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CP Final > BRS Booknotes > Flashcards

BRS Booknotes Flashcards

1
Q

Arteries contain what volume

A

Stressed volume

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2
Q

Arterioles have the highest __________ in the CV system

A

Resistance

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3
Q

What controls the arterioles of the skin, splanchnic, and renal circulation

A

α1

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4
Q

What controls the arterioles of the skeletal muscle

A

β2

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5
Q

What has the largest cross sectional area in the circulation

A

Capillaries

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6
Q

What volume is present in veins

A

Unstressed volume

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7
Q

What receptor is present on veins

A

α1

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8
Q

Capacitance is ___________ of stiffness

A

Inverse

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9
Q

How do you calculate capacitance

A

Volume/pressure

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10
Q

How do you calculate the velocity of blood

A

Flow/area

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11
Q

Which blood vessels have higher capacitance

A

Veins

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12
Q

Capacitance __________ with age

A

Decreases

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13
Q

What is the most important determinant of pulse pressure

A

Stroke volume

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14
Q

How do you calculate the mean arterial pressure

A

Diastolic pressure + 1/3 pulse pressure

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15
Q

How can one estimate the LA pressure

A

Inserting a catheter into the pulmonary arterioles near the capillaries and measuring pressure here approximates the LA pressure

Pulmonary wedge pressure

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16
Q

What does the p wave represent

A

Atrial depolarization

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17
Q

Where does the atria repolarize

A

QRS complex

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18
Q

What does the PR interval represent

A

Initial depolarization of the ventricles

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19
Q

What does the PR interval depend on

A

Depends on velocity through AV node

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20
Q

What increases the PR interval? Decreases?

A

Parasympathetic; sympathetic

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21
Q

What does the QRS complex represent

A

Ventricular depolarization

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22
Q

What does the QT interval represent

A

Entire ventricle depolarization and repolarization

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23
Q

What does the ST interval represent

A

Isoelectric

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24
Q

What does the T wave represent

A

Ventricle repolarization

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25
Q

What determines the resting membrane potential

A

K conductance

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26
Q

What is phase 0 in normal contraction

A
  • upstroke of AP

- increased Na conductance causes Na influx

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27
Q

What is the peak of phase 0

A

Na equilibrium

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28
Q

What is phase 1 of normal ap

A

K efflux from fast channels and brief repolarization

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29
Q

What is phase 2 of the normal AP

A

Plateau of the AP

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30
Q

What causes the plateau at phase 2

A

K goes out but Ca comes in so repolarization stalls

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31
Q

What happens at phase 3 of normal AP

A

Repolarization continues as Ca conductance decreases but the slow K channels open so the K drives repolarization

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32
Q

What is phase 4 of normal AP

A

Resting potential

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33
Q

What has the fastest action potential

A

SA node > AV node > purkinje fibers

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34
Q

What are the AV node and purkinje fibers called

A

Latent pacemakers

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35
Q

Why is the SA node the pacemaker

A

It has an unstable resting potential

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36
Q

How is the nodal AP different from normal ones

A

There is no phase 1 or 2

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37
Q

What is phase 0 of the nodal AP

A

Ca influx which is the same as the AV node

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38
Q

What is phase 3 of the nodal AP

A

Repolarization; K flows in

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39
Q

What is phase 4 of nodal AP

A

Na influx called If; turned off by repolarization

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40
Q

What determines the conduction velocity

A

Ca influx during depolarization

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41
Q

What portion of the heart has the fastest conduction velocity

A

Purkinje

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42
Q

What is the difference between absolute and effective refractory period

A

Absolute means no AP can be initiated

Effective means no AP can be conducted

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43
Q

What is the relative refractory period

A

The period where AP is not likely but can be initiated with more force

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44
Q

What is a chronotropic change

A

Change in HR

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45
Q

What is a negative chronotropic change

A

Decreases in HR caused by decrease in SA node firing

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46
Q

What is a positive chronotropic change

A

Increase in HR caused by increase in SA nodal firing

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47
Q

What is a dromotropic change

A

Change in conduction velocity

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48
Q

What is a negative dromotropic change

A

Slower speed through AV node and longer PR interval

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49
Q

What is a positive dromotropic change

A

Faster conduction through AV node and shorter PR interval

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50
Q

What portions of the heart have vagal innervation? What does it do

A

SA node, atria, AV but NOT ventricles

Parasympathetic vagal innervation

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51
Q

What is the mechanism of negative chronotropic change

A

Decreases in HR due to slowing phase 4 depolarization (Na entering cells of AV and SA node)

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52
Q

What is the mechanism of negative dromotropic changes

A

Slower conduction through AV node; more K out and less Ca in

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53
Q

What is the mechanism of positive chronotropic changes

A

Faster phase 4 depolarization from faster I_f which is the Na flow responsible for phase 4 at SA node

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54
Q

What is the mechanism of positive dromotropic change

A
  • faster conduction through AV node
  • ventricle filling can be compromised
  • increased Ca current
  • decreased RR interval
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55
Q

Contractability is called what

A

Inotropism

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56
Q

What causes an increase in contractability

A

Increasing intracellular Ca

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57
Q

What is a normal ejection fraction

A

60%

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58
Q

What does a positive inotropic activity? Negative inotropic activity

A

Increase in contractability; decrease in contractability

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59
Q

What causes positive inotropism

A

Increased HR
Increased sympathetic activity via β1 receptor
Cardioglycosides (digitalis)

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60
Q

How does increased HR cause positive inotropism

A

Causes a building of Ca intracellular concentration = positive staircase or Bowditch staircase

Postextrasystolic potentiation = next beat is stronger from extra Ca in the cell and causes an extra boost of power from the Ca

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61
Q

What does increased sympathetic activity do for inotropism? What receptor is used

A

Increases; β1

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62
Q

How does increased sympathetic activity increase inotropism

A
  1. Increases influx of Ca with each AP

2. Increases Ca pump activity (phospholamban)

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63
Q

What do cardioglycosides do? What else are they called

A

Positive inotropism; digitalis

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64
Q

How do cardioglycosides cause positive inotropism

A

They inhibit the Na/K ATPase this leaves more Na inside the cell. Since intracellular Na is higher, the Na/Ca pump doesn’t bring in as much Na which leaves intracellular Ca high

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65
Q

What things cause positive inotropism

A

Inreased HR
Increased sympathetic activity via β1
Digitalis

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66
Q

What causes negative inotropism? How does it work

A

Parasympathetic activation via vagus N with ACh on muscarinic receptors. This causes a decrease of Ca flow during phase 2

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67
Q

What is preload related to

A

RA pressure

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68
Q

What increases preload

A

Increases in venous return causing increased end-diastolic volume and increases fiber length

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69
Q

What is afterload

A

Aortic pressure (or pulmonary A pressure) working against ventricular ejection

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70
Q

What increases afterload

A

Increases in pulmonary A pressure or aorta pressure

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71
Q

Increased length of sarcomeres causes increased __________ and allows for _________ cross bridges to form

A

Tension; more

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72
Q

When is contraction velocity maximal

A

When there is no afterload

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73
Q

As afterload increases, velocity of ejected blood ____________

A

Decreases

74
Q

Increased end diastolic volume causes

A

Increased SV and CO
Increased venous return
Increased preload

75
Q

Increased end diastolic volume causes ________ ventricle fibers which causes (increased/decreased) tension

A

Stretched; increased

76
Q

Venous return is directly correlated to what

A

Cardiac output

77
Q

Upward shift in CO means what? Downward shift means what

A

Increased contractility; decreased contractility

78
Q

Increased contractility (increases/decreases) CO

A

Increases

79
Q

At point 1 in ventricular pressure volume loops what valve is closing

A

AV valves close

80
Q

At point 2 in ventricular pressure-volume loops what is happening with valves

A

Semilunar valves open

81
Q

What is happening with valves at point 3 in ventricular pressure volume loops

A

Semilunar valves closes

82
Q

What happens at point 4 of pressure volume loops

A

AV valves open

83
Q

From 1–>2 in pressure volume loop is called

A

Isovolumetric

84
Q

What happens at 2–>3 in pressure volume loops

A

SV is ejected

-width (Δ x-axis) is the SV

85
Q

Point 3 in pressure volume loops is what general cardiac event

A

Diastole

86
Q

What causes the semilunar valves to close

A

When pressure in the artery is higher than ventricle

87
Q

When does isovolumetric contraction occur

A

3–>4 in pressure volume loops

88
Q

What event marks 4–>1 in pressure volume loops

A

Ventricular filling

89
Q

When does mitral valve open

A

LV pressure < LA pressure

90
Q

What does increased preload cause

A

increased SV by F-S relationship (increased width on X axis)

Caused by increased end diastole volume

91
Q

What causes increased end diastole volume

A

Decreased venous capacitance and/or increased venous return

92
Q

How does increased afterload manifest on pressure-volume loop

A

‘Skinnier’ graphs; decreased width

93
Q

Why does afterload decrease SV

A

The ventricle is ejecting blood against pressure so some energy of contraction goes into opposing that force

94
Q

What causes increased afterload

A

Increases in aortic or pulmonary a BP

95
Q

Increased contractility manifests as what on pressure-volume loop

A

Increased height and width of the curve

96
Q

The intersection of vascular function and cardiac curve is what

A

Venous return and CO since venous return = CO

97
Q

Where can you find mean systemic pressure on vascular/cardiac function graphs

A

Where the venous return intersects the x axis

98
Q

What is mean systemic pressure approximately equal to

A

RA pressure with no flow

99
Q

How do you obtain mean sytemic pressure

A

Stop the heart and wait for the pressure to equilibrate

100
Q

What increases the mean systemic pressure

A

Increase in blood volume or decrease in venous capacitance

101
Q

The slope of venous return is a function of what

A

Arteriole pressure

102
Q

Depressing the vascular/cardiac graph causes

A

Same CO
Decreased flow —> increased TPR (total peripheral resistance)
Caused by increased arteriole constriction and increased RA pressure (preload)

103
Q

Depressing vascular cardiac graphs is called what for venous return

A

CCW rotation of venous return

104
Q

Stretching the vascular cardiac graph vertically results in __________ CO and __________TPR

A

Increased; lower

105
Q

Vertically stretching vascular cardiac graph is named what in the vascular system

A

CW rotation of venous return

106
Q

CW rotation of venous return does what to RA pressure and arteriole pressure

A

Decrease; decrease

107
Q

Increases in TPR causes what changes

A

Decreased CO decreased venous return

108
Q

How do you calculate SV

A

End diastolic volume - end systolic volume

109
Q

How do you calculate CO

A

SV*HR

110
Q

What is normal EF? How do you calculate it

A

0.6; SV/end-diastolic-volume

or

(EDV-ESV)/(EDV)

111
Q

How do you calculate stroke work? What is the primary energy source?

A

Pressure*SV

Fatty acids

112
Q

The tension of ventricles α ________

A

Cardiac O2 consumption

113
Q

What causes cardiac O2 to increase

A
  1. Increase afterload
  2. Increase size of heart
  3. Increase in contractility
  4. Increase HR
114
Q

How do you calculate cardiac output without stroke volume

A

(O2 consumed in body)/([O2]pulmonary v - [O2]pulmonary a)

115
Q

What immediately proceeds atrial systole

A

P wave

116
Q

Atrial systole causes what change in venous pressure graph

A

A wave (increase)

117
Q

In ventricular hypertrophy, atrial systole causes what

A

4th heart sound

118
Q

Isovolumetric contraction happens during what

A

QRS

119
Q

What causes the first heart sound

A

AV valves

120
Q

What is a split 1st heart sound

A

Mitral valve can shut faster than tricuspid

121
Q

How much blood is ejected during isovolumetric contraction

A

None, the aortic valve is closed so no blood leaves

122
Q

What portion of heart contraction has the highest ventricular pressure

A

Rapid ventricular contraction

123
Q

What ends rapid ventricular contraction

A

T wave

124
Q

What happens with the atria during rapid ventricular contraction

A

Atrial filling begins

125
Q

When is the remainder of the SV ejected

A

During reduced ventricular ejection

126
Q

What wave on the venous pulse correlates to reduced ventricular ejection

A

V wave

127
Q

What is the second heart sound? What happens when it’s split

A

Aortic and pulmonic valve close; inspiration can interrupt pulmonary valve

128
Q

During what stage on contraction do we see the dicrotic notch

A

Isovolumetric ventricular relaxation

129
Q

What phase starts with the AV valves opening

A

Rapid ventricular filling

130
Q

What is the third heart sound

A

Mitral valve opening; normal in kids, but means disease in adults

131
Q

What is the longest phase of the cardiac cycle

A

Reduced ventricular filling

132
Q

What are the 7 phases of the cardiac cycle

A 
Atrial systole
Isovolumetric ventricular contraction
Rapid ventricular ejection
Reduced ventricular ejection
Isovolumetric ventricular relaxation
Rapid ventricular filling 
Reduced ventricular filling (diastasis)
133
Q

What is the dicrotic notch also called

A

Incisura

134
Q

What is the fast method of altering arterial pressure? Slow?

A

Baroreceptors

Slow is RAAS

135
Q

Where are the baroreceptors located

A

They are stretch receptors located in the walls of the carotid sinus near the bifurcation of the common carotid arteries

136
Q

What is the primary mechanism of baroreceptors

A

Fast and neural

137
Q

What are the general steps in the baroreceptor reflex

A
  1. Decrease in arterial pressure
  2. Decreased stretch decreases the firing rate of the carotid sinus nerve (hering’s nerve CN IX)
  3. This new level of stretch is compared to the set point in the vasomotor center (about 100 mm Hg)
  4. The vasomotor center decreases parasympathetic (vagal) outflow to the heart and increases sympathetic flow to the heart and blood vessels
138
Q

What are the four ways that arterial pressure can be raised quickly

A

Increase HR
Increase contractility and stroke volume
Increase vasoconstriction of the arterioles
Increase vasoconstriction of the veins

139
Q

How does contractility and stroke volume increase BP

A

When they are both raised this raises CO which increases arterial pressure

140
Q

What does the valsava maneuver do? What is it

A

It is trying to expire against a closed glottis

This increases interthoracic pressure which decreases venous return, this decreases Pa, baroreceptors detect change and increase sympathetic activity to blood vessels and heart

141
Q

What produces the greatest response from baroreceptors

A

Rapid changes in pressure

142
Q

What is unique about the baroreceptors in the aortic arch

A

They respond to increases in pressure but not decreases

143
Q

How does RAAS regulate blood pressure

A

Changes in blood volume

144
Q

What does renin do

A

Enzyme from the kidney which converts angiotensinogen to angiotensin I

145
Q

What converts angiotensin I to II? Why is this important

A

Angiotensin converting enzyme (ACE) is in the lungs and angiotensin II is the active form

146
Q

What degrades angiotensin II

A

Angiotensinase

147
Q

What are the steps in the renin-angiotensin-aldosterone system

A
  1. Decrease in renal perfusion pressure causes juxtaglomerular cells of the afferent arteriole to secrete renin
  2. Renin converts angiotensinogen to angiotensin I in the plasma
  3. ACE converts I to II in the lungs
148
Q

What is the ultimate effect of ace inhibitors

A

Block the conversion of angiotensin I to II which decreases blood pressure

149
Q

What do angiotensin receptor antagonists do

A

They block the effect of angiotensin II by binding to the receptors and thus cause a decrease in pressure

150
Q

What are the 4 effects of angiotensin II

A
  1. Stimulates the synthesis and secretion of aldosterone in the adrenal cortex
    • this increases Na reabsorption which increases blood volume (water follows ions) and increases blood pressure
    • slow because protein syn is slow
  2. Increases Na-H exhange in proximal convoluted tubule
    • angiotensin II and aldosterone both increase Na retention (angiotensin is direct aldo is indirect)
    • angiotensin II leads to contraction alkalosis
  3. Increases thirst and water intake
  4. Causes vasoconstriction of the arterioles and thus increases TPR (total peripheral resistance) and BP
151
Q

What follows cerebral ischemia

A

Increase in PCO2 in brain tissue

152
Q

What reaction is associated with cerebral ischemia

A

Cushing reaction

153
Q

What are the effects of cerebral ischemia

A

Intense peripheral constriction to shunt blood to brain (too much blood is shifted)
Mean arterial pressure can rise to life-threatening levels

154
Q

What is the cushing reaction

A

A response to cerebral ischemia which is marked by increases in intercranial pressure. This compresses cerebral blood vessels and causes ischemia and increases PCO2 which causes vasomotor to increase sympathetic outflow to heart and blood vessels

155
Q

How do the peripheral receptors respond to blood gas

A

They consume lots of O2 and are sensitive to decreases do they signal vasomotor center to increase vasoconstriction and increase TPR and Pa

156
Q

What is vasopressin

A

ADH, causes increase in BP

157
Q

What does vasopressin mainly react to

A

Large loss of BP (hemorrhage)

158
Q

What causes vasopressin release

A

Decreased pressure in atria cause posterior pituitary to release vasopressin

159
Q

What are the two effects of vasopressin

A
  1. Potent vasoconstrictor that increase TPR by activating V1 receptors on arterioles
  2. Increases water reabsorption in renal distal tubule and collecting ducts by activating V2 receptors
160
Q

What increases filtration (movement of fluid out of capillaries)

A 
Increased Pc
-increased Pa
-increased Pv
-arteriolar dilation
-venous constriction
Decreased Pi
Decreased πc
-decreased protein concentration in the blood
Increased πi
-caused by inadequate lymphatic function
161
Q

What is the fluid effect of histamine

A

Causes increase in arterial dilation and venous constriction which both cause local edema

162
Q

Which factor of starling forces does histamine change

A

Increase in Pc

163
Q

What is active hyperemia

A

Blood flow to an organ α metabolic activity

164
Q

The MoA of NO involves what enzyme and intermediate

A

Guanylate cyclase; cGMP

165
Q

NO is one form of

A

Endothelial-derived relaxing factor

166
Q

What stimulates production of NO

A

Circulating ACh

167
Q

What causes reactive hyperemia

A

Removal of an occlusion

168
Q

Bradykinin causes what? What are its other effects similar to

A

Arterial dilation and venous constriction; histamine

169
Q

Serotonin is released in response to

A

Vascular damage

170
Q

Serotonin is believed to be related to vascular spasms which are related to

A

Migraines

171
Q

What does serotonin do to vessels

A

Arterial constriction and released in response to blood vessel damage

172
Q

Which prostaglandin is a dilator

A

Prostacyclin and E series prostaglandins

173
Q

Which prostaglandins are vasoconstrictors

A

F-series prostaglandins; thromboxane A2

174
Q

Hypoxia and adenosine cause what CV effects

A

Vasodilation

175
Q

Cerebral circulation exhibits what hyperemia

A

Active and reactive

176
Q

What is the most important vasodilator for cerebral circulation

A

CO2

177
Q

Vasoactive compounds don’t act on

A

Cerebral circulation

178
Q

β2 is responsible for

A

Vasodilation

179
Q

What are the local vasodilators related to exercise

A

Lactate, adenosine, K+

180
Q

Cutaneous sympathetic nerves are primarily responsible for

A

Temperature regulation; more flow through cutaneous = more dissipation

CP Final (14 decks)

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