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BRS Phys > Ch 3 > Flashcards

Ch 3 Flashcards

1
Q

What is stressed volume?

A

Blood volume contained in arteries

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2
Q

What vessels are the site of highest resistance in the CV system?

A

Arterioles

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3
Q

What vessels have the highest total cross sectional and surface area?

A

Capillaries

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4
Q

What vessels contain the highest proportion of blood in the CV system?

A

Veins

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5
Q

What is unstressed volume?

A

Blood volume contained in veins

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6
Q

What is the formula for velocity of blood flow?

A

v = Q/A Q = blood flow
A = cross sectional area

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7
Q

How is velocity related to cross sectional area in vessels?

A

Inversely proportional

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8
Q

What is the formula for flow?

A

Q = delta P / R delta P = pressure difference
R = resistance

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9
Q

What is Poiseuille’s equation?

A

R = 8nl/(pi)r^4 R = resistance
n = viscosity
l = vessel length
r = vessel radius

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10
Q

How is vessel resistance related to vessel radius?

A

Vessel resistance is inversely proportional to vessel radius to the 4th power

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11
Q

How is vessel resistance related to blood viscosity?

A

Directly proportional

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12
Q

How is vessel resistance related do vessel length?

A

Directly proportional

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13
Q

What happens to total resistance when arteries are added in parallel? In series?

A

Parallel - resistance decreases Series - resistance increases

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14
Q

What does Reynolds number predict?

A

Whether blood flow will be turbulent or laminar

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15
Q

What does an increased Reynolds number mean?

A

There will be a greater tendency for turbulent blood flow

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16
Q

What two factors increase Reynolds number?

A

Decreased blood viscosity Increased blood velocity (decreased vessel radius)

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17
Q

What is compliance?

A

The ability of a vessel to distend to handle increases in volume

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18
Q

How is compliance related to elastance?

A

Inversely proportional - the more elastic fibers in a vessel, the less compliant (able to handle volume) it will be

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19
Q

What is the formula for vessel compliance?

A

C = V/P V = volume
P = pressure

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20
Q

Do veins have greater or lesser compliance than arteries?

A

Greater. Thus, they hold more volume at any given moment.

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21
Q

What happens to vessel compliance with age?

A

Decreases, because arteries become stiffer and less distensible.

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22
Q

What is pulse pressure?

A

The difference between systolic and diastolic blood pressure

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23
Q

What is the most important determinant of pulse pressure?

A

Stroke volume

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24
Q

What is the equation for mean arterial pressure?

A

MAP = 1/3 (systolic pressure) + 2/3 (diastolic pressure)

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25
Q

What is used to estimate left atrial pressure?

A

Pulmonary wedge pressure

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26
Q

What does the P wave represent?

A

Atrial depolarization

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27
Q

What is the PR interval?

A

The measurement from the beginning of the P wave to the beginning of the QRS complex.

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28
Q

What is the QT interval?

A

The interval from the beginning of the Q wave to the end of the T wave.

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29
Q

What is the main determinant of cardiac myocyte RMP (phase 4)?

A

K+ conductance

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30
Q

What causes cardiac myocyte phase 0 (depolarization)?

A

Inward current of sodium ions

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31
Q

What is cardiac myocyte phase 0?

A

Depolarization

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32
Q

What is cardiac myocyte phase 1?

A

Brief initial repolarization

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33
Q

What causes cardiac myocyte phase 1 (brief initial repolarization)?

A

Outward current of potassium ions coupled with decreased inward current of sodium ions

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34
Q

What is cardiac myocyte phase 2?

A

Plateau phase

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35
Q

What causes cardiac myocyte phase 2 (plateau)?

A

Inward calcium current balanced by outward potassium current

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36
Q

What is cardiac myocyte phase 3?

A

Repolarization

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37
Q

What causes cardiac myocyte phase 3 (repolarization)?

A

Outward current of potassium ions

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38
Q

What is SA node phase 0?

A

Upstroke of the action potential

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39
Q

What causes SA node phase 0 (action potential upstroke)?

A

Inward current of calcium ions

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40
Q

What is SA node phase 3?

A

Repolarization

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41
Q

What causes SA node phase 3 (repolarization)?

A

Outward current of potassium ions

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42
Q

What is SA node phase 4?

A

Resting membrane potential (slow depolarization)

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43
Q

What causes slow depolarization in SA node cells (phase 4)?

A

Leaky inward sodium channels (If)

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44
Q

What causes SA node phases 1 and 2?

A

Nothing - they don’t exist!

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45
Q

Where in the heart is conduction velocity the fastest?

A

Purkinje system

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46
Q

Where is conduction velocity the slowest?

A

AV node

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47
Q

What is the order, from fastest to slowest, of conduction velocity for heart tissues?

A

Purkinje fibers -> Atria -> Ventricles -> AV node

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48
Q

What are chronotropic effects?

A

Those that change heart rate

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49
Q

What changes firing rate to cause chronotropic effects?

A

SA node

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50
Q

What are dromotropic effects?

A

Those that change conduction velocity, primarily in the AV node

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51
Q

How does Ach slow heart rate (negative chronotropic effect)?

A

Decreases the rate of phase 4 depolarization through decreased inward sodium current in the SA node

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52
Q

How does Ach cause negative dromotropic effects (increased PR interval)?

A

Decreased inward calcium current and increased outward potassium current

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53
Q

How does NE speed heart rate (positive chronotropic effect)?

A

Increases the rate of phase 4 depolarization through increased inward sodium current in the SA node

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54
Q

How does NE cause positive dromotropic effects (shortened PR interval)?

A

Increased inward calcium current

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55
Q

What is the function of intercalated disks in cardiac myocytes?

A

Maintenance of cell-cell adhesion

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56
Q

What is the function of gap junctions in cardiac myocytes?

A

Allow for rapid electrical spread of action potentials - account for the heart’s behavior as an electrical syncytium

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57
Q

Explain cardiac myocyte excitation-contraction coupling.

A
  1. Action potential spreads from cell membrane to T tubules 2. Calcium conductance is increased during phase 2 of the action potential. Enters the myocyte through L type calcium channels.
  2. Calcium entry triggers calcium release from the SR (calcium induced calcium release)
  3. Calcium binds to troponin C, moving tropomyosin out of the way, allowing actin and myosin to bind.
  4. Relaxation occurs when calcium is re-accumulated into the SR by a calcium ATPase pump
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58
Q

What is contractility (inotropy)?

A

The intrinsic ability of cardiac muscle to develop force at a given muscle length

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59
Q

What ion plays the main role in determination of cardiac contractility?

A

Calcium

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60
Q

How does sympathetic stimulation increase contractility (2 ways)?

A
  1. Increases the inward calcium current during phase 2 of the myocyte action potential. 2. Causes phosphorylation of phospholamban, which activates SERCA, increasing calcium reuptake into the SR, allowing for more calcium release with subsequent beats.
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61
Q

What is the function of phospholamban?

A

Inhibits SERCA

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62
Q

In what phosphorylation state is phospholamban active?

A

Dephosphorylated

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63
Q

What effect does epinephrine have on phospholamban?

A

Phosphorylates it, relieving phospholamban’s inhibition on SERCA, allowing SERCA to take up more calcium for release on subsequent beats (increased contractility).

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64
Q

Explain the mechanism by which cardiac glycosides (digoxin) increase contractility.

A
  1. Inhibition of Na/K ATPase increases intracellular sodium. 2. Increased intracellular sodium reduces the activity of SERCA (which antiports sodium with calcium, reducing calcium concentration in the cell), thus increasing intracellular calcium.
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65
Q

What effect do cardiac glycosides (digoxin) have on contractility?

A

Increase it

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66
Q

What is the MOA for cardiac glycosides (digoxin)?

A

Inhibit Na/K ATPase in cardiac myocytes.

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67
Q

What happens to EDV as venous return increases?

A

Increases

68
Q

What is preload?

A

The pressure, created by end diastolic volume, which stretches (lengthens) ventricular myocytes

69
Q

What happens to stroke volume with increased preload?

A

Increases

70
Q

What determines afterload for the LV? RV?

A

LV - aortic pressure RV - pulmonary artery pressure

71
Q

Why does increased EDV cause increased SV?

A

Increased EDV results in increased ventricular fiber length, which increases tension and force of contraction

72
Q

What happens to SV with increased afterload?

A

Decreases

73
Q

What happens to SV with increased contractility?

A

Increases

74
Q

What happens to ESV with increased afterload?

A

Increases

75
Q

What happens to EDV with increased preload?

A

Increases

76
Q

What happens to ESV with increased contractility?

A

Decreases

77
Q

What happens to EDV with increased contractility?

A

No change

78
Q

What is mean systemic pressure?

A

Right atrial pressure when there is “no flow” in the CV system. Measured when the heart is stopped experimentally.

79
Q

How do you determine mean systemic pressure on a vascular function curve?

A

Mean systemic pressure is the point at which the vascular function curve intersects the x-axis

80
Q

What are the axes on a vascular function curve?

A

x axis- RA pressure or EDV y axis - CO or venous return

81
Q

What two measurements are represented on a vascular function curve?

A

CO and Venous return

82
Q

What determines the slope of the venous return curve on a vascular function curve?

A

Arteriolar resistance

83
Q

What changes only the venous return curve on a vascular function curve?

A

Changes in blood volume

84
Q

What changes only the CO curve on a vascular function curve?

A

Changes in inotropy

85
Q

What changes both CO and venous return on a vascular function curve?

A

Changes in TPR

86
Q

What effect do positive inotropic agents have on CO?

A

Increase

87
Q

Which one of these can change mean systemic pressure: changes in blood volume, changes in TPR, or changes in CO?

A

Changes in blood volume (shifts the x-intercept on a vascular function curve)

88
Q

What effect does an increase in TPR have on CO and venous return?

A

Decreases BOTH

89
Q

What effect does a decrease in TPR have on CO and venous return?

A

Increases BOTH

90
Q

What is the formula for stroke volume?

A

SV = EDV - ESV

91
Q

What is the formula for CO?

A

CO = HR * TPR

92
Q

What is a normal ejection fraction?

A

55%

93
Q

What is the formula for ejection fraction?

A

EF = SV/EDV = (EDV-ESV)/EDV

94
Q

What effect does increased blood volume have on mean systemic pressure?

A

Increases it

95
Q

What effect does hemorrhage have on mean systemic pressure?

A

Decreases it

96
Q

What is ejection fraction?

A

The fraction of EDV ejected in each heartbeat

97
Q

What is stroke work?

A

The work the heart performs on each beat

98
Q

What is the formula for LV stroke work?

A

Stroke work = aortic pressure * stroke volume

99
Q

What 4 things increase cardiac O2 demand?

A

Increased afterload Increased heart size

Increased contractility

Increased HR

100
Q

What does the Fick principle measure?

A

Cardiac output

101
Q

What is the Fick principle formula?

A

CO = O2 consumption / [O2 pulmonary vein - O2 pulmonary artery] Peripheral arterial blood is used to estimate pulmonary vein O2
Peripheral venous blood is used to estimate pulmonary artery O2

102
Q

What causes S4?

A

Atria contracting against a stiff walled ventricle

103
Q

What causes the a wave on a venous pressure tracing?

A

Atrial systole

104
Q

What causes S1?

A

Closure of the AV valves

105
Q

Which AV valve closes first and may contribute to splitting of S1?

A

Mitral

106
Q

What causes the c wave on a venous pressure tracing?

A

Ventricular contraction causing the tricuspid valve to bulge into the RA

107
Q

What causes the v wave on a venous pressure tracing?

A

Venous return against a closed tricuspid valve

108
Q

What causes x descent on a venous pressure tracing?

A

Atrial relaxation leading to rapid atrial filling due to decreased atrial pressure

109
Q

What causes y descent on a venous pressure tracing?

A

Emptying of atria into the ventricle after opening of the tricuspid valve

110
Q

What causes S2?

A

Closure of aortic/pulmonary valves

111
Q

What causes S3?

A

Rapid ventricular filling (volume overload)

112
Q

What signals the onset of isovolumetric relaxation?

A

Aortic valve closure (S2)

113
Q

Which semilunar valve closes first?

A

Aortic

114
Q

What signals the onset of isovolumetric contraction?

A

AV valve closure (S1)

115
Q

How do venodilators like NO decrease myocardial O2 demand?

A

Decrease preload

116
Q

How do vasodilators decrease myocardial O2 demand?

A

Decrease afterload

117
Q

Which organ gets 100% of CO?

A

Lungs

118
Q

Which organ gets the largest share of systemic CO?

A

Liver

119
Q

Which organ gets the highest blood flow per gram of tissue?

A

Kidney

120
Q

Which organ has the highest A-V O2 difference?

A

Heart - O2 extraction is nearly 80%

121
Q

What happens to blood viscosity in anemia? Does this increase or decrease the risk for turbulent flow?

A

Viscosity decreases. This increases the risk for turbulent flow.

122
Q

What happens to blood viscosity in polycythemia?

A

Increases

123
Q

Explain the baroreceptor reflex

A
  1. A decrease in arterial pressure decreases stretch on walls of carotid sinus. 2. Decreased stretch decreases firing rate of carotid sinus nerve (CN IX)
  2. CN IX feeds back to the vasomotor center to cause increased HR, increased contractility/SV, increased arteriolar vasoconstriction, and increased venoconstriction- all of which increase arterial pressure back toward normal.
124
Q

What effect on blood flow does a Valsalva maneuver have?

A

Decreases venous return, causing a decreased CO and arterial pressure

125
Q

What do aortic arch baroreceptors respond to?

A

Increases in BP (not decreases)

126
Q

What nerve transmits information from teh carotid baroreceptors?

A

CN IX

127
Q

What enzyme catalyzes the conversion of angiotensinogen to angiotensin I?

A

Renin

128
Q

What causes renin release?

A

Decrease in renal perfusion pressure or increase in sodium concentration, sensed by the juxtaglomerular apparatus Also mediated through activation of beta-1 receptors on the kidney

129
Q

What converts angiotensin I to angiotensin II? Where?

A

ACE, in the lungs

130
Q

What four effects does angiotensin II have?

A
  1. Causes release of aldosterone 2. Increases sodium/hydrogen exchange in the PCT, causing increased sodium reabsorption
  2. Increases thirst
  3. Causes vasoconstriction of the arterioles, increasing TPR
131
Q

What is the Cushing reaction?

A

Increased ICP causes compression of cerebral blood vessels, leading to cerebral ischemia and increased sympathetic outflow, which causes hypertension. Increased sympathetic activation also causes increased HR, which, along with HTN, causes baroreceptor activation, leading to bradycardia.

132
Q

What is the triad seen in the Cushing reaction?

A

Hypertension, bradycardia, respiratory depression

133
Q

What do chemoreceptors in carotid and aortic bodies respond to?

A

Decreased O2

134
Q

ADH binding to V1 receptors causes…

A

Gq activation, leading to vasoconstriction

135
Q

ADH binding to V2 receptors causes…

A

Gs activation, leading to insertion of water channels in collecting ducts, increasing water reabsorption

136
Q

Under what circumstances does ADH play a role in regulation of blood pressure?

A

Hemorrhage

137
Q

What causes ANP release?

A

Increase in blood volume sensed by atria

138
Q

What are the 3 functions of ANP?

A

Causes relaxation of smooth muscle (decreased TPR) Causes excretion of sodium and water

Inhibits renin secretion

139
Q

What is the Starling equation?

A

Fluid movement = Kf (out) - (in) = Kf (Pc + pi if) - (Pif + pi c)

Where Kf = filtration coefficient, Pc = capillary hydrostatic pressure, pi IF = interstitial fluid oncotic pressure, Pif = interstitial fluid hydrostatic pressure, and pi c = capillary oncotic pressure.

140
Q

How does arteriolar dilation cause edema?

A

Increases capillary hydrostatic pressure

141
Q

How does venous constriction cause edema?

A

Increases capillary hydrostatic pressure

142
Q

How does heart failure cause edema?

A

Increases capillary hydrostatic pressure

143
Q

How does liver failure cause edema?

A

Decreased plasma colloid oncotic pressure

144
Q

What is the MOA of endothelium-derived relaxing factor?

A

Production of cGMP causes vascular smooth muscle relaxation, leading to vasodilation

145
Q

What is autoregulation?

A

Maintenance of constant blood flow to an organ in the face of changing blood pressure

146
Q

Which 3 organs exhibit autoregulation?

A

Brain, heart, kidney

147
Q

What is active hyperemia?

A

Increased blood flow to an organ in response to increased metabolic demand

148
Q

What is reactive hyperemia?

A

Increased blood flow to an organ in response to a period of reduced blood flow

149
Q

What are the two hypotheses that explain local control of blood flow?

A

Myogenic hypothesis Metabolic hypothesis

150
Q

What is the myogenic hypothesis of autoregulation?

A

Vascular smooth muscle contracts when it is stretched. Therefore, when blood flow is increased to an organ, the increased stretch will cause vasoconstriction, maintaining constant blood flow.

151
Q

What is the metabolic hypothesis of autoregulation?

A

Production of vasodilator metabolites (O2, K+, adenosine, lactate) by metabolic activity in tissues causes vasodilation and increased blood flow in response to increased need.

152
Q

According to the metabolic hypothesis, what happens with a spontaneous increase of blood flow to a particular organ?

A

It “washes out” vasodilator metabolites, causing vasoconstriction and maintenance of blood flow

153
Q

What are the most important factors for determining autoregulation in the heart?

A

Local metabolites - CO2, adenosine

154
Q

What is the most important local vasodilator for cerebral circulation?

A

CO2

155
Q

What are the 3 most important vasodilator substances in skeletal muscle?

A

Lactate, adenosine, and K+

156
Q

What is the most important regulator of blood flow to skeletal muscle at rest?

A

Sympathetic nervous system

157
Q

What is the most important regulator of blood flow to skeletal muscle during exercise?

A

Local metabolic mechanisms - local vasodilator substances adenosine, K+, lactate

158
Q

What is the principal function of cutaneous sympathetic innervation to the skin?

A

Temperature regulation

159
Q

What happens to TPR during exercise?

A

Decreases (skeletal muscle vasodilation due to buildup of vasodilator metabolites lactate, adenosine, and K+)

160
Q

What happens to the arteriovenous O2 difference during exercise?

A

Increased due to increased O2 consumption by tissues

161
Q

What happens to renin in response to hemorrhage?

A

Increases

162
Q

What happens to aldosterone in response to hemorrhage?

A

Increases (save volume to raise BP)

163
Q

What happens to ADH in response to hemorrhage?

A

Increases (save volume and cause vasoconstriction to raise BP)

164
Q

What happens to angiotensin I and II in response to hemorrhage?

A

Increase (increase TPR to raise BP)

165
Q

What happens to epinephrine and norepinephrine in response to hemorrhage?

A

Increase (increase TPR to raise BP)

BRS Phys (6 decks)

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