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

A: Liver and Kidney B: patients with.. ventricular tachyarrhythmias, ventricular ectopy previous MI C: [Class 1C]

pharm: 10-12 Antiarrhythmias Drugs Flashcards by Brian McCalister

Procainamide

A: Mechanism (2)

B: Effect (4)

C: Antiarrhythmia Class

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

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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Procainamide

A: Clinical Application (2)

B: Route of Admin (3)

C: Metabolized into ______ and is eliminated by ______

*[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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Procainamide

Side Effects (3)

B: How is Quinidine related to Procainamide?

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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A: How is DISOPYRAMIDE related to Procainamide?

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

C: Adverse Effects (3)

D: Indication

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.

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

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

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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Lidocaine

A: Mechanism

B: Effect (2)

C: Antiarrhthymia Class

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

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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Lidocaine

A: Indication (2)

B: route of admin for Arrhythmias

C: Metabolization

D: Side Effects (3)

[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

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

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Mexiletine

A: _____ Active _____ analog!

B: Adverse Effects

C: Indications (3)

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

B: SE similar to Lidocaine

Chronic Pain
Diabetic Neuropathy
Nerve Injury

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Flecainide

A: MOA

B: Effect on Action Potential (2)

C: Indication (2)

A: [Na+ and K+ channel] blockade

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

[Supraventricular Arr in pt with normal hearts]
Maintains NSR

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Flecainide

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

A: Liver and Kidney

B: patients with..

ventricular tachyarrhythmias,
ventricular ectopy
previous MI

C: [Class 1C]

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Propafenone

A: MOA (2)

B: Structural similarity to _____ but with weak______ activity.

C: Indication

D: Adverse effects (4)

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

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

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

D: Adverse effects/toxicity:

sinus bradycardia (from β-blockade).
bronchospasm (from β-blockade).
Metallic taste
constipation.

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Propranolol

A: MOA

B: Effect (4)

A: [Class 2 General β-blocker]

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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Propranolol

B: Adverse Effects (5)

C: Contraindications

D: How is it related to DM pts?

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

*Pulmonary Dz Pts

*Pts with bradycardia or AV Block

D: May mask tachycardia associated with hypOglycemia in diabetic patients

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Amiodarone

A: MOA (4)

B: Effect (3)

C: Antiarrhthymia Class

A: “Amy BLOCKED the NBC-K channel”

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

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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Amiodarone

A; Indication (Oral vs. IV)

B: Adverse Effects (5)

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

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

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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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)

” Nervous Barry Protects Carrie “

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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Dronedarone is a _____ analogue of Amiodarone

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

B: Indications (2)

C: Contraindications

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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Sotalol

A: MOA (2)

B: Indications (2)

C: Antiarrhthymic Class

[General β-blocker] (L-isomer only)
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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Verapamil

A: MOA

B: Effect (3)

B2: Which tissue does it affect most?

C: Clinical Application (3)

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

[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).

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

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Verapamil

A: Antiarrhythmic Class

B: Metabolism

C: Adverse Effects (8)

A: Class 4

B: Extensive Hepatic –> can cause Liver Dysfunction

C: “ 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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A: How is Diltiazem compared to Verapamil

B: Additional uses of Diltiazem (3)

C: Antiarrhythmic class of Diltiazem

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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ADENOSINE

A: MOA (2)

B: Antiarrhythmic Class

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

Study These Flashcards

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

B: NO CLASS

C: Atrial ; Action similar to ACh

MAGNESIUM

A: MOA (2)

B: Antiarrhythmic Class

Study These Flashcards

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

B: NO CLASS

POTASSIUM

A: MOA (HYPER vs. hypOkalemia)

B: Antiarrhythmic Class

Study These Flashcards

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

B: NO CLASS

**[DIGITALIS CARDIAC GLYCOSIDE]** A: MOA B: Antiarrhythmic Class

A:Inhibit [Na+/K+-ATPase], ---\> affects Na+- Ca++ exchange, increase intracellular Ca++ B: **NO CLASS**

**ADENOSINE** *Effect (2)*

* Primarily acts on atrial tissues, * slows AV node conduction and increases AV node refractoriness---\> produces transient cardiac arrest

**MAGNESIUM** *Effect (2)*

* Anti-arrhythmic effects in some patients with normal Mg+ levels. * May inhibit afterdepolarizations.

**POTASSIUM** *Effect (HYPER vs. hypOkalemia)*

* Hyperkalemia--\> slows conduction (may lead to re-entrant arrhythmias and AV nodal block). * Hypokalemia---\>enhances ectopic automaticity, lengthens action potential duration which can lead to EADs (torsades de pointes).

**[DIGITALIS CARDIAC GLYCOSIDES]** *Effect (2)*

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

**MAGNESIUM** * A: Indication (2)* * B: Route of Admin*

* Digitalis induced arrhythmias with hypOmagnesemia * * torsade des pointes **potential** tx B: IV

**POTASSIUM** * A: Indication* * B: Route of Admin (2)*

* Maintain normal plasma K+ B: IV or PO

**ADENOSINE** *Indication*

* Converts [paroxysmal supraventricular tachycardia] to sinus rhythm

**[DIGITALIS CARDIAC GLYCOSIDES]** *Indication (2)*

* Atrial arrhythmias (atrial flutter/afib). * In (atrial flutter/afib) parasympathomimetic effects slow AV nodal conduction,----\>slows excessively high ventricular rates.

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

A: **Rapid** IV bolus (initially 6 mg) B: Theophylline/Caffeine C: Dipyridamole D: - Flushing - SOB

**[DIGITALIS CARDIAC GLYCOSIDES]** ## Footnote 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: 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.

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

Action Potential Duratioin (Phase 2) (QT)

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: **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

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

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

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**?

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] * "Antiarrhythmics are better acting when the **M-Lid** is up frequently"* C: Antiarrhythmics CAN STILL ACT ON NORMAL Cells with "RESTING" Na+ channel M-Lids! ---\> Drug induced Arrhythmia!

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

* Reduce Conduction Velocity by DEC rate and magnitude of [Phase 0 Fast Action Potential Upstroke] * May also affect K+ channels ---\> Prolonged Repolarization ---\> Prolonged Action Potential Duration B: Procainamide / Quinidine / Disopyramide

A: What is **NAPA**? B: Antiarrhythmic Class C: Elimination (2) D: Adverse Effects (3)

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!

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: 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)

_Non-Pharmacologic_ Anti-Arrhythmic Therapies **Radiofrequency ablation / Cryoablation** A: MOA B: Indication

Radiofrequency ablation / Cryoablation A: interrupts reentrant / accessory pathway B: used frequently to **replace** anti-arrhythmic drug therapies

_Non-Pharmacologic_ Anti-Arrhythmic Therapies **Electrical cardioversion** Indications (2)

- atrial fibrillation - ventricular tachycardia and fibrillation

_Non-Pharmacologic_ Anti-Arrhythmic Therapies **Implantable Cardioverter Defibrillator (ICD)** Indication

vFib

_Non-Pharmacologic_ Anti-Arrhythmic Therapies **Vagal Maneuver** A: Examples (3) B: MOA C: Indication

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)

Drugs used for Conversion to sinus Rhythm? (3)

"_Adele_ and _Ami_ *converted* me to _Flex_" Adenosine / Amiodarone/ Flecainide

Drugs used for **_Maintenance_** of sinus rhythm (4)

"Maintain ur **F**-**PAD** man" Amiodarone / Dronedarone / Flecainide / Propafenone

Drugs used for **V**entricular Rate Control (4)

" **V EDP**" Diltiazem/**V**erapamil / Propranolol/Esmolol

Which Drugs for: Ventricular tachycardia in patients without heart disease (2)

"Ur having VTach *without* Heart Dz..? Go to **LA**" **L**idocaine **A**miodarone

Which Drugs for: AV Block (2)

Atropine Pacemaker

Which Drugs for: aFib (3)

Diltiazem/Verapamil / Propranolol

Which Drugs for: VENTRICULAR FIBRILLATION!

Defibrillation with or without [Amiodarone or Lidocaine]

**Propranolol** Indications (6)

" Propranolol uses **VARAMA** cream " 1. **V**t Rate Control 2. **A**trial arr 3. **R**einfarct POST MI tx 4. **A**fterDepolarization (*EAD/DAD)* tx 5. **M**aintains Sinus Rhythm 6. **A**V Nodal Re-entry tx

pharm: 10-12 Antiarrhythmias Drugs Flashcards

(54 cards)