Pharm #7 - Anti-Arrhythmics Flashcards Preview

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Flashcards in Pharm #7 - Anti-Arrhythmics Deck (50):
1

Procainimide:

MOA & effect

CLASS 1A drug

Block Na & K channels

- slows upstroke of AP and conduction
- PROLONGS QRS
- direct depressant actions on SA/AV nodes
(use/state dependent)

2

Procainimide

- clinical application

atrial and ventricular arrhythmias

2nd choice for ventricular arrhythmias after acute MI ((after lidocaine and amiodarone) )

3

Adverse effects of Procainimide

Why?

Adverse effects/toxicity:

Ganglion blocking properties,
risk of hypotension
Anti-cholinergic effects
Induction of torsade de pointes arrhythmia (NAPA) !!
Long term: Lupus erythematosus syndrome (arthritis, pleuritis…)
in 30% of all patients

adverse effect of tornadoes de points due to metabolite NAPA !
- eliminated renally (need to dose adjust)

4

Quinidine:

MOA

Adverse Effects

Actions similar to procainamide (Na channel blocker)

Indications: Same as procainamide

Rarely used because of cardiac and extra-cardiac


adverse effects:
- stronger anticholineric
- cinchonism: HA, dizziness, tinnitus

Ganglion blocking properties, risk of hypotension
(>> procainamide)

Anti-cholinergic effects, increases sinus rate and AV conduction,

may require co-administration of drugs that slow AV conduction

Induction of ventricular fibrillation and torsade de pointes !!


5

Disopyramide

MOA

What does it need to be coadministered with?


similar to procainamide

Anticholinergic effects >> than procainamide & quinidine
- increase sinus rate and AV conduction and requires co-administration of drugs that slow AV conduction

Negative inotropic effects may induce HF
- most exctra cardiac effects result from atropine like actions

6

Disopyramide

Approved for?

Approved only for ventricular arrhythmias

not drug of 1st or 2nd choice

7

What are the three Class1A drugs?

1. Procainamide
2. Quinidine
3. Disopyramide

8

MOA of Class 1B drugs

Which drugs fall into this class (2)

MOA: fast kinetics, reduction of AP potential duration

1. lidocaine
2. mexiletine

9

Lidocaine

MOA

Effect

Na channel blockade

(use/state dependent drug action)

effect: rapid kinetics at normal resting potential:

No effect on conduction,
recovery from block between action potential

Selective depressing of conduction in depolarized (ischemic) cells

10

Lidocaine

clinical use

DOC?

highly effective for ventricular arrhythmias after MI

DOC: tx of Ventricular tachycardia and fibrillation after cardioversion in setting of ischemic/infarction

PROPHYLACTIC TX not recommended

11

Lidocaine

PK: how is it metabolized?


Side effect?

EXTENSIVE first pass metabolism by liver
(2 hr half life)
- least cardiotoxic drug!

Neurologic side effects due to local anesthetic properties (paresthesia,
tremors,
nausea,
lightheadedness,
hearing disturbances,
slurred speech, convulsions)


Large doses may induce hypotension probably through effects
on myocardial contractility

12

Mexiletine

MOA
Class

Unique off label use?

Class 1 B
(Class I B: fast kinetics, APD decreases)

- Na channel blockade

orally active lidocaine analogue

Actions/adverse effects similar to lidocaine

Off label use: CHRONIC PAIN (diabetic neuropathy, nerve injury)

13

Which drug is IV only, mexiletine or lidocaine?

LIDOCAINE!

Mexilitine is oral (used off label for chronic pain associated with diabetic neuropathy)

14

CLass 1 C drugs (2)

MOA

Flecainamide
Propafenone

- slow kinetics, NO EFFECT ON APD

15

Flecainamide

MOA

effect

Na and K channel block

no effects on APD even tho K channel blocked

NO ANTICHOLINERGIC EFFECTS!

16

What are class 1 a effects on

1. kinetics
2. APD

Class 1B?
Class 1 C?

1. intermediate kinetics
increase APD

2. Fast kinetics, decrease APD

3. Slow kinetics, no effect on APD

17

What drugs are in the class1A antiarrhythmics? (3)

Drugs: Procainamide, Quinidine, Disopyramide

18

Clinical use for Class 1C drugs (1)
- state the 2 drugs

CLinical: Supraventricular arrhythmias in patients with otherwise normal hearts

1. flecainamide
2. propafenone

19

PK for flecainamide (elimination)

half life?

Well absorbed, half-life 20 hrs, elimination: liver and kidney

20

flecainamide (class 1c)

adverse effects/ contraindications (3)

increases mortality in patients with ventricular tachyarrhythmias , MI, and ventricular ectopy (contraindication!)

21

Propafenone
-class
-MOA
(has some ___ activity which is significant to remember)

CLass1C (slow conduction, no change in APD)

Potent blocker of Na+ channels with slow kinetics, may also block K+ channels


-similar structurally to propranolol with weak B blocking activity!!! (bronchospasm, bradycardia etc)

22

Propafenone

Indications

adverse effects/toxicity

Indication: Supraventricular arrhythmias in patients with NORMAL hearts

adverse effects/toxicity:
arrhythmogenic
sinus bradycardia/bronchospasm **
- metallic taste & constipation

23

All Class 1 C anti- arrhythmic drugs are only indicated for what? State the 2 drugs

Supraventricular arrhythmia

- flecainamide
-propafenone

24

Class 2 anti- arrhythmic drugs are what?

B- Blockers

25

Propranolol

- MOA (selective or non)
- effect

MOA: inhibit normal sympathetic effects that act through B receptors

NON SELECTIVE

Effect:
-reduces HR
- decrease pacemaker currents (SA automaticity)
- reduces conduction
-decreases catecholamine induced DAD and EAD mediated arrhythmias

26

Which is the non selective Class 2 B-blocker?

Selective?

- propranolol

- esmolol (shorter half life, IV, 9 min)

SVT!!!

27

Propranolol

-clinical (4)

- prevention of recurrent infarction & sudden death after MI

- Afib
- Afluter
- AV node re-entry

28

Propranolol

side effects (5)

- bradycardia
- reduced exercise capacity
- HF
-hypotension
-AV block

29

Propranolol

Contraindications (4)

- sinus bradycardia
-AV block

- bronchospasm in asthmatics or COPD patients!

- masks tachycardia associated with hypoglycemia in diabetic patients

30

State the 3 class 3 Anti-Arrhythmic Drugs


- moa?

- strong effects at ___ and risk of what?

Amiodarone
Dronedarone
Soltalol

(ADS for 3)

- typically block K+ currents causing prolonged APD

ECG: QT-prolongation

May also enhance inward current
(Na+ channels)

Delayed repolarization leads to
prolongation of action potential duration and prolongation of refractory period


Least effects at fast heart rates (although desirable)

- strong effects at low heart rates (risk of Torsades des pointes)

31

Amiodarone

-MOA
- effect (main point)

MOST IMPORTANT DRUG!!!!

- blocks K+ channels

- also Na, Ca, and B-receptors

Effect: prolong APD
- prolong refractoriness
-slows conduction
-suppresses abnormal automaticity and can slow normal sinus automaticity

PROLONGS QT and QRS complex!

32

Amiodarone

-clinical effect

(oral & IV)

ORAL:

recurrent venricular tachycardia or fibrillation resistant to other drugs
-also Afib (maintains sinus rhythm)


IV: DOC for out of hospital cardiac arrest
- termination of vtachy or fibrillation

33

What is unique out AMiodarone metabolism

50% of drug 3-10 days (still remains)

-Highly lipophilic, accumulation in several organs (heart, lung, liver, cornea)

34

Amiodarone

- adverse effects
(MAIN 1 is_____)

- bradycardia
-heart block in patents with SA/AV node disease

MAIN: Pulmonary toxicity (pulmonary fibrosis in 1%), hepatic toxicity

-Photodermatitis (skin discoloration)
Cornea microdeposits in almost all patients

-Blocks conversion of T4 to T3, source of inorganic iodine:
Hypo- and hyperthyroidisms**

35

Which drug has the following adverse effect:

Pulmonary toxicity (pulmonary fibrosis in 1%), hepatic toxicity

-Photodermatitis (skin discoloration)
Cornea microdeposits in almost all patients

-Blocks conversion of T4 to T3, source of inorganic iodine:
Hypo- and hyperthyroidisms**

AMiodarone (class 3)

36

2 drugs that are both drug of choice for ventricular tachy or fibrillation

amiodarone

lidocaine

37

dronedarone

- moa
- indications

contraindication

MOA: Class 3 (block Na, K and Ca channels and prolong AP)

- structural analogue of amiodarone without done atoms to eliminate effects on thyroxine metabolism (hypo/hyperthyroidism)

Indications: Atrial Fib/ Flutter

Contraindicated: severe HF!

38

Which drug is: contraindicated in severe or recently decompensated symptomatic heart failure

Dronedarone (class 3)

39

Soltalol

- moa
-class
Indications

MOA: B blocker (non-selective)

Indications: Ventricular and supraventricular arrhythmias
- maintenance of sinus rhythm in patients with Afib

40

Class 4 Drugs MOA

(2)

Ca channel blockers (non-dihydropyridines)

- verapamil
- diltiazem

41

Verapamil
-moa
-class

effect: (AV, SA, HR)

- moa: blocks activated and inactivated L type Ca channels in the heart

- Class 4

Effect: use/state dependent action
- major effects in slow response tissues (SA/AV node)
- directly slows AV node conduction and increases AV node refractoriness
- slows SA node automaticity
lower HR & increase PR

42

Verapamil

Clinical Use (DOC)
(3)

DOC for SUPRAVENTRICULAR ARRHYTHMIA

- re-entry arrhythmias/tachycardias involving AV node

- slows ventricular rate in Afib/flutter

43

Verapamil
- metabolized by what? (careful)

side effects:
(3 main)

- LIVER --> careful with liver failure

side effects:
1- VASODILATION & negative inotropic effects
(verapamil has negative inotropic so need to make sure a patient doesn’t have a ventricular tachycardia!!!
(SVT is fine, but not VT!!!)

2-AV block in patients with AV nodal disease or in high doses (treated with atropine or b-receptor stimulants)

3. Heart block in patients with b-adrenoceptor blockers !!!

Constipation, nervousness, vasodilation, peripheral edema

44

Contraindication for verapamil:

ventricular tachycardia (lead to hypotension & negatove inotropic effects)

45

Diltiazem

- MOA
-Class
- Indication (2 others than verapamil)

- MOA: Class 4 Calcium channel blocker

- block L type calcium channels

- lower cardioselectivity (also affects calcium channels in vasculature and causes relaxation)

- HTN & Angina Pectoris

46

Adenosine:

- MOA
-Effect
-DOC

MOA: increase K conductance (hyper polarization ) and inhibits Ca currents via purigenic receptors

Effect: atrial tissues to slow AV node conduction & increase AV node refractoriness

- produce transient cardiac arrest

DOC: PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA

47

Which drug is DOC for PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA

Adenosine

- IV bolus injection! (lasts seconds since causes heart to temporarily block)

48

Adenosine:


- adverse effect

Flushing and shortness of breath, sinus bradycardia, sinus pauses, AV block,
decrease in blood pressure


- Pharmacokinetics and dosage:

Half-life of seconds, rapid IV BOLUS dose required (initially 6 mg i.v.)

Less effective with theophylline/caffeine, potentiated by dipyridamole

49

Cardiac Glycosides:

Digitalis
MOA

- inhibit Na/K ATPase

- affect Na/Ca exchange
- increase intracellular Ca

EFFECT: positive inotropic actions (used in HF)

- parasympathotomimetic effects: increase AV node refractoriness & slow AV ode conduction

(use for atrial arrhythmias and Afib/flutter)

50

Lidocaine is only available in what form?

IV

-extensive LIVER METABOLISM  thus cannot take orally (need IV!)