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MSP Problem Set #4
1. While in the Wooden Center during class one day you run into Dr. Middlekauff. After
30mins of sweating next to her on the stair climber, you start to think about your increase
in CO during this exercise. You remember that CO=HR X SV. Just then Dr.
Middlekauff hands you this chart (see below) and says “Since you skipped class, why
don’t you summarize the effects of exercise for me.” Jee…. thanks.
Increase/Decrease and why
Heart rate

Stroke volume

Cardiac output

Arteriole pressure
 (slight)
Pulse pressure
 (due to increased stroke volume)
Systemic vascular resistance
 (due to vasodilation of skeletal muscle
AV O2 difference
beads)
 (due to increased O2 consumption)
2. You are ready to faint, but Holly just keeps on going. You ask her what her HR is and
are surprised to find out that your HR is the same as yours (you are both wearing heart
monitors). How can you both have the same HR and different CO?
Her stroke volume is larger because she is well trained.
CO (H.M.)=SV X HR
CO (you)= SV X HR
3. After you finish, you feel your legs and they are firm and warm (increase blood flow to
those legs). How does this happen? (Hint: your explanation should include something
about metabolites and pumps)
Interstitial K+, hyperosmolarity, hypoxemia, and adenosine mediate metabolic
vasodilation. These all increase muscle blood flow and lead to capillary recruitment,
which will decrease diffusion of nutrients.
Muscle pump: as muscles flex it will squeeze blood out of the veins. Then when the
muscle relaxes, the vein will now have negative pressure therefore can “suck” blood
through the capillaries. This will facilitate blood flow to the muscles.
4. Now you really start wondering about the reflex systems that control your circulation
during exercise. When you ask Holly about this, she whips out this chart and tells you to
fill in as much as you can (what is it with these charts?).
Central
command
Muscle
metaboreflex
Arteriole
Baroreflex
Heart
HR by
 vagal
 SNA
Kidney
XXXXXXXX
HR
and SNA
and
contract by  vasoconstrict
SNA and
 RAAS
vagal
 vagal and XXXXXXX
SNA
because BP.
Skeletal Muscle Splanchnic Bed
XXXXXXXX
XXXXXXXX
 SNA and
vasoconstrict
(ask about how
working
muscles
get
blood)
XXXXXXXX
X
SNA
and
vasoconstrict
and
venoconstrict
XXXXXXXX
NOTE: these
receptors are
usually reset to
allow a higher
BP
than
normal
Fill in effects of each reflex mechanism on these tissues/vascular beds
5. You and Holly have such a great time together you decide to train for the LA marathon
(a few months away). What will be the changes that allow your body to make it the 26.2
miles?
Central changes: cardiac mass, vascularity and ventricular cavity size increase.
Resting HR decreases BUT resting CO does not change. The difference is the larger
stroke volume upon training.
O2 delivery is dependent on cardiac output and max CO increases with training (again
this is due to an  in SV)
Peripheral Mechanisms: changes within the skeletal muscle:
1. New capillary growth
2. Increased mitochondria
3. Increased myoglobin
These changes will enhance oxygen exchange within the muscle and enhance use of
energy substrates.
6. Mr. Salvador, a 60-year-old male, comes to your preceptor's office with a chief
complaint of fainting. He reports that he fainted a week ago while on the toilet
"reading his paper" and 3 days ago when he picked up his golf bag with everything in
it. Your preceptor is taking care of another patient at the moment and he has asked
you to take this patient's history till he comes back. However, thinking about your
recent physiology lectures, you find yourself capable of more than just taking a
history. For example, you can explain the reason behind this patient's fainting spells.
Well, go on!
Bowel movements and lifting heavy objects are associated with an increase in
intrathoracic pressure. Normally, this increase in intrathoracic pressure causes
an exertion of pressure upon the thoracic aorta. This initially raises mean
arterial pressure which leads to a reflex bradycardia, or slowing of the hear
(Phase 1). With sustained raised intrathoracic pressure, the venous return falls
and end-diastolic volume is lowered. Due to Starling's law, the lower volume
leads to impaired stoke volume, further reduced blood pressure, and a reflex
sympathetic response resulting in Phase 2 tachycardia and vasoconstriction.
When the pressured breath is released (Phase 3), the mechanical drop in
intrathoracic pressure makes the periaortic pressure drop. The last phase,
Phase 4, is caused by the surge of venous return into the thorax from the
previously hindered vena cavae. In this phase, you see increasing blood pressure
(due to Starling again: increased filling leads to increased contractility/stroke
volume). In the setting of high sympathetic tone from Phase 2, this additional
blood pressure increased triggers the arterial baroreceptors and a vagal reflex
finally slows the heart. Phases 2 and 4 are useful markers for the competence of
the baroreflex because they require blood pressure (mechanical stretch, actually)
detection and sympathetic response. If a neurological disorder (inappropriate
vagal or sympathetic response) were present, there would be a continuing
pressure fall in Phase 2 or no bradycardia in Phase 4.
7. Mrs. Hypochondriac filled her prescription for a beta-blocker and a diuretic, which
she received from her doctor for her mild hypertension. However, since she thought
that 2 drugs were not enough, she visited another physician and talked her into giving
her another drug for her hypertension. The second doctor prescribed a vasodilator.
So, she took her 3 medicines, and happily went about her business. A couple of days
later, she overslept and when she got out of her bed and rushed to the bathroom
quickly so she wouldn't be late for work, she felt lightheaded and got a "head rush,"
and was about to fall when she grabbed on to the sink. How could a vasodilator
combined with a beta-blocker and diuretic lead to her faintness upon standing? What
is the phenomenon called? How would you detect it on physical exam?
A mixture of these drugs, a vasodilator, a volume reducer, and a sympathetic
reflex blocking agent, can severely reduce the response to orthostatic changes in
blood pressure. The phenomenon is orthostatic hypotension, which can be found
by taking blood pressure while the patient is in both the standing and supine
position. A difference of over 15 mmHg is indicative of this condition.
8. When we stand what happens to the central venous pressure? What does this do to
stroke volume, cardiac output, and blood pressure?
There is postural displacement of venous blood. Approximately 500 ml of blood
shifts from the thorax into the lower extremities. This isn't because the blood
flows backward in vena cava because the valves prevent this. The heart keeps
pumping blood forward and gravity and more importantly the high capacitance
of the venous system to accommodate the venous pooling prevents the blood
from reaching all the way up to the heart again. It takes approximately 600 ml
of additional venous blood in the standing position to open all the valves. During
this time preload is decreased. This leads to a decreased contractility by the
Frank-Starling mechanism. Stroke volume is decreased by 40%. This results in
a decrease in cardiac output and pulse pressure.
9. What are the components of the compensatory mechanisms involved in postural
changes? Explain.
a. Muscle pump: skeletal muscles of the legs and the venous valves. The
skeletal muscle contraction sends the venous blood back up to the heart and
the valves prevent blood's return backward.
b. Respiratory pump: during inspiration, venous blood is essentially sucked
back into the thorax, increasing venous return and preload. (because
intrathoracic pressure decreases)
c. Neural: changes in sympathetic and vagal efferent neural activity supports
blood pressure. Arterial baroreflexes sense a decrease in blood pressure and
the cardiopulmonary baroreceptors sense a decline in LVEDP. This leads to
decreased inhibitory nerve firing from the baroreceptors.
Efferent
sympathetic nerve activity now may increase. In the heart, efferent
sympathetic nerve activity increases and efferent vagal activity decreases,
leading to an increase in heart rate and contractility; efferent sympathetic
nerve activity is increased to the splanchnic circulation, leading to splanchnic
vasoconstriction and venoconstriction; efferent sympathetic nerve activity in
increased to the skeletal muscle, leading to muscle vasoconstriction; and
finally, anti-diuretic hormone secretion is increased, serving to increase
blood volume in the log run.
10. Fill in the following blanks with the selections:
a) increase
b) decrease
c) do not change
d) Receptor control is very specific. Changes to different stimuli are modulated
in certain receptors in various fashions. In response to an increased arterial
blood pressure, arterial baroreceptors, (much like Cardiopulmonary
baroreceptors), ___A___ their firing rate to decrease sympathetic nervous
system activity (SNA) to afford a decreased blood pressure, while a decreased
arterial blood pressure will cause the receptors to __B__ their firing rate to
affect SNA. Arterial chemoreceptors (much like Muscle metaboreceptors) on
the other hand, use a different modality to affect SNA. In response to
decreasing CO2 in the blood arterial chemoreceptors ___B_____ their firing
rate to afford decreased SNA.
11. Differentiate between the terms threshold vs. sensitivity of firing for a receptor.
Threshold is the minimum pressure at which a receptor begins to fire, whereas
sensitivity is the change in receptor firing per change in stimulus.
12. Clinical Situations:
Please describe what effects on Sympathetic Nervous System Activity and
Parasympathetic Nervous System Activity (increase vs. decrease) will occur TO
COMPENSATE in the following clinical scenarios.
a) Hemorrhage:
SNA __UP
PSNA ___DOWN
b) Asphyxiation:
HINT: Think Vagus!
SNA __ UP
PSNA___UP___
13. Explain why that when both Arterial and Cardiopulmonary Baroreceptors are cut, that
Blood Pressure gradually increases.
Blood pressure increases because of increased sympathetic outflow due to the
removal of inhibitory effects of the ABR and the CPBR.
14. What is the essential cardiac difference in the Arterial Baroreceptor Reflex vs.
Arterial Chemoreceptor Reflex?
ABR Reflex elicits a tachycardic response whereas ACR Reflex elicits a
bradycardic response.
15. Last week, we discussed sinus arrhythmia as a normal change in heart rate that
occurs in normal patients during breathing. Now, understanding the presence of
baroreceptors and chemoreceptors and lung stretch receptors, explain the cycle of
sinus arrhythmia.
From a normal intrathoracic pressure during the exhalation phase, in
inhalation, intrathoracic pressure drops markedly, (increased Pulmonary
Capillary Storage volume decreases return to the Left side of the Heart) as a
result, LVEDP drops, decreasing CPBR outflow, furthermore, the transient
decreased CO due to decreased Stroke Volume drops ABR outflow, the
combined effect drops the inhibition of SNA and inhibitory effects of the PSNA
through the Vagus, but MOST IMPORTANTLY, the lung stretch receptors
afford a drop in efferent vagal outflow to the heart, which causes the heart rate
to transiently increase in inspiration.
15. Explain how increased SNA during exercise does not afford vasoconstriction in the
metabolically active muscle beds.
THINK MUSCLE METABOREFLEX! Metabolites released during exercise
cause vasodilation of the vessel beds.
Extra credit:
After your stellar performance in the LA Marathon, you decide to try a triathlon. You go
for a swim at Sunset Rec for about 1 hour (completely submerged). Afterwards, you
relieve your bladder of its contents and check the osmolarity with you handy pocket
osmometer. You very accurate meter tells you that your urine is iso-osmolar to your
plasma. Why? (think in general terms and this question can be answered in one sentence)
The  in “atmospheric” pressure on the on your body will  the intravascular pressuer
( volume) and will signal to renal systems to dump volume.
TUTORS: ADDRESS Afferent vs. Efferent tracts in neural reflex system.