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pharm sci exam 2 > Waldrop > Flashcards

Waldrop Flashcards

0
Q

Resting HR

A

60-100 pbm

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1
Q

Main pace maker cell

Channels?

A

SA node

Channels are Ica Ik and If

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2
Q

Secondary pacemakers
Rate?
Channels?

A

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

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3
Q

Purkinje fibers

A

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

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4
Q

Normal conduction of the heart

A

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

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5
Q

Why is conduction slowed through the av node?

A

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

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6
Q

What affects the QT interval?

A

Potassium blockers

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7
Q

What effects the PR interval?

A

Calcium channel blockers

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8
Q

Resting phase

A

Activation gate closed

Inactivation gate open

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9
Q

Activated phase

A

Activation gate open
Inactivation gate open
Sodium in

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10
Q

Inactivated state

A

Activation gate open
Inactivation gate closed
Sodium entry blocked
Potassium excreted

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11
Q

Recovery state

A

Inactive back to resting state

Dependent on cell membrane voltage being neg

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12
Q

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

A

Prolonged the. Tissue is harder to depolarize

Good anti arrhythmic

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13
Q

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

A

Inactive state

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14
Q

Arrhythmias are due to what?

A

Disturbances in impulse formation and/or conduction

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15
Q

What has the highest rate of spontaneous formation?

A

SA node

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16
Q

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

A

Hypo kalemia

Increase autonomic ns activation

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17
Q

Impulse formation

A

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

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18
Q

After depolarization

A

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

19
Q

EAD

A

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

20
Q

DAD

A

Occurs at fast hr and associated wit calcium overload

Can be from digoxin overload or excessive SMS activity

21
Q

Impulse conduction

A

Due to block or reentry

22
Q

Block

A

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

23
Q

First degree block

A

Abnormal long PR interval

24
Q

Second degree block

A

Every other p wave is able to conduct through av node

2:1

25
Q

Third degree block

A

Complete heart block

26
Q

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

A

Rabbit ears or prolonged qrs interval

27
Q

Re-entry

A

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

28
Q

Fibrillation

A

Reentry circuits may be random and meander through myocardial tissue

29
Q

Three conditions required for reentry

A
  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)
30
Q

2 methods to treat reentry circuits

A

1 speed conduction around depressed tissue

2 increase the effective refractory period of depressed area

31
Q

Bidirectional block

A

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

32
Q

How do drugs that treat arrhythmias prolong refractory period?

A

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

33
Q

Atrial fibrillation

A

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

34
Q

Treat a fib via rhythm control

A 
Class 1 sodium blocking and class three potassium blocking 
Corrects reentry 
Makes tissue refractory
35
Q

A fib treatment for rate control

A 
Class 4 and class 2 and digoxin 
Slows av node
36
Q

Rate control

A

Controls av node

Makes more resistant to signals

37
Q

Rhythm control

A

Converts back to normal sinus rhythm

38
Q

Premature ventricular contractions

A

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

39
Q

Ventricular tachycardia

A

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

40
Q

Sinus bradycardia

A

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

41
Q

Sinus tachycardia

A

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

42
Q

Mesolithic e

A

Used for neuropathies

43
Q

Lidocaine

A

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

44
Q

Quinidine

A

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

45
Q

Interactions of quinidine

A

3a4 inhib
Inhibits 2d6
Decreases clearance of digoxin

46
Q

ADR of quinidine

A

Diarrhea
Cinchonism
Antimuscarinic effects

pharm sci exam 2 (7 decks)

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