, and may be used in arrhythmias associated with MI. It’s action on ganglions may cause hypotension

A

Procainamide. It directly depresses the activities of SA and AV nodes.

  • Has ganglion-blocking properties, reduces peripheral vascular resistance and may cause hypotension
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17
Q

Explain how sympathetics increase HR.

A

Beta 1 –> increased AC –> increased cAMP –> increased funny channel flow rate and decreased calcium channel threshold –> increased pacemaker speed.

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18
Q

Explain how parasympathetic slows heart rate

A

M2 –> decreased AC and increased K opening –> slow funny current, higher threshold (via less cAMP/PKA for Ca channel), and lower resting potential

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19
Q

What causes an early afterdepolarization?

A

Afterdepolarization is another rapid depolarization during phase 2 and 3 of the previous AP. this is caused by impaired K channels and prolonged repolarization period

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20
Q

Torsades de pointes is commonly seen in _

A

Long QT syndrome (prolonged repolarization)

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21
Q

Which antiarrhythmic drugs are long-QT inducing?

A

Class 1A or Class 3

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22
Q

What is a delayed afterdepolarization?

A

Another partial depolarization during phase 4 (hyperpolarized). Due to increased cytosolic Ca++.

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23
Q

What are some indication for procainamide?

A
  • WPW, PAC, PVC, A-fib, V-tach, A-flutter
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24
Q

what AE are associated with procanamide?

A
  • QT interval prolongation
  • Induction of torsade de pointes arrhythmias and syncope
  • excessive inhibition of conduction
  • Lupus syndrome with arthritis, pleuritis, pulmonary disease, hepatitis and fever
  • nausea/diarrhea
  • agranulocytosis
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25
Q

What are some indication for Quinidine

A
  • Restore rhythm in a-fib/flutter pts with noral to arrhythmic hearts.
  • Sustained ventricular arrhythmia (MAT, PAC, PVC, V-tach)
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26
Q

What AE are associated with quinidine

A
  • QT interval prolongation
  • Torsade de pointes and syncope
  • excessive slowing of conduction
  • GI effects
  • HA/dizziness/tinnitus
  • thrombocytopenia, hepatitis, fever
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27
Q

Disopyramide is used for

A

treatment of recurrent V-arrhythmias

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28
Q

what AE are associated with disopyramide

A
  • QT interval prolongation,
  • Torsade de pointes
  • syncope
  • negative inotropic effect – > HR
  • excessive depression of cardiac conduction
  • Atropine-like symptoms: Urinary retention, dry mouth, blurred vision, constipation, exacerbation of glucoma
29
Q

What is the MOA of lidocaine?

A
  • blocks inactivated Na channel (use dependence) - selectively blocks conduction in depolarized tissue, making damaged tissue completely electrically silent
  • rapid kinetics so dissociates fast and has no effect on cardiac conductivity in normal tissue.
30
Q

What is the indication for lidocaine?

A
  • mono and polymorphic ventricular tachycardias. esp useful in arrhythmia after MI.
31
Q

What adverse effects are associated with lidocaine?

A

This is the least toxic Class 1 drugs

  • CV: hypotension in pts w/ HF
  • Neuro: paresthesias, tremor, slurred speech, convulsion
32
Q

What is mexiletine used for?

A

V-arrhythmias

- relieve chronic pain, esp pain due to DM neuropathy and nerve injury

33
Q

What AE are associated with mexiletine?

A
  • tremor
  • blurred vision
  • nausea
  • lethargy
34
Q

What is Flecainide used for?

A

In pts with normal hearts to treat SVA including AF, PSVT (AVNRT, AVRT)
- Life threatening V-arrhythmias, such as sustained V-tach

35
Q

What AE are associated with Flecainide?

A

Severe exacerbation of V-arrhythmia when given to pts with: preexisting Vtach, MI, or V-ectopic rhythms

36
Q

What is propaenone used for?

A

Prevent paroxysmal AF and SVT in pts w/o structural disease

- sustained Varrhythmias

37
Q

What AE are associated with Propafenone?

A
  • Exacerbation of V-arrythmias
  • metallic taste
  • constipation
38
Q

Propafenone should not be combined with what hepatic enzyme inhibitors as the risk of proarrhythmia may be increased?

A

CYP2D6 and CYP3A4

39
Q

What is the indication of propranolol?

A
  • Arrhythmias associated with stress
  • re-entrant arrhythmias that involve AV node (AVNRT, AVRT)
  • A-fib and flutter
  • Arrhythmias associated with MI
40
Q

What class 2 drug is short acting (10mins) and is used as continuous iv infusion with rapid onset and termination of its action

A

Esmolol

41
Q

What is esmolol used for?

A
  • SVA
  • arrhythmias associated with thyrotoxicosis
  • Myocardial ischemia or AMI with arrhythmia
  • used as adjunct in general anesthesia to control arrhythmias in perioperative period
42
Q

1 blocks potassium channels, but also has adrenolytic activity (causes peripheral vasodilation) and is known to block inactivated Na channel; causes bradycardia, slows AV conduction

A

Amiodarone

43
Q

Amiodarone is used for

A

V-arrhythmia.

- A-fib (not FDA approved)

44
Q

_ is known to have maintained drug effects even 1-3 months after discontinuation

A

Amiodarone

45
Q

What AE are associated with amiodarone?

A
  • AV block and bradycardia
  • Fatal pulmonary fibrosis
  • hepatitis
  • photodermatitis, deposits in skin, blue grey skin discoloration in sun exposed areas
  • optical neuritis: deposit of drugs in places like cornea and other eye tissues
  • Blocks thryoxine to Triiodothyroine –> hypo or hyperthyroidism
46
Q

what is the dronedarone?

A

1 Blocks multiple K channels;

  • Block Na current
  • Blocks L-type Ca current
  • Prolongs AV refractory period and PR interval
  • stronger antiadrenergic effects than amiodarone
47
Q

what is dronedarone used for?

A

A-fib/flutter. Not as effective as amiodarone in maintaing sinus rhythm

48
Q

What AE are associated with dronedarone?

A
  • Worsen HF
  • GI issues
  • not as severe AE as amiodarone (no iodine moiety, shorter half life, less drug interaction)
49
Q

Dronedarone is contraindicated in pts with _

A

decompensated HF

50
Q

what is sotalol used for?

A

It is a Class 3 antiarrhythmic drug (K channel blocker) that is used to treat life-threatening ventricular arrhythmias and maintenance of sinus rhythm in pts with afib.

51
Q

what AE are associated with sotalol (Class 3 antiarrhythmic drug Channel blocker)

A

depression of cardiac function, provokes torsade de pointes

52
Q

what is the MOA of dofetilide?

A
  • blocks rapid component of the delayed rectifier potassium current- effect is more pronounced at lower heart rates.
53
Q

What antiarrhythmic clas 3 drug is eliminated by the kidney and a very narrow therapeutic window and thus dose needs to be adjusted based on creatinine clearance.

A

Dofetilide

54
Q

what is the indication for dofetilide?

A

Converts AF to sinus rhythm and maintain sinus rhythm after cardioversion

55
Q

what AE is associated with Dofelitide?

A

QT interval prolongation and increased risk of ventricular arrhythmias

56
Q

what are cardioactive CCB (class 4 antiarrhythmic) used for?

A
  • prevention of paroxysmal SVT

- rate control in AF and atrial flutter

57
Q

what adverse effects are associated with CBB’s used as antiarrhythmics?

A
  • negative inotrophy
  • AV block
  • SA node arrest
  • bradyarrhythmias
  • Hypotension
    _ constipation (verapamil)
58
Q

What is the MOA for adenosine?

A
  • Activates K current and inhibits Ca and funny currents, causing marked hyperpolarization and suppression of action potentials in pacemaker cells.
  • inhibits AV conduction and increase nodal refractory period
59
Q

What is adenosine used for?

A

conversion to sinus rhythm in Paroxysmal SVT

60
Q

What AE are associated with adenosine?

A
  • SOB
  • Bronchoconstriction
  • chest burning
  • AV block
  • Hypotension
61
Q

what drugs or classes or drugs are known to cause long QT syndrome and torsade de pointes arrhytmias?

A
  • Antiarrhythmic drugs - classes 1A and 3 (amiodarone very rarely induces TdPs)
62
Q

Digoxin induced arrhthmias (tachy and ectopic rhythms) is a type of triggered activity resulting from delayed afterdepolarization which occurs during phase_1_ , as a result of increased cytosolic 2 due to it’s overload. This overload is primarily spontaneous release of 3 from SR which activates 4 exchange leading to a net depolarizing current.

A
  1. 4
  2. Ca++
  3. Ca++
  4. 3Na/Ca
63
Q

Explain the mechanism of digoxin-induced bradyarrhythmia

A

Central parasympathominetic activity and accentuation of vagal effects on the heart

64
Q

How is digoxin-induced arrhythmias treated?

A

Cancel digoxin
anti-digoxin ab (digibind, digifab)
- K supplement to upper normal levels

65
Q

Both sotalol and esmolol are beta blockers but they are in different categories of antiarrhythmic drugs. which one is known to prolong QT interval?

A

Sotalol. It’s a K channel blocker and thus prolong AP duration and AT interval on ECG and prolongs refractory period.

66
Q

Slowing of atrioventricular conductivity is likely done by diltiazem or nifedipine?

A

Diltiazem

67
Q

Pt develops sinus bradycardia, what drug is known to be safe and effective in normalizing HR in these type of patients?

A

Atropine

68
Q

With the use of quinidine, indicate what changes are seen in:
A. PR interval
B. QRS interval
C. QT interval

A

A. slight decrease (quinidine is known to have antimuscarinic effect thus enhance AV conductance)
B. moderate increase
C. greater increase.

69
Q

A pt with afib has a rate of 280/min with a ventricular rate of 140 with a 2:1 nodal transmission. After tx with a drug the atrial rate slowed to 180 but the ventricular rate also increased to 180. Which drug was most likely given?

A

Disopyramide (class 1A)

Cardiovascular Med II Final (9 decks)

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