Antiarrythmics (Cardio and Renal 2) Flashcards by G V

4 classes of Antiarrhythmics

Na+ Channels Blockers
Beta Blockers
K+ Channels Blockers
Calcium channel Blocker

1 & 3 - big guns for life threatening situations

2 and 4 - toy guns

How well did you know this?

Not at all

Perfectly

Antiarrhythmics: Miscellaneous Drugs

Adenosine
Digoxin
Magnesium Sulfate

How well did you know this?

Not at all

Perfectly

Heart Action Potentials - Phase 0

Depolarization

Increase Na+ current

How well did you know this?

Not at all

Perfectly

Heart Action Potentials - Phase 1

Overshoot
Initial repolarization inactivation of Na+ channel
Decrease K+

How well did you know this?

Not at all

Perfectly

Heart Action Potentials - Phase 2

Plateau
Increase Ca2+
Decrease K+ currents

How well did you know this?

Not at all

Perfectly

Heart Action Potentials - Phase 3

Repolarization

Decrease K+ current

How well did you know this?

Not at all

Perfectly

Heart Action Potentials - Phase 4

Resting potential

Maintained by Na+/K+ ATPase Pump

How well did you know this?

Not at all

Perfectly

Electrophysiological Properties of the Heart (1 of 4) - Responsiveness

Capacity of a cell to depolarize

Depends on the # of Na+ channels in ready state

How well did you know this?

Not at all

Perfectly

Electrophysiological Properties of the Heart (2 of 4) - Conductance

Rate of spread of an impulse (conduction velocity)

Depends on: Vmax, Threshold potential, and resting membrane potential

How well did you know this?

Not at all

Perfectly

Electrophysiological Properties of the Heart (3 of 4) - Automaticity

Ability to spontaneously depolarize

How well did you know this?

Not at all

Perfectly

Electrophysiological Properties of the Heart (4 of 4) - Refractoriness (Refractory HTN)

Inability to respond to a stimulus

How well did you know this?

Not at all

Perfectly

Electrophysiological Properties of the Heart - Refractoriness

Effective Refractory Period (ERP) - Period during which no stimulus of any size will produce a response (Arrhythmia: Decrease ERP -> formation of premature impulse)

Relative Refractory Period (RRP) - a STRONG impulse may elicit a response

Measuring Refractory: ERP / Action Potential Duration (APD)

Decreased ERP –> Formation of premature impulses

How well did you know this?

Not at all

Perfectly

The sodium channel exists in 3 states

Resting or ready state
Open or active state
Inactivated or refractory state

How well did you know this?

Not at all

Perfectly

The sodium channel is a voltage channel with 2 gates:

M (activating)

2. h (inactivating) gate

How well did you know this?

Not at all

Perfectly

Mechanism of Arrhythmia Formation: Abnormalities in impulse Formation

SA Node: Increase symp –> Tach

SA Node: increase parasym –> brady

Purkinje fibers

How well did you know this?

Not at all

Perfectly

Mechanism of Arrhythmia Formation: Abnormalities in impulse Conduction (2)

Ectopic foci

Re-entry mechanisms

How well did you know this?

Not at all

Perfectly

Mechanism of Arrhythmia Formation: Conduction block (A-V block) - 3 types

1st Degree - prolonged PR Interval (> .20 sec)

2nd Degree:
Mobitz I - Above AV node = intermittent failure of AV conduction
*PR lengthens before beat is dropped

Mobitz II - Unpredictable loss of AV conduction
      * Constant PR interval, but beats are dropped

3rd Degree - Failure of any impulses to be conducted from atria to ventricles
* Atria and Ventricle beat independently of each other (all over the place)

How well did you know this?

Not at all

Perfectly

Na+ channel Blockers Class 1A

Quinidine, Procainamide, and Disopyramide

Activated Na+ channel

Decrease Vmax, and prolong APD (Action Potential Duration)
- Slowing rate of AP, prolong AP, and increasing ventricular ERP

Na+ channel Blockers 1A: Quinidine

*Increase APD and ERP in atria, ventricles, and purkinje fibers of His –> Phase 0 Shortened

Anticholinergic effect: Increase heart rate and conduction

Alpha blocking effect: vasodilation and reflex tachycardia

Na+ channel Blockers 1A: **Quinidine Side Effects

GI: NVD

CV: Increase QT interval (Torsades de Pointes)

Thrombocytopenia

**Cinchonism: tinnitus, loss of hearing, GI upset, diplopia

Na+ channel Blockers 1A: Quinidine Drug Interactions

Antacids increase quinidine absorption

***Displaces digoxin from tissue binding sites

Decrease Vd

Na+ channel Blockers 1A: Procainamide

Less anticholinergic
No alpha blocking activity

Active metabolite NAPA –> Prolongs the duration of AP and little effect on max polarization of Purkinje Fibers

Na+ channel Blockers 1A: Procainamide Side Effects

Agranulocytosis (Order CBC if pt. comes in with cough with any med causing agranulocytosis)

SLE like syndrome

Na+ channel Blockers 1A: Disopyramide

The most anticholinergic –> *Greater anti-ionotropic effect

Na+ Channel Blockers: 1B MOA and Uses

Inactivated Na+ channel No effect on Vmax, but decrease APD Uses: Preference for ischemic tissues (partially depolarized) Increase threshold of VFib Slow conduction in hypoxic and ischemic tissue

Na+ Channel Blockers: 1B Drugs (3)

Lidocaine Tocainide Mexiletine

Na+ Channel Blockers 1B: Lidocaine (3)

1. Rx: V-Tac after MI, or digitalis toxicity 2. Least cardiotoxic 3. Shortens Phase 3 repols and decreases APD

Na+ Channel Blockers 1B: Mexiletine and Tocainide

Given orally Pulmonary toxicity (Pulmonar fibrosis)

Na+ Channel Blockers Class 1C MOA

Both Na+ Channels Marked decrease of Vmax, but no effect on APD

Na+ Channel Blockers Class 1C: Drugs

Flecainide, Propafenone, Moricizine Pro-arrhythmic effects: can worsen existing arrhythmia Increase in sudden death and cardiac arrest after MI

Class 2: Beta Blockers Drugs (4)

Propanolol Acebutalol Esmolol: half life of 8 minutes; given IV for emergency in SVT Metoprolol

Class 2: Beta Blockers MOA (3)

Decrease SA and AV nodal conduction Decrease the slope of phase 4 depolarization Used as prophylaxis Post-MI and to rx SVTs

Class 3: K+ Channel Blockers MOA

Increase APD and ERP Prolong repolarization and lengthen phase 2 (prolonging relaxation of heart)

Class 3: K+ Channel Blockers Drugs (5)

Amiodarone Ibutilide Dofetilide Dronaderone Sotalol

Class 3: K+ Channel Blockers - Ibutilide and Dofetilide MOA (3)

Selectively block outward potassium channel called *delayed rectifier potassium channels Prolong ventricular repolarization and increase the QT interval Used for pharmacological cardioversion of atrial fibrillation and flutter

Class 3: K+ Channel Blockers: Amiodarone MOA (5)

Mimics class 1, 2, 3, and 4 Binds to Na+ channel (inactivated) Blocks K+ and Ca2+ channels Non-competitive inhibitor of B receptors *Half-life: 25-60 days

Class 3: K+ Channel Blockers: Amiodarone Side Effects (5)

* Pulmonary fibrosis * Hepatotoxicity * Smurf skin (Bluish pigmentation of skin) * Hypothyroidism 5% & hyperthyroidism 2% * May cause torsades de pointes

Class 3: K+ Channel Blockers: Sotalol MOA (4)

*Beta blockers & K+ channel blockers Class 2: Decrease heart rate and AV conduction Class 3: Prolongs APD and ERP *Rx of life threatening V arrhythmia

Class 3: K+ Channel Blockers: **Sotalol Side Effects

Headache, depression, and impotence **Careful with asthmatic

Class 4: Calcium channel blockers MOA

Decrease SA and AV nodal conduction Decrease slope of phase 4

Class 4: Calcium channel blockers: Drugs

Verapamil Diltiazem Rx: PSVT due to AV nodal re-entry *Contraindicated in atrial tachycardia due to WPW (tissue problem)

Unclassified Anti-arrythmics: Adenosine MOA

Vasodilatation causing bradycardia --> reflex tachycardia Rx of PSVT Antagonist: Theophylline

Torsades de Pointes

Management Discontinue the drug prolonging the QT K+ channel blockers, thioridazine, TCAs Correct hypokalemia and hypomagnesemia Magnesium is indicated