LEC EXAM #3 CHP 11 Flashcards

1
Q

Cardiac muscle tissue characteristics: (4)

A
  • automaticity
  • extended contraction time
  • long absolute refractory period
  • nervous system alters contraction force and rate
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2
Q

Automaticity:

A
  • contraction without neural stimulation

- controlled by pacemaker cells (SA node)

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3
Q

In what way does cardiac muscle tissue have a long absolute refractory period?

A

Prevention of wave summation and tetanic contractions of cell membranes

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4
Q

Does cardiac or skeletal muscle tissue have a longer contraction time?

A

Cardiac

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5
Q

2 kinds of cardiac cells:

A
  • pacemaker cells (auto rhythmic/myogenic cells)

- contractile cells

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6
Q

Intercalated discs:

A

Hold cells together

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7
Q

Gap junctions:

A

Ports that allow ions to spread from one cell to another

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8
Q

Pacemaker cells are found:

A
  • SA node (sets pace/rate)
  • AV node
  • Bundle of HIS
  • Purkinjee fibers
  • Bundle branches
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9
Q

What do pacemaker and contractile cells have in common?

difference?

A
  • both rely on K+, Ca2+, Na+, and CI-

- different AP’s

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10
Q

4 characteristics of pacemaker cells:

A
  • spontaneously depolarize
  • slow to depolarize/hit threshold
  • autorhythmic
  • do NOT contract
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11
Q

Pacemaker cell AP

Phase 0: (2)

A
  • Ca rushes in

- increases depolarization

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12
Q

Pacemaker cell AP

Phase 3:

A

K leaves

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13
Q

Pacemaker cell AP

Phase 4:

A

Na rushes in

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14
Q

Pacemaker cells depolarized by:

A

Ca rushing in

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15
Q

Contractile cells characteristics:

A
  • low RMP= -96 mv
  • gets impulse from pacemaker cells via gap junctions
  • depolarize-> contract
  • long absolute refractory period
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16
Q

Do pacemaker cells or contractrile cells have a longer absolute refractory period (depol)?

A

Contractile

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17
Q

Why do contractile cells have a longer absolute refractory period?

A

Because Ca is rushing in at the same time as K is leaving, leading to a plateau PHASE 2

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18
Q

Cardiac muscle cell contraction occurs:

A

In contractile cells only

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19
Q

Provides Ca for cardiac muscle contraction:

important bitch

A

ECF and SR

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20
Q

Main function of sarcoplasmic reticulum?

A

To store Ca

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21
Q

Less Ca (in cardiac muscle cell contraction) =

A

less force generated

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22
Q

Heart failure channel blocker would be:

A

Calcium

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23
Q

What is the secondary active transport in cardiac muscle cell relaxation?

A

Calcium being forced out by Na coming in

sodium-calcium antiport

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24
Q

Cardiac tissue is innervated by:

A

Autonomic nervous system at SA node

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25
Q

What is absolute refractory period responsible for?

A

Not generating an AP

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26
Q

How do contractile cells communicate?

A

SA node spreads through the atria

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27
Q

AV node is responsible for what during contraction?

A

Takes the impulse from the atria to the ventricles

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28
Q

Why do we need relaxation to occur?

A

To refill with enough blood

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29
Q

Once contractile cells get an impulse, what happens?

A
  • Ca from skeletal muscle is released from endoplasmic reticulum
  • binds troponin to move tropomyosin out of the way
  • myosin binds to active site
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30
Q

Where do we get Ca for skeletal muscle contraction?

A

Sarcoplasmic reticulum

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31
Q

Alpha and beta adrenergic cardiac tissue receptors bind:

A

Nor-epi + Epi (hormone) and increase depolarization of pacemaker cells

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32
Q

Epi has higher affinity for:

A

Beta adrenergic receptors

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33
Q

What happens to your HR when nor-epi and epi bind to alpha and beta receptors?

A
  • increase in HR
  • increase in SV
  • increase in CO
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34
Q

Nor-epi has higher affinity for:

A

Alpha adrenergic receptors

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35
Q

Sympathetic hormones:
receptors:

Parasympathetic hormones:
receptors:

A

NE + Epi
Alpha + Beta adrenergic

Ach
Muscarinic cholinergic

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36
Q

What happens to your HR when Ach bind to muscarinic cholinergic receptors?

A
  • decrease in HR
  • decrease in SV
  • decrease in CO
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37
Q

Phenoxybenzamine:

A

Antagonistic drug that binds to alpha adrenergic receptors

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38
Q

Propranolol:

A

Antagonistic drug that binds to beta adrenergic receptors

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39
Q

Atropine:

A

(from deadly night shade)

antagonistic drug that binds to muscarinic cholinergic receptor

40
Q

How would phenoxybenzamine effect HR?

A

Unable to bind to alpha adrenergic receptor to nor-epi so slight decrease in HR

41
Q

Lead 1:

A

RA (-) LA (+)

42
Q

How would atropine effect HR?

A

blocks Ach and causes an increase in HR

43
Q

How would propranolol effect HR?

A

Since we have more beta receptors, greater decrease in HR

44
Q

Lead 2:

A

RA (-) and LL (+)

45
Q

Lead 3:

A

LA (-) and LL (+)

46
Q

Which lead shows the bulk of the electrical current?

A

Lead 2

47
Q

“0” on an EKG represents:

A

Isoelectric line= no electrical activity

48
Q

When waveform deflects up (pos deflection)->

A

Electrical activity is going towards positive lead (lLL)

49
Q

When waveform defects down (neg deflection)->

A

Electrical activity is going towards negative lead (RA)

50
Q

P wave shows:

A

Atrial depol

51
Q

Before the atria depolarizes, what has to depolarize?

A

SA node

52
Q

QRS interval shows:

A

Ventricle depol

53
Q

T wave shows:

A

Ventricle repol

54
Q

Where is the P wave depolarizing towards?

A

LL

Positive deflection

55
Q

Interval has ____

Segments have no ____

A

Waves

56
Q

If SA node is damaged, can the heart still beat?

A

Yes, but the rate will be slower and the AV node takes over

57
Q

Cardiac cycle:

A

period between the start of one heartbeat and the beginning of the next

58
Q

Cardiac cycle consists of:

A

Systole + diastole

59
Q

Atria cardiac cycle:

A
  1. atria passively fill (end of diastole)
  2. atria contract (start of systole)
  3. atria eject blood into ventricles (end of systole)
  4. atria relax (start of diastole)
60
Q

Ventricular cardiac cycle:

A
  1. ventricles passively fill as atria fill and contract (end of diastole)
  2. atria contract (start of systole)
  3. atria eject blood into ventricles (end of systole)
  4. atria relax (start of diastole)
61
Q

What is happening at diastole?

A

Blood is filling into the atria and ventricles

62
Q

What is the “lub” sound in the heart?

A

Blood hitting the closed AV valves, pressure is built up

63
Q

What is the “dub” sound in the heart?

A

Blood hitting the shut semilunar valves

64
Q

During systole, what happens to BP?

A

increases

65
Q

During diastole, what happens to BP?

A

decreases

66
Q

Blood flows from:

A

high -> low pressure

67
Q

What dictates blood flow throughout the heart?

A

Contractions and valves

68
Q

Does all the blood get ejected from the ventricles when it contracts?

A

NO

69
Q

Where is pressure higher?

A

Ventricles

70
Q

Ventricles contract every:

A

270 milliseconds (0.2 secs)

71
Q

Contraction for heart time:

A

370 milliseconds

72
Q

How is SV calculated?

A

EKG, ultrasound, prob into neck

73
Q

Tachycardia:

A

Fast rhythm

74
Q

Bradycardia:

A

Slow rhythm

75
Q

Be able to talk through the steps of the Wigger diagram:

A
  • P wave depolarizes
  • Increase in atrial pressure-> atrial systole
  • blood is pushed into ventricles as a result of the LA contracting
  • increase in ventricular volume
  • QRS complex causes ventricular depol
  • isovolumetric contraction occurs resulting in the AV and semilunar valves closing as the ventricles build up in pressure
  • semilunar valve opens causing ejection
  • causes a decrease in ventricular volume
  • T wave causes ventricles to repolarize
  • ventricle relaxation + isovolumetric relaxation
  • ventricles able to fill again
76
Q

Ventricular filling (phase 1)

A
  • blood->relaxed atria->av valves->ventricles

- atria contract-> blood going into ventricles

77
Q

Isovolumetric contraction (phase 2)

A
  • ventricles begin contracting
  • all valves closed
  • no blood flowing=same volume
78
Q

Ventricular ejection (phase 3):

A
  • ventricles contract

- blood ejects into aorta + pulmonary arteries

79
Q

Isovolumetric relaxation (phase 4)

A
  • semilunar shut

- AV valves open and ventricles passively fill with blood until they contract again

80
Q

During ventricular contraction the aorta:

A

Stores energy by stretching (pressure reservoir)

81
Q

Aortic pressure is higher than ventricular pressure during:

A

Diastole

82
Q

During ventricular diastole the aorta:

A

Releases pressure to maintain blood flow to body

83
Q

MAP=

A

profusion pressure to organs

84
Q

EDV:

A

End-diastolic volume

85
Q

ESV:

A

End-systolic volume

86
Q

Equation to get SV?

A

EDV-ESV=SV

87
Q

Starling’s law:

A

Increase EDV by increasing venous return via:

  • skeletal muscle pump
  • respiratory pump
  • sympathetic nervous system
  • arterial vasoconstriction
88
Q

Dicrotic notch shows:

A

Semilunar valves closing

89
Q

Equation to get CO?

A

SVxHR=CO

90
Q

What does increasing venous return result in? (starling’s law cont.)

A
  • increase stretch of cardiac fibers
  • increase strength of contraction
  • increase SV
91
Q

Starling’s law causes:

A

Stroke volume to increase

92
Q

How do we measure resting HR? (3)

A

3 sec method
6 sec method
R-R method

93
Q

PT interval:

A

heart contracts, systole

94
Q

PT segment:

A

heart resting, diastole

95
Q

Why is an AP not possible during absolute refractory period?

A

Because Na v.g.v. are sealed shut