Waldrop

Question 0

Resting HR

Answer 0

60-100 pbm

Question 1

Main pace maker cell

Channels?

Answer 1

SA node

Channels are Ica Ik and If

Question 2

Secondary pacemakers
Rate?
Channels?

Answer 2

Av node
Rate 50-60 pbm
Channels- Ica, Ik, If

Question 3

Purkinje fibers

Answer 3

In ventricles
Fire 30-40 bpm
Channels Ina, Ica, Ik, If

Question 4

Normal conduction of the heart

Answer 4

SA node depolarizers, goes to av node via intermodal pathways, depolarization spreads across atria, conduction slows through av node, depolarization move to apex of heart from apex back up

Question 5

Why is conduction slowed through the av node?

Answer 5

To allow for blood to fill in order to be contracted out

Question 6

What affects the QT interval?

Answer 6

Potassium blockers

Question 7

What effects the PR interval?

Answer 7

Calcium channel blockers

Question 8

Resting phase

Answer 8

Activation gate closed

Inactivation gate open

Question 9

Activated phase

Answer 9

Activation gate open
Inactivation gate open
Sodium in

Question 10

Inactivated state

Answer 10

Activation gate open
Inactivation gate closed
Sodium entry blocked
Potassium excreted

Question 11

Recovery state

Answer 11

Inactive back to resting state

Dependent on cell membrane voltage being neg

Question 12

If a drug stabilizes the inactive state, what happens to the recovery time?

Answer 12

Prolonged the. Tissue is harder to depolarize

Good anti arrhythmic

Question 13

What type of tissue do anti arrhythmic prefer to bind to?

Answer 13

Inactive state

Question 14

Arrhythmias are due to what?

Answer 14

Disturbances in impulse formation and/or conduction

Question 15

What has the highest rate of spontaneous formation?

Answer 15

SA node

Question 16

What mechanisms alter the rate of impulse formation resulting in arrhythmias?

Answer 16

Hypo kalemia

Increase autonomic ns activation

Question 17

Impulse formation

Answer 17

Spontaneous formation of an action potential due to significant If or sodium leak restricted to SA node, AV node, and perkinje fibers

Question 18

After depolarization

Answer 18

Impulses that interrupt phase 3 or phase 4 of cardiac myocytes action potential

Question 19

EAD

Answer 19

Occurs at low hr when action potential duration or QT interval is long and can occur with potassium blockers or congenital abnormalities

Question 20

DAD

Answer 20

Occurs at fast hr and associated wit calcium overload

Can be from digoxin overload or excessive SMS activity

Question 21

Impulse conduction

Answer 21

Due to block or reentry

Question 22

Block

Answer 22

Increase pns activity may depress av node so conduction from atria to ventricles is slowed or prevented treat with anti muscarinic aka atropine

Question 23

First degree block

Answer 23

Abnormal long PR interval

Question 24

Second degree block

Answer 24

Every other p wave is able to conduct through av node | 2:1

Question 25

Third degree block

Answer 25

Complete heart block

Question 26

Right or left ventricular block can cause what on the EKG?

Answer 26

Rabbit ears or prolonged qrs interval

Question 27

Re-entry

Answer 27

When one impulse renters and excites areas of heart more than once Abnormality- accessory bypass tract from atria to ventricles bypasses the AV node

Question 28

Fibrillation

Answer 28

Reentry circuits may be random and meander through myocardial tissue

Question 29

Three conditions required for reentry

Answer 29

1. Obstacle to homogenous condition (not traveling at same speed) 2 unidirectional block 3 conduction time around the block (must be long enough so area is no longer refractory and can conduct in retrograde fashion)

Question 30

2 methods to treat reentry circuits

Answer 30

1 speed conduction around depressed tissue | 2 increase the effective refractory period of depressed area

Question 31

Bidirectional block

Answer 31

Good bc conduction is fast around the depressed tissue it gets to other side while that tissue is still refractory

Question 32

How do drugs that treat arrhythmias prolong refractory period?

Answer 32

1 delay recovery by prolonging the inactivation state of voltage gated sodium channels 2 prolong depolarization by blocking potassium channels

Question 33

Atrial fibrillation

Answer 33

Erratic atrial muscle depolarizations with multiple foci Irregular irregularly tracing No p wave on EKG and no pattern with Qrs

Question 34

Treat a fib via rhythm control

Answer 34

``` Class 1 sodium blocking and class three potassium blocking Corrects reentry Makes tissue refractory ```

Question 35

A fib treatment for rate control

Answer 35

``` Class 4 and class 2 and digoxin Slows av node ```

Question 36

Rate control

Answer 36

Controls av node | Makes more resistant to signals

Question 37

Rhythm control

Answer 37

Converts back to normal sinus rhythm

Question 38

Premature ventricular contractions

Answer 38

Skipped beat Wide weird qrs followed by a pause Can be uni or multi focal

Question 39

Ventricular tachycardia

Answer 39

Rapid succession of depolarizations resulting from ventricular foci originating at ventricular pacemaker

Question 40

Sinus bradycardia

Answer 40

Lower heart rhythm than norm originating from sinus node less than 60 bpm

Question 41

Sinus tachycardia

Answer 41

Heart rhythm from sinoatrial node with elevated rate of impulses greater than 100 bpm

Question 42

Mesolithic e

Answer 42

Used for neuropathies

Question 43

Lidocaine

Answer 43

Used for ventricular arrhythmias Not for prophylaxis Binds alpha 1 glycoprotein Increased in stress so levels vary when pt goes back to normal

Question 44

Quinidine

Answer 44

Class1/3 Accelerates AV node b/c anti muscarinic Makes it easier for abnorm impulses to reach ventricles

Question 45

Interactions of quinidine

Answer 45

3a4 inhib Inhibits 2d6 Decreases clearance of digoxin

Question 46

ADR of quinidine

Answer 46

Diarrhea Cinchonism Antimuscarinic effects