1
Q
What’s a typical EF%?
Trained athletes can get up to ___% EF during exercise.
Heart failure patients have an EF below ___%.
A
~60%
- 85%
- 40%
2
Q
Increasing preload has what effect on max tension developed?
A
None
3
Q
Increasing preload has what effect on m. shortening?
A
Increased
4
Q
Increasing preload has what effect on EDP?
A
Increased (bottom curve, further right)
5
Q
How does increased afterload affect m. shortening?
A
Decreased
6
Q
How does increased afterload affect pressure development before ejection?
A
Increased (therefore increased energy consumption)
7
Q
How does decreased contractility affect SV?
A
Decreased
8
Q
How does decreased contractility affect m. shortening?
A
Decreased
9
Q
How does increased contractility affect ejection velocity?
A
Increased
10
Q
How would increased contractility affect ESV? ESP?
A
Decreased ESV
Increased ESP
11
Q
What issue would lead to systolic heart failure?
What issue would lead to diastolic heart failure?
How would each affect the P-V diagram?
A
- Decreased ventricular contractility (lowers active tension line)
- Decreased ventricular compliance (increases resting tension line)
12
Q
What heart murmur could you possibly hear during diastolic heart failure?
A
S4 (atrial kick into stiff ventricle)
13
Q
How does an increase in end-diastolic pressure affect ventricular filling?
A
Decreases it
14
Q
Would a decrease in ventricular compliance affect filling?
A
Yes, would decrease it
15
Q
How would a-fib affect EDV?
A
Decreased (loss of atrial kick)
16
Q
Would a dilated ventricle affect afterload?
A
*Yes, dilated heart –> increased wall tension –> increased afterload
17
Q
How would tachycardia affect contractility? How would it affect ventricular filling time?
A
- Increase it (Treppe)
- Decrease it
18
Q
What areas contribute to the volume of the central venous pool?
A
Corresponds approximately to the volume enclosed by the right atrium and the great veins in the thorax.
19
Q
What is the venous return?
What would it be at S-S conditions?
A
- RATE at which blood returns to the thorax from the peripheral vascular beds, i.e. blood entering the central venous pool.
- S-S venous return = CO
20
Q
Define CO w/r/t the central venous pool.
A
Rate at which blood leaves the central venous pool and is pumped out of the heart.
21
Q
Which is higher, right CO or left CO?
A
=
L contracts stronger because blood going thru higher pressure circuit
22
Q
Define mean circulatory pressure in a detailed way.
A
- (Pmc) is the mean pressure that exists in the circulatory system when cardiac output stops and the pressures within the vascular system redistributes.
- It represents the relationship between the volume of blood in the circulation compared to the functional capacity of the system.
- It is influenced by the volume of circulating blood and the smooth muscle venous tone of the system (which determines the capacity of the system).
- It is a measure of the fullness of the circulatory system.
- Pmc is normally about 7 mm Hg
23
Q
How does blood flow change when mean circulatory pressure = CVP?
A
Stops! (death)
24
Q
How does increasing CO affect CVP?
A
Decreases CVP
25
What would happen at negative CVP?
Transmural pressure collapses the large veins resulting in zero venous return.
26
What's the general theme of ways to influence venous return?
You want to alter the pressure gradient between peripheral and central venous pressure. (Higher pressure in periphery pushes it in)
- CVP analogous to R atrial pressure
27
What are some ways to increase peripheral venous pressure?
- Increase symp vasoconstriction
- Increase blood volume (e.g. water retention)
- SkM pumps
28
What are some ways to decrease CVP?
- Resp pump
| - Cardiac suction
29
How would hemorrhage affect venous return? Why?
Decrease (decreased blood volume)
30
How would transfusion affect venous return? Why?
Increase (increased blood volume)
31
How would an increase in venous tone (symp stim) affect CVP?
Increase it
32
What would be a side effect of long-term heart failure due to the elevated CVP (to compensate for the decreased contractility)?
Edema
33
How would arterial vasoconstriction affect TPR? What would be a negative side effect?
- Increases TPR, shunting blood to the heart (improves BP)
| - Bad side effect: peripheral ischemia
34
What is the maximum survivable blood loss?
About 40% of total blood volume (~2L)
35
Sole function of the arterial side is to control ___________. Function of the venous side if to control ___________.
Pressure
| Volume
36
What is blood flow proportional to? What is it inversely proportional to?
- * Proportional to pressure gradient and radius^4
- Inversely proportional to vessel length and fluid viscosity
* Resistance is the opposite, also pressure gradient doesn't affect it. * Pressure gradients generally held constant via feedback mechs
37
What is shear stress? What's it analogous to?
Resistance to movement between laminae (pressure)
38
What is shear rate? What's it analogous to?
Relative velocities between laminae (velocity of blood flow)
39
What's the difference b/w a Newtonian and non-Newtonian fluid?
- Viscosity changes in non-Newtonian fluid, over a range of shear rates and stresses (velocities and pressures)
40
As velocity of blood flow increases, viscosity _____________ due to less interactions between components.
Decreases
41
Define HCT.
| What's a nl range?
Aka packed cell volume (PCV), is the volume % of RBCs in blood.
- 35-50%
42
Would HCT be high or low in anemia? How would this affect viscosity?
Low. Would decrease viscosity.
43
Define axial streaming.
Tendency of RBCs to accumulate in axial laminae (center) at high shear rates (high velocities).
44
Define plasma skimming.
Tendency of smaller vessels (
45
Would you expect to see a higher HCT in larger or smaller vessels? Why?
Larger (will increase up to a certain extent and then level out)
- Plasma skimming/axial streaming occurs in smaller vessels
* Therefore HCT measurement depends on the vessel you take the sample from
46
What does hereditary spherocytosis result in? Why?
Anemia
| - Sphere shaped RBCs can't enter smaller caps
47
What type of flow is silent?
Laminar flow
48
What are murmurs and bruits a sign of?
Turbulent flow
49
What are Korotkoff sounds?
Based on changes in the velocity of blood flow, --> production of turbulent flow
50
What types of events could produce turbulent flow?
Damage to endothelial lining or thrombi
51
Based on the Reynold's equation, what part of the circulatory system is most likely to develop turbulent flow?
Aorta (* largest diameter)
52
How would increasing cross-sectional area affect blood flow velocity?
Would decrease it (finger on hose)
| * Caps would shoot higher velocity but we have way more of them
53
In terms of velocity of flow, what can happen if the flow is too fast (stenosis) or too slow (aneurysm)?
* - Too fast (stenosis) --> can cause vessel to collapse due to decrease in static pressure
- Too slow (aneurysm) --> can cause vessel to dilate and rupture due to increase in static pressure
54
Blood flow doesn't always follow it's pressure gradient, but instead follows an energy gradient. Explain with the example of stenosis.
*Low P w/in stenosis (due to higher velocity) --> high P out of stenosis (due to lower velocity)
55
Why can a bike tire withstand greater pressure than a car tire?
Mainly because bike tire has less wall tension due to smaller radius.
56
Which type of vessel has the largest cross-sectional area? What about the largest volume?
- caps
| - vv
57
How do you calculate pulse pressure? What does pulse pressure actually represent?
Systolic - diastolic P's
| - Represents the force the heart generates when it contracts
58
What parts of the circ system have no pulse pressure?
Caps and veins
59
Where in the circ system do you see the greatest drop in pressure?
Arterioles
60
Why is MAP closer to diastolic P?
Heart spends more time in diastole
61
Where is pulse pressure widest?
| What else happens as you move away from the heart?
In vessels furthest from the heart
b) high frequency components damped (incisura/notch).
c) systolic peak increased and waveform narrowed.
d) late diastolic hump in waveform.
62
What are some possible causes of why pulse pressure widens as you move farther from the heart?
a) reflection at branch points.
b) vascular tapering (vascular beds become smaller)
c) * decrease in arterial compliance
63
What are the major differences b/w arterial and venous walls?
* - Arterial walls have internal elastic lamina (tunica intima) and external elastic lamina (tunica media).
- Arterial walls have more smooth m. in the tunica media
- Venous walls have a more develop CT layer in the tunica adventitia
64
What would you find in both arterial and venous walls?
- Tunica intima w/endothelial cell layer
- Tunica media w/smooth m.
- Tunica adventitia w/CT, some smooth m cells, + vaso vasorum
65
Rank the compliance characteristics of the smooth m, collagen (CT), and elastic lamina layers.
1. Most compliant: elastic lamina
2. Smooth m
3. Collagen/CT
66
Explain the characteristics of a continuous capillary and where it might be found.
Continuous endothelial cells; no fenestrations in capillary wall; tight junction b/w cells.
- Continuous basal lamina.
- Found in muscle, connective tissues
67
Explain the characteristics of a fenestrated capillary and where it might be found.
Continuous endothelial cells with fenestrations w/ or w/o diaphragms
- Continuous basal lamina.
- Found in kidney, intestine, where sieves are needed
68
Explain the characteristics of a discontinuous (sinusoidal) capillary and where it might be found.
Discontinuous endothelial cells separated by wide spaces
- *Discontinuous basal lamina.
- Found in liver (proteins), bone marrow (WBCs), spleen (RBCs), so bigger things can pass
69
How much smooth m, elastic tissue, and fibrous CT do caps have?
None
70
How much smooth m, elastic tissue, and fibrous CT do venules have?
Just some fibrous CT (none of the others)
71
What vessels have the greatest wall thickness:diameter ratio? What does this mean?
Precap sphincters
| - They have the greatest control of diameter and thus flow
72
Veins have a small thickness:diameter ratio. Therefore, what does a vein do?
Regulate volume more than flow or pressure
73
What is hydraulic filter (you know it)?
The volume ejected from the LV during systole is temporally stored by the distension of the elastic vascular component of the aorta. After systole ends, the distended aortic wall recoils and thereby acts as a secondary pump to maintain constant flow during diastole. This process is dependent on the compliance characteristics of the aortic wall.
74
A low compliant aorta is an independent risk factor for _________.
*CHF
75
What determines our diastolic pressure?
*TPR status (therefore doesn't change much during exercise)
76
As as compliance decreases w/age (increased collagen and decreased elastin), a given increase in volume elicits a (smaller or larger) (increase or decrease) in pressure?
larger increase
77
How would decreased compliance affect pulse pressure
Widen
78
What is a wide pulse pressure an independent risk factor for?
What else does it contribute to?
CHF
| - Contributes to systolic hypertension, cardiac hypertrophy, aortic dilation, and low exercise tolerance
79
Why are aa considered resistance vessels?
Aa exhibit a relatively constant low compliance (shallow slope) throughout the physiological pressure range.
- Recall, smaller diameter will increase resistance
80
Why are vv considered capacitance vessels?
Vv exhibit a relatively high compliance (steeper slope) in the physiological pressure range (
81
Why can saphenous vv sometimes be used as grafts in CABG?
Arterial pressure is high at the coronary aa. At high pressure, venous compliance decreases to a level closer to arteries (because they're full). Therefore, a vein could be used to replace an artery at a high P.
82
How fast does the pressure pulse wave travel as compared to blood flow?
The arterial Pressure Pulse (wave) travels down the aorta at 5 meters/sec and increases to about 10-15 meters/sec in the small arteries. In contrast, blood flow travels at about 1 meter/sec (Radial pulse, not flow but energy).
83
As compliance decreases down the arterial tree, the velocity of propagation of the pressure pulse _________.
Increases (makes sense visually)
84
Define MAP (not the equation)
Average pressure existing in the aorta and proximal arterial system during one cardiac cycle.
MAP = Diastolic Pressure + 1/3 Pulse Pressure
85
What 2 major factors determine BP?
*CO and TPR (= MAP + CVP)
86
____________ primarily affects systolic P.
*CO
87
____________ primarily affects diastolic P.
*TPR
88
Which is more constant, CO or TPR?
TPR
89
Does the baroreceptor reflex affect CO, TPR, both, or neither?
Both
90
How would sepsis affect BP?
Drops it dangerously low.
-Sepsis comes about from the presence of toxins in the blood, leading to overall relaxation of resistance and your pressure completely drops
91
Give some eg's of things that affect arterial compliance.
Arterial vasculature, age, blood volume, sympathetic tone, pregnancy.
92
Does blood V affect SV? Arterial compliance?
Yes, yes
93
What are some e.g.s of metabolites that could cause vasodilation?
K+, adenosine, CO2, H+
94
Does the heart increase O2 extraction during exercise?
No
95
What is the reason systolic P increases during exercise?
*Increased SV (+ symp vasoconstriction)
96
What are the 3 pre-capillary resistance vessels?
a. Arterioles
b. Metarterioles (shunts blood past caps)
c. Precapillary sphincter
97
What are the characteristics of cap blood flow?
a. low velocity
- Allows for proper O2 release
b. intermittent (vasomotion)
c. direction (pressure gradients)
d. not uniform
e. Rouleaux formation
- RBCs get in line w/each other
98
Why do you have lower hydrostatic P in your lungs?
*Because you don't want filtration to occur because the edema would make it difficult for gas exchange.
99
Why does albumin contribute a disproportionately large amount to blood's oncotic pressure?
Even though blood ptns are 51% albumin, since it attracts Cl- (and therefore Na+), it accounts for 65% of its oncotic pressure.
100
Why does arterial pressure have a larger affect on cap hydrostatic pressure than does venous pressure?
- Arterial pressure exerts a relatively small effect on capillary hydrostatic pressure because of significant pre-capillary resistance (prevents P from being transferred into capillary).
- Venous pressure exerts a relatively larger effect on capillary hydrostatic pressure because of little post-capillary resistance. Easy for this pressure to back up system and cause larger affect on hydrostatic pressure.
101
What endothelial factors cause vasodilation?
- Prostacyclins
- Endothelium-Derived Relaxing Factor (EDRF)
- Nitric Oxide (NO)
- Metabolites (K+, adenosine, H+, CO2)
102
What endothelial factor causes vasoconstriction?
Endothelin (ET)
103
How does prostacyclin cause vasodilation? (don't need to know yet)
cAMP > PKA > P'lates MLCK (inhibited) > decreased P'lation of MLC > decreased actin/myosin interaction
104
How does NO cause vasodilation? (don't need to know yet)
cGMP > PKG > P'lates MLCK (inhibited) > decreased P'lation of MLC > decreased actin/myosin interaction
105
How does endothelin cause vasoconstriction? (don't need to know yet)
PLC > IP3 (released) > ^[Ca2+] > Ca/Calmodulin activates MLCK via P'lation > P'lated myosin binds actin
106
What's the main fcn of the lymphatic system?
Collects and returns interstitial fluid to the circulatory system.
107
What are the main characteristics of the lymph system?
- Unidirectional flow
- Valves
- Thinner
- Non-fenestrated endothelium
108
What factors govern lymph flow?
a) amount of capillary filtration
b) skeletal muscular activity
c) lymphatic unidirectional valves
109
What are some precipitating factors of peripheral edema? (think about it, not that hard)
a) reduction in plasma protein concentration (serum albumin
110
How could CHF cause peripheral edema?
Right ventricle weakened > blood backs up in systemic veins > increases hydrostatic P (+ decreased oncotic P) > fluid leaves
111
Gives some causes of edema (think about liver, kidneys...).
a) CHF
b) mechanical obstruction of venous return
c) renal disease - loss of protein
d) liver disease - lack of protein (albumin) synthesis
e) burn – increases capillary permeability.
112
What is basal tone?
Amount of vascular contraction found under resting conditions without neural or hormonal (extrinsic) influences. Pretty low.
- Theoretical reference point.
113
Active mechanisms induce a change in vascular resistance (toward/away) from the basal arterial tone. Passive mechanisms induce a change in vascular resistance (toward/away) the basal arterial tone.
away, toward
114
Would you see more TPR in basal tone or resting sympathetic tone?
Resting sympathetic tone
115
Most sympathetically innervated things use NE (adrenergic) for their post-synaptic NT but some use ACh (cholinergic). What are the ones that use ACh?
* SkM (?), piloerectors (hairs during shivering), sweat glands --> vasodilation (rather than the usual vasoconstriction)
- Also, Adrenal cortex is stimulated w/ACh and releases epi/NE directly into bloodstream (modified post-ganglionic post-synaptic symp neuron)
116
What 3 NT's can stimulate adrenergic receptors?
Epi, NE, isoproterenol
117
Stimulation of alpha receptors on bv's causes _______________.
Vasoconstriction
| - *Coronary and cerebral vessels have little sympathetic vasoconstrictor innervation
118
Stimulation of beta-1 and beta-2 receptors on the heart causes _______________.
Increased HR and contractility
119
Stimulation of beta receptors on bv's causes _______________.
Vasodilation
120
What do parasympathetic cholinergic fibers innervate?
| What do they NOT innervate?
* Parasympathetic fibers innervate a limited number of blood vessels: cerebral, some viscera including splanchnic, genitalia (think viagra), bladder and large bowel; causes vasodilation.
- Skeletal muscle and cutaneous vessels are NOT innervated by parasympathetic nerves.
121
What do sympathetic cholinergic fibers innervate?
| What do they NOT innervate?
Postganglionic sympathetic fibers that release acetylcholine on effectors (exceptions). Ex. Sweat glands of non-apical skin to indirectly induce vasodilation.
122
Baroreceptor nerve firing frequency is _________ by an increase in arterial pressure and _________ by a decrease in arterial pressure.
increased, decreased
123
Which is more sensitive to changes in BP, carotid sinus or aortic sinus?
Carotid sinus is more sensitive
124
In the baroreceptor reflex, where the vasomotor centers located to which CN's IX and X communicate w/?
Medulla
125
What is the BP threshold (#) for activation of the sinus nerve impulses?
What is nl MAP?
~50 mmHg
| ~100 mmHg
126
How do baroreceptors behave in HTN?
The threshold is increased and the receptors are less sensitive to changes in transmural pressure
- So 100mmHg in normotensive people might get a certain firing rate, but 110mmHg in HTN people elicit that same firing rate.
127
What would be the symp and parasymp response to hypoxia?
In the CV system, peripheral chemoreceptors only play a role during severe hypoxia (they are not activated during normal fluctuations in PaO2 levels). These signals stimulate efferent sympathetic and parasympathetic nerve activity to cause vasoconstriction and bradycardia, respectively.
* In real life, however, hypoxia induces tachycardia because the increase in ventilation acts via stretch receptors in the lung to centrally inhibit efferent vagal nerve activity (resulting in an increase heart rate).
128
In terms of chemoreceptor response, are the effects of the CV or resp system bigger?
Resp system
129
During hypoxia, how would concurrently increasing the CO2 levels change the response?
Would lead to stronger response sooner
130
What part of blood vessels is responsible for the control of total peripheral resistance, arterial and venous tone, and the distribution of blood flow throughout the body?
Vascular smooth muscle
131
What are the 2 primary mechs that are hypothesized to be responsible for bv autoregulation?
1. Myogenic hypothesis
| 2. Metabolic hypothesis
132
Define the myogenic hypothesis.
Vascular smooth muscle contracts in response to stretch and relaxes in response to a reduction in stretch.
133
Define the metabolic hypothesis.
Metabolic activity produces substances (adenosine, H+, and CO2) that relax vascular smooth muscle (shows that affected tissue is active and metabolizing food, so requires more blood).
- The concentration of these inhibitory metabolites in the microvascular bed depends on the level of blood flow. When pressure is increased there is a brief increase in blood flow which removes the inhibitory metabolites and thereby allows the resistance vessels to constrict. As they constrict, resistance increases and flow decreases.
- Conversely, when pressure is decreased, less blood flow allows an accumulation of inhibitory metabolites causing vessels to dilate. Dilation decreases resistance and increases flow.
134
What organs possess strong autoregulation?
* Heart, brain, kidneys, SkM
135
What organs possess weak autoregulation?
* Splanchnic region
136
What organs possess little autoregulation?
* Skin, lungs
137
When increasing flow via increased pressure gradient (but not changing vessel diameter/resistance) such as w/exercise, how would local endothelial cells respond? How does this compare to the myogenic response?
- They would release vasodilators to further increase the flow via positive feedback (NO, EDRF, prostacyclins) to these SkMm.
- In the myogenic response, if the vessel was stretched the vessel would constrict, but this would probably be over-riden by the local regulation
138
What is active (functional) hyperemia?
What factors are responsible for this type of control?
What types of tissues would it be seen in?
Increased blood flow caused by enhanced tissue activity.
- K+, inorganic phosphate, and interstitial osmolarity are among the factors responsible for this type of control.
- e.g. cardiac m, skeletal m
139
What is reactive (passive) hyperemia
Brief arteriole occlusion leads to a transient increase in blood flow. Thus, metabolic debt increases blood flow.
140
What's a reperfusion injury? (not on test)
Tissue damage caused when blood supply returns to the tissue after a period of ischemia or lack of oxygen (anoxia, hypoxia, s/p angioplasty).
- the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than restoration of normal function.
- Activated endothelial cells produce more reactive oxygen species but less nitric oxide following reperfusion, and the imbalance results in a subsequent inflammatory response.
141
What are the 5 major classes of shock?
1. Cardiogenic Shock (associated with heart problems)
2. Hypovolemic Shock (caused by inadequate fluid volume). AKA Hemorrhagic Shock.
3. Anaphylactic Shock (caused by allergic reaction)
4. Septic Shock (associated with infections)
5. Neurogenic Shock (caused by damage to the nervous system)
142
What is shock?
Low blood perfusion to tissues resulting in cellular injury and inadequate tissue function (life-threatening). The typical signs of shock are low blood pressure, rapid heart rate, and signs of poor end-organ perfusion.
143
What are some causes of cardiogenic shock?
- Dysrhythmias caused by complete heart block (v-tac, bradycardia)
- Cardiac tamponade (fluid in pericardium)
144
In hemorrhagic shock (hypovolumic shock), how much blood loss typically occurs before sx appear?
10-20%
145
Why does anaphylactic shock lead to fluid loss?
Allergic rxn: after an initial exposure to a substance like bee sting toxin, the person's immune system becomes sensitized to that allergen. On a subsequent exposure, an allergic reaction occurs with massive release of histamines and subsequent vasodilation.
146
Why does septic shock lead to fluid loss?
Inflammatory/immune response to severe infection/sepsis: e.g. a bacteriotoxin causes the leakage of plasma into tissues (vasodilation, increased cap permeability), resulting in hypovolemia.
147
How could neurogenic shock possibly arise?
E.g. an acute spinal cord injury that blocks sympathetic activity.
FHB Cardio
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