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πŸ„ΌπŸ’Š CARDIO PATH/RX > pharm: 10-12 Antiarrhythmias Drugs > Flashcards

pharm: 10-12 Antiarrhythmias Drugs Flashcards

1
Q

Procainamide

A: Mechanism (2)

B: Effect (4)

C: Antiarrhythmia Class

A

A: Blocks [Na+ Phase 0] and K+ channels

B:

  • Slow upstroke of AP and conduction
  • Prolongs QRS complex
  • Direct depressant actions on [SA/AV nodes]
  • use/state-dependent

C: [Class 1A]

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2
Q

Procainamide

A: Clinical Application (2)

B: Route of Admin (3)

C: Metabolized into ______ and is eliminated by ______

A

A:

*[Atrial Arrhythmias]

*[2nd choice for Ventricle Arrhythmias after acute MI]

B: PO / IV / IM

C: Metabolized into NAPA and eliminated via RENAL

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3
Q

Procainamide

Side Effects (3)

B: How is Quinidine related to Procainamide?

A
  • Torsades des pointes,
  • hypOtension
  • Anticholinergic effects

B: Similar to Procainamide AND SAME CLASS but with stronger anticholinergic effects. Rarely used due to cardiac and other (HA/tinnitus) adverse effects.

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4
Q

A: How is DISOPYRAMIDE related to Procainamide?

B: Effects (2); What does this require to work?

C: Adverse Effects (3)

D: Indication

A

A: Similar to Procainamide but anticholinergic effects >> Procainamide and Quinidine,

B: Its Anti-cholinergic effects INC [sinus rate and AV conduction] but requires co-administration of drugs that slow AV conduction.

C:

*Negative inotropic effects,

*may induce heart failure.

*extra-cardiac side effects from atropine-like actions.

D: Approved only for ventricular arrhythmias, Not drug of 1st or 2nd choice

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5
Q

A: Class 1 Antiarrhythmic Drugs are _______ that have a ______ action

B:

  • Name the 3 Subtypes
  • Describe their rate of kinetics
  • Effect on action potential
A

A: Class 1 Antiarrhythmic Drugs are [Na+ Channel Blockers] that have a [local anesthetic] action

B: 3 Subtypes

1A: Intermediate kinetics and [prolongs action potential]

1B: FAST kinetics and [DEC action potential duration]

1C: Slow kinetics and [NO EFFECT ON ACTION POTENTIAL]

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6
Q

Lidocaine

A: Mechanism

B: Effect (2)

C: Antiarrhthymia Class

A

A: [Na+ Phase 0 Blocker] w/[Use-state dependent action]

B:

  • Generally no effect on overall conduction (since recovery from block occurs between action potential).
  • Selective depression of conduction in [depolarized ischemic cells] (Na+ channels can’t be in RESTING state)

C: [Class 1B]

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7
Q

Lidocaine

A: Indication (2)

B: route of admin for Arrhythmias

C: Metabolization

D: Side Effects (3)

A

A:

  • [ventricular arrhythmias after MI].
  • [1st choice - [Vtach and fib] after cardioversion in the setting of ischemia/infarction]

B: IV ONLY in Arrhythmias

C: First Pass-Hepatic metabolism

D:

(x) Least cardiotoxic in Class 1
(x) Neurological SE from local anesthetic properties
(x) hypOtension with large doses

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8
Q

Mexiletine

A: _____ Active _____ analog!

B: Adverse Effects

C: Indications (3)

A

A: Orally Active Lidocaine analog! (is also Class 1B)

B: SE similar to Lidocaine

C:

  • Chronic Pain
  • Diabetic Neuropathy
  • Nerve Injury
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9
Q

Flecainide

A: MOA

B: Effect on Action Potential (2)

C: Indication (2)

A

A: [Na+ and K+ channel] blockade

B:

  • K+ blocker but has NO EFFECTS ON ACTION POTENTIAL DURATION
  • No Anticholinergic Effects

C:

  1. [Supraventricular Arr in pt with normal hearts]
  2. Maintains NSR
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10
Q

Flecainide

  • A: Elimination (2)*
  • B: Contraindications (3)*
  • C: Antiarrhythmia class*
A

A: Liver and Kidney

B: patients with..

  • ventricular tachyarrhythmias,
  • ventricular ectopy
  • previous MI

C: [Class 1C]

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11
Q

Propafenone

A: MOA (2)

B: Structural similarity to _____ but with weak______ activity.

C: Indication

D: Adverse effects (4)

A

A: [Class 1C] Potent blocker of Na+ channels, / may also block K+ channels.

B: Structural similarity to propanolol with weak Ξ²-blocking activity.

C: Used for [supraventricular arrhythmias] in patients with otherwise normal hearts.

D: Adverse effects/toxicity:

  • sinus bradycardia (from Ξ²-blockade).
  • bronchospasm (from Ξ²-blockade).
  • Metallic taste
  • constipation.
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12
Q

Propranolol

A: MOA

B: Effect (4)

A

A: [Class 2 General Ξ²-blocker]

B:

  • inhibits sympathetic influences on cardiac electrical activity.
  • DEC heart rate by DEC pacemaker currents (SA node automaticity)
  • reduces conduction
  • decreases [catecholamine induced DAD] and [EAD mediated arrhythmias]
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13
Q

Propranolol

B: Adverse Effects (5)

C: Contraindications

D: How is it related to DM pts?

A

B:

(x) Bradycardia
(x) DEC excercise capacity
(x) Heart Failure
(x) hypOtension
(x) AV Block

C:

*Pulmonary Dz Pts

*Pts with bradycardia or AV Block

D: May mask tachycardia associated with hypOglycemia in diabetic patients

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14
Q

Amiodarone

A: MOA (4)

B: Effect (3)

C: Antiarrhthymia Class

A

A: β€œAmy BLOCKED the NBC-K channel”

[Blocks Na+ / Beta receptors / Ca+ / K+ channels]

B:

  • Prolongation of action potential duration (QT interval) by prolonging refractoriness
  • slows conduction (prolongs QRS)–> suppresses abnormal automaticity
  • can slow normal sinus automaticity.

C: [Class 3]

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15
Q

Amiodarone

A; Indication (Oral vs. IV)

B: Adverse Effects (5)

C: Explain how it is related to Thyroid problems (2)

A

A: Oral: [Recurrent VTach or Fib that’s resistant to other drugs] and afib

  • IV*:
  • [1st choice-out of hospital Cardiac Arrest]
  • Termination of VTach or VFib

B:

  • Highly lipophilic–> accumulation in several organs (heart, lung, liver, cornea).
  • Bradycardia and heart block in patients with SA/AV node disease.
  • Pulmonary and hepatic toxicity,
  • photodermatitis,
  • cornea microdeposits.

C: Structural analogue of thyroid hormone–>blocks conversion of T4 to T3,

-source of inorganic iodine: Hypo- and hyperthyroidisms

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16
Q

Describe What the Antiarrhythmia Classes below are

A: Class 1 (A vs. B vs. C)

B: Class 2

C: Class 3

D: Class 4

D2: What sites do Class 4 act? (3)

A

” Nervous Barry Protects Carrie β€œ

Class 1: Na+ channel Blockers (A vs. B vs. C)

Class 2: Beta Blockers

Class 3: Prolongs action potential duration typically as a K+ channel blocker

Class 4: [Ca+ L-type channel blockers - Non-Dihydropyridine]

[Vascular smooth m. / cardiac myocytes / SA-AV Node]

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17
Q

Dronedarone is a _____ analogue of Amiodarone

A: What is the differences and what was it desinged for?

B: Indications (2)

C: Contraindications

A

A: Structural analogue of amiodarone but without iodine atoms,. Designed to eliminate effects on thyroxine metabolism.

B: Indications: atrial fibrillation/flutter.

Contraindicated in severe or recently decompensated symptomatic heart failure.

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18
Q

Sotalol

A: MOA (2)

B: Indications (2)

C: Antiarrhthymic Class

A

A:

  1. [General Ξ²-blocker] (L-isomer only)
  2. inhibits delayed rectifyer and possibly other K+ currents

B: Indications:

  • [Ventricular and supraventricular arrhythmias].
  • [Maintenance of sinus rhythm in patients with afib]

C: Class 3

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19
Q

Verapamil

A: MOA

B: Effect (3)

B2: Which tissue does it affect most?

C: Clinical Application (3)

A

A: blocks activated and inactivated [L-Type Ca+ channels] in the heart

B:

  • [Directly slows AV node conduction] and [increases AV node refractoriness],
  • slows SA node automaticity.–> Lowers heart rate and INC PR-interval
  • Use/state-dependent action.

B2: Major effects in slow- response tissues- (i.e. SA/AV node).

C:

  1. [1st choice- Supraventricular arrhythmias]
  2. Re-entry arrhythmias/tachycardias involving AV node.
  3. Slows ventricular rate in atrial flutter/fib
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20
Q

Verapamil

A: Antiarrhythmic Class

B: Metabolism

C: Adverse Effects (8)

A

A: Class 4

B: Extensive Hepatic –> can cause Liver Dysfunction

C: β€œ Verapamil has HORRIBLE PLANCH!”

  • Vasodilation after IV injection
  • Negative inotropic effects–> CHF
  • hypOtension and fib in Vtach or [L vt dysfunction] pts
  • Heart block with pt on b-blockers
  • AV block in pts with nodal dz or high dose (tx w/atropine or beta blockers)
  • Lassitude (lack of energy)
  • Peripheral Edema
  • Constipation
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21
Q

A: How is Diltiazem compared to Verapamil

B: Additional uses of Diltiazem (3)

C: Antiarrhythmic class of Diltiazem

A

Similar to Verapamil but with lower cardioselectivity,

B: used also for

  • HTN
  • Angina
  • Exercise Tolerability INCREASE by [decreasing angina freq. and myocardial demand]

C: Class 4

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22
Q

ADENOSINE

A: MOA (2)

B: Antiarrhythmic Class

C: What tissue does it mainly act? What compound is it similar in action to?

A

A: Increases K+ conductance (hyperpolarization) and inhibits [camp-Ca+ currents] both via purinergic receptors

B: NO CLASS

C: Atrial ; Action similar to ACh

23
Q

MAGNESIUM

A: MOA (2)

B: Antiarrhythmic Class

A

A: Inhibits [Na+,K+-ATPase] and [Na+/ K+/ Ca+ channels]β€”> alters membrane surface charge

B: NO CLASS

24
Q

POTASSIUM

A: MOA (HYPER vs. hypOkalemia)

B: Antiarrhythmic Class

A

A:

  • Hyperkalemia; depolarizes resting membrane potential
  • Hypokalemia; decreases K+ permeability

B: NO CLASS

25
Q

[DIGITALIS CARDIAC GLYCOSIDE]

A: MOA

B: Antiarrhythmic Class

A

A:Inhibit [Na+/K+-ATPase], β€”> affects Na+- Ca++ exchange, increase intracellular Ca++

B: NO CLASS

26
Q

ADENOSINE

Effect (2)

A
  • Primarily acts on atrial tissues,
  • slows AV node conduction and increases AV node refractorinessβ€”> produces transient cardiac arrest
27
Q

MAGNESIUM

Effect (2)

A
  • Anti-arrhythmic effects in some patients with normal Mg+ levels.
  • May inhibit afterdepolarizations.
28
Q

POTASSIUM

Effect (HYPER vs. hypOkalemia)

A
  • Hyperkalemia–> slows conduction (may lead to re-entrant arrhythmias and AV nodal block).
  • Hypokalemiaβ€”>enhances ectopic automaticity, lengthens action potential duration which can lead to EADs (torsades de pointes).
29
Q

[DIGITALIS CARDIAC GLYCOSIDES]

Effect (2)

A
  • Positive inotropic actions (used widely in heart failure)
  • Parasympathomimetic effects: increase AV nodal refractoriness and slow AV node conduction.
30
Q

MAGNESIUM

  • A: Indication (2)*
  • B: Route of Admin*
A
  • Digitalis induced arrhythmias with hypOmagnesemia
    • torsade des pointes potential tx

B: IV

31
Q

POTASSIUM

  • A: Indication*
  • B: Route of Admin (2)*
A
  • Maintain normal plasma K+

B: IV or PO

32
Q

ADENOSINE

Indication

A
  • Converts [paroxysmal supraventricular tachycardia] to sinus rhythm
33
Q

[DIGITALIS CARDIAC GLYCOSIDES]

Indication (2)

A
  • Atrial arrhythmias (atrial flutter/afib).
  • In (atrial flutter/afib) parasympathomimetic effects slow AV nodal conduction,β€”->slows excessively high ventricular rates.
34
Q

ADENOSINE

  • A: Route of Admin*
  • B: Deactivating factors*
  • C: Potentiating factors*
  • D: Adverse Effects (2)*
A

A: Rapid IV bolus (initially 6 mg)

B: Theophylline/Caffeine

C: Dipyridamole

D:

  • Flushing
  • SOB
35
Q

[DIGITALIS CARDIAC GLYCOSIDES]

A: Elimination by the ______ with a______ therapeutic window.

B: drug interactions (3)

B2: Which conditions enhance toxic effects? (2) .

C:Adverse Effects (4)

D: How do you Reverse Severe digitalis toxicity

A

A: Eliminated by the kidney with a Narrow therapeutic window.

B: Many drug interactions (amiodarone, verapamil, flecainide)!!! B2: Hypokalemia/magnesemia enhance toxic effects.

C:

  • Loss of appetite
  • visual disturbances (yellow-green),
  • drowsiness/depression.
  • Development of arrhythmias (DAD).

D: Severe digitalis toxicity can be reversed by digoxin antibodies.

36
Q

What is the primary determinant of the ventricular muscle refractory period?

A

Action Potential Duratioin (Phase 2) (QT)

37
Q

A: hypOkalemia and Acidosis can each cause what change to the SA Node?

B: EAD usually occurs at ____ HR from the _______

C: DAD usually occurs at ____ HR from the _____

A

A: Disturb Impulse Formation and cause premature stimulation –> INC HR

B: EAD (early afterdepolarization) usually occurs at SLOW HR from the [Phase 2 Plateau]

C: DAD (Delayed afterdepolarization) usually occurs at FAST HR from the Resting Potential

38
Q

4 Main Ways Antiarrhythmic Drugs can treat Arrhythmia in the [SA/AV node]

A
  1. Reduction of phase 4 slope
  2. Increase [max. Resting Potential]
  3. Increase of threshold potential
  4. Increase of action potential duration
39
Q

Explain what [Use-dependent or state-dependent] drug action actually means

B: Example (2)

C: Why should tx of asymptomatic or minimally symptomatic arrhythmias DISCOURAGED AGAINST?

A

channels used frequently or inactivated are more susceptible to being blocked! ,

B: e.g.

  • during fast tachycardia (many channel activations/inactivations)
  • [ischemic /infarcted tissues due to more positive resting potentia]
  • β€œAntiarrhythmics are better acting when the M-Lid is up frequently”*

C: Antiarrhythmics CAN STILL ACT ON NORMAL Cells with β€œRESTING” Na+ channel M-Lids! β€”> Drug induced Arrhythmia!

40
Q

A: How do Antiarrhythmic Class 1: [Na+ channel Phase 0 blockers] work? (2)

B: Name the 3 [Class 1 Antiarrhythmics] that actually INC Action Potential Duration

A
  • Reduce Conduction Velocity by DEC rate and magnitude of [Phase 0 Fast Action Potential Upstroke]
  • May also affect K+ channels β€”> Prolonged Repolarization β€”> Prolonged Action Potential Duration

B: Procainamide / Quinidine / Disopyramide

41
Q

A: What is NAPA?

B: Antiarrhythmic Class

C: Elimination (2)

D: Adverse Effects (3)

A

A: Metabolite from [Class 1 Procainamide]

B: Is actually Class 3! and

C: eliminated via Liver and Kidney(requires dose reduction in renal failure )

D:

  • hypOtension
  • Torsade De pointes
  • Lupus Erythematosus with long term usage!
42
Q

A: Which 3 Antiarrhthymic drugs cause [EKG: QT Prolongation]?

B: Why (what class)?

C: This Antiarrhthymic class works better with which Heart Rate (fast vs slow)?

A

A: Amiodarone / Dronedarone / Sotalol

B: These are CLASS 3 - Antiarrhythmics –> Prolongs Action Potential Duration as a K+ channel Blocker

C: WORKS BETTER WITH SLOW HR (even tho this may cause Torsades De Pointes)

43
Q

Non-Pharmacologic Anti-Arrhythmic Therapies

Radiofrequency ablation / Cryoablation

A: MOA

B: Indication

A

Radiofrequency ablation / Cryoablation

A: interrupts reentrant / accessory pathway

B: used frequently to replace anti-arrhythmic drug therapies

44
Q

Non-Pharmacologic Anti-Arrhythmic Therapies

Electrical cardioversion​

Indications (2)

A
  • atrial fibrillation
  • ventricular tachycardia and fibrillation
45
Q

Non-Pharmacologic Anti-Arrhythmic Therapies

Implantable Cardioverter Defibrillator (ICD)

Indication

A

vFib

46
Q

Non-Pharmacologic Anti-Arrhythmic Therapies

Vagal Maneuver

A: Examples (3)

B: MOA

C: Indication

A

Vagal maneuvers

A: carotid sinus message, [diving reflex (cold water on face)], [Valsalva maneuver].

B: slows conduction through AV node.

C: Acute treatment for paroxysmal supraventricular tachycardia (PSVT)

47
Q

Drugs used for Conversion to sinus Rhythm? (3)

A

β€œAdele and Ami converted me to Flex”

Adenosine / Amiodarone/ Flecainide

48
Q

Drugs used for Maintenance of sinus rhythm (4)

A

β€œMaintain ur F-PAD man”

Amiodarone / Dronedarone / Flecainide / Propafenone

49
Q

Drugs used for Ventricular Rate Control (4)

A

” V EDP”

Diltiazem/Verapamil / Propranolol/Esmolol

50
Q

Which Drugs for:

Ventricular tachycardia in patients without heart disease (2)

A

β€œUr having VTach without Heart Dz..? Go to LA”

Lidocaine

Amiodarone

51
Q

Which Drugs for:

AV Block (2)

A

Atropine

Pacemaker

52
Q

Which Drugs for:

aFib (3)

A

Diltiazem/Verapamil / Propranolol

53
Q

Which Drugs for:

VENTRICULAR FIBRILLATION!

A

Defibrillation with or without [Amiodarone or Lidocaine]

54
Q

Propranolol

Indications (6)

A

” Propranolol uses VARAMA cream β€œ

  1. Vt Rate Control
  2. Atrial arr
  3. Reinfarct POST MI tx
  4. AfterDepolarization (EAD/DAD) tx
  5. Maintains Sinus Rhythm
  6. AV Nodal Re-entry tx

πŸ„ΌπŸ’Š CARDIO PATH/RX (22 decks)

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