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Anatomy > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Cardiac and smooth muscle are similar how?

A

“Unitary” contract as a unit.

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2
Q

Where are intercalated disc located?

A

Convoluted borders (only found in the heart tissue)

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3
Q

How are the convoluted borders/intercalated disc beneficial to the heart tissue?

A

increase gap junctions (increased surface area)

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4
Q

What do cardiac muscle and skeletomuscular tissue have in common?

A

sarcomere & striated pattern (d/t actin and myosin alignment)

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5
Q

the different in cardiac muscle cell and skeletomuscular?

A

Only one cell nuclei

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6
Q

Fibroblast

A

cells that create scar tissue

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7
Q

Tx for CHF

A

ACEi and ARB - prevent growth factor causing too much scar tissue.

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8
Q

What component of RASS is the growth factor?

A

Angiotensin II

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9
Q

Syncytial connections

A
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10
Q

The majority of the heart cells are?

A

cardiac myocytes

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11
Q

What do conduction tissue lack?

A

Myofibrils, tissue specialized to generate APs

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12
Q

What kind of neuron can conduct AP faster?

A

large neuron more than a small neuron.

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13
Q

Endocardium

A

innermost layer of heart

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14
Q

Endocardium lining

A

one cell layer thick and composed of endothelial cells.

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15
Q

Myocardium

A

bulk of the muscle wall

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16
Q

Pericardium (4)

A

Epicardium, pericardial space, parietal pericardium, fibrous pericardium

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17
Q

what layer are the vessels in the heart?

A

Coronary art. and vein run along the epicardium

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18
Q

Epicardium also called

A

visceral layer

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19
Q

What cells and tissue in the epicardium

A

mesothelial cells and connective tissue

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20
Q

Pericardium space (cavity)

A

between the parietal and epicardium layer

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21
Q

Fluid found in the pericardial space

A

mucus and fluid

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22
Q

Parietal pericardium

A

can stretch (inner layer of sac)

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23
Q

fibrous pericardium

A

leather like material (like dura)

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24
Q

What can constrict the heart

A

Fluid accumulation in the fibrous pericardium

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25
Q

Where do MIs occur often?

A

Subendocardium

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26
Q

Cardiac sarcomeres at rest

A

not relaxed at an optimal degree (eliminating H band)

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27
Q

Frank-starling law and heart

A

preload is needed to increase the force of contraction

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28
Q

Ventricular Vrm

A

-80mV

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29
Q

Ventricular AP threshold

A

-70 mV

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30
Q

Purkinje Fiber Vrm

A

-90 mV

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31
Q

Purkinje fiber AP threshold

A

-70 mV

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32
Q

Intrinsic Purkinje fiber HR

A

20-40 bpm

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33
Q

Oculocardiac reflex

A

V & X stimulation = severe bradycardia

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34
Q

iCa, iNa, iK mean?

A

current crossing over resistance

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35
Q

duration of cardiac muscle AP

A

about 200 msec

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36
Q

normal HR

A

72 bpm

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37
Q

AP every sec for 72 bpm

A

0.83 sec

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38
Q

HR without nervous system influence

A

110 bpm

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39
Q

SA node + sympathetic (only)

A

120 bpm (10 bpm increase)

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40
Q

SA + vagal influence (only)

A

60 - 62 bpm

41
Q

AV node instrinsic rate

A

40-60 bpm

42
Q

Purkinje fibers instinct rate

A

15-30 bpm

43
Q

Normal AP difference (magnitude)

A

100 mV

44
Q

EKG (y-axis) Small box:

A

0.1 mv

45
Q

EKG (Y axis) larger box:

A

0.5 mV

46
Q

EKG (x-axis) small box:

A

0.04 sec

47
Q

EKG (X-axis) big box:

A

0.2 sec

48
Q

EKG (X Axis) 5 big boxes:

A

1 sec

49
Q

Net magnitude of EKG

A

1.5 mV

50
Q

P wave (boxes & deflection)

A

Positive deflection ( 2 boxes up and 2 boxes long)

51
Q

Atrium repolarization

A

end of the S wave (buried in QRS)

52
Q

QRS wave duration

A

0.06 sec

53
Q

Tall QRS

A

misplacement of leads or heart tissue is enlarged. (hypertrophy of vent)

54
Q

Prolonged QRS

A

dilated cardiomyopathy

55
Q

j point

A

isoelectric point, point of reference for infarct.

56
Q

unhealthy tissue and T wave

A

Chronic depolarization in post T wave, ischemic myocardium

57
Q

QT interval

A

0.25-0.35 secs

58
Q

R to R interval

A

usually 0.83 sec

59
Q

HR Formula

A

60 sec/ R-R interval (sec)

60
Q

Lusitropy

A

how fast repolarization of ventricles

61
Q

SA nodal tissue threshold

A

-40 mV

62
Q

SA nodal Vrm

A

-55mv

63
Q

HCN Channel

A

hyperpolarization + cyclic nucleotide

64
Q

HCN channel ion

A

Na+ primary / Ca++ secondary

65
Q

cAMP

A

cyclic nucleotide

66
Q

Beta agonist

A

increase HR by opening more HCN channels

67
Q

hyperkalemia

A

increase HR by making Vrm more positive.

68
Q

Hypercalcemia

A

decrease HR (make threshold more positive)

69
Q

hypocalcemia

A

decrease threshold potential = faster HR

70
Q

Diastolic depolarization

A

Phase 4 AP of nodal tissue

71
Q

Phase 0 of Nodal tissue

A

lack VG Na+

72
Q

Density of HCN channels

A

SA node (highest) AV node (less) Vent. (least)

73
Q

sec for normal conduction of heart

A

0.22 sec

74
Q

Interatrial bundle

A

Bachmann’s bundle

75
Q

SA to AV node (sec)

A

0.03 sec

76
Q

AV node to Bundle of His

A

0.12 sec

77
Q

Bundle of His to bundle branches

A

0.01 sec

78
Q

lead II placement

A

(-) R arm & (+) L ft

79
Q

Lead I placement

A

(-) R arm & (+) L arm

80
Q

lead III placement

A

(+) L ft & (-) L arm

81
Q

Einthoven’s Triangle

A

aVR, aVL, aVF

82
Q

Mean axis deviation

A

59 degrees

83
Q

Right axis deviation

A

More than 59 degree

84
Q

left axis deviation

A

less than 59 degrees

85
Q

EKG diagnose WHAT

A

3 lead EKG

86
Q

EKG diagnose WHERE

A

12 lead EKG

87
Q

Einthoven’s Law

A

Lead I + Lead III = lead II

88
Q

Einthoven’s law is based on what?

A

equilateral triangle

89
Q

What does Einthoven’s law provide clinicals with?

A

help check the accuracy of ECG recordings and detect possible errors in lead placement.

90
Q

When do you see the most positive deflection on the EKG?

A

when tissue is 50% depolarized and 50% at rest.

91
Q

How do Ca++ channel blockers work?

A

Ca channel blockers inhibit “the calcium component” in phase 4 (diastolic depolarization) of nodal action potential, slowing the HR.

antagonizing the L type calcium channels, preventing CICR from SR.

92
Q

Beta Agonist stimulation in heart tissue?

A

synthesis of cAMP

cAMP activated PK-A

PK-A phosphorylates:
- L type channels
- Troponin I
- Phospholamban

93
Q

Phosphorlyated phospholamban

A

Loses its inhibitory effect on SERCA, which accelerates calcium reuptake into SR.

(+) chronotropic

94
Q

Effect the lusitropy of the heart?

postive and negative?

A
  • Phospholamban ( + chronotropy)

shorter ST segment

Negative lusitropy would be the unphosphrylation of phospholamban

95
Q

Phosphorylation of Trop I

A

increase Ca++ sensitivity of contractile proteins

increasing cycling rate of cross bridge generation

(+) inotropic effect

96
Q

Phosphorylation of L type Ca++ channels

A

increases sensitivity (chronotropic influence) of channel and easier to open.

This will increase the amount of calcium coming inside during an AP.

(+) inotropic and chronotropic

97
Q

How does L type Ca++ channels contribute to EAD or DAD?

A

too much beta adrenergic activity = heart attacks by an increase in sensitivity by the phosphorylation of L type Ca channel .

too much sensitivity of L-type calcium channels is BADDDD : causing an MI

98
Q

inhibition of PDe:

A

will increase the cAMP availability = increasing activity of PKA = phosphorylation of -lamban, Trop I, L CA++

Anatomy (7 decks)

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