Antiarrhythmatic Drugs and CHF

Question 1

Therapeutic Mechanism of Quinidine?

Answer 1

1) Block Na+ channels- decreases excitability and decreases conduction velocity in fast tissue.
2) Block K+ channels- prolonged refractory period which can inhibit reentry arrhythmias.

Question 2

Cardiotoxic effect of quinidine

Answer 2

Risk of arrhythmias increases with lengthening of QRS and Q-T intervals.

Question 3

Most common cardiac side effect of quinidine is quinidine syncope: Describe…

Answer 3

Lightheadedness and fainting caused by quinidine-induced torsade de pointes. Usually resolves but can degenrate into ventricular fibrillation.

Question 4

Extracardiac side effects of quinidine

Answer 4

GI disturbances, cinchonism (tinnitus, dizziness, blurred vision, headaches), and rerely thrombocytopenia, hepatitis, angiodema, fever.

Question 5

Actions of K+ channel blockade:

Answer 5

Lengthens action potentials which lengthens refractory period and can therefore interrupt re-entry arrhythmias.

Question 6

ECG of K+ channel blockers:

Answer 6

Lengthened Q-T interval

Question 7

Cardiac Side Effects of K+ channel blockers

Answer 7

Torsade de pointe- lengthened AP can produce early after- depolarization

Question 8

K+channel blockers:

Answer 8

Quinidine, NAPA (procainamide metabolite), sotalol, dofetilide

Question 9

Uses of Ca2+ channel inhibition

Answer 9

Reduces excitability of slow AV nodal and SA nodal tissue. Used for reducing ventricular rate during atrial tachyarrhythmias.

Question 10

ECG changes with Ca2+ channel inhibition

Answer 10

Lengthened P-R interval

Question 11

Cardiac Side effects for Ca2+ channel inhibition

Answer 11

• SA and AV nodal block- beta blockers (propranolol), sotalol, Calcium channel blockers (diltiazem and verapemil), amioderone
• Negative inotropic effect- beta blockers, calcium channel blockers

Question 12

NA+ channel inhibition uses:

Answer 12

Inhibits excitability in fast tissue, used principally for ventricular or supra-ventricular arrhythmias involving fast tissue.

Question 13

ECG changes in Na+ channel inhibition

Answer 13

Lengthened QRS (except lidocaine)

Question 14

Cardiac side effects for NA+ channel blockers

Answer 14

Can cause arrhythmias (especially potent Na channel blockers such as flecainimide)

Question 15

Class 1a: Na+ and K+ channel block drug

Answer 15

Quinidine- Weak anti muscarinic

Question 16

Class 1a: Na+ channel blocker:

Answer 16

Procainamide- weaker K channel blocker (NAPA) and muscarinic block than quinidine

Question 17

SE of Procainamide:

Answer 17

Hypotension, lupus, GI disturbances, hepatitis, fever. Rare agranulocytosis and rash.

Question 18

Class 1B Drug that blocks NA+ channels in depolarized tissue

Answer 18

Lidocaine- little effect on healthy tissue

Question 19

Half life of lidocaine:

Answer 19

1-2 hours; IV or IM

Question 20

Side effects of lidocaine

Answer 20

CNS ( paresthesis, drowsiness, tinnitus, blurred vision; toxic levels: convulsions, unconsciousness, respiratory arrest).

Question 21

Class 1c potent and selective Na+ channel blocker

Answer 21

Flecainamide

Question 22

SE of Flecainamide

Answer 22

Significantly pro-arrhythmic, enhanced risk of death with long term use

Question 23

Class II: Beta-adrenergic receptor blockade drug

Answer 23

Propranolol- Beta blockers reduce beta stimulation of Ca channels and thus act much like Ca channel blockers

Question 24

Side effects of propranolol

Answer 24

• SA and AV block,
• Sudden withdrawal may worsen angina and arrhythmias due to receptor up-regulation,
• shortness of breath

Question 25

Class III: K+ channel block drug

Answer 25

Amiodarone- K channel block, Ca channel block, use-dependent block of Na channels, alpha and beta receptor block

Question 26

Side Effects of Amiodarone

Answer 26

1) Corneal and skin deposits
2) GI disturbances
3) Neurological SE
4) Hypotension (due to Ca Channel block)
5) Life-threatening pulmonary toxicity
6) Liver toxicity
7) Thyroid dysfunction

Question 27

Half life of amiodarone

Answer 27

Long (Up to 3 months)

Question 28

Drug interactions of amiodorone

Answer 28

• SA/AV block when combined with Ca channel blockers or beta blockers.
• Increases plasma level of many anti-arrythmic drugs

Question 29

A K channel blocker and beta blocker

Answer 29

Sotalol

Question 30

K channel blocker SE of Sotalol

Answer 30

Torsades de pointes

Question 31

Beta blocker SE of Sotalol

Answer 31

SA and AV block, sudden withdrawal may worsen angina and arrhythmias due to receptor up-regulation, shortness of breath

Question 32

K- Channel Blocker causing Torsades de Pointes

Answer 32

Dofetilide

Question 33

Class IV: Ca2+ channel blockade drugs

Answer 33

Verapamil and diltiazem

Question 34

SE of Verapamil and diltiazem

Answer 34

1) SA or AV block
2) Negative inotropic effect
3) Constipation (inhibition of gut motility)
4) Peripheral edema (vasodilation from Ca blockers)
5) CNS effects (lassitude, vervousness, dizziness, headache).

Question 35

IV half life of Verapamil and diltiazem

Answer 35

4 minutes

Question 36

Activation of adenosine does what?

Answer 36

Activates K+ channels to hyperpolarize AV nodal tissue by opening K+ channels. Short time of action (seconds)

Question 37

Therapeutic effect of digoxin

Answer 37

Positive inotropic effect

Question 38

Mechanism of digoxin

Answer 38

1) Direct membrane effect: inhibits Na/K ATPase

2) Indirect effect: Parasympathomimetic