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M3 Pharm B2 > Antiarrythmics (Cardio and Renal 2) > Flashcards

Antiarrythmics (Cardio and Renal 2) Flashcards

1
Q

4 classes of Antiarrhythmics

A
  1. Na+ Channels Blockers
  2. Beta Blockers
  3. K+ Channels Blockers
  4. Calcium channel Blocker

1 & 3 - big guns for life threatening situations

2 and 4 - toy guns

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2
Q

Antiarrhythmics: Miscellaneous Drugs

A

Adenosine
Digoxin
Magnesium Sulfate

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3
Q

Heart Action Potentials - Phase 0

A

Depolarization

Increase Na+ current

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4
Q

Heart Action Potentials - Phase 1

A

Overshoot
Initial repolarization inactivation of Na+ channel
Decrease K+

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5
Q

Heart Action Potentials - Phase 2

A

Plateau
Increase Ca2+
Decrease K+ currents

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6
Q

Heart Action Potentials - Phase 3

A

Repolarization

Decrease K+ current

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7
Q

Heart Action Potentials - Phase 4

A

Resting potential

Maintained by Na+/K+ ATPase Pump

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8
Q

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

A

Capacity of a cell to depolarize

Depends on the # of Na+ channels in ready state

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9
Q

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

A

Rate of spread of an impulse (conduction velocity)

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

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10
Q

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

A

Ability to spontaneously depolarize

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11
Q

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

A

Inability to respond to a stimulus

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12
Q

Electrophysiological Properties of the Heart - Refractoriness

A

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

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13
Q

The sodium channel exists in 3 states

A
  1. Resting or ready state
  2. Open or active state
  3. Inactivated or refractory state
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14
Q

The sodium channel is a voltage channel with 2 gates:

A
  1. M (activating)

2. h (inactivating) gate

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15
Q

Mechanism of Arrhythmia Formation: Abnormalities in impulse Formation

A

SA Node: Increase symp –> Tach

SA Node: increase parasym –> brady

Purkinje fibers

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16
Q

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

A

Ectopic foci

Re-entry mechanisms

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17
Q

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

A

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)

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18
Q

Na+ channel Blockers Class 1A

A

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

19
Q

Na+ channel Blockers 1A: Quinidine

A

*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

20
Q

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

A

GI: NVD

CV: Increase QT interval (Torsades de Pointes)

Thrombocytopenia

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

21
Q

Na+ channel Blockers 1A: Quinidine Drug Interactions

A

Antacids increase quinidine absorption

***Displaces digoxin from tissue binding sites

Decrease Vd

22
Q

Na+ channel Blockers 1A: Procainamide

A

Less anticholinergic
No alpha blocking activity

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

23
Q

Na+ channel Blockers 1A: Procainamide Side Effects

A

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

SLE like syndrome

24
Q

Na+ channel Blockers 1A: Disopyramide

A

The most anticholinergic –> *Greater anti-ionotropic effect

25
Q

Na+ Channel Blockers: 1B MOA and Uses

A

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

26
Q

Na+ Channel Blockers: 1B Drugs (3)

A

Lidocaine
Tocainide
Mexiletine

27
Q

Na+ Channel Blockers 1B: Lidocaine (3)

A
  1. Rx: V-Tac after MI, or digitalis toxicity
  2. Least cardiotoxic
  3. Shortens Phase 3 repols and decreases APD
28
Q

Na+ Channel Blockers 1B: Mexiletine and Tocainide

A

Given orally

Pulmonary toxicity (Pulmonar fibrosis)

29
Q

Na+ Channel Blockers Class 1C MOA

A

Both Na+ Channels

Marked decrease of Vmax, but no effect on APD

30
Q

Na+ Channel Blockers Class 1C: Drugs

A

Flecainide, Propafenone, Moricizine

Pro-arrhythmic effects: can worsen existing arrhythmia

Increase in sudden death and cardiac arrest after MI

31
Q

Class 2: Beta Blockers Drugs (4)

A

Propanolol

Acebutalol

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

Metoprolol

32
Q

Class 2: Beta Blockers MOA (3)

A

Decrease SA and AV nodal conduction

Decrease the slope of phase 4 depolarization

Used as prophylaxis Post-MI and to rx SVTs

33
Q

Class 3: K+ Channel Blockers MOA

A

Increase APD and ERP

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

34
Q

Class 3: K+ Channel Blockers Drugs (5)

A

Amiodarone

Ibutilide

Dofetilide

Dronaderone

Sotalol

35
Q

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

A

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

36
Q

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

A

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

37
Q

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

A
  • Pulmonary fibrosis
  • Hepatotoxicity
  • Smurf skin (Bluish pigmentation of skin)
  • Hypothyroidism 5% & hyperthyroidism 2%
  • May cause torsades de pointes
38
Q

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

A

*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

39
Q

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

A

Headache, depression, and impotence

**Careful with asthmatic

40
Q

Class 4: Calcium channel blockers MOA

A

Decrease SA and AV nodal conduction

Decrease slope of phase 4

41
Q

Class 4: Calcium channel blockers: Drugs

A

Verapamil

Diltiazem

Rx: PSVT due to AV nodal re-entry

*Contraindicated in atrial tachycardia due to WPW (tissue problem)

42
Q

Unclassified Anti-arrythmics: Adenosine MOA

A

Vasodilatation causing bradycardia –> reflex tachycardia

Rx of PSVT

Antagonist: Theophylline

43
Q

Torsades de Pointes

A

Management

Discontinue the drug prolonging the QT

K+ channel blockers, thioridazine, TCAs

Correct hypokalemia and hypomagnesemia

Magnesium is indicated

M3 Pharm B2 (10 decks)

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