Antiarrhythmic Drugs- Leah (3)* Flashcards
Anti-arrhythmic effects (4)
1) Decreased automaticity
2) Decrease/ restore, block conduction
3) Make ERPs homogeneous OR…
4) ^ ERP –> slow heart rate
Describe the four classes of arrhythmia drugs:
- Class I- Na Channel block
- Class II- B block
- Class III- K+ block/ ^ APD/ERP
- Class IV- Ca++ channel block
How do Na channel blockers effect heart rate/rhythm? (3)
- DECREASE depolarization
(phase 0 slope decreased on AP plot for MYOCYTES) - DECREASE conduction + automaticity
(Decrease phase 4 slope on AP plot for pacemaker cells SA/AV) - Intuitive: increase THRESHOLD for AP
Most common cause of persistent arrhythmias?
How do infarctions facilitate this process (3)
Anatomical re-entry = heterogenous ERP
- INFARCTION = SLOWER conduction + ERP
- Normal conduction does not initially pass through infarcted site (longer ERP)
- Conduction RE-ENTERs infarct @ wrong time/ wrong direction after ERP is over
Risk associated with drugs that increase effective refractory period?
Relevance (2)?
***Torsades de points: polymorphic V Tach–> fatal V Fib
- Many drugs that increase QT are reserved for emergency or fatal arrhythmias
- Not used in asymptomatic arrhythmias because of their high risk
Type I drugs are “state dependent”: what does this mean?
Describe the three subclasses of type 1 anti-arrhythmic drugs.
- Na channel blockers are state dependent.
- Only bind Na channels in the open/ active state.
- Disassociate from inactive/ closed channels with varying speed
- Speed of disassociation determines subclass.
1A- moderate effects
1B- small effects because (rapidly disassociate)
1C- large effects (slowly disassociate)
What are three class 1A drugs? Which is actually used in practice? Why?
- Procainamide***
- Quinidine
- Disopyramide
“(I)A QUeen PROClaims DISO’s PYRAMID.”
- PROCAINAMIDE is still used
- IA drugs have some anti-Ach effects –> may ^AV conduction–> unpredictable effects
- May increase or decrease AV conduction
PROCAINAMIDE: lowest anti-ach effects
DISCOPYRAMIDE: highest anti-Ach effects
(L Dose may precipitate CHF: no longer used)
What are two class 1B drugs? When are they effective?
- Lidocaine***
- Mexiletine
“I’d Buy LIDdy’s MEXIcan Tacos”
I would NOT. I heard they make you delirious & might even give you seizures.
- Only effective in the diseased heart
- In a normal heart, they rapidly disassociate from inactive Na channels, have little efficacy.
What are two class IC drugs? Important limiting factor in their use
- Flecainide***
- Propafenone
“Can I have Fries Please”
- *Cannot be used in patients with an organic heart disease
- INCREASES CHF MORTALITY
- Only used for patients with an idiopathic refractory arrythmia
Three important class II drugs? Range of use for this class (4)?
- Propranolol (non selective)
- Esmolol (selective)
- Metoprolol (selective)
**Widest range of use; Not labeled for “only emergencies”.
Tx: CHF, postMI, PVCs, SV arrhythmias (afib/flutter)
Class III drugs (5)
Common side effect of this class?
- AMIODARONE ***most important, always on boards.
- Drondarone
- Ibutilide
- Dofetilide
- Sotalol* (Amiodarone substitute)
“AIDS”
- Because this class increases APD/ERP predominately, most drugs increase QRS/QT
- ^ risk of torsade
- Most reserved for emergency/refractory cases*
Most important class IV drug:
Verapamil
*Widest range of use second to B blocks
When might atropine and isoproterenol be used to treat arrythmias? How long are patients treated with these drugs?
Bradycardia, AV blocks
(When heart rate needs to INCREASE)
* Short-term until pacemaker is placed
What are three “vagomimetics” used to treat arrythmias?
What are their uses?
- Valsalva
- Carotid sinus massage
- Digoxin
- Valsalva and carotid massage mimic increased BP; may terminate PSVT
- Digoxin slows ventricular rate in a-flutter/fib
Why? Because AV node NEEDS Na/K pump for action potential. Digoxin increases contraction BUT decreases AP rate for AV node!!
Adenosine: Cardiac effects (2) / MOA Cardiac use/DOC (1) ROA (1) ADR (3) CI + Replacement drug (2):
Effects/MOA:
^ K+ out of cell–> Hyperpolerization–> DECREASE automaticity + AV conduction
Use: DOC terminates PSVT
ROA: IV only (w/ short half life)
ADR: Bronchospasm, Flushing, Impending Doom
CI: COPD, Asthma (use verapamil)
Two drugs that markedly prolong QT on ECG:
Procainamide (I-A), amiodarone (III)
Three drugs that markedly increase QRS on ECG:
Procainamide (I-A)
Flecainide (I-C)
Amiodarone (III)
Most class I-IV anti-arrythmics slow down AV conduction and increase PR interval on ECG. What are two exceptions?
- Procainamide/ Class 1A.
- anti-Ach properties make AV node effects unpredictable
- PR could increase, decrease, or remain the same. - Lidocaine/Class 1B:
- Rapidly disassociate from Na channels
- Often leave the PR interval unchanged
What drug classes cause increased risk of torsades?
Class 1A
Class III
*I believe dronadrone also causes torsades, yes! Sorry–forgot to respond earlier!
Effects of all class 1, 2, and 4 drugs on:
Conduction Phase 0 slope on AP plot Automaticity APD ERP
- Decrease conduction
- Decrease automaticity
- Decrease phase 0 slope on AP plot
- ^ APD
- ^ ERP
Effects of class 3 drugs on: Conduction Automaticity ARP ERP
+ important caveat
On their own, “class 3” drugs only ^ ERP/APD
HOWEVER, most drugs in this class have mixed mechanisms allowing them to also decrease conductivity/ automaticity
Ex: amiodarone has class III effects mainly, but it also has class I/IV activity
Two drugs in the cardiac unit that may cause a reversible lupus-like syndrome?
Procainamide; Hydralazine
Procainamide: Class Use ROA ADRs (4) Active metabolite
1A
Emergency ventricular arrythmias
IV/oral
ADRs:
- ^QT/torsades esp with hypokalemia
- LUPUS
- AGRANULOCYTOSIS
- leukopenia
Active metabolite: NAPA (also has Na blocking properties)
Lidocaine: Class Use(2) ROA ADRs (2)
- Class 1B
- Digoxin arrythmia/ life threatening ventricular arrythmia
- IV only (first pass elimination)
- delirium and seizures
