Antiarrhythmic Drugs- Nordgren Flashcards by Alisha Lindberg

What ion causes depolarization (phase 0 of AP) in atrial, purkinje, and ventricular cells?

Na+ current

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What ion causes depolarization (phase 0 of AP) in SA and AV nodal cells?

Ca2+ current

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Describe the different phases of Na channel positions

Resting = activation gate closed, inactivation gate open

Activated = both gates open

Inactivated= activation gate still open, but inactivation gate closes

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What causes repolarization in all cell types?

Efflux of K+

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Define refractory period

the time between phase 0 and sufficient recovery of Na+ channels in phase 3 to allow another action potential to occur

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What happens to Na channel recovery time at more positive (depolarized) membrane potential?

Recovery time will increase (it will be slower at more depolarized potentials)
Increases refractory period of cell

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What are the two mechanisms that can produce an arrhythmia?

Disturbances in impulse formation or impulse conduction

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Define State-Dependent Drugs

Bind readily to activated or inactivated channels
Phase 0 = activated
Phase 2 = inactivated
Bind poorly or not at all to rested channels

**Prevents drug binding in this state and/or promotes drug dissociation from receptors when channels become rested

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What are the three drugs in Class IA?

Quinidine
Procainamide
Disopyramide

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How does the action potential curve shift in response to drugs in Class IA?

Moderate decrease in slope of phase 0

Takes longer for repolarization (some effect on K+ channels)

Increase AP duration
Increase EFP
Increase QT interval

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What is a noted side effect of the drugs in class IA?

Increasing the QT interval can lead to torsades de point

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Specific side effect of procainamide?

Reversible SLE-like syndrome

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List the three drugs in Class IB

Mexiletine
Tocainide
Lidocaine

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How does the action potential curve shift in response to drugs in class IB?

Slightly decrease slope of phase 0
Quickens repolarization (opens K+ channels)

Decreases AP duration
Decrease ERP
Shortens QT interval

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Which of the class I subytpes is best for ventricular arrythmias post MI?

Class IB

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List the three drugs in Class IC

Flecainide
Propafenone
Moricizine

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How does the action potential curve shift in class IC?

Drastically decreases slope of phase 0

No effect on refractory period or duration of action potential

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What are the three components of rhythm?

Rate of impulse
Site of origin
Conduction (transport) of impulse

What can cause an early afterdepolarization?

Early afterpolarization occurs DURING the action potential and interrupts orderly repolarization of myocytes.

Caused by

opening of more Ca2+ channels in late phase 2
Opening of Na+ channels in early phase 3
Inhibition of K+ channels

What can cause delayed afterdepolarization?

Occurs AFTER action potential, when nearly or fully repolarized but before another action potential would normally occur. Can be caused by:

Elevated cytoslic Ca2+ levels -> overload of SR causes spontaneous release of Ca2+ and leads to depolarizing current

Are early afterdepolarizations exacerbated at fast or slow HRs?

Slow HRs

Are delayed afterdepolarization exacerbated at fast or slow HRs?

Fast HRs

Increased HR -> increased intracellular Ca2+ -> overload of SR causes spontaneous release of Ca2+ and leads to a depolarizing current

Procainamide

Class IA
Induction of torsades de points
Long term use can cause SLE-like syndrome

Quinidine

Class IA

Torsade de pointes

Disopyramide

Class IA | Loading dose NOT reccommended because of risk of percipitating heart failure

Lidocaine

Class 1BUsed for prevention of ventricular fibrillation AFTER cardioversion in the setting of acute ischemia. Prophylactic use may actually increase totally mortality → DO NOT DO IT!

Mexiletine

Class IBSignificant efficacy in relieving chronic pain, especially due to diabetic neuropathy and nerve injury (off-label use)

Flecainide

Class IC Drastically decreases slope of phase 0, Potent blocker of Na+ and K+ channels with SLOW UNBLOCKING KINETICS (but does not prolong the AP or QT-interval)

Propafenone

Class IC | Weak B-blocking activity

Amiodarone

Class III K+ blockerToxicity = bradycardia and heart block in patients w/ pre-existing SA or AV node disease • Drug accumulates in tissues → DOSE RELATED PULMONRY TOXICITY!!!!

Dofetilide

Class III K+ blocker | Contraindicated in long QT, bradycardia, hypokalemia

Ibutilide

Class III K+ channel blocker but also slow inward Na+ activator - delays repolarization

Verapail

Class IV Ca+ channel blocker Blocks both activated and inactivated L-type Ca2+ channels, so greater affect in tissue that fires frequently, those less polarized, or nodal tissue. Contraindicated in WPW

Nitroglycerine

synergistic hypotension with phsophodiesterase type 5 inhibitors such a Vardenafil (Viagra, Cialis, Levitra)

What are the three drug classes used for angina?

Nitrates- venodilation Ca2+ Channel blockers - decrease HR and contractility B-Blockers- decrease HR, BP and contractility

How do Class IA drugs effect an EKG?

Increase QT interval, Increase QRS duration

How do class IB drugs effect an EKG?

Decrease QT in Purkinje Cells

How do class IC drugs effect an EKG?

Slight increase in PR interval (effect on AV nodal cells) | Increase QRS duration

What do Propranolol and Esmolol do to EKG?

Increase PR interval (because they block calcium currents to increase length of phase 4 in Pacemaker cells)

What does Amiodarone do to EKG?

Increases PR, Increases QRS, Increases QT | Note: Amiodarone is also a sodium channel blocker, calcium channel blocker, and weak beta blocker!

Ibutilide and Dofetilide effect on EKG?

Increase QT interval (only block K+)!

Sotalol effect on EKG?

Increase PR and Increase QT

Adenosine effect on EKG?

Increases PR (adenosine suppress L type calcium channels in nodal tissue).