# STUDENT QUESTIONS CARDIOVASCULAR PHYSIOLOGY

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```					              STUDENT QUESTIONS: CARDIOVASCULAR PHYSIOLOGY

Student: I am having trouble with a hemodynamics concept that I hope you can clarify for me.
The question is, essentially, if the diameter of a vessel is increased, what happens to Reynolds’s
number?
I can see the explanation going either way, which is where I'm getting confused...
If the diameter is increased, then the velocity goes down, because velocity is proportional to
1/(r2). If velocity goes down, then Reynolds’s number should also go down. So, it seems like
velocity has a bigger effect on Reynolds’s number than the diameter.
However, could it also not be, that if the diameter is increased, there is more room for turbulence,
thereby increasing Reynolds’s number?
Similarly, if the diameter of a vessel is decreased, will the Reynolds’s number go up (according
to manipulation of the equations), or will it go down (according to the seemingly logical
explanation)?
Please let me know if there is a better way of looking at this.
Always first, write down an equation. Notice that Re is directly proportional to D. Hence, it is
no surprise that turbulence may happen in the aorta.
The biggest determinant of Re is the flow velocity. Where there is a high velocity, such as at a
stenosis, turbulence is prone to happen. This is the basic concept underlying bruits and murmurs.
What is of concern is your use of the term “diameter goes up or it goes down”. Are you referring
to hemodynamics in a single vessel that is dilating or constricting? On the other hand, are you
comparing the hemodynamics of a large vessel compared to that of a smaller vessel? Make sure
of the question that you ask.

Student: I'm having a few issues with hemodynamics again. Please let me know if my
understanding is correct...
In the aorta, the velocity is large, causing turbulence.
In the whole system of capillaries, the cross sectional area increases, so velocity as a whole
decreases, when compared to the aorta.
However, in each single capillary, since the cross sectional area is much smaller than the aorta,
each single capillary will have a larger velocity than the aorta.
This large velocity in each single capillary causes a high shear rate, leading to a decrease in
viscosity.
-this high shear rate in each capillary is larger than the shear rate in the aorta. Thus, there will
be higher turbulence in each individual capillary, when compared to the aorta.
Please let me know if this reasoning is correct, or where I need to change my thinking.
Your reasoning is not quite correct on two accounts:
Velocity in a capillary is low (See diagram from class). One would expect the shear rate to be
low but it is actually higher than expected, due to plasma skimming - The Fahraeus-Lidqvist
effect.
Remember that the velocity = Q/Cross-sectional area.
You have to take flow rate into account. Recall that flow rate (Q) is actually very low in an
individual capillary. Hence, velocity has to be much lower than in the aorta.
One is often prone to forget that in parallel branches, flow rate has to decrease.
Student:
I had a quick question about circulation, that is part of the small group assignments. The right
and left carotid arteries are in series, correct? I thought you had said that all of the circulation is
in series, except for vessels going into different organs. Since the question (case 3, question 5)
tells us to assume these arteries are both going to the brain, doesn't that make them in series?
Also, I thought that blood flow to the liver was in parallel to blood flow to the spleen or any
other organ, but that the blood flow through each organ is in series. But how about the
microcirculation of the liver and that of the spleen-- are these two microcirculations in parallel or
series with each other? Or is the capillary circulation only in series when looke at as a whole, so
that their main systemic arteries are in series with the main systemic veins?
Many students are initially tripped up by this.
Blood flow through each individual carotid artery is in series.
The left and right carotid arteries do not have a common origin accordingly, they are in parallel
to the brain.
You are correct in saying that organs receive their blood supply in parallel.
Individual capillaries are in parallel within a capillary bed. This is why the bed has such a low
total resistance. Capillary beds within an organ are generally parallel to each other; except for
the kidney (always there is an exception to the rule), which has two major capillary beds in series.

Student
I have a question involving a conceptual conflict. Reynolds number tells us that a fluid with an
extremely low viscosity will most likely be turbulent. Turbulent flow requires a greater pressure
to keep the flow rate constant. Otherwise, at constant pressure, the flow rate drops (?).
You are correct in your statement that turbulent flow requires a greater driving pressure to keep
flow rate concept. Because of the “bombardment’ of molecules against the vessel wall with
turbulence, potential energy is lost. A higher potential is needed to keep the flow constant.
Think of it this way, if you take your foot off the gas, the speed drops.
Certain cars require more pressure on the gas pedal to obtain a specific speed. But if you take
your foot off the gas, irrespective of the make of car, the car still slows down.
Recall that Poiseuille’s law tells us that a fluid with an extremely low viscosity has decreased
resistance, and decreased resistance brings increased flow rate.

Student:
I was reviewing the lecture today and wanted to know if my way of viewing the IV plot was
correct or off base. I am thinking of the IV plot as the type (inward vs. outward) and amount of
current at a certain membrane potential. So then, if we know what a membrane potential is, we
can assume how a (rectifier) channel will be acting in regards to that ion. I guess my main
question is, the IV plot does not necessarily plot out in real time the effect of the current on the
membrane potential, but only the effect of the membrane potential on the channel (and current).
There is no “time” component on an IV plot. Channel conductance changes with membrane
potential and so does the driving force on the current. This is why an I-V plot is so helpful in
explaining the behavior of a channel.
Perhaps it is the term "rectifying" that is confusing. The IV plots of individual channels are all
different. Today I explained to you the meaning of the term "rectification".
What is confusing is the fact that a) the channel can conduct an inward or an outward current
depending on the driving force and the membrane potential. This is unusual.
And b) the channel prefers to conduct inward (and outward if it is an outward rectifier). Read
my notes slowly once again. The IV plot of the Na channel does not show rectification, hence, it
is a straightforward voltage gated channel.
By having an inward rectifier, the cell can easily maintain the resting membrane potential at a
certain level and protect the cell from extraneous influences. I.e., it can compensate for small
depolarizations as well as for large hyperpolarizations.

Student
I have a question about Figure 15 in your lecture today. I was under the impression that when
you decrease Ica-L channel activity the threshold will become more positive, making it more
difficult to reach threshold for the action potential (and further away from MDP), and the
opposite happens during sympathetic control. However, in the graph for parasympathetic it
shows the threshold (in the dotted line) going down and the threshold going up in the
sympathetic control graph. Can you explain why this is so? Am I getting the channels and/or
effects confused?
You are not confused about the channels. However, concepts in the figure may be confusing.
Figure 15 shows the autonomic effects by means of which heart rate may be adjusted. It does
show correctly that down regulation of I_Ca_L slows the heart (sympathetic effects are
opposite). However, it does not show you the actual change in threshold of the AP. This is
actually shown in Figure 13. Thus, while you understand the concepts nicely, the figure from a
textbook shows the effects but does not provide you with actual explanations. What Figure 15
does show is that down regulation of ICa_L will give a lower AP amplitude and a slowing of the
heart. As you have said, pushing the threshold to a more positive value will slow the heart.

Student
"AV nodal cells have long refractory periods (because of slow depolarization and slow
conduction), which inhibits atrial tachycardias from reaching the ventricle."
Does this mean that ventricular tachycardia is caused by a problem in the AV node? Specifically,
something that speeds up its conduction--or maybe by the functional loss of the AV node
altogether, such that the fast SA node potential speeds right by like somebody running a red
light?
A ventricular tachycardia may arise from ectopic sites within the ventricle (AV node plays no
role). But many ventricular tachycardias may be generated by atrial impulses that bypass the AV
node through e.g., abnormal conduction sites such as, the bundle
of Kent. Typical in WWP syndrome ( like your "running a red light" analogy. May I use it in
future?).

Student:
This student had a problem with the diagram showing the ventricular depolarizing vectors.
The vectors spread as I have indicated, over both ventricles. The first, is from left to right across
the septum, then towards the apex, followed by the anti-clockwise depolarization of the lateral
walls. Vectors do not cancel out, but the left ventricle, with its larger mass, dominates the
electrical events (vectors). Thus, although there are vectors o both ventricles, the EKG only sees
the dominant vector. That is why one cannot see e.g., atrial repolarization on the EKG.

Student: Regarding the Wiggers diagram.
First, why does ventricular volume increase in phase A--and then decrease?? Where does that
blood go, since only the mitral and tricuspid valves are open?
Your textbook is the only one that I know of that shows this happening. Others don't show this
because the effect is slight and not important for our discussion. When the AV valves start to
close against the pressure in the ventricle, some blood "slips back" into the atrium and
ventricular volume SLIGHTLY decreases. Think of this as putting a lid on an overfilled plastic
container. The fluid can slip back out of the container when you press down.

Student:
We talked about heart murmurs, specifically systolic and diastolic murmurs. Do these only refer
to the aortic and pulmonary valves? If so, how do you diagnose problems with the AV valves? If
not, do valve problems always come in pairs?
You realize that a murmur is not caused by a valve closing, but by turbulence. Accordingly, a
murmur can be caused during the ejection of blood into either the pulmonary or aortic valves.
This would be a systolic murmur. The velocity is high when you have to eject against an
increased load (such as a stenosis). Systolic murmurs occurs between S1 and S2.
During diastole you will not have an ejection murmur but you may have a regurgitant murmur.
These occur after S2. This may be through either the semilunar valves or the AV valves (the
latter caused by mitral or tricuspid stenosis). You have to know the cardiac cycle to determine
the timing. This is off course much more clinical information that you need for M1.

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 views: 8 posted: 9/15/2011 language: English pages: 4