Cardio 10 Deck 3

Question 1

Arrhythmias are caused by

Answer 1

physiological and/or anatomical consequences to prevent normal cardiac action potentials.

Question 2

Normal HR depends on

Answer 2

the intrinsic electrical impulses initiated at the sinoatrial (SA) node and conducted to the AV node and over the ventricles.

Question 3

Absolute refractory period

Answer 3

Regardless of the strength of a stimulus, the cell cannot be depolarized.

Question 4

Relative refractory period

Answer 4

Stronger-than-normal stimulus can induce depolarization

Question 5

Refractoriness

Answer 5

State of the cardiac cell which determines depolarization.

Question 6

Damaged heart cells

Answer 6

may maintain a constant rate of refractoriness or may not be refractory at all.

Question 7

Spontaneously depolarizing cells

Answer 7

SA nodes, AV nodes, His-Purkinje, special atrial cells

Question 8

Automaticity

Answer 8

Ability of a heart cell to spontaneously depolarize and generate an action potential

Question 9

Automaticity may be

Answer 9

altered, enhanced, decreased by:

Cell damage, biochemical disturbance, pharmacological agents, environmental toxins

Question 10

Automacity is the target

Answer 10

Target for antiarrhythmic drugs

Question 11

Reentry Phenomena

Answer 11

Reentry is the cause of some arrhythmias.

It depends on two anatomically or physiologically distinct electrical pathways.

Question 12

Normally, impulses from the

Answer 12

AV node are conducted down both pathways in the same direction, bifurcating to cover the entire ventricle.

Sometimes this will get interupted and go out of order and this is wher eyou will have atopic irregular beats. Reentry phenomena

Question 13

Reentry Phenomena

If a block is encountered

Answer 13

by the action potential in one of the pathways, then the impulse can only be conducted down the other pathway.

The impulse can return to the initial point of bifurcation and reexcite the myocardium

Question 14

Short-circuiting conducting tissue can occur

Answer 14

and cause premature contraction.

PVC and PAC

Question 15

If reentry is

Answer 15

repetitive, sustained ventricular arrhythmias, such as ventricular tachycardia, can occur.

Question 16

Class I: sodium channel blockers

MOA

Answer 16

A: lengthen the duration of action potential
B: shorten the duration of action potential
C: minimally increase action potential

Question 17

Class II: beta blockers

MOA

Answer 17

Reduce adrenergic activity in the heart
Sotalol: considered a class II and III drug

Question 18

Class III: potassium channel blockers

MOA and example

Answer 18

Prolong effective refractory period and reduce speed of conduction
Amiodarone

Question 19

Class IV calcium channel blocker MOA

Answer 19

Block the influx of calcium, reduce contractility (negative inotropism), decrease SA and AV node conduction
Significantly reduce afterload but little effect on preload

Question 20

Class IV calcium channel blocker example

Answer 20

Verapamil, diltiazem, bepridil

Question 21

potassium will

Answer 21

prolong the effect of refractory period to reduce the speed of conduction. This can stop the heart.

Question 22

I. Membrane-stabilizing agents (sodium channel blockers)

examples A,B,C

Answer 22

Quinidine, procainamide, disopyramide
Lidocaine, phenytoin
Encainide, Iorcainide, flecainide

Question 23

Beta blocker examples

Answer 23

Propranolol, metoprolol, sotalolol, and others

Question 24

III. Agents that prolong duration of the action potential (potassium channel blockers)

examples

Answer 24

Amiodarone, bretylium

Question 25

. Agents that prolong duration of the action potential (potassium channel blockers)

examples

Answer 25

Amiodarone, bretylium

Question 26

IV. Calcium channel blockers

examples

Answer 26

Verapamil, diltiazem, bepridil

Question 27

Pharmacological management of arrhythmias requires

Answer 27

an office that is prepared, ready, and able to handle emergencies.

Question 28

Drugs for arrhythmias you will see these patients for

Answer 28

infections, depression, anemia, fatigue, and so on. Be aware of actions and adverse drug interactions.

Question 29

Beta Adrenergic Blockers various types include

Answer 29

include nonspecific beta antagonists, selective beta-antagonists, and those with or without intrinsic sympathomimetic activity (ISA)

Question 30

Beta blockers are commonly seen in

Answer 30

In post-MI patients, cardioselective agents without ISA are preferred.

Question 31

some beta blockers are used as

Answer 31

aniarrhythmics

Question 32

Drugs with ISA may help

Answer 32

avoid a decrease in cardiac output (CO) and HR. May be preferred for patients who experience bradycardia with other BBs.

Question 33

Beta Adrenergic Blockers more effective in

Answer 33

African American and older patients

Question 34

BBs may NOT be

Answer 34

abruptly withdrawn, because it will increase beta receptor sensitivity

Question 35

BB are no longer

Answer 35

first-line HTN drug choice

Question 36

Amiodarone class

Answer 36

III antiarrhythmic

Question 37

Amiodarone onset of action

Answer 37

oral – 2 days to 3 weeks

Question 38

Amiodarone duration of action

Answer 38

7 to 50 days

Question 39

Amiodaraone excreted in

Answer 39

feces, 1% in urine

Question 40

Amiodarone watch out for

Answer 40

for use of grapefruit juice!

inhibits the absorption and will cause the pts to get the wrong dose.

Question 41

Dose of Amiodarone

Answer 41

Ventricular arrhythmias: 800 to 1,600 mg twice daily for 1 to 3 weeks, then decreased to 300 to 400 mg twice daily, maintenance 400 mg/day

Question 42

Amiodarone ARR

Answer 42

thyroid, neurological, blue skin discoloration, bradycardia, lung damage not evident until advanced

Question 43

Amiodarone drug interactions

Answer 43

many

Question 44

For All Antiarrhythmics Monitoring

Answer 44

Potassium, blood urea nitrogen (BUN), creatinine, therapeutic drug levels
Electrocardiography (ECG)

Question 45

For All Antiarrhythmics Patient education

Answer 45

Take exactly as prescribed; do not double doses.
Be aware of food–drug interactions.
Monitor HR for regularity of rate and rhythm.
Monitor BP at home.