Antiarrhythmics Flashcards

(47 cards)

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?

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
Which drug has a low potential for EAD and Torsade de Point: Procainamide or Amiodarone?
Amiodarone
26
Amiodarone: Uses
(1) Suppress atrial and ventricular premature beats | (2) Suppress atrial fibrillation and ventricular tachycardias
27
Amiodarone: Adverse Effects
(1) T1/2 13-103 days; pulmonary fibrosis (2) Tremor (3) Thyroid dysfunction (4) Photosensitivity
28
What are the Ca channel blockers?
Verapamil, Diltiazem
29
Why is Nifedipine not used for anti-arrhythmic drugs?
It has no direct effect on the heart
30
What Ca channel blockers do?
- Decrease Ca entry which decreases automaticity (S-A, A-V node) and decreases conduction in A-V node
31
Ca channel blockers: Uses
(1) Supraventricular tachycardia | (2) Slows ventricular rate by decreasing A-V conduction during atrial tachycardias
32
Ca channel blockers: Adverse Effects
(1) Bradycardia (2) Decrease Contractility (3) Decrease BP
33
What does DIgoxin do?
Decreases A-V conduction by increasing parasympathetic activity
34
When is it good to use digoxin?
When you have a patient with heart failure and arrythmias (it's a 2 for 1)
35
Digoxin- Uses
Slow or prevent acceleration of ventricular rate during atrial tachycardias
36
What does Adenoside do?
Decreases A-V conduction (by activating adenosine receptors)
37
Adenosine- Uses
Supraventricular tachycardia involving the A-V node
38
What is Adenosine a good choice for antiarrhythmic drugs?
Very short half life (10sec); IV only used as a big bolus dose which terminates the arrhythmia rapidly
39
Indications for sinus bradycardia?
(1) Atropine | (2) Pacemaker
40
Indications for sinus tachycardia?
(1) Beta-blocker
41
Indications for AF?
(1) Cardioversion (2) Amiodarone (3) Na channel blocker (4) Ca or B blocker or Digoxin
42
Indications for Atrial Flutter?
(1) Cardioversion (2) Amiodarone (3) Na channel blocker (4) Ca or B blocker or Digoxin
43
Indicatinos for PSVT?
(1) Adenosine (2) Ca or Beta blocker (3) Digoxin
44
Indications for Symptomatic PVC?
(1) Na channel blocker | (2) Beta blocker
45
Indications for VT (with MI)
(1) Lidocaine (2) Amiodarone (3) Other Na or K channel blocker
46
Indications for VF?
(1) Cardioversion (2) Amiodarone (3) other Na or K channel blockers
47
What is the pathway of excitation and action potentials?
S-A node --> atria -->A-V node --> purkinje fibers --> ventricular muscle