Anti-arrhythmia drugs

Question 1

What is occurring during phase 0 of action potential in cardiac electrical system fast response fibers?

Answer 1

Activate NA channels open and Na moves into the cell

Question 2

What is occurring during phase 1 of action potential in cardiac electrical system fast response fibers?

Answer 2

Na channels inactivated and K moves outward

Question 3

What is occurring during phase 2 of action potential in cardiac electrical system fast response fibers?

Answer 3

Ca inward balanced by K outward - plateau

Question 4

What is occurring during phase 3 of action potential in cardiac electrical system fast response fibers?

Answer 4

Inactivation of Ca channels
Repolarization –> K outward

Question 5

What is occurring during phase 4 of action potential in cardiac electrical system fast response fibers?

Answer 5

Resting membrane potential by Na/K ATPase pump

Question 6

What is occurring during phase 0 of action potential in cardiac electrical system slow response fibers?

Answer 6

Activation of L-type Ca channels –> Ca inward

Question 7

What is occurring during phase 3 of action potential in cardiac electrical system slow response fibers?

Answer 7

K outward –> repolarization

Question 8

What is occurring during phase 4 of action potential in cardiac electrical system slow response fibers?

Answer 8

Na and Ca inward –> K outward
Pacemaker current

Question 9

4 properties of the electrophysiology of the heart

Answer 9

Responsiveness
Conductance
Automaticity
Refractoriness

Question 10

Equation that illustrates measure of refractoriness of the heart electrical system

Answer 10

ERP/APD
ERP = effective refractory period
APD = action potential duration

Question 11

Result of increase SyNS activity in SA node

Answer 11

Tachycardia

Question 12

Result of increase PsNS activity in the SA node

Answer 12

Bradycardia

Question 13

General mechanism of Vaughn Williams class I antiarrhythmic drugs

Answer 13

Na channel blockers

Question 14

Mechanism of Vaughn Williams class Ia antiarrhythmic drugs

Answer 14

Block activated Na channel to decrease Vmax and prolong ADP

Anticholinergics

Question 15

Anticholinergic effect on the heart

Answer 15

Increase HR and conduction

Question 16

Adverse effects of quinidine

Answer 16

Cinchonism
Increase QT interval –> Torsades de pointes
Displace digoxin –> decrease VD
Antacids increase absorption

Question 17

Symptoms of cinchonism

Answer 17

Tinnitus
Hearing loss
GI upset
Diplopia

Question 18

Adverse effects of procainamide

Answer 18

Agranulocytosis
SLE like syndrome –> slow acetylators

Question 19

Drugs included in Vaughn Williams class Ia antiarrhythmic drugs

Answer 19

Quinidine - also an alpha blocker
Procainamide - least anticholinergic
Disopyramide - most anticholinergic

Question 20

Mechanism of Vaughn Williams class Ib antiarrhythmic drugs

Answer 20

Decrease APD and no effect on Vmax
Increase threshold of V fib
Slow conduction in hypoxic and ischemic tissue
Preference for ischemic tissue

Question 21

Drugs included in Vaughn Williams class Ib antiarrhythmic drugs

Answer 21

Lidocaine –> least cardiotoxic
Tocainide
Mexiletine

Question 22

Cardiovascular uses of lidocaine

Answer 22

V tach after MI
Digitalis toxicity

Question 23

Adverse effects of lidocaine

Answer 23

Drowsiness
Paresthesia
Convulsions –> toxic doses

Question 24

Mechanism of Vaughn Williams class Ic antiarrhythmic drugs

Answer 24

Both Na channels to markedly decrease Vmax with no effect on APD

Question 25

Drugs included in Vaughn Williams class Ic antiarrhythmic drugs

Answer 25

Flecainide Propafenone Moricizine

Question 26

Clinical uses of Vaughn Williams class Ic antiarrhythmic drugs

Answer 26

Life threatening V tach or V fib Refractory SVTs

Question 27

Adverse effects of Vaughn Williams class Ic antiarrhythmic drugs

Answer 27

Pro-arrhythmic effect Increase risk for sudden death and cardiac arrest by decreasing LV function after MI

Question 28

Mechanism of Vaughn Williams class 2 antiarrhythmic drugs

Answer 28

Beta-blocker that decrease SA and AV node conduction --> decrease slope of phase 4 depolarization

Question 29

Clinical uses of Vaughn Williams class 2 antiarrhythmic drugs

Answer 29

Prophylaxis for ventricular arrhythmias post MI SVTs

Question 30

Adverse effects of Vaughn Williams class 2 antiarrhythmic drugs

Answer 30

Proarrhythmic Can cause AV block

Question 31

Mechanism of Vaughn Williams class 3 antiarrhythmic drugs

Answer 31

K channel blockers that increase ADP and ERP. Prolong repolarization and lengthen phase 2.

Question 32

Drugs included in Vaughn Williams class 3 antiarrhythmic drugs

Answer 32

Amiodarone Dofetilide Ibutilide Sotalol Dronedarone

Question 33

Mechanism of amiodarone

Answer 33

Binds to and inactivates Na channel Blocks K and Ca channels Non-competitive inhibition of beta receptors

Question 34

Half-life of amiodarone

Answer 34

25-60 days

Question 35

Clinical uses of amiodarone

Answer 35

A fib V tach Use with anticoagulant

Question 36

Adverse effects of amiodarone

Answer 36

Pulmonary fibrosis Hepatotoxicity Bluish discoloration of skin Hypothyroidism in 5% Hyperthyroidism in 25% Torsades de pointes

Question 37

Mechanism of dofetilide and ibutilide

Answer 37

Selectively block outward K channel (delayed rectifier K channel). Results in prolonged ventricular repolarization and increase QT interval.

Question 38

Uses of dofetilide and ibutilide

Answer 38

Pharmacological cardioversion --> A fib and A flutter

Question 39

Mechanism of sotalol

Answer 39

Beta blocker and K channel blocker - Decrease HR and AV conduction - Prolongs APD and ERP

Question 40

Antiarrhythmic uses of sotalol

Answer 40

A fib Life threatening ventricular arrhythmias

Question 41

Adverse effects of sotalol

Answer 41

Torsades de pointes HA Depression Impotence

Question 42

Contraindication of sotalol

Answer 42

Asthma

Question 43

Ca channel blockers used for arrhythmias

Answer 43

Diltiazem Verapamil

Question 44

Mechanism of Ca channel blockers in arrhythmia

Answer 44

Decrease SA and AV nodal conduction Decrease slope of phase 4

Question 45

Anti-arrhythmic use of Ca channel blockers

Answer 45

PSVT due to AV nodal reentry

Question 46

Adverse effects of Ca channel blockers

Answer 46

Orthostatic hypotension Reduce CO Lower extremity edema Constipation

Question 47

Drug interactions of verapamil

Answer 47

Displaces digoxin, increasing its toxicity

Question 48

Drug interaction of Ca channel blockers

Answer 48

Pro-arrhythmic AV block is used with beta blockers

Question 49

Condition in which Ca channel blockers should be used with caution

Answer 49

A tach due to WPW

Question 50

Rapid acting AV nodal blocker with a half-life of 30 seconds

Answer 50

Adenosine

Question 51

Adenosine receptors and their effect

Answer 51

A1 --> Gi coupled --> decrease SA and AV nodal rate A2a --> Gs coupled --> vasodilate A2b --> Gq coupled --> bronchoconstrict

Question 52

Clinical use of adenosine

Answer 52

Drug of choice for PSVT

Question 53

Antagonist of adenosine

Answer 53

Theophylline

Question 54

Adverse effects of adenosine

Answer 54

Flushing SOB Burning sensation in chest

Question 55

Anti-arrhythmic uses of digoxin

Answer 55

Control ventricular rates in A fib and A flutter

Question 56

Arrythmias caused by drugs that prolong QT intervals

Answer 56

Torsades de pointes

Question 57

Treatment for Torsades de pointes

Answer 57

Discontinue causative agent Magnesium sulfate and potassium

Question 58

Some drugs that can cause torsades de pointes

Answer 58

Amiodarone Quinidine Sotalol Thioridazine TCAs