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PHYS III > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

1
Q

Which disease is the # 1 cause of death?

A

Cardiovascular Disease

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2
Q

Major underlying cause of ischemia I due to:

A

Atheroscerosis (plaquing)

Artery Spasm

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3
Q

Causes of Inflamation

A

High blood cholesterol (dyslipidemia)

recruitment &expression of pro-inflammatory cytokines

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4
Q

Inflammatory pathways promote:

A

Thrombosis

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5
Q

Thrombosis is responsible for:

A

MI & most strokes

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6
Q

The Nervous System can modulate

A

Inflammation

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7
Q

Hemostasis is:

A

Prevention of blood loss

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8
Q

Mechanisms of hemostasis:

A

Vascular Spasm
Formation of platelet plug
Blood coagulation
Fibrous tissue growth to seal

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9
Q

Vascular Constriction associated with:

A

Trauma

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10
Q

SNS induced constriction from pain is caused by:

A

Neural Reflexes

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11
Q

Responsible for most of the constriction

A

Local myogenic spasm

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12
Q

Local humoral factors include:

A

Thromboxane A2 from platelets (especially important in smaller vessels)

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13
Q

Platelets contain:

A 
Contractile proteins (actin & myosin)
Enzymes
Calcium
ADP & ATP
Thromboxane A2
Serotonin
Growth Factors
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14
Q

Platelet Cell Membrane Contains:

A

Glocoproteins (adhere to damaged area

Phospholipids containing platelet factor 3 (initiates clotting)

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15
Q

Mechanism of Platelet Activation:

A

When platelets contact damaged area they:

  1. Swell
  2. Irregular form w/ irradiating processes protruding from surface
  3. Contractile proteins contract causing granule release
  4. Secrete ADP, Thromboxane A2, & Serotonin
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16
Q

Thromboxane A2 is a/an:

A

Vasoconstrictor &

Potentiates the release of granule contents

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17
Q

Platelets are important in:

A

Minute ruptures

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18
Q

A lack of platelets is associated with:

A

Small hemorrhagic areas under the skin and throughout internal tissues

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19
Q

Platelets have a half-life of:

A

8-12 days

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20
Q

Platelets primarily eliminated by:

A

Macrophage action (mostly occurs in spleen)

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21
Q

On average there are ______platelets per ul

A

150,000-300,000

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22
Q

Role of Endothelium:

A

Prevents platelet aggregation
Produces PGI2
Produces factor VIII

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23
Q

PGI2’s role in endothelium:

A

Its a vasodilator
Stim. Platelet adenyl cyclase which suppresses release of granules
limits platelet extension

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24
Q

Factor VIII’s role in endothelium:

A

Clotting

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25
Q

Aspirin blocks:

A

Thromboxane A2 & prostacyclin production by inhibiting fatty acid cyclooxygenase which converts arachidonic acid to PGG2 & PGH2

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26
Q

Anticoagulants prevent:

A

Clots from forming via:
Chelators (tye up calcium)
Heparin (complexes w/ Antithrombon III)
Dicumarol (Inhibits Vit. K dependent factors; II, VII, IX, X aka Cumadin/ warfarin)

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27
Q

Dissolving clots that have already formed is called:

A

Lysis of Clots

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28
Q

The inactive form of plasmin which circulates in the blood

A

Plasminogen

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29
Q

Endogenous Activators of Plasminogen are found in:

A

Tissues, plasma, & urine

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30
Q

Exogenous Activators of Plasminogen:

A

Streptokinase

Tissue Plasminogen Activator (tPA)

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31
Q

Most of the frank tissue damage associated w/ infarction occurs via:

A

Reperfusion

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32
Q

Reperfusion associated w/

A

Formation of highly reactive oxygen species w/ unpaired electrons (free radicals)

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33
Q

Free radicals are generated when:

A

pressure on tissues relieved & again perfused w/ blood

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34
Q

The ability to open up alternate routes of blood flow to compensate for a blocked vessel

A

Collateralization

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35
Q

The formation of new blood vessels

A

Angiogenesis

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36
Q

Collateralization occurs via:

A

Angiogenesis
Vasodilation
SNS stimulation (may impede via vasoconstriction and/ or augment via the release of NPY)

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37
Q

Extrinsic mechanism of thrombosis:

A

Initiated by chemical factors released by damaged tissues

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38
Q

Intrinsic mechanism of thrombosis:

A

requires only components in blood trauma to blood exposure to collagen (or foreign surface)

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39
Q

Clotting Factors:

A 
I - fibrinogen
II - Prothrombin
III -Thromboplastin
IV - Calcium
V - Proaccelerin
VII - Serum prothrombin conversion accelerator
VIII - Antihemphilic factor (A)
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40
Q

Clotting Factors Cont:

A 
IX - Antihemophilic factor (B)
X - Stuart factor
XI - Antihemophilic factor (C)
XII - Hageman factot
XIII - Fibrin stab. Factor
Prekallikrein 
High molecular weight kininogen
Platelets
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41
Q

Hepatocytes (liver’s) role in clotting:

A 
Liver synthesizes 5 clotting factors;
I - fibrinogen
II - Prothrombin
VII - SPCA
IX - AHF B
X - Stuart factor
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42
Q

Hepatocytes (liver’s) role in clotting Cont.:

A

Coumarin depresses liver formation of II, VII, IX, & by blocking action of Vit K

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43
Q

Hemphilia is sex linked on the _____chromosome

A

X Chromosome

mostly men

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44
Q

85 % of Hemophilia cases occur due to a defect in:

A

Factor VIII

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45
Q

15 % of Hemophilia cases occur due to a defect in:

A

Factor IX

46
Q

Key step to clotting is the conversion of:

A

Fibrinogen to fibrin which requires thrombin

47
Q

Autoimmune disorder where the body makes antibodies against phospholipids in cell membranes

A

Antiphospholipid antibody syndrome

48
Q

Antiphospholipid antibody syndrome causes ______ to form

A

Clots

49
Q

Amino acid in the blood that may irritate blood vessels prompting atherosclerosis.

A

Homocysteine

50
Q

Homocysteine levels can be reduced by taking

A

folic acid, B6 and B12

51
Q

Produced 2-8 months after birth spontaneously

A

Agglutinins

52
Q

Immediate Hemolysis in mismatched transfusions

A

less common

53
Q

Delayed Hemolysis in mismatched transfusions

A

More common

54
Q

Syncytium =

A

many acting as one

55
Q

Intercalated discs create

A

low resistance pathways connecting cells end to end

56
Q

Na+

A

Inc. at depol

Dec. at repol

57
Q

Ca++

A

Inc. at depol

Dec. at Repol

58
Q

K+

A

Dec. at DepolInc. at repol

59
Q

Tetradotoxin blocks fast Na+ channels selectively changing a fast response into

A

a slow response

60
Q

During resting membrane potential ______ and ____ are closed and ____ channels are open

A

Na+ and Ca++ closed

K+ open

61
Q

If the Na+/K+ pump is inhibited, what accumulated?

A

Ca+

62
Q

Ca+ accumulation in the cardiac cell _____contractile strength

A

Increases

63
Q

Absolute Refractory Period

A

Unable to re-stim cardiac cell

Occurs during the plateau

64
Q

Relative Refractory Period

A

Requires a supra-normal stimulus

Occurs during repol

65
Q

Normal pacemaker of the heart

A

SA node

66
Q

The SA node is:

A

less (-) at Er, has a leaky membrane to Na+ and Ca++, and contracts feebly

67
Q

Cells of the AV node and perkinje system are under overdrive suppression by the

A

SA node

68
Q

Delays the wave of depolarization from entering the ventricle

A

AV node

69
Q

Allows the atria to contract slightly ahead of the ventricles

A

AV node

70
Q

Slow conduction velocity due to smaller diameter fibers

A

AV node

71
Q

AV node may act as a slower pacemaker in absence of

A

SA nodr

72
Q

AS Heart Rate Inc, cycle length:

A

decreases

73
Q

At a resting heart rate systole is ____diastole

A
74
Q

During systole perfusion of the myocardium is restricted by the

A

contracting cardiac muscle compressing blood vessels

75
Q

Isovolumic contraction and ejection

A

Systole

76
Q

Isovolumic relaxation, rapid inflow, diastasis, atrial systole

A

Diastole

77
Q

Volume of ventricles at the end of filling

A

End Diastolic Volume

78
Q

Volume in ventricles at the end of ejection

A

End Systolic Volume

79
Q

Volume ejected by ventricles

A

Stroke Volume

80
Q

% of EDV ejected

A

Ejection Fraction (SV/EDV * 100)

81
Q

Normal Ejection Fraction

A

50-60%

82
Q

Stretch on the wall prior to contraction

A

Preload

83
Q

Changing aortic BP during ejection of blood from the left ventricle

A

Afterload

84
Q

Associated with atrial contraction

A

A wave

85
Q

Associated with ventricular contraction

A

C wave

86
Q

Associated with atrial filling

A

V wave

87
Q

LV pressure > Aortic pressure =

A

Aortic Valve open

88
Q

Aortic pressure > LV pressure =

A

Aortic valve closed

89
Q

AV valves

A

Mitral and tricuspid

90
Q

Semilunar valves

A

Aortic and pulmonic

91
Q

Valve not opening fully

A

Stenoic

92
Q

Valve not closing fully

A

Insufficient/leaky

93
Q

Valve creates vibrational noise

A

murmor

94
Q

Systolic Heart Murmur =

A

Aortic and pulmonary stenosis + mitral & tricuspid insufficiency

95
Q

Diastolic Murmur

A

Aortic and pulmonary insufficiency + mitral & tricuspid stenosis

96
Q

Both Systolic and Diastolic Murmur =

A

Patent ductus arteriosis combined valvular defect

97
Q

Law of Laplace

A

At a given operating pressure as ventricular radius INC, developing wall tension also INC.

98
Q

Anything that effects the heart rate

A

Chronotropic

99
Q

Anything that effects conduction velocity

A

Dromotropic

100
Q

Anything that effects strength of contraction

A

Inotropic

101
Q

Within physiologic limits the heart will pump all the blood that returns to it without allowing excessive damming of blood in veins

A

Frank-Starling Law of the Heart

102
Q

Mechanism of Frank-Starling:

A

Increased venous return causes increased stretch of cardiac muscle fibers

103
Q

Increased stretch of cardiac muscles causes:

A

An increase in cross-bridge formation, calcium influx, and stretch on SA node

104
Q

When cardiac fibers are stretched and the force of contraction is increased, this is called

A

Heterometric autoregulation

105
Q

3 methods of Heterometric Autoregulation:

A

Flow induced
Pressure induced
Rate induced

106
Q

Flow induced means:

A

inc. stroke volume maintained as EDV dec.

107
Q

Pressure induced means:

A

Inc. in aortic BP will Inc. force of contraction

108
Q

Rate induced means:

A

Inc. HR will Inc. force “treppe”

109
Q

Stretch on SA node will:

A

Increase Ca+/Na+ permeability, increases HR

110
Q

Sympathetic innervation:

A

Increases HR, strength of contraction, and conduction velocity

111
Q

Parasympathetic innervation:

A

Decreases HR, strength of contraction, conduction velocity

PHYS III (1 decks)

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