Cardio: Antiarrhythmics Flashcards
1
Q
Na+ Channel blockers - Antiarrhythmics
Block fast Na+ channels
thereby reducing the rate of Phase 0 depolarization
prolonging the effective refractory period
increasing the threshold of excitability
and reducing Phase 4 depolarization
A
- (3) Class I antiarrhythmics
- Class IA
- Class IB
- Class IC
2
Q
Class IA: Drugs
A
-
Quinidine (Muscarinic and α antagonist = Atropine)
- SEx: reflex tacycardia
- Used for Atrial Fibrillations
- Digitilize pt.** w/ Digoxin to slow AV node conduct.**
- Procainamide
- Disopyramide
- “The Queen Proclaims Diso’s pyramid”
3
Q
Class IA: Mechanism
A
- Moderate block of Na+ channels; prolong APs
- Fast Na+ Channels
- *Slow Conduction →
- ↑** APD - action potential duration
- ↑ ERP = effective refractory period
-
*Prolongation of the QRS and * QT interval
- → Torsades
- Possible Heart block
- At low doses, anticholinergic (vagolytic) effects predominate, and may increase conduction velocity in the AV node and accelerate HR
4
Q
Class 1A: Clinical Use
A
- Both Atrial Fibrillation to prevent passage to ventricular arrhythmias (use w/ Digoxin)
- especially re-entrant and ectopic SVT and **VT **and can be used to maintain Sinus rhythm
5
Q
Class IA: Toxicity
A
- Cinchonism (Quinidine = tinnitus, ringing of the ears and dizziness, headache, GI dysfunction, ocular disfunction)
-
Procainamide = Reversible SLE-like syndrome (w/ slow acyelators = +ANA, +Antihistone)
- Hematotoxity (CBCs monitored), Torsades
- Heart Failure (Disopyramide)
- Thrombocytopenia
-
Torsades de pointes due to increased QT interval
- “Twisting of the spikes”
- w/ Digoxin → monitor ECG
- w/ Hyperkalemia → enhances effects
6
Q
Class IB: Drugs
A
- **Lidocaine **(Only used IV due to first-pass)
- Post-MI
- Open-Heart Surgery
- Digoxin toxicity
- SEx: CNS toxicity, Least Cardiotoxic!!
- Mexiletine (Oral)
- Tocainide (Oral)
7
Q
Class IB: Mechanism
A
- Fast Na+ Channels (↓ INa)
-
Shorten the duration of the Refractory period
→ Blocks inactivated channels (slow conduction in hypoxic and ischemic heart)
→ ↓ APD - due to slow Na channels during the plateau phase - plateau gets shorter - more narrow - Preferentially affect ischemic or depolarized Purkinje and Ventricular tissue
- Phenytoin can also fall into the class IB category
8
Q
Class IB: Clinical Use
A
- Suprress Acute ventricular arrhythmias
(especially post-MI)- IB is Best post-MI
- Little effect on conduction velocity so it has little effect on atrial function
- Digitalis-induced arrhythmias
9
Q
Class IB: Toxicity
A
- CNS stimulation / depression
- Cardiovascular depression
10
Q
Class IC: Drugs
A
-
Flecainide (Tambocor)
- Limited use because of its proarrhythmogenic effects leading to sudden cardiac death
- Propafenone
- Class IC:
- “Can I have Fries** P**lease”
11
Q
Class IC: Mechanism
A
- Strongly blocks fast Na+ and K+ channels
- especially His-Purkinje tissue
- No effect on APD
- No ANS effects
- Significantly prolongs refractory period in AV node
- Minimal effect on AP duration
12
Q
Class IC: Clinical Use
A
- ULTIMATE - Last ditch use
- Treat SVTs
- Including Paroxysmal **Atrial fibrillation **and Atrial flutter
- Only as a last resort in refractory VT
13
Q
Class IC: Toxicity
A
- Flecainide = Proarrhythmic actions –> use of these drugs is limited, cautious use is recommended may cause SCD
- Contraindicated in post-MI
- Structural and Ischemic
- IC is Contraindicated in structural and ischemic heart disease
14
Q
Class II: Drugs
A
ß-blockers
- Propranolol (non-selective)
- Carvedilol
- Metroprolol
- Esmolol (Selective)
- Atenolol
- Timolol
- “PC MEAT”
15
Q
Class II: Mechanism
A
- β-adrenoceptor antagonists and act by reducing sympathetic stimulation
- Depress automaticity
- ↓ SA and AV nodal activity by decreasing cAMP
- *decreased *Ca2+ currents
- ↓ slope of phase 4 (repolarization)
- AV node particularly sensitive
- *Increase *PR interval
- Esmolol very short acting