pharm: 10-12 Antiarrhythmias Drugs Flashcards
Procainamide
A: Mechanism (2)
B: Effect (4)
C: Antiarrhythmia Class
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]
Procainamide
A: Clinical Application (2)
B: Route of Admin (3)
C: Metabolized into ______ and is eliminated by ______
A:
*[Atrial Arrhythmias]
*[2nd choice for Ventricle Arrhythmias after acute MI]
B: PO / IV / IM
C: Metabolized into NAPA and eliminated via RENAL
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.
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.
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
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: 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]
Lidocaine
A: Mechanism
B: Effect (2)
C: Antiarrhthymia Class
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 canβt be in RESTING state)
C: [Class 1B]
Lidocaine
A: Indication (2)
B: route of admin for Arrhythmias
C: Metabolization
D: Side Effects (3)
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
Mexiletine
A: _____ Active _____ analog!
B: Adverse Effects
C: Indications (3)
A: Orally Active Lidocaine analog! (is also Class 1B)
B: SE similar to Lidocaine
C:
- Chronic Pain
- Diabetic Neuropathy
- Nerve Injury
Flecainide
A: MOA
B: Effect on Action Potential (2)
C: Indication (2)
A: [Na+ and K+ channel] blockade
B:
- K+ blocker but has NO EFFECTS ON ACTION POTENTIAL DURATION
- No Anticholinergic Effects
C:
- [Supraventricular Arr in pt with normal hearts]
- Maintains NSR
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]
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 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.
Propranolol
A: MOA
B: Effect (4)
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]
Propranolol
B: Adverse Effects (5)
C: Contraindications
D: How is it related to DM pts?
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
Amiodarone
A: MOA (4)
B: Effect (3)
C: Antiarrhthymia Class
A: βAmy BLOCKED the NBC-K channelβ
[Blocks Na+ / Beta receptors / Ca+ / K+ channels]
B:
- Prolongation of action potential duration (QT interval) by prolonging refractoriness
- slows conduction (prolongs QRS)β> suppresses abnormal automaticity
- can slow normal sinus automaticity.
C: [Class 3]
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 thatβs resistant to other drugs] and afib
- IV*:
- [1st choice-out of hospital Cardiac Arrest]
- Termination of VTach or VFib
B:
- Highly lipophilicβ> 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 hormoneβ>blocks conversion of T4 to T3,
-source of inorganic iodine: Hypo- and hyperthyroidisms
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)
β Nervous Barry Protects Carrie β
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]
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.
Sotalol
A: MOA (2)
B: Indications (2)
C: Antiarrhthymic Class
A:
- [General Ξ²-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
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
B:
- [Directly slows AV node conduction] and [increases AV node refractoriness],
- slows SA node automaticity.β> Lowers heart rate and INC PR-interval
- Use/state-dependent action.
B2: Major effects in slow- response tissues- (i.e. SA/AV node).
C:
- [1st choice- Supraventricular arrhythmias]
- Re-entry arrhythmias/tachycardias involving AV node.
- Slows ventricular rate in atrial flutter/fib
Verapamil
A: Antiarrhythmic Class
B: Metabolism
C: Adverse Effects (8)
A: Class 4
B: Extensive Hepatic β> can cause Liver Dysfunction
C: β Verapamil has HORRIBLE PLANCH!β
- Vasodilation after IV injection
- Negative inotropic effectsβ> 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
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
ADENOSINE
A: MOA (2)
B: Antiarrhythmic Class
C: What tissue does it mainly act? What compound is it similar in action to?
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
A: Inhibits [Na+,K+-ATPase] and [Na+/ K+/ Ca+ channels]β> alters membrane surface charge
B: NO CLASS
POTASSIUM
A: MOA (HYPER vs. hypOkalemia)
B: Antiarrhythmic Class
A:
- 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], β> 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 refractorinessβ> 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)
- Hyperkalemiaβ> 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).
[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,β->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]
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 β> 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]
- Reduction of phase 4 slope
- Increase [max. Resting Potential]
- Increase of threshold potential
- 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]
- βAntiarrhythmics are better acting when the M-Lid is up frequentlyβ*
C: Antiarrhythmics CAN STILL ACT ON NORMAL Cells with βRESTINGβ Na+ channel M-Lids! β> 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 β> Prolonged Repolarization β> 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 β> 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 cardioversionβ
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)
βAdele and Ami converted me to Flexβ
Adenosine / Amiodarone/ Flecainide
Drugs used for Maintenance of sinus rhythm (4)
βMaintain ur F-PAD manβ
Amiodarone / Dronedarone / Flecainide / Propafenone
Drugs used for Ventricular Rate Control (4)
β V EDPβ
Diltiazem/Verapamil / Propranolol/Esmolol
Which Drugs for:
Ventricular tachycardia in patients without heart disease (2)
βUr having VTach without Heart Dz..? Go to LAβ
Lidocaine
Amiodarone
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)
β Propranolol uses VARAMA cream β
- Vt Rate Control
- Atrial arr
- Reinfarct POST MI tx
- AfterDepolarization (EAD/DAD) tx
- Maintains Sinus Rhythm
- AV Nodal Re-entry tx
