How many classes of antiarhythmic drugs are there?

What are the classes?

4

- Class 1(A, B, C): sodium channel blockers

- Class II: B blockers

- Class III: potassium channel blockers

- Class IV: calcium channl blockers

What phase does fast sodium channels open -> Na enters cell?

What phase does slow calcium channels open -> Ca enters cell?

What is the voltage that calcium channels open?

What phase does potassium channels open -> K exits cell?

What happns duing phase 3?

[image]

Phase 0

Phase 2

-40 mV

Phase 3

Repolarization

What does the P wave indicate?

What does the PR interval indicate?

What does the R wave indicate?

What does the t wave indicate?

What does the QT interval indicate?

[image]

Arial depolarization

Time required to conduct AP thru atria & AV node

Ventricular depolarization

Ventricular repolarization

Duration of ventricular AP

1) Acute myocardial infarctions (heart attack)

2) Anesthetized patient

3) Digitalis/Congestive heart failure

What are the 2 major causes of arrhythmias?

1) Abnormal automaticity (spontaneous AP\depolarization of phase 4)

2) Abnormal impulse conduction -> retrograde conduction from block or reentry

What is the treatment of abnormal automaticity? 2

What is the treatment of abnormal impulse conduction? 2

- Decrease slope of phase 4 -> harder to depolarize

- Raise treshold

- Slow conduction

- Increase refractory period

What are the 3 changes in potential that cause arrhythmias?

 [image]

1) Slope of phase 4 increases

2) Threshold potential is more negative

3) Maximum diasolic potential is more positive

- Early afterdepolarization

- Late afterdpolarization

1) Unidirectional block -> retrograde conduction

2) Reentry of ventricular tissue

What drugs cause arrhythmias?

What are the general effects of antiarrhythmic drugs at regular doses?

What are the effects of antiarrhythmic drugs at higher doses?

Every drug can

- Surpress ectopic automaticity (premature atrial contractions)

- Surpress abnormal conduction

- Depress conduction

- Product drug induced arrhythmias

What do class I drugs target?

What states do they work on?

What phase in the action potential does it affect?

Why?

Sodium channel blockers

Open & inactive state

Phase 0

Because that is when sodium channels are open to enter the cell

- QUINIDINE

- Disopyramide (Norpace)

- Procainamide (Pronestyl)

- Open

- Inactive

What phases do class IA drugs effect?

What effect do they have on the AP?

What is their rate of dissociation?

- Phase 0

- Phase 3

Lengthen AP

Slow

What cells do class 1A effect the most?

Why?

Rapidly firing cells

Na channels are open more/longer than normal cells

- Tachyarrhythmias

- Reentry

- SA/AV block

- Arrhythmogenic (causes arrhythmias)

Why is Quinidine not used for long term management of patients?

What is quinidine metabolized by?

What is the preffered usage of quinidine?

- Reduces survival

- Narrow thereputic window between appropriate does & arrhythmiagenic dose

Cytochrome P450

Acute treatment of arrhythmias

- LIDOCAINE

- Mexilentine (Mexitil)

What phase does 1B/Lidocaine effect?

How does 1B/Lidocaine effect the AP?

Phase 3

Shortens duration of AP

- Ventricular arrhythmias after MI

- Blocking reentry

- Arrhythmogenic

- Some CNS (numbness & tingling -> seisures)

What type of channels do class 1C drugs target?

Sodium channels (blocker)

- Flecainide (Tambocor)

- Propafenone (Rhythmol)

What is the rate of dissociation of class 1C drugs?

What type of cell do they affect the most (firing)?

VERY SLOW

Normally firing cells

- Arrhythmogenic

- Aggravates CHF by decreasing force of contraction

What drugs shifts the AP this way?

[image]

What drugs shifts the AP this way?

[image]

What drugs shifts the AP this way?

[image]

- PRORANOLOL (Inderal)

- Esmolol (Brevibloc)

- Metoprolol (Lopressor)

What phase do class II drugs effect?

What is their major effect?

Phase 4

Decreases HR

- Prolong life in people w arrhythmias

- Tachyarrhythmias

- Reduces mortality after MI

- Slow cardiac reduction

- Reduce cardiac remodeling

- Reduce release of renin -> decrease angiotensis II

What type of channels do class III drugs effect?

How do class III drugs effect AP?

K channels (blocker)

Prolong AP duration

- AMIODARONE (Coradarone)

- Sotalol

What do toxic levels of class III drugs cause?

What does the EKG look like?

- Arrythmias

Torsade de pointes (polymorphic tachycardia): twisting of the points

What type/class drug shifts the AP this way?

[image]

What class drug is Amiodarone?

What are the effects of amiodarone toxicity?

Class 3

- Bradycardia

- Heart block

- Heart failure

- PULMONARY FIBROSIS

- Verapamil

- Diltiazem (Cardiezem)

What AP phase do class IV drugs effect?

How do class IV drugs effect conduction?

Phase 4: slows depolarization

Slows AV node conduction

- Open

- Resting

- Atrial dysrhythmias

- Control reentry

- Hypotension

- Aggravate CHF

- Heart block

- Negative inotropic effect

- Adenosine (Adenocard)

- Magnesium sulfate

- Enhances K conductance

- Inhibits cAMP induced Ca influx

- Paroxysmal supraventricular tachycardia

- Only used in emergencies: chemical defib

- Control seizures in preeclampsia & eclampia

- Cardiac glycoside-induced arrhythmias

- Polymorphic ventricular tachycardia

- Propranolol (class II)

- Verapamil (class IV)

- Propranolol (class II)

- Verapamil (class IV)

- Epinephrine

- Lidocaine