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Patho Fall 2019 > Ex2 L5 CVS > Flashcards

Ex2 L5 CVS Flashcards

1
Q

Force the muscle can generate is dependent on

A

Length of muscle

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2
Q

Optimal length of muscle

A

Resting length

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3
Q

Bicep muscle is example of

A

Length-tension relationship

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4
Q

Optimal length of cardiac muscle

A

The more stretched it is (more filled ventricle = more force)

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5
Q

Cardiac muscles are physically coupled via

A

Desmosome

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6
Q

Cardiac muscles are coupled via

A

Physically + electrically

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7
Q

Cardiac muscle cells are coupled electrically via

A

Gap junctions

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8
Q

Autorhythmic cells

A

Spontaneously fire action potentials

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9
Q

Unique aspect of autorhythmic cells

A

They require no triggering event

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10
Q

Instead of action potential, autorhythmic cells have

A

Pace (maker) setter potential

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11
Q

Responsible for all triggering events of cardiac muscle

A

Autorhythmic cells

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12
Q

What makes pace setter cell different from other cells?

A

Constant leak of sodium into cell

“Leak sodium channels”

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13
Q

Why do pace maker cells not have a stable membrane potential?

A

Leak sodium channels

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14
Q

What helps slow depolarization move to threshold?

A

T-type calcium channels

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15
Q

Responsible for slow depolarization of cardiac cells

A

Leaky sodium channels

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16
Q

At threshold, what channels open?

A

Long-type Calcium Channels

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17
Q

Once L calcium channels open, what happens?

A

Calcium rushes into cell, fast depolarization

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18
Q

At peak of self-induced action potential, what occurs?

A

Calcium channels close
Potassium channels open
Potassium moves out of cell

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19
Q

Repolarization of autorhythmic cells occurs as a result of

A

Potassium channels open, Ca2+ channels close

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20
Q

What happens during Repolarization of autorhythmic cells

A

K moves out of cell

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21
Q

Cardiac action potential - rapid depolarization is due to

A

Opening of “fast” Na+ channels

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22
Q

Difference between AP of normal cells vs cardiac cells

A

Plateau phase, no discernible repolarization phase

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23
Q

Trigger of depolarization in cardiac cells

A

Autorhythmic cells

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24
Q

After depolarization of cardiac cells, what happens?

A

Sodium channels close

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25
Q

After depolarization + Na channels close, what occurs?

A

Plateau phase

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26
Q

Plateau phase of cardiac cells

A

Calcium channels open - ca2+ move in

Potassium channels open - K moves out

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27
Q

Main difference between normal AP and cardiac AP is a result of

A

Sustained depolarization - d/t Calcium

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28
Q

Sustained depolarization allows for

A

Enough time for all cardiac cells (intercalated together) to depolarize as a single unit

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29
Q

Important for both autorhythmic and cardiac cells

A

Calcium

30
Q

Locations of autorhythmic cells

A
  1. SA node
  2. AV node
  3. Bundle of His (septum)
31
Q

Pathway of autorhythmic cells

A

SA —> AV —> Bundles of His

32
Q

Characteristic of Bundle of His

A

Deep fibers - Purkinje fibers — penetrate into walls of both ventricles (contraction at same time)

33
Q

Wave of APs - direction in heart

A

Begins at apex of heart and moves up ventricular wall

34
Q

SA Node is also known as

A

Pacemaker of heart

35
Q

What happens if SA node is too slow?

A

AV node will “fire first”

Ventricles do not benefit from atrial contraction

36
Q

Reason for difference in frequency between autorhythmic cells

A

Length of time cells spend in slow depolarization phase

37
Q

SA node speed

A

70-80 APs/minute

38
Q

AV node speed

A

40-60 APs/minute

39
Q

Bundle of His speed

A

20-40 APs/minute

40
Q

Time between SA —> AV node firing

A

AV nodal delay

100 ms

41
Q

Reason for AV nodal delay

A

Time to allow maximal filling of ventricles

42
Q

Where does the SA node firing go?

A
  1. Interarterial pathway (to LA)
  2. Intermodal pathway (to AV node)
  3. RA
43
Q

What defines systole/diastole

A

Ventricular contraction

44
Q

P wave

A

Depolarization of SA node + atria

45
Q

T wave

A

Repolarization of ventricles

46
Q

QRS complex

A

Depolarization of both ventricles

47
Q

Pause between P and QRS complex

A

AV Nodal Delay

48
Q

ECG without P wave

A

AV node fired before SA node

SA too slow or silent for a beat

49
Q

Pause between QRS and T wave

A

Blood is moving from ventricles into arteries

50
Q

ECG represents

A

Electrical events in heart

51
Q

R-R interval

A

Heart rate

52
Q

Passive filling occurs during

A

Ventricular + atrial diastole

53
Q

Ventricular filling is mostly

A

Passive

54
Q

Last bit of blood that goes into ventricles at end of diastole

A

Atrial kick

55
Q

Contraction of ventricles occurs

A

Following QRS

56
Q

Both AV valves shut when?

A

Ventricular pressure rises above atrial pressure

57
Q

First heart sound

A

AV valve closure

58
Q

All valves are shut

A 
Isovolumetric contraction
(Ventricles are contracting against constant volume)
59
Q

Aortic valve opening occurs

A

When ventricular pressure surpasses aortic pressure

60
Q

Ventricular ejection

A

Occurs after ventricular pressure > aortic pressure, arterial/pulmonic valve opens, rush of blood into aorta

61
Q

T wave

A

Repolarization/relaxation of ventricles

Decrease in V pressure

62
Q

Measure of cardiac performance

A

Ejection fraction

63
Q

Difference between SV and CO

A 
SV= one beat
CO = one minute
64
Q

Aortic/pulmonic valve closure

A

V pressure < aortic pressure

65
Q

Second heart sound

A

Aortic/pulmonic valve closure

66
Q

Isovolumetric relaxation

A

Atrial pressure < ventricular pressure < aortic pressure; all valves shut

67
Q

Dicrotic notch

A

Aortic valve shuts —> bump in aortic pressure

68
Q

Systolic blood pressure is an indirect measurement of

A

Ventricular pressure

69
Q

DBP is an indirect measure of

A

Conditions of arteries (elasticity)

Total Blood volume

70
Q

Cardiac suction

A

Dip in atrial pressure (atria are filling while ventricles are emptying)

Patho Fall 2019 (13 decks)

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