Ch 3 Flashcards
(165 cards)
1
Q
What is stressed volume?
A
Blood volume contained in arteries
2
Q
What vessels are the site of highest resistance in the CV system?
A
Arterioles
3
Q
What vessels have the highest total cross sectional and surface area?
A
Capillaries
4
Q
What vessels contain the highest proportion of blood in the CV system?
A
Veins
5
Q
What is unstressed volume?
A
Blood volume contained in veins
6
Q
What is the formula for velocity of blood flow?
A
v = Q/A Q = blood flow
A = cross sectional area
7
Q
How is velocity related to cross sectional area in vessels?
A
Inversely proportional
8
Q
What is the formula for flow?
A
Q = delta P / R delta P = pressure difference
R = resistance
9
Q
What is Poiseuille’s equation?
A
R = 8nl/(pi)r^4 R = resistance
n = viscosity
l = vessel length
r = vessel radius
10
Q
How is vessel resistance related to vessel radius?
A
Vessel resistance is inversely proportional to vessel radius to the 4th power
11
Q
How is vessel resistance related to blood viscosity?
A
Directly proportional
12
Q
How is vessel resistance related do vessel length?
A
Directly proportional
13
Q
What happens to total resistance when arteries are added in parallel? In series?
A
Parallel - resistance decreases Series - resistance increases
14
Q
What does Reynolds number predict?
A
Whether blood flow will be turbulent or laminar
15
Q
What does an increased Reynolds number mean?
A
There will be a greater tendency for turbulent blood flow
16
Q
What two factors increase Reynolds number?
A
Decreased blood viscosity Increased blood velocity (decreased vessel radius)
17
Q
What is compliance?
A
The ability of a vessel to distend to handle increases in volume
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
19
Q
What is the formula for vessel compliance?
A
C = V/P V = volume
P = pressure
20
Q
Do veins have greater or lesser compliance than arteries?
A
Greater. Thus, they hold more volume at any given moment.
21
Q
What happens to vessel compliance with age?
A
Decreases, because arteries become stiffer and less distensible.
22
Q
What is pulse pressure?
A
The difference between systolic and diastolic blood pressure
23
Q
What is the most important determinant of pulse pressure?
A
Stroke volume
24
Q
What is the equation for mean arterial pressure?
A
MAP = 1/3 (systolic pressure) + 2/3 (diastolic pressure)
25
What is used to estimate left atrial pressure?
Pulmonary wedge pressure
26
What does the P wave represent?
Atrial depolarization
27
What is the PR interval?
The measurement from the beginning of the P wave to the beginning of the QRS complex.
28
What is the QT interval?
The interval from the beginning of the Q wave to the end of the T wave.
29
What is the main determinant of cardiac myocyte RMP (phase 4)?
K+ conductance
30
What causes cardiac myocyte phase 0 (depolarization)?
Inward current of sodium ions
31
What is cardiac myocyte phase 0?
Depolarization
32
What is cardiac myocyte phase 1?
Brief initial repolarization
33
What causes cardiac myocyte phase 1 (brief initial repolarization)?
Outward current of potassium ions coupled with decreased inward current of sodium ions
34
What is cardiac myocyte phase 2?
Plateau phase
35
What causes cardiac myocyte phase 2 (plateau)?
Inward calcium current balanced by outward potassium current
36
What is cardiac myocyte phase 3?
Repolarization
37
What causes cardiac myocyte phase 3 (repolarization)?
Outward current of potassium ions
38
What is SA node phase 0?
Upstroke of the action potential
39
What causes SA node phase 0 (action potential upstroke)?
Inward current of calcium ions
40
What is SA node phase 3?
Repolarization
41
What causes SA node phase 3 (repolarization)?
Outward current of potassium ions
42
What is SA node phase 4?
Resting membrane potential (slow depolarization)
43
What causes slow depolarization in SA node cells (phase 4)?
Leaky inward sodium channels (If)
44
What causes SA node phases 1 and 2?
Nothing - they don't exist!
45
Where in the heart is conduction velocity the fastest?
Purkinje system
46
Where is conduction velocity the slowest?
AV node
47
What is the order, from fastest to slowest, of conduction velocity for heart tissues?
Purkinje fibers -> Atria -> Ventricles -> AV node
48
What are chronotropic effects?
Those that change heart rate
49
What changes firing rate to cause chronotropic effects?
SA node
50
What are dromotropic effects?
Those that change conduction velocity, primarily in the AV node
51
How does Ach slow heart rate (negative chronotropic effect)?
Decreases the rate of phase 4 depolarization through decreased inward sodium current in the SA node
52
How does Ach cause negative dromotropic effects (increased PR interval)?
Decreased inward calcium current and increased outward potassium current
53
How does NE speed heart rate (positive chronotropic effect)?
Increases the rate of phase 4 depolarization through increased inward sodium current in the SA node
54
How does NE cause positive dromotropic effects (shortened PR interval)?
Increased inward calcium current
55
What is the function of intercalated disks in cardiac myocytes?
Maintenance of cell-cell adhesion
56
What is the function of gap junctions in cardiac myocytes?
Allow for rapid electrical spread of action potentials - account for the heart's behavior as an electrical syncytium
57
Explain cardiac myocyte excitation-contraction coupling.
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.
3. Calcium entry triggers calcium release from the SR (calcium induced calcium release)
4. Calcium binds to troponin C, moving tropomyosin out of the way, allowing actin and myosin to bind.
5. Relaxation occurs when calcium is re-accumulated into the SR by a calcium ATPase pump
58
What is contractility (inotropy)?
The intrinsic ability of cardiac muscle to develop force at a given muscle length
59
What ion plays the main role in determination of cardiac contractility?
Calcium
60
How does sympathetic stimulation increase contractility (2 ways)?
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.
61
What is the function of phospholamban?
Inhibits SERCA
62
In what phosphorylation state is phospholamban active?
Dephosphorylated
63
What effect does epinephrine have on phospholamban?
Phosphorylates it, relieving phospholamban's inhibition on SERCA, allowing SERCA to take up more calcium for release on subsequent beats (increased contractility).
64
Explain the mechanism by which cardiac glycosides (digoxin) increase contractility.
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.
65
What effect do cardiac glycosides (digoxin) have on contractility?
Increase it
66
What is the MOA for cardiac glycosides (digoxin)?
Inhibit Na/K ATPase in cardiac myocytes.
67
What happens to EDV as venous return increases?
Increases
68
What is preload?
The pressure, created by end diastolic volume, which stretches (lengthens) ventricular myocytes
69
What happens to stroke volume with increased preload?
Increases
70
What determines afterload for the LV? RV?
LV - aortic pressure RV - pulmonary artery pressure
71
Why does increased EDV cause increased SV?
Increased EDV results in increased ventricular fiber length, which increases tension and force of contraction
72
What happens to SV with increased afterload?
Decreases
73
What happens to SV with increased contractility?
Increases
74
What happens to ESV with increased afterload?
Increases
75
What happens to EDV with increased preload?
Increases
76
What happens to ESV with increased contractility?
Decreases
77
What happens to EDV with increased contractility?
No change
78
What is mean systemic pressure?
Right atrial pressure when there is "no flow" in the CV system. Measured when the heart is stopped experimentally.
79
How do you determine mean systemic pressure on a vascular function curve?
Mean systemic pressure is the point at which the vascular function curve intersects the x-axis
80
What are the axes on a vascular function curve?
x axis- RA pressure or EDV y axis - CO or venous return
81
What two measurements are represented on a vascular function curve?
CO and Venous return
82
What determines the slope of the venous return curve on a vascular function curve?
Arteriolar resistance
83
What changes only the venous return curve on a vascular function curve?
Changes in blood volume
84
What changes only the CO curve on a vascular function curve?
Changes in inotropy
85
What changes both CO and venous return on a vascular function curve?
Changes in TPR
86
What effect do positive inotropic agents have on CO?
Increase
87
Which one of these can change mean systemic pressure: changes in blood volume, changes in TPR, or changes in CO?
Changes in blood volume (shifts the x-intercept on a vascular function curve)
88
What effect does an increase in TPR have on CO and venous return?
Decreases BOTH
89
What effect does a decrease in TPR have on CO and venous return?
Increases BOTH
90
What is the formula for stroke volume?
SV = EDV - ESV
91
What is the formula for CO?
CO = HR * TPR
92
What is a normal ejection fraction?
55%
93
What is the formula for ejection fraction?
EF = SV/EDV = (EDV-ESV)/EDV
94
What effect does increased blood volume have on mean systemic pressure?
Increases it
95
What effect does hemorrhage have on mean systemic pressure?
Decreases it
96
What is ejection fraction?
The fraction of EDV ejected in each heartbeat
97
What is stroke work?
The work the heart performs on each beat
98
What is the formula for LV stroke work?
Stroke work = aortic pressure * stroke volume
99
What 4 things increase cardiac O2 demand?
Increased afterload Increased heart size
Increased contractility
Increased HR
100
What does the Fick principle measure?
Cardiac output
101
What is the Fick principle formula?
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
What causes S4?
Atria contracting against a stiff walled ventricle
103
What causes the a wave on a venous pressure tracing?
Atrial systole
104
What causes S1?
Closure of the AV valves
105
Which AV valve closes first and may contribute to splitting of S1?
Mitral
106
What causes the c wave on a venous pressure tracing?
Ventricular contraction causing the tricuspid valve to bulge into the RA
107
What causes the v wave on a venous pressure tracing?
Venous return against a closed tricuspid valve
108
What causes x descent on a venous pressure tracing?
Atrial relaxation leading to rapid atrial filling due to decreased atrial pressure
109
What causes y descent on a venous pressure tracing?
Emptying of atria into the ventricle after opening of the tricuspid valve
110
What causes S2?
Closure of aortic/pulmonary valves
111
What causes S3?
Rapid ventricular filling (volume overload)
112
What signals the onset of isovolumetric relaxation?
Aortic valve closure (S2)
113
Which semilunar valve closes first?
Aortic
114
What signals the onset of isovolumetric contraction?
AV valve closure (S1)
115
How do venodilators like NO decrease myocardial O2 demand?
Decrease preload
116
How do vasodilators decrease myocardial O2 demand?
Decrease afterload
117
Which organ gets 100% of CO?
Lungs
118
Which organ gets the largest share of systemic CO?
Liver
119
Which organ gets the highest blood flow per gram of tissue?
Kidney
120
Which organ has the highest A-V O2 difference?
Heart - O2 extraction is nearly 80%
121
What happens to blood viscosity in anemia? Does this increase or decrease the risk for turbulent flow?
Viscosity decreases. This increases the risk for turbulent flow.
122
What happens to blood viscosity in polycythemia?
Increases
123
Explain the baroreceptor reflex
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)
3. 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
What effect on blood flow does a Valsalva maneuver have?
Decreases venous return, causing a decreased CO and arterial pressure
125
What do aortic arch baroreceptors respond to?
Increases in BP (not decreases)
126
What nerve transmits information from teh carotid baroreceptors?
CN IX
127
What enzyme catalyzes the conversion of angiotensinogen to angiotensin I?
Renin
128
What causes renin release?
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
What converts angiotensin I to angiotensin II? Where?
ACE, in the lungs
130
What four effects does angiotensin II have?
1. Causes release of aldosterone 2. Increases sodium/hydrogen exchange in the PCT, causing increased sodium reabsorption
3. Increases thirst
4. Causes vasoconstriction of the arterioles, increasing TPR
131
What is the Cushing reaction?
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
What is the triad seen in the Cushing reaction?
Hypertension, bradycardia, respiratory depression
133
What do chemoreceptors in carotid and aortic bodies respond to?
Decreased O2
134
ADH binding to V1 receptors causes...
Gq activation, leading to vasoconstriction
135
ADH binding to V2 receptors causes...
Gs activation, leading to insertion of water channels in collecting ducts, increasing water reabsorption
136
Under what circumstances does ADH play a role in regulation of blood pressure?
Hemorrhage
137
What causes ANP release?
Increase in blood volume sensed by atria
138
What are the 3 functions of ANP?
Causes relaxation of smooth muscle (decreased TPR) Causes excretion of sodium and water
Inhibits renin secretion
139
What is the Starling equation?
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
How does arteriolar dilation cause edema?
Increases capillary hydrostatic pressure
141
How does venous constriction cause edema?
Increases capillary hydrostatic pressure
142
How does heart failure cause edema?
Increases capillary hydrostatic pressure
143
How does liver failure cause edema?
Decreased plasma colloid oncotic pressure
144
What is the MOA of endothelium-derived relaxing factor?
Production of cGMP causes vascular smooth muscle relaxation, leading to vasodilation
145
What is autoregulation?
Maintenance of constant blood flow to an organ in the face of changing blood pressure
146
Which 3 organs exhibit autoregulation?
Brain, heart, kidney
147
What is active hyperemia?
Increased blood flow to an organ in response to increased metabolic demand
148
What is reactive hyperemia?
Increased blood flow to an organ in response to a period of reduced blood flow
149
What are the two hypotheses that explain local control of blood flow?
Myogenic hypothesis Metabolic hypothesis
150
What is the myogenic hypothesis of autoregulation?
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
What is the metabolic hypothesis of autoregulation?
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
According to the metabolic hypothesis, what happens with a spontaneous increase of blood flow to a particular organ?
It "washes out" vasodilator metabolites, causing vasoconstriction and maintenance of blood flow
153
What are the most important factors for determining autoregulation in the heart?
Local metabolites - CO2, adenosine
154
What is the most important local vasodilator for cerebral circulation?
CO2
155
What are the 3 most important vasodilator substances in skeletal muscle?
Lactate, adenosine, and K+
156
What is the most important regulator of blood flow to skeletal muscle at rest?
Sympathetic nervous system
157
What is the most important regulator of blood flow to skeletal muscle during exercise?
Local metabolic mechanisms - local vasodilator substances adenosine, K+, lactate
158
What is the principal function of cutaneous sympathetic innervation to the skin?
Temperature regulation
159
What happens to TPR during exercise?
Decreases (skeletal muscle vasodilation due to buildup of vasodilator metabolites lactate, adenosine, and K+)
160
What happens to the arteriovenous O2 difference during exercise?
Increased due to increased O2 consumption by tissues
161
What happens to renin in response to hemorrhage?
Increases
162
What happens to aldosterone in response to hemorrhage?
Increases (save volume to raise BP)
163
What happens to ADH in response to hemorrhage?
Increases (save volume and cause vasoconstriction to raise BP)
164
What happens to angiotensin I and II in response to hemorrhage?
Increase (increase TPR to raise BP)
165
What happens to epinephrine and norepinephrine in response to hemorrhage?
Increase (increase TPR to raise BP)
