Antidysrhythmics/Inotropics

Question 1

Atropine use

Answer 1

To treat bradycardia

Question 2

movement of ions across the cardiac cell membrane results in..

Answer 2

AP (action potential) generation

Question 3

AP leads to..

Answer 3

Contraction of myocardial muscle

Question 4

Supraventricular tachycardia

Answer 4

120-250 BPM

Paroxysmal: Episodic, starts suddenly and returns to normal within 24 hr

Persistent: Episodes > 7 days. Tx needed

Permanent: lasts more than a year despite meds

Question 5

Supraventricular dysthymias affect ventricle contraction rate, thus..

Answer 5

AV block is desirable

Question 6

Which is more dangerous? Ventricular dysrhythmias or supraventricular?

Answer 6

Ventricular

Question 7

Vaughan Williams Classificatiom

Answer 7

Categorizes antidysrhythmia drugs

Class I: Na channel blockers

Class II: B blockers

Class III: K channel blockers

Class IV: Calcium channel blockers

other: adenosine, digoxin

Question 8

Class I: Na Channel Blockers

Answer 8

Block Na Channels. Slow depolarization.

Question 9

Class Ia: Na channel blockers

Answer 9

quinidine
•Slows atrial and ventricular rates
•Used for acute onset atrial fibrillation

Question 10

Class Ib: Na channel blockers

Answer 10

Class Ib: lidocaine (IV)
•Blocks sodium channels
•Used for ventricular dysrhythmias only

Question 11

Class II: B-adrenoceptor antagonists (beta blockers)

Answer 11

Metaprolol

Reduce or block sympathetic nervous system stimulation
•AV block

Question 12

Class III: Potassium Channel Blockers

Answer 12

Amiodarone

Prolong repolarization

Amiodarone is very effective but 75% have serious adverse effects if used >6 months (lung fibrosis..)
10% fatal

Used for resistance to other drugs

Question 13

Class IV: Calcium Channel Blockers

Answer 13

Diltiazem, verapamil
•Inhibits Ca cell entry
•Acts on AV node - reduces conduction velocity (AV block)

Question 14

Unclassified Antidysrhythmics

Answer 14

Digoxin
Adenosine

Both decrease AV conduction

Question 15

Digoxin

Answer 15

AV block
Slows HR

Question 16

Adenosine

Answer 16

Slows conduction through AV node

•for SVT

•Short half-life: 10-20 seconds

Only administered as fast IV push

May cause asystole for a few seconds

Question 17

Nursing implications

Answer 17

Clients taking B-blockers OR digoxin + other agents should be taught to take their own radial pulse for 1 full minute

•notify their physician if the pulse is less than 60 bpm before taking next dose

Question 18

Inotropic: Digoxin

Answer 18

Cardiac glycoside

•Positive inotropic (increased contractility)

•Negative chronotropic (reduced HR at SA node)

•Negative dromotropic (reduced AV node conduction)

Question 19

Inotropics:
3 S’s of Digoxin Action

Answer 19

•Positive inotropic (increased contractility) - STRENGTHEN

•Negative chronotropic (reduced HR at SA node) - SLOWS

•Negative dromotropic (reduced AV node conduction) - SLOWS

Question 20

Digoxin Effects

Answer 20

-increased stroke volume, and therefore cardiac output
-Promotion of diuresis due to improved kidney perfusion

Question 21

Digoxin indications

Answer 21

•Heart failure
•supraventricular dysrhythmias (atrial fibrillation and atrial flutter)

Question 22

Digoxin Adverse Effects

Answer 22

•Narrow therapeutic window
•Drug levels must be monitored
•Low potassium levels increase toxicity
•Generalized malaise
•GI: anorexia, nausea, vomiting, diarrhea
•Coloured vision: seeing yellow
•Dysrhythmias: bradycardia. MUST take apical pulse.

Question 23

Digoxin Toxicity

Answer 23

•Life threatening dysrhythmias
•Digoxin immune Fab therapy used as antidote. Binds to digoxin.

Factors increasing risk for toxicity:
•Low K (diuretics)

Question 24

Digoxin: Client Care Implicatioms

Answer 24

•Assess apical pulse full 1 min (less than 60, more than 120=no give. or less than 90 in infant)
•Labs: potassium, renal
•Slow rate could be sign of toxicity
•Hold dose and notify prescriber if: anorexia, nausea, vomiting, diarrhea or visual disturbances