Antiarrhythmics Flashcards

1
Q

What are the 5 phases of fast response action potentials?

A
Phase 0: opening of sodium channels in the membrane
Phase 1: Repolarization
Phase 2: Influx of Ca into the cell
Phase 3: Opening of K channels
Phase 4: Resting membrane potential
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2
Q

Where do the fast response action potentials occur? Are they Ca or Na dependent?

A

Atrial tissue, His-purkinje tissue system, and ventricle tissue; Na dependent

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3
Q

Where do the slow response action potentials occur? Are they Ca or Na dependent?

A

Those that occur in S-A, A-V nodes ; Ca dependent

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4
Q

What are the 4 classes of anti-arrhythmic drugs? What are the “others” in anti-arrhythmic drugs?

A

(1) Sodium channel blockers
(2) Beta-blockers
(3) K channel blockers
(4) Ca channel blockers
Others- digoxin, adenosine

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5
Q

What are the sodium channel blockers? Are they mild, moderate, or high blockers?

A

(1) Procainamide- moderate
(2) Lidocaine- minimum
(3) FLecainide- strong

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6
Q

What does Procainamide do?

A
  • Moderate Na channel blocker
    ~ Decreases conduction which decreases reentry (of the fast action potentials)
    ~ Decreases automaticity which decreases ectopic beats (in low doses)
  • Moderate K channel blocker
    ~increases APD which decreases reentry
    ~ excessive increase in APD= EAD and Torsade de Pointe (10-20% of patients)
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7
Q

T/F Procainamide is not dose dependent.

A

FALSE; at high doses it becomes pro-arrhythmic

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8
Q

Procainamide- Uses

A

(1) Atrial, ventricular premature beats
(2) Atrial flutter, fibrillation (prevents re-occurrence by suppressing reentry that causes them)
(3) Ventricular tachycardia/fibrillation (prevents the re-occurrence)

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9
Q

Procainamide- Adverse Effects

A

(1) Cardiac suppression
(2) Ganglion block (hypotension)
(3) Lupus-like syndrome (fever, joint pain)

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10
Q

What does Lidocaine do?

A
  • Minimal sodium, channel blockade and phase 0 depression

~ decreases automaticity (selectively decreases ventricular abnormal pacemakers)

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11
Q

Lidocaine- Uses

A

(1) Ventricular arrhythmias only (fast action potentials)
(2) VPC, Vent. Tachyardia: associated with MI
(3) Digoxin-induced ventricular arrhythmias

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12
Q

T/F Lidocain is ineffective against atrial arrhythmias

A

TRUE

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13
Q

Lidocaine- Adverse Effects

A

High doses causes CNS symptoms (agitation, convulsions)

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14
Q

How is Lidocaine given?

A

IV only due to rapid first pass metabolism int he liver

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15
Q

What dose Flecainide do?

A
  • Strong Na channel blocer (decreases phase 0)
    ~ decreases conduction (fast action potentials)
    ~ decreases automaticity
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16
Q

Flecainide: Uses

A

(1) Atrial tachyarrythmias in the absence of heart disease

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17
Q

Who is contraindicated to use Flecainide?

A

Patients with ventricular heart disease

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18
Q

Flecainide: Adverse Effects

A

(1) Cardiac suppression: bradycardia

(2) Pro-arrhythmic

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19
Q

What are the Beta blockers?

A

Propranolol, Metoprolol

20
Q

What do Beta blockers do?

A
  • Decrease automaticity and decrease conductino in A-V node

~blocks sympathetic tone int he A-V node

21
Q

Beta blockers- Uses

A

(1) Supraventricular tachyarryhtmias
(2) Catecholamine induced arrhythmias
(3) Slows ventricular rate during atrial tachycardias (by decreasing conduction of A-V node)
(4) post MI patients because it increases the sympathetic drive which lowers the chance of other arrythmias

22
Q

Beta blockers- Adverse Effects

A

(1) Bradycardia
(2) decrease contractility (C.O)
(3) Decrease BP

23
Q

What are the K channel blockers?

A

Amiodarone

24
Q

What does Amiodarone do?

A
  • K-channel block which increases APD which suppresses reentry
  • Na-channel block which decreases conduction which suppresses reentry
  • decreases automaticity which decreases ectopic beats
25
Q

Which drug has a low potential for EAD and Torsade de Point: Procainamide or Amiodarone?

A

Amiodarone

26
Q

Amiodarone: Uses

A

(1) Suppress atrial and ventricular premature beats

(2) Suppress atrial fibrillation and ventricular tachycardias

27
Q

Amiodarone: Adverse Effects

A

(1) T1/2 13-103 days; pulmonary fibrosis
(2) Tremor
(3) Thyroid dysfunction
(4) Photosensitivity

28
Q

What are the Ca channel blockers?

A

Verapamil, Diltiazem

29
Q

Why is Nifedipine not used for anti-arrhythmic drugs?

A

It has no direct effect on the heart

30
Q

What Ca channel blockers do?

A
  • Decrease Ca entry which decreases automaticity (S-A, A-V node) and decreases conduction in A-V node
31
Q

Ca channel blockers: Uses

A

(1) Supraventricular tachycardia

(2) Slows ventricular rate by decreasing A-V conduction during atrial tachycardias

32
Q

Ca channel blockers: Adverse Effects

A

(1) Bradycardia
(2) Decrease Contractility
(3) Decrease BP

33
Q

What does DIgoxin do?

A

Decreases A-V conduction by increasing parasympathetic activity

34
Q

When is it good to use digoxin?

A

When you have a patient with heart failure and arrythmias (it’s a 2 for 1)

35
Q

Digoxin- Uses

A

Slow or prevent acceleration of ventricular rate during atrial tachycardias

36
Q

What does Adenoside do?

A

Decreases A-V conduction (by activating adenosine receptors)

37
Q

Adenosine- Uses

A

Supraventricular tachycardia involving the A-V node

38
Q

What is Adenosine a good choice for antiarrhythmic drugs?

A

Very short half life (10sec); IV only used as a big bolus dose which terminates the arrhythmia rapidly

39
Q

Indications for sinus bradycardia?

A

(1) Atropine

(2) Pacemaker

40
Q

Indications for sinus tachycardia?

A

(1) Beta-blocker

41
Q

Indications for AF?

A

(1) Cardioversion
(2) Amiodarone
(3) Na channel blocker
(4) Ca or B blocker or Digoxin

42
Q

Indications for Atrial Flutter?

A

(1) Cardioversion
(2) Amiodarone
(3) Na channel blocker
(4) Ca or B blocker or Digoxin

43
Q

Indicatinos for PSVT?

A

(1) Adenosine
(2) Ca or Beta blocker
(3) Digoxin

44
Q

Indications for Symptomatic PVC?

A

(1) Na channel blocker

(2) Beta blocker

45
Q

Indications for VT (with MI)

A

(1) Lidocaine
(2) Amiodarone
(3) Other Na or K channel blocker

46
Q

Indications for VF?

A

(1) Cardioversion
(2) Amiodarone
(3) other Na or K channel blockers

47
Q

What is the pathway of excitation and action potentials?

A

S-A node –> atria –>A-V node –> purkinje fibers –> ventricular muscle