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Flashcards in Antiarrhythmic Drugs Deck (28)
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1
Q

What are the classes of anti-arrhythmic?

A
  • I - Sodium channel Blockers
    • Ia - Moderate phase 0 depression and slowed conduction (2+), prolong repolarization
    • Ib - Minimal phase 0 depression and slow conduction (0-1+); shorten repolarization
    • Ic - Marked phase 0 depression and slow conduction (4+); little effect on repolarization
  • II - Beta-Adrenergic Blockers
  • III - Potassium Channel Blockers (prolong repolarization)
  • IV - Calcium Channel Blockers
2
Q

What is the mechanism of Class I drugs?

A
  • Act on fast response cells
  • Reduce membrane responsiveness
  • Increase threshold for AP firing Reducing Vmax (depress conduction velocity)
  • Prolong effective refractory period (ERP)
3
Q

What is a Class 1A Drug? What are its direct effects? What are its indirect effects? What are its indications?

A

Qunidine

  • Direct: Increase AP threshold, ERP; Decrease Vmax
  • Indirect effects: Blocks K channels leading to early afterdepolarizations (EADs), vagolytic effect
  • Use: A-Flutter/fib, Prevention of V-Tach/Fib
4
Q

What are Quinidne’s side effects? Where is it metabolised? Can it be used with renal failure?

A
  • SE: GI effects - Diarrhea, cramps; Vagolytic in heart, P450 inhibition, Proarrythmic for other arrythmias, reduces renal clearance of digitalis
  • Liver metabolism
  • Tolerated in patients with renal failure
5
Q

What is a Class 1B Drug? What are its direct effects? What are its SE? What are its indications?

A

Lidocaine

  • Direct: Increase AP threshold; Decreases Vmax/Na channel activity at high HR, AP duration, ERP SE: Dizziness, seizures
  • Use: V-Tach, Digitalis inudced arrhythmias, Safe with long QT patinets
6
Q

What is a Class 1C Drug? What are its direct effects? What is its major SE? What is its indication?

A

Flecainide

  • Direct: Increase AP threshold; decrease Vmax/conduction velocity; variable effects on ERP; Slow Na channel dissociation
  • SE: Pro-arrhythmic
  • Use: Life-threatening situations where supraventricular and ventricular arrhythmias are resistant to other drugs
7
Q

What are some class II drugs and their specific kinetics? What is their mechanism? Which part of the action potential do they affect?

A
  • Drugs: Propranolol - Long acting, oral Esmolol - Short acting, IV
  • Mechanism: Competitive inhibitor of catecholamines for the beta-adrengergic receptors of cardiac cells
  • Affects phase 4 (diastolic) depolarization in the presence of catecholamines
8
Q

What are the indications for beta-blockers? What are the major side effects?

A
  • All atrial arrhythmias, V-Tach/Fib when there are high levels of catecholamines
  • Most useful antiarrhythmic drugs due to safety and wide clinical applications
  • Safe for long QT syndrome patients because they do not prolong repolarization in ventricular tissues
  • Major side effects - Negative inotropic effect, heart block, bradycardia, bronchospasm
9
Q

What are some class III drugs? What is the general mechanism? What is the most common target? What is the main common effect?

A

Amiodarone, Sotalol

  • Main mechanism: K+ Channel Block, prolongs AP repolarization; reverse use-dependence
  • Target: IKr (hERG channel)
  • Effect: Increased ERP
10
Q

What are the channel actions of amiodarone? What are its effects? What are its indications? What are its major side effects?

A
  • Potent K+ channel blockers, modest Na+, Modest Ca2+, Modest Beta-blocker
  • Effect: Potent K+ channel blocker, Increased AP duration, ERP
  • Use: V-Tach/Fib, prevention of recurrent paroxysmal A-Fib/Flutter SE: Triggered arrhythmias (EADs), rarely Torsades de Pointes; Altered thyroid function/hypothyroidism, pulmonary fibrosis often irreversible
11
Q

What are the actions of Sotalol? What are the indications of Sotalol? What is the most serious side effect?

A
  • Actions: Main: IKr block, Beta-blocking secondary actions
  • Uses: V-Tach/Fib. Supraventricular tach, A-Fib
  • Side effect: Triggered arrhythmias, Torsades de Pointes
12
Q

What is this?

A

Torsade de Pointes

13
Q

What are some Class IV drugs and the family they belong to?
What is their primary mechanism?
What are the major effects?
What are the indications?

A

Diltiazem (Benzothiazepines), Verapamil (Phenylalkylamines)
Mechanism: Acts primarily on slow response cells (SA & AV node), dependent on Ca2+ influx for depolarization
Increase threshold for AP firing in nodal cells, nodal cell refractory period; depress conduction velocity in the SA and AV nodes
Uses: A-Tach (Paroxysmal supraventricular tachycardia); Rarely for V-Tach

14
Q

Why are 1,4-DHPs not generally used for arrythmias?

A

They target vascular instead of cardiac cells; instead prescribed for treatment of angina to releieve arterial spasms

15
Q

What are the major side effects of Ca2+ blockers?
Common
Specific (Nifedipine, Verapamil, Diltiazem)

A

Common: Negative chronotropic effect - decreases SA node automaticity (bradycardia)
Negative inotropic effect - decreases Ca2+ influx during plateau of ventricular AP
Hypotension - Decreases Ca2+ influx into vascular smooth muscle cells

Peripheral edema (N-type mostly)
Constipation (V especially)
With digitalis to slow AV node leading to heart block (V&D)
Increase plasma digitalis levels by competiting for renal excretion (V&D)

16
Q

What is the mechanism of adenosine?
What is the indication?

A
  • Mechanism: Very rapidly activates K+ channels to slow phase 4 depolarization at AV node (Half-life of 10 seconds)
  • Blocks cAMP-enhanced Ca2+ channel activity in AV node
  • Use: Supraventricular Tachycardia - Slows AV conduction and heart rate
17
Q

What is digoxin?
What is its mechanism?
What is its indication?

A

Digitalis Glycoside
Mech: Enhances vagal parasympathetic activity to slow conduction at the AV node
Use: A-Fib, Supraventricular Tachycardia to control ventricular response rate

18
Q

What ECG pattern is this?

A

Normal Sinus Rhythm

19
Q

What ECG pattern is this?

A

Sinus Tachycardia

20
Q

What ECG pattern is this?

A

Atrial Fibrilation

21
Q

What ECG pattern is this?

A

Ventricular Tachycardia

22
Q

What ECG pattern is this?

A

Ventricular Fibrillation

23
Q

What ECG pattern is this?

A

Ventricular Asystole (Flat line)

24
Q

What are the three main mechanisms of arrhythmias?

A
Increased automaticity (Inappropriately excitable cells)
Triggered automaticity (Normal AP is interrupted or followed by an abnormal depolarization; afterdepolarizations)
Re-entry (Abnormal impulse conduction)
25
Q

What changes can occur in increased automaticity?

A

Slope of phase 4 is increased
Threshold potential is more negative
Maximum diastolic potential (MDP) is more positive

26
Q

What is Early Afterdepolarization (EAD)?
What exacerbates it?
What can it result in?

A

Depolarization that interrupts repolarization
Exacerbated by slow rate/long QT syndrome
Torsades de Pointes results

27
Q

What is Delayed Afterdepolarization?
What exacerbates it?

A

Depolarization after repolarization
Exacerbated by fast rates, high intracellular Ca 2+, digitalis toxicity, catecholamines, ischemia

28
Q

What is re-entry?
What causes functionally defined re-entry?
Where can anatomic re-entry occur?

A

Re-excitation of a localized region of tissue from the same impulse (Current goes backwards)
Functionally defined: Ischemia and hypoxia
Anatomic: AV node