Test 3: lecture 2 Flashcards

1
Q

action potential curve of skeletal muscle

A

depolarization

repolarization

hyperpolarization

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2
Q

absolute refractory period

A

no additional signal can happen

(waiting for sodium channels to re-set)

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3
Q

relative refractory period

A

second action potential can start but needs to be much stronger

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4
Q

•In reference to the graph below illustrating the contraction of a skeletal muscle fiber over time, what do you think would happen if a second action potential was triggered at the time where the big green arrow is pointing?

A.Nothing because the action potential is still in its refractory period

B.The next contraction would produce a higher tension due to summation

C.The fiber would relax more quickly

D.The next tension/time curve would have a plateau

A

B.The next contraction would produce a higher tension due to summation

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5
Q

____ cardiac cells are not autorhythmic, but do conduct action potentials

A

contractile cardiac cells

(generate force)

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6
Q

___ cardiac cells provide a pathway for spreading excitation through the heart

A

autorhythmic

pacemaker cells

conduction fibers

*don’t generate much contractile force)

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7
Q

the main job of auto-rhythmic cardiac cells is ___

A

pacemaker (create action potential)

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8
Q

how is action potential of fast response action potentials different from skeletal muscles

A

the repolarization phase is much longer (plateau)

2-3 msec

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9
Q

fast response action potentials in the heart are driven by ___

A

voltage gated Na+ channels

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10
Q

slow response AP is driven by __

A

Ca2+ (L-type Ca2+ channels)

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11
Q

what kind of AP do autorhythmic cardiac cells produce

A

slow response AP

(Calcium driven pump)

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12
Q

what kind of AP do contractile cardiac cells produce

A

fast-response AP

Na+ driven

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13
Q

___ potentials lead to spontaneous action potentials

A

•Pacemaker

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14
Q

P acemaker potentials lead to spontaneous action potentials due to hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (funny current) and ___calcium channels

A

T-type

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15
Q

why no hyper-polarization in fast response AP

A

resting at -90

almost at equilibrium potential for potassium (-94)

(normal muscle resting is at 70 so when potassium is repolarizing it is trying to get to its happy place at -94 and causes hyperpolarization)

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16
Q

how do hyperpolarization-activated cyclic nucleotide-gated (HCN) channels work?

A

opened during hyperpolarization

opens and lets sodium into the cell causing a slow depolarization (will get about half way pacemaker potential → other half to threshold by T-type Calcium channels)

“funny current”

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17
Q

how does pacemaker potential work?

A

hyperpolarization-activated cyclic nucleotide-gated (HCN) channels open during hyperpolarization and lets sodium into the cell causing a slow depolarization

about half way, Ttype Ca channels will open and get “pacemaker” cell to threshold

where L-type Ca channels open

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18
Q

___ cause spontaneous depolarization of pacemaker cells

A

hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (sodium channels triggered by hyperpolarization)

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19
Q

how does ANS effect pacemaker potential

A

effects cyclic nucleotide production

which effect hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (sodium channels)

will change slope. very steep → fast HR. low slope → slow HR

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20
Q

what causes plateau for AP in contractile cardiac cells

A

K leaving and Calcium entry are even for a little keeping same charge

calcium channels close but K continues to leave and cell will repolarize

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21
Q

why no summation is contractile cardiac cells

A

AP and contraction same length

(can not receive another AP until contraction is done)

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22
Q

I Kr

A

rapidly activated delayed rectifying potassium current

more potassium leave cell causing repolarization

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23
Q

I Ks

A

slowly activating delayed rectifying potassium current

potassium leave cell cause rapid depolarization

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24
Q

I K1

A

inward rectifying potassium current

potassium trying to get to -94 happy place

(can move potassium in or out)

resting potential for contractile cardiac ell at -90

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25
Q

steps of AP in pacemaker cells

A

Phase 4 (pacemaker potential)

  • If: funny current, HCN channel- sodium into cell (slight depolarization
  • ICa2+ (T): calcium current, T-type voltage gated channel (calcium into cell slowly- slight depolarization)

Phase 0:

•ICa2+ (L): calcium current, L-type voltage gated channel (rapid calcium into cell- fast depolarization (not as fast as Na but faster then T type calcium)

Phase 1 and 2 are absent

Phase 3:

•Ik: potassium current (K out of cell → repolarization), delayed rectifier potassium (although there are several potassium channels here)•

Also important: IKACh: rectifying potassium current that is important for parasympathetic regulation of HR

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26
Q

explain

A

4: pacemaker potential : HCN (Na in slowly), T-type Ca (calcium in slowly)

hits threshold → stage 0

Ltype Ca (calcium in faster)

stage 3: calcium close, K open (K leave cell)

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27
Q

intercalated disks

A

Desmosomes provide structural strength

  • Cells are electrically linked through gap junctions
  • The heart behaves as a functional syncytium
  • Anisotropic conduction
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28
Q

how is electrical current conducted from cell to cell in the heart

A

intercalated disks

desmosomes (gap junctions)

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29
Q

anisotropic conduction

A

1 direction movement of electrical current

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30
Q

functional syncytium means __

A

heart cells will beat at same time cause electrical signal is passed through gap junctions at intercalated disks

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31
Q

conduction through the heart

A
32
Q

___ is the pacemaker of the heart

A

SA (sinoatrial node)

33
Q

•The ___ is the only pathway through which the signal can pass between the atria and the ventricles

A

AV node

atrioventricular node

34
Q

there is a slight ___ in transmission from SA to AV node

A

delay

(allow blood to move into ventricles)

35
Q

what causes the delay in transmission from SA to AV node

A

reduction in gap junctions sending signals

reduction in diamter

36
Q

___ provides for unidirectional passage of action potential through the atria to ventricles

A

AV node

37
Q

___ act as an auxiliary pacemaker if needed

A

AV node

38
Q

what is the pathway of the spread of AP through the heart

A

SA→AV→ bundle of his → perkinji fibers

39
Q

If any pacemaker/conduction cell can initiate its own action potential, then why is the SA node the heart’s “pacemaker”?

A

to keep everything in order

unidirectional blood flow

Because of the hierarchy of normal automaticity and the concept of overdrive suppression!

SA node will spontaneously fire faster then other places

40
Q

activity of the Na/K pump is dependent on the__ node

A

SA

try to keep up with the 70-80 AP per min

if SA stops working, AV node only does 40-60 AP per min but Na/K at same level making cell more negative → hyperpolarization→ makes it harder for the cell to reach threshold → takes longer for pacemaker potential to reach threshold

41
Q

explain overdrive suppression

A

there are enough Na/K pumps to maintain AP for the SA node at 70-80 AP/min

this amount of Na/K makes the cell hyper polarized which makes it harder for other cardiac cells to spontaneously fire

42
Q

abnormally high heart rate

A

tachycardia

•Classified based on site of origin (atrial tachycardia, sinus tachycardia, junctional tachycardia, ventricular tachycardia)

43
Q

abnormally low heart rate

A

bradycardia

44
Q

dysfunction of the SA node

A

sick sinus syndrome

45
Q

depolarizations during the refractory period

A

Afterdepolarizations

46
Q
  • Early afterdepolarizations (EAD): occur during phase__
  • Delayed afterdepolarizations (DAD): occur during phase __
A

2-3

4

47
Q

early afterdepolarization happens when?

A
48
Q

what happens with delayed afterdepolarization

A
49
Q

•a complete block; no atrial action potentials conducted to ventricles

A

3rd degree block

50
Q

: some atrial action potentials conducted to ventricles

A

2nd degree block

51
Q

•all atrial action potentials transmitted to ventricles, however the delay at the AV node is abnormally long

A

1st degree block

52
Q
A

unidirectional block

reentry of AP back into atria

53
Q

abnormal parallel signaling through the heart

A

reentry

unidirectional block

  • Most common mechanism of arrhythmias
  • Caused by a block and/or slowed conduction

Anatomically defined•Wolff-Parkinson-White Syndrome

Functionally definedIschemia, pH alterations

54
Q

•Length and amplitude of waves of the ECG depend on two factors

A

:•Size of the sum of potentials•Synchronicity of potentials

55
Q

explain

A

if you look from A → B the ions closest to you are more positive, then the ions closer to B (1st line)

if you look from C→ D the ions have = charge → straight line

56
Q

P wave=

A

atrial depolarization

left to right = more + on right = bump up

57
Q

Q wave

A

early ventricular depolarization

(left side faster then right→ right side not depolarized yet→ from left side = more negative then right → downward bump

58
Q

R wave

A

ventricular depolarization

depolarization from inside to outside, at this time but ventricles not the same width → + deflection toward the apex (left) → left more + then right = positive spike

59
Q

S wave

A

later ventricular depolarization

last bit of ventricles depolarize → from left to right → left negative = small negative spike

60
Q

T wave

A

ventricular repolarization

(repolarization from apex to base, left to right ) repolarization = positive out of the cell = left more + → positive bump

61
Q

QRS=

A

ventricular depolarization

62
Q

why positive T wave?

A

repolarization of ventricle

= cell becoming more negative = loss + (cell lose K+)

the K channels in the apex of the heart faster then the K channels in the base therefore repolarization left → right gives a + bump

63
Q

Einthoven’s law

A

Any two of the three bipolar limb leads determine the third one.

Lead I + Lead III = Lead II

bipolar limb leads

64
Q

P-Q segment

A

no bump

time after P but before Q

65
Q

intervals vs segments

A

intervals include wave

segments time inbetween wave

66
Q
A

60 sec/0.75 sec= 80 beats per min

67
Q

draw ECG for tachycardia

A

short T-P segment

68
Q

draw ECG for bradycardia

A

long T-P segment

69
Q

draw ECG for 1st degree AV block

A

•First-degree block: all atrial action potentials transmitted to ventricles, however the delay at the AV node is abnormally long

long P-Q interval

70
Q

draw ECG for 2nd degree AV block (type 1)

A

•Second-degree block: some atrial action potentials conducted to ventricles

type 1= most AP gets through but each time longer and longer then resets

PR progressively longer then resets→ eventually AV might take over and there will be a skipped P wave

71
Q

draw ECG for 3rd degree AV block

A

•Third-degree block: a complete block; no atrial action potentials conducted to ventricles

AV node will trigger on its own -40 AP/min, can combine together

no obvious pattern, SA on its own, AV on its own

72
Q
A

ST segment

73
Q

Can atrial repolarization be observed on an ECG if there is a separation between atrial and ventricular depolarization (i.e. during a block?)

A

in theory yes

atrial repolarization occurs during ventricle depolarization (QRS) if there is heart block atria and ventricle beating on there own pace

there could be a chance to see the repolarization of atria if timing is correct

TA wave -Blue line - wide and shallow and negative = left side more - then right side (same direction as depolarization wave)

74
Q

when on an ECG is the plateau phase in the ventricles occuring?

A

ST interval

75
Q

can atrial repolarization be observed on an EKG if there is a separation between atrial and ventricular depolarization (i.e during a block)?

A

yes during 3rd degree heart block, atria and ventricles contract at different patterns, Atria by the SA and ventricles by the AV node.

in a normal EKG atria repolarization occurs during the QRS, so you can’t see it

during block the random rhythm, may allow the repolarization to be seen- (negative wave, repolarization occurs in same direction as depolarization)