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Physiology I Block 3 > Cardio 7.13 > Flashcards

Cardio 7.13 Flashcards

1
Q

second degree heart block

A

P wave is not always followed by QRS

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2
Q

describe mobitz type I

A

a second degree heart block

PR interval gets progressively longer and then QRS will drop

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3
Q

describe motbitz type II

A

randomly dropped QRS

PR interval the same and then random drop of QRS

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4
Q

mobitz type II thought to reflect damage to

A

specialized conduction system

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5
Q

which is worse mobitz type I or II

A

II

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6
Q

what happens to AP with hyperkalemia

A

it shortens - it promotes potassium conductance so increased potassium current

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7
Q

what happens to rate of rise with yperkalemia

A

slowed - this is the sodium current

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8
Q

what happens to AP with hyperkalemia

A

shortens AP duration

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9
Q

as you depol cell you switch from what for sodium channels

A

to inactivated state

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10
Q

how do you get from inactivated state to closed state

A

negative resting membrane potential again

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11
Q

QRS you don’t want bigger than

A

2 little boxes (80)

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12
Q

peaked t wave

A

cells really sensitive to high potassium (hyperkalemia) so they repol fast and you get peak t wave (pg 205)

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13
Q

causes of conduction block

A

closure of gap junctions

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14
Q

what could cause closure of gap junctions

A

ischemia
low pHi
high Cai

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15
Q

what happens to pH during ischemia

A

low

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16
Q

why is pH low in ischemia

A

CO2 increases

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17
Q

what happens to calcium in ischemia

A

increases - can close gap junctions

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18
Q

lidocaine does what

A

blocks sodium channels

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19
Q

cocaine does what

A

blocks sodium channels

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20
Q

sodium channel blockers used to block pain and also as

A

antiarthmia

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21
Q

sodium current (INa) produces upstroke of

A

everything but SA and AV, so atrial ventricular, Hi-spurkinje myocytes

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22
Q

inhibition of Ica by medications

A

decreases upstroke of AV and SA nodes, would think it would also decrease AP duration

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23
Q

Ica produces

A

upstroke of SA and AV nodal cells

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24
Q

Ach blocks

A

calcium current

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25
Q

Ach affects

A

conduction velocity through AV nodes and contractability of atria

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26
Q

what is most common caues of tachycardia

A

re-entry

27
Q

how can you get unidirectional conduction

A

dead cells that can’t fire AP - you end up with one cell trying to activate a bunch and i isn’t ble to do that (pg 210)

28
Q

what is reentry

A

AP is re-entering in spacial area (like dog chasing its tail)

29
Q

when wave fronts come through ventricles what normall yhappens

A

collide come togther, activate, and extinguish (but in re-entry it doesn’t extinguish)

30
Q

re-entry in AV node would cause

A

ventricles to fire at fast rate

31
Q

micro-rentry you would see in

A

ventricular fibrulation

32
Q

two broad types of reentry and reentrant arrhytmias

A

anatomical & functional (spiral waves)

33
Q

what do you need for re-entry to proceed

A

excitable gap

34
Q

put a premature beat in and what happens

A

anatomical reentry (ppt 210) there is video

35
Q

look at anatomical reentry

A

pg 215

36
Q

describe reentrant ventricular tachycardia

A

very fast HR lower CO
QRS wider than normal and no distinguishable P or T waves
pg 216

37
Q

if there is bypass track what syndrome can develop

A

wolff-parkinson white syndrome

38
Q

what is bypass track

A

band of muscle tat connects atria directly to ventricle

39
Q

describe wolff parkinson white syndrome

A

fast AP conduction via accessory pathway (bypass track_ - short PR interval. pre-excitation with delta waves

40
Q

What does WPW stand for

A

wolff-parkinson-white syndrome

41
Q

what is delta wave

A

ramp like start to R wave, no Q wave

42
Q

Look at WPW

A

pg 217

43
Q

pt with WPW pre-disposed to what

A

pre-disposed to re-entrant ventricular tachycardia

44
Q

what does AVRT stand for

A

atrioventricular reentrant ventricular tachycardia

45
Q

how might you treat WPW

A

can identify the bypass track and put catheter and apply frequency nd destroy the accessory pathway

can also reduce calcium current, so it slows AV node, so can give pt calcium channel blockers

46
Q

adenosine is

A

fast channel calcium blocker

47
Q

atrial flutter characterized by

A

“saw-tooth”atrial activity

48
Q

atrial flutter describe

A

crazy re-entry through the atria every time it fires - goingso fast it’s not contributing to ventricle filling

49
Q

how to identify atrial flutter

A

the saw tooth pattern of p waves

50
Q

atrial flutter can degrade into

A

atrial fibrulation

51
Q

Ventricular fibrillation can be caused easily by

A

even small hit to tet

or electrecutted

52
Q

VF stands for

A

ventricular fibrillation

53
Q

SCA stands for

A

sudden cardiac arrest

54
Q

who is at risk for SCA

A

pts with coronary artery disease
pts with heart failure
pts with inherited channelopathies causing ventricular arrhythmia

55
Q

most widespread sustained arthymia

A

atrial fibrillation

56
Q

AF stands for

A

atrial fibrillation

57
Q

describe AF

A

no visible P waves

ventricular firing often fast and irregular

58
Q

look at AF

A

pg 225

59
Q

what is missing in ECG in AF

A

p wave

60
Q

why isn’t there P wave in AF

A

P wave is b/c of normal coordinated propegation of AP through atria - so you might get little squiggle but no discernible p wave.

61
Q

how do you treat arrhythmia

A

Electrical Cardioversion

Antiarrhythmic Drugs

Catheter Ablation

Implanted Rhythm Devices

62
Q

defibrilation

A
  • put electrodes on chest (v fib)
63
Q

cardioversion

A

apply shock and convert to normal sinus

64
Q

ccardioversion vs. defibrillation

A

cardioversion apply shock during QRS

Physiology I Block 3 (14 decks)

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