Flashcards in Antiarrhythmic Drugs- Leah (3)* Deck (50):
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:
1. Class I- Na Channel block
2. Class II- B block
3. Class III- K+ block/ ^ APD/ERP
4. Class IV- Ca++ channel block
How do Na channel blockers effect heart rate/rhythm? (3)
1. DECREASE depolarization
(phase 0 slope decreased on AP plot for MYOCYTES)
2. DECREASE conduction + automaticity
(Decrease phase 4 slope on AP plot for pacemaker cells SA/AV)
3. 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?
***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?
"(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?
"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
"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)?
1. Propranolol (non selective)
2. Esmolol (selective)
3. 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?
1. AMIODARONE ***most important, always on boards.
5. Sotalol* (Amiodarone substitute)
*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:
*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?
2. Carotid sinus massage
* 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!!
Cardiac effects (2) / MOA
Cardiac use/DOC (1)
CI + Replacement drug (2):
^ 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:
Most class I-IV anti-arrythmics slow down AV conduction and increase PR interval on ECG. What are two exceptions?
1. Procainamide/ Class 1A.
- anti-Ach properties make AV node effects unpredictable
-PR could increase, decrease, or remain the same.
2. Lidocaine/Class 1B:
-Rapidly disassociate from Na channels
-Often leave the PR interval unchanged
What drug classes cause increased risk of torsades?
*I believe dronadrone also causes torsades, yes! Sorry--forgot to respond earlier!
Effects of all class 1, 2, and 4 drugs on:
Phase 0 slope on AP plot
-Decrease phase 0 slope on AP plot
Effects of class 3 drugs on:
+ 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?
Emergency ventricular arrythmias
1. ^QT/torsades esp with hypokalemia
Active metabolite: NAPA (also has Na blocking properties)
-Digoxin arrythmia/ life threatening ventricular arrythmia
- IV only (first pass elimination)
-***delirium and seizures***
How is mexiletine different than lidocaine?
Same other than:
orally effective + some GI ADRs
In what cases are lidocaine and mexilitine contraindicated?
Seizures/ hepatic disease
Use: deadly ventricular arrythmias/ SVT IN THE ASBENCE OF ORGANIC HEART DISEASE
How does Propafenone differ from Flecainide?
Propafenone has some Beta blocking properties
Three important ADRs to keep in mind for B-blockers when using them to treat cardiac patients
1) Bronchospasm- (only B1 selective for asthma/COPD pts)
2)CHF/ AV block
3) Insulin induced hypoglycemia + loss of hypoglycemic tachycardia
Most common uses (2)
IV admin POST OP for control of:
Atrial arrythmias (sinus tacky/ or Afib/flutter)
Very short half life
Class III, with some I and IV properties
**DOC: emergency ventricular arrythmias**
1. Pulmonary fibrosis
3. Hypo/hyper thyroid
4. QT ^/ torsades
5. AV block + bradycardia
6. Corneal microdeposits, photosensitivity
7. Blue/gray nose + cheeks
("DIRTY" drug due to having multiple mechanisms)
Half life amiodarone
Very long because it is a lipophilic drug (up to 107 days)
Class III with some class I activity
Liver injury/ CHF
24 hr t1/2
*INCREASES CHF MORTALITY = RARELY USED*
Tx: A flutter/ fib
*HIGHEST TORSADES DUE TO SINGULAR K+ ACTIVITY = RARELY USED*
Class III/ II (non-cardioselective BBer Ends in --olol!!!!!!!!!)
Tx: V tach
*CAN REPLACE AMIODARONE IN INTOLERANT PATIENTS*
Use: atrial arrhythmia (SVA, PSVT, AFIB /flutter)
Drug of choice for ventricular arrythmias (commonly used by paramedics)
What drugs cannot be in patients with organic heart disease (2)
Which drug has an active metabolite "NAPA"?
What drugs cause delirium and seizures (2)?
Drug that is lipophilic and has an extremely long half life?
Drug that may cause pulmonary fibrosis
Four pro-arrythmic conditions:
1) Conduction block/re-entry
2) Any change in effective refractory period (ERP)
3) Increased automaticity (i.e. abnormal foci)
4) After depolarization
2. CHF/ AV block
3. Constipation (Why? Because it blocks SM calcium release NONspecifically! Stops GI SM contraction too!!)
Contra: Sick Sinus Syndrome
1. B-blockers (^ - inotropic effects)
2. Digoxin (double decrease in AV cndxn)
4. CYP3A4s (cimetidine)
"same 4 listed in the vasodilator lecture!!"
Drugs causing Long QT
1. AntiArrhythmics (class Ia, III)
2. AntiBiotics (macrolides)
3. Anti"C"ycotics (haloperidol)
4. AntiDepressants (TCAs)
5. AntiEmetics (ondansetron)
Drugs contraindicated in Asthmatics/COPD
1. non-specific Beta Blockers
What is ondansetron?
Why is it relevant to this deck of cards?
At a party with alcohol and feeling queasy?
Keep ON DANCing with ONDANSetron.
****It prolongs QT like many of the anti- arrhythmics, ^ Torsades risk.
Drug of choice for PVST?