Download Cardiac Output Venous Return

Circulatory
Physiology
As a Country Doc
Episode 3
Cardiac Output
and
Venous Return
Patrick Eggena, M.D.
Novateur Medmedia, LLC.
Circulatory
Physiology
As a Country Doc
Episode 3
Cardiac Output
and
Venous Return
Patrick Eggena, M.D.
Novateur Medmedia, LLC.
i
Copyright
This Episode is derived from:
Course in Cardiovascular Physiology by Patrick Eggena, M.D.
© Copyright Novateur Medmedia, LLC. April 13, 2012
The United States Copyright Registration Number: PAu3-662-048
Ordering Information via iBooks:
ISBN 978-0-9663441-2-7 Circulatory Physiology as a Country Doc,
Episode 3: Cardiac Output and Venous Return
Contact Information:
Novateur Medmedia, LLC
39 Terry Hill Road, Carmel, NY 10512
email: [email protected]
Credits:
Oil Paintings by Bonnie Eggena, PsD.
Music by Alan Goodman from his CD Under the Bed,
Cancoll Music, copyright 2005 (with permission).
Illustrations, movies, text, and lectures by Patrick Eggena, M.D.
Note: Knowledge in the basic and clinical sciences is constantly changing. The reader is advised to carefully consult the instructions and informational material included in the package inserts of each drug or therapeutic agent before administration. The
Country Doctor Series illustrates Physiological Principles and is not intended as a guide to Medical Therapeutics. Care has been
taken to present correct information in this book, however, the author and publisher are not responsible for errors or omissions
or for any consequence from application of the information in this work and make no warranty, expressed or implied, with respect to the contents of this publication or that its operation will be uninterrupted and error free on any particular recording device. Novateur Medmedia, LLC shall not be held liable for any punitive damages resulting from the use or inability to use this
work. This work is copyrighted by Novateur Medmedia, LLC. Except to store and retrieve one copy of the work, you may not
reproduce, decompile, reverse engineer, modify or create derivative works without prior written permission by Novateur Medmedia, LLC.
ii
iii
This Episode is dedicated to Bonnie and
to our children Kendra and Brandon and
to our grandchildren Basia, Anika, and August.
iv
Foreword
This is the third of three episodes in the Circulatory Physiology Series. Each episode
starts with a case where the student finds himself or herself in the imaginary world of a
Country Doctor who is called upon to manage a clinical problem related to a 50-minute lecture given by the author to First Year Medical Students. Video tapes of these lectures are
divided into short segments which are interwoven with relevant chapters of the author’s
ebook, “Medical Physiology of the Heart-Lung-Kidney.”
v
About the Author
The author was born in London in 1938. His parents had fled from Germany in 1933
after his father was wrongly accused of burning down the Reichstag in Berlin as Hitler
was rising to power. When War broke out, the author’s family was interned on the Isle
of Man and, after the War ended, transported back to Germany. There the author
grew up on a farm, attended Gymnasium, and emigrated to America at the age of 18.
Shortly after arriving in the US he was drafted into the Army and sent overseas where
he served as a Medic. Upon returning to the US he attended Kenyon College and
then Medical School at the University of Cincinnati. After serving as a house officer
at the Cincinnati General Hospital he started a career in Medical Research, first as an
NIH post-doctoral fellow at the Brookhaven National Laboratories and the University
of Copenhagen and then as an Established Investigator of the American Heart Association at the Mount Sinai School of Medicine. There he rose through the academic
ranks to Professor of Physiology & Biophysics and served for 5 years as Acting Chairman of the Department.
He chaired the Physiology Course for more than 20 years, taught all aspects of
Physiology, and participated in the Art and Science of Medicine courses for First and
Second Year Medical Students.
After retiring from teaching and research, the author returned to living on a farm
with his wife and horses. Once a week he functions as an Emergency Physician in a
nearby hospital --alone for the 16-hour night shift -- where he applies his understanding of Physiology to everyday patient care at the bedside.
Students at The Mount Sinai Medical School showed their appreciation for his teaching by awarding him The Excellence in Teaching Award on twelve occasions. Student
comments and evaluations relating to the episodes published here are given on the
next pages.
vi
Student Evaluations
People Comments Report
Printed: 4/5/2010
Patrick Eggena
Comments about Educator: Please provide any constructive feedback about this educator.
Dr. Eggena is the best teacher I have ever had. I always felt secure that he would explain things
thoroughly and logically and address our questions effectively. He is so familiar with the material,
and its application to clinical practice, that I think he knows how to anticipate students' questions
and confusion, and that makes him an excellent teacher. I also thought his text book and the supplemental practice programs online were invaluable resources. I feel that Eggena has given me a
very firm grasp of the basics of cardiopulmonary physiology, and I'm very grateful to have had him
as a teacher.
I thought Dr. Eggena was great. It was really helpful to have both his book and his computer program to supplement lectures - with 3 ways to learn the same information (and in the same order!) it
is hard not to eventually understand each concept. The computer program with quizzes was especially useful. Lectures were clear and well organized.
Dr. Eggena is one of the finest teachers I've yet experienced. His patience and thorough explanations allowed me a deep understanding of the material, while his focus on the practical aspects of
each topic left me with a sense of competency that I will remember in the coming years. I enjoyed
each of his lectures and have a deep respect for his dedication to providing study materials for students beyond the lectures and his wonderful text book. This has been an exciting and memorable
learning experience.
Great lecturer, very clear.
Very clear lectures. Keep up the good work!
Great professor, very knowledgeable, patient, clear, concise.
Dr. Eggena was very thorough and clear in his explanations of cardiovascular and pulmonary physiology. His handouts were very helpful, as were his multimedia programs.
vii
People Comments Report Printed: 9/28/2011
Patrick Eggena
Comments about Educator: Please provide any constructive feedback about this educator.
Oh my goodness, where to begin? Dr. Eggena is PHENOMENAL. He is so old-school using
his projector and sharpie, drawing schematics and graphs he's obviously done a million
times, and has such a story-teller's voice. But that's what makes him GREAT. More professors shoiuld realize that maybe the powerpoint isn't the best format to teach, that maybe a
less recently available form of technology would be a better teaching aide. More professors
should give up trying to find a working dry erase board marker and switch to projectors and
sharpies. On top of that, to have created a multimedia program and quizes that reinforce
the material in such an entertaining way! Really I can't think of anything negative to say except that Dr. Eggena's lectures didn't extend to the whole of physiology and that his multimedia program did not have anything on kidneys, endocrine, GI, etc.
I found some of his lectures to be a little too fast paced, and unclear in some points. But he
has a definite great rapport with the students, seems to really care about teaching, and his
multimedia programs and multitude of practice questions were invaluable.
One of the best professors I have had yet. Very clear explinations, always happy to answer
questions. A kind and approachable professor with clear clinical applications.
A truly masterful educator. And physician. excellent
Great instructor!
Eggena is the best. So clear! good
Fantastic teacher.
Once I got the hang of it, his outlines were helpful and it was a change to draw along during
class rather than just typing away on a computer. His multimedia programs were also immensely helpful and the only reason I passed.
Dr. Eggena was a phenomenal educator and lecturer. I truly learned a lot from him regarding cardio and respiratory physiology. His online material was very helpful in studying for
quizzes and exams. Thanks for a great semester!
Dr. Eggena was great. He went quickly but clearly through the material, and he always presented concepts in terms of actual patient care, which made it all seem real.
viii
Performance Analysis Report
Report Notes:
1
Printed: 9/28/2011
School of Medicine Evaluation System
Subject: Patrick Eggena
Activity Group: Physiology
Starting Request Date: 12/01/2010
Ending Request Date: 09/28/2011
Location: Mt. Sinai
Clarity of presentation
Using the lecture/educator list above to link this instructor with the lecture (s)he gave, please rate their clarity of presentation.
Average:
Minimum:
Maximum:
Non-Zero Count:
Scale:
Standard Dev:
4.35
2
5
138
1 to 5
0.74
Answer Value: Answer Choices:
2
Choice Count:
Percentage:
1
0
1%
0%
2%
0
1
Unable to Evaluate
Unacceptable
2
Below Average
3
3
Average
13
9%
4
Very Good
55
40%
5
Superior
67
48%
Rapport with students
Please rate this educator's rapport with students.
Average:
Minimum:
Maximum:
Non-Zero Count:
Scale:
Standard Dev:
4.62
3
5
138
1 to 5
0.52
Answer Value: Answer Choices:
3
Choice Count:
Percentage:
0
Unable to Evaluate
1
1%
1
2
Unacceptable
Below Average
0
0
0%
0%
3
Average
2
1%
4
Very Good
48
35%
5
Superior
88
63%
Quality of Tracking
Please rate this educator's overall quality of teaching.
Average:
Minimum:
Maximum:
Non-Zero Count:
Scale:
Standard Dev:
4.51
2
5
138
1 to 5
0.63
Answer Value: Answer Choices:
Choice Count:
Percentage:
0
Unable to Evaluate
1
1%
1
Unacceptable
0
0%
2
Below Average
1
1%
3
4
Average
Very Good
7
50
5%
36%
5
Superior
80
58%
Page 1 of 1
Performance Analysis Report
Report Notes:
1
Printed: 4/5/2010
School of Medicine Evaluation System
Subject: Patrick Eggena
Activity Group: Physiology
Time Frame Start Date between: 01/11/2010 and 04/05/2010
Clarity of presentation
Please rate this educator's clarity of presentation.
Average:
Minimum:
Maximum:
Non-Zero Count:
Scale:
Standard Dev:
4.38
3
5
136
1 to 5
0.62
Answer Value: Answer Choices:
2
Choice Count:
Percentage:
0
Unable to Evaluate
0
0%
1
Unacceptable
0
0%
2
3
Below Average
Average
0
10
0%
7%
4
Very Good
65
48%
5
Superior
61
45%
Rapport with students
Please rate this educator's rapport with students.
Average:
Minimum:
Maximum:
Non-Zero Count:
Scale:
Standard Dev:
4.68
3
5
136
1 to 5
0.50
Answer Value: Answer Choices:
3
Choice Count:
Percentage:
0
Unable to Evaluate
0
0%
1
Unacceptable
0
0%
2
Below Average
0
0%
3
4
Average
Very Good
2
40
1%
29%
5
Superior
94
69%
Quality of Tracking
Please rate this educator's overall quality of teaching.
Average:
4.57
Minimum:
3
Maximum:
5
Answer Value: Answer Choices:
Non-Zero Count:
136
Scale:
1 to 5
Standard Dev:
0.58
Choice Count:
Percentage:
0
Unable to Evaluate
0
0%
1
Unacceptable
0
0%
2
Below Average
0
0%
3
Average
6
4%
4
Very Good
47
35%
5
Superior
83
61%
Page 1 of 1
1
The Country Doctor
The Case
The Case
12
The Discussion
Kay: “Doc, it was good that you were
holding on to him when he stood up and
we took his blood pressure.”
Doc: “Yes, Kay --we had to be prepared
for him to faint. He did so once before
when he stood up and hurt himself --could
have happened again.”
Kay: “By how much does blood pressure
have to drop before you call it orthostatic hypotension?”
Doc: “Systolic pressure has to fall by at
least 10%.”
Kay: “and pulse increase by 10%?”
Doc: “Yes - Mr. Bach’s pulse increased in
response to the pressure drop --after his
Kay --your nurse is taking night courses to become a nurse practitioner. She comes along
when you are making house calls.
baroreceptor reflex kicked in.”
Kay: “The sensors for this are in the carotid sinus?”
Doc: “Yes --and in the wall of the aorta.
Stretch receptors. High pressure receptors
that are tonically active -- less so when
pressure drops. The response is fast
--really fast.”
Kay: “But not with Mr. Bach. His reflex
was slow --really slow.”
Doc: “That’s his problem. That’s why he
fainted. That’s his chief complaint. It’s why
his daughter called us.”
Kay: “So as he stood up, blood pooled
in his legs, less returned to his heart,
his heart pumped less to his brain, and
he fainted. All due to a sluggish baroreceptor!?”
Doc: “Yes, Kay --that’s his problem in a nutshell.”
13
Kay: “His nerves from the carotid sinus
something that depleted his blood vol-
to the vasomotor center in the medulla
ume? That can also cause orthostatic
and back out to the veins were probably
hypotension, can’t it -- Doc?”
not conducting impulses fast enough?”
Doc: “Yes for sure. Very common. If his
Doc: “Could be. Patients with peripheral
veins are nearly empty, tensing up on them
neuropathy, for example, tend to faint on
won’t increase pressure by much. But is
standing up suddenly. They have problems
plasma volume depletion a likely explana-
with nerve conduction.
tion here --considering his blood pressure?”
Kay: “Like in patients with diabetes?”
Kay: “No --he was not in shock --not
Doc: “Yes --diabetic neuropathy is a quite
with a systolic pressure of 160 mmHg
common cause of orthostatic hypoten-
and with the strong pulse that he had.”
sion.”
Kay: “How about medicines?”
Doc: “Yes --patients receiving medicines
for hypertension --quite common --especially alpha-1-adrenergic blockers.”
Kay: “I did an internship on a psychiatric
ward. Many of the antipsychotic medicines do this also.”
Doc: “Not uncommon side effect of medicines. But we did ask his daughter if he
had diabetes or was taking any medicines
for hypertension or for his PTSD from the
Korean War, and she said “No”.”
Kay: “But what if he was dehydrated or
bleeding internally or had diarrhea or
Doc: “His strong pulse is called a Corrigan
pulse or a water-hammer pulse. It was
due to his high pulse pressure.”
Kay: “You mean the large difference between his systolic and diastolic blood
pressure?”
Doc: “Yes, it was quite large because of
his great stroke volume.”
Kay: “It’s as if he were exercising and all
that blood was going to his muscles.
But it wasn’t. So why did he have such
large stroke volumes?”
Doc: “Well --you listened to his heart.
What did you hear?”
14
Kay: “I heard --with your help --an early
flow among other properties of blood,
decrescendo diastolic murmur and a lit-
such as viscosity and density.”
tle pre-systolic sound, which you said
was called an Austin Flint murmur. But
what do these murmurs have to do with
his large stroke volume?”
Doc: “He has aortic insufficiency. His aortic valve doesn’t close properly, so blood
regurgitates back into his left ventricle during diastole. This produces the decrescendo murmur right after the second
heart sound.”
Kay: “The murmur did get louder as he
leaned forward and exhaled.”
Doc: “Yes, that brought his heart closer to
your stethoscope. Still, it’s difficult to hear
this murmur. Diastolic murmurs aren’t as
loud as systolic murmurs.”
Kay: “Okay, so this murmur indicates
that blood flows backwards across his
aortic valve?”
Doc: “Yes -- and his left ventricle, therefore, fills during diastole from two sides -blood coming through the mitral valve as
usual and blood flowing backwards
through an incompetent aortic valve.”
Kay: “And this resulted in a large enddiastolic volume which produced the
large stroke volume and the large pulse
pressure.”
Doc: “Right.”
Kay: “The other murmur, the presystolic one, must have been due to mi-
Kay: “Why is this?”
tral stenosis. Right?”
Doc: “Higher velocity of flow during sys-
Doc: “Sort of, but his mitral valve is not
tole. More turbulence. Higher Reynold’s
number.”
Kay: “Higher what?”
Doc: “Reynold’s number --a way of estimating when turbulence is likely to occur.
This is a dimensionless number which
takes into account the velocity of blood
really damaged as, for example, in rheumatic fever. Here we have a functional
murmur.”
Kay: “A flow murmur?”
Doc: “Well, what happens is this. One of
the leaflets of the mitral valve can’t open
properly because it is kept partially shut by
15
a jet of blood flowing backwards through
Doc: “Yes --wet crackles from pulmonary
the damaged aortic valve. So when the
edema. Why were his lungs wet?”
left atrium contracts toward the end of diastole blood ejected through the mitral
Kay: “Blood was backing up into his
valve becomes turbulent and creates the
lungs because his left ventricle couldn’t
pre-systolic murmur, the so-called Austin
handle the load?”
Flint murmur.”
Kay: “His left ventricle is working hard
--has been for a long time --and now it
is hypertrophied. Right?”
Doc: “How do you know that it is hypertrophied?”
Kay: “Because the S-wave in lead V1
plus the R-wave in V5 is greater than 35
mm. --- You taught me that the other
day. But I don’t understand why the ST
segment is depressed in lead V5.”
Doc: “Left ventricular strain --sloping of
the ST segment --indicates endocardial
ischemia.”
Kay: “Is his left ventricle failing?”
Doc: “Well, what do you think? What did
Doc: “Blood wasn’t really backing up, but
a higher pressure was required to fill his
left ventricle because it was hypertrophied
and stiff.”
Kay: “So more blood was filtered across
the capillaries in the lungs because capillary pressure was increased?”
Doc: “Yes --and the lymphatics couldn’t
quite handle the increased load. Couldn’t
return all the extra fluid around his alveoli
back to the circulation.”
Kay: “I asked him if he got short of
breath when he lies down, and he said
“Yes”. And he said that he slept with
his head on three pillows.”
Doc: “Why did he use several pillows?”
you hear when you listened to his lungs?”
Kay: “I know, this is called orthopnea
Kay: “His lungs didn’t sound normal.
legs moving back into his lungs at
Where those wet rales I heard?”
night.”
and it is due to the edema fluid in his
16
Doc: “And also, when he lies flat more of
Doc: “Yes --to move fluid from his lungs
his lungs are below the level of the tricus-
back into his feet.”
pid valve. So hydrostatic pressure is
higher in more lung capillaries than usual
Kay: “And he also said that he can’t
and more fluid is filtered into the interstitial
make it all the way up the stairs to his
spaces around the alveoli.”
bedroom without having to stop several
times because he runs out of breath.”
Kay: “So more of his lung is under water?”
Doc: “Yes, he has dyspnea on exertion or
DOE for short.”
Doc: “Yes, so-to-speak.”
Kay: “Doc, I noticed that the residents in
Kay: “He also said that he has asthma
the hospital tend to speak in abbrevia-
attacks at night which adds to his prob-
tions and broken sentences to one-
lem with breathing. But I didn’t hear any
another, why is this?”
wheezing when I listened to his lungs.”
Doc: “They are usually in a rush and sort of
Doc: “He has cardiac asthma which is dif-
know how to complete a sentence started
ferent from regular asthma.”
by one of their colleagues without it being
Kay: “How so?”
Doc: “In cardiac asthma it is edema fluid
that wells up from the alveoli into the bron-
vocalized. A lot of medicine is repetition.”
Kay: “Alright, so what’s with Mr. Bach’s
DOE?”
chioles distending their walls and imped-
Doc: “When he gets ready to climb the
ing air flow. This shortness of breath that
stairs, his pre-motor cortex sends im-
comes on at night is called paroxysmal
pulses over several pathways all the way
nocturnal dyspnea or PND for short.”
down to the muscles in his legs that are go-
Kay: “He said that these attacks were so
bad sometimes that he had to sit up
with his legs dangling over the side of
the bed.”
ing to do the work. Arterioles dilate and as
muscle start to contract pre-capillary
sphincters click open in response to metabolic by-products such as carbon dioxide
and adenosine that are released from cells.
And his leg muscles get warm from the
17
heat generated from the brake down of
Kay: “He feels short of breath --is dysp-
ATP molecules and this along with release
neic -- because he is not getting
of endothelial relaxing factors dilates ves-
enough oxygen. Right?”
sels even more. These mechanisms furnish Mr. Bach’s leg muscles with the oxy-
Doc: “You might think so because he is, in-
gen and nutrients needed to climb the
deed, not getting enough oxygen. But air-
steps.”
hunger --or not being able to catch ones
breath -- is due to the excessive work that
Kay: “Okay, Doc --got it. What next?”
Doc: “Now all this extra blood that rushes
to his leg muscles in arteries comes back
out in his veins and is returned to the right
ventricle which pumps more into his
lungs.”
Kay: “Well, that happens to all of us
when we exercise. So what is different
with Mr. Bach?”
his inspiratory muscles have to do to distend his alveoli which have become stiffer
because of the surrounding edema fluid. It
is this extra work that gives him the sensation of dyspnea. It’s a subjective feeling
--a little bit like pain.”
Kay: “That’s interesting. Now I also noticed that his neck veins were distended. I guess this means that his
right ventricle was also failing. But
Doc: “You have a normal cardiac reserve,
why? It wasn’t working overtime like
where your left ventricle pumps about 5
his left ventricle?”
liters/minute at rest, but on exercising can
pump perhaps 15 liters/minute or more.
But Mr. Bach does not have much of a cardiac reserve. His heart can pump just
about enough blood to get by at rest.”
Kay: “And so the blood that is not
pumped by the left ventricle is left in
the lungs and takes his breath away?”
Doc: “Yes --he becomes dyspneic. Hence
the term dyspnea on exertion.”
Doc: “Kay, but it was. It was also working
much harder because left ventricular failure invariably leads eventually to right
heart failure.”
Kay: “Why is that?”
Doc: “When the left ventricle fails and fluid
accumulates in the lungs, the amount of
oxygen in blood decreases and this
causes arterioles in the lung to constrict.”
18
Kay: “But I thought blood vessels re-
muscle that behave in some respects simi-
laxed when oxygen is lacking. Isn’t this
lar to hemoglobin in that they change their
how more blood flows to tissues that
conformation depending on the amount of
need it? Remember, “autoregulation”
oxygen bound to them.”
we talked about yesterday?”
Kay: “And this conformational change
Doc: “Big difference between autoregula-
with little oxygen around causes the
tion in peripheral tissues and in the lung.
contraction?”
In the lung a decrease in oxygen tension
causes constriction of blood vessels, not
relaxation.”
Kay: “But why?”
Doc: “Eventually, yes --but first the conformational change in the protein closes a potassium channel so that potassium diffusion out off the smooth muscle cell is
slowed.”
Doc: “ If a section of the lung is not getting
oxygen because a bronchus is plugged
Kay: “And that moves the membrane po-
with mucus, you don’t want to have blood
tential away from the potassium equilib-
flowing to that section of lung. It won’t
rium potential of -90 mV. Right? We
pick up any oxygen or get rid of any car-
learned about the Nernst Equation and
bon dioxide. In fact, blood flowing through
membrane potentials not long ago in
an unventilated section of lung is like a
class.”
right-to-left shunt -- allowing unoxygenated venous blood to flow straight into the
Doc: “Good, Kay --the membrane poten-
arterial circulation as if you had poked a
tial becomes less negative at which point a
hole in the interventricular septum. So no,
voltage-gated calcium channel in the mem-
the response to hypoxia is reversed in the
brane opens and calcium ions flood the
lung.”
cell and make it contract.”
Kay: “But how do blood vessels in the
Kay: “And this increases the resistance
lung sense that oxygen is low and that
against which the right ventricle has to
they ought to constrict?”
eject its stroke volume?”
Doc: “There are receptor proteins in the
membranes of pulmonary vascular smooth
19
Doc: “ Yes -- pulmonary resistance, that is
Doc: “Not quite. In a sphere, like an alveo-
the afterload on the right ventricle, in-
lus or ventricle, it’s twice the radius. But
creases and it eventually fails.”
you’re right, wall tension will be increased
Kay: “What do you mean by “fails”?”
Doc: “Fails to ejected 2/3rds of its enddiastolic volume.”
Kay: “So his right ventricle is not contracting fast enough?”
Doc: “Yes, not fast enough in the time it
has to contract during systole.”
Kay: “So what happens?”
so that more ATP molecules and more oxygen and more coronary blood flow will be
needed to force the blood out. Nothing is
for free.”
Kay: “But doesn’t the ventricle eventually hypertrophy?”
Doc: ”Yes, it does, and with hypertrophy
wall tension is distributed over more sarcomeres. This decreases overall wall tension. But now the ventricle becomes
stiffer -- more difficult to fill.”
Doc: “It increases its end-diastolic volume.”
Kay: “So his CVP has to go up?”
Kay: “A bigger heart?”
Doc: “Yes --his neck veins should have
been filled to no more than about 8 cm
Doc: “Yes --the ventricular chamber dis-
above his sternum.”
tends and with the help of the FrankStarling mechanism manages to eject a
Kay: “That’s because the tricuspid valve
bigger stroke volume.”
is zero and it is about 5 cm below the
Kay: “But that requires more energy and
more work. Doesn’t it?”
sternum?”
Doc: “Right. Total pressure about 13 cm
H2O or roughly 10 mmHg.”
Doc: “Yes, it’s inefficient because of the
LaPlace equation.”
Kay: “Specific gravity of mercury is
about 13?”
Kay: “I remember: Wall tension equals
pressure times radius.
Doc: “Yes, Kay, if I remember correctly.”
20
Kay: “So blood then started flowing
Doc: “As edema fluid distends the intersti-
backwards into his legs causing his
tial spaces, elastic tissues in these spaces
edema?”
are stretched and create a back-pressure
which eventually stops more fluid from en-
Doc: “No --blood keeps flowing toward the
tering this compartment.”
heart even when the CVP is high. The only
difference is that a higher pressure is now
Kay: “But won’t his plasma volume be
required in foot capillaries to keep blood
depleted by the amount of extra fluid
moving upwards to the heart.”
ending up in his feet and legs?”
Kay: “Doc, that’s what I’m saying. Blood
Doc: “His plasma volume is kept at a near
flows backwards into the feet to raise
normal level by his kidneys.”
pressure to keep blood moving.”
Doc: “No --nothing flows backwards.
There are one-way valves in the large veins
that keep that from happening. No -blood stays in the feet. Won’t move until
enough has accumulated to generate the
recoil pressure required to move blood
Kay: “How do his kidneys do that?”
Doc: “As fluid is lost to interstitial spaces,
less blood is returned to the right atrium
where low pressure baroreceptors in the
subendocardium sense the decrease in
blood volume.”
against gravity up to the heart.”
Kay: “Plasma volume receptors?”
Kay: “And the increase in capillary pres-
Doc: “Yes --but the body can’t measure
sure then causes more fluid to be fil-
blood volume, it only has sensors for pres-
tered into the interstitial spaces of Mr.
sure. But these low pressure receptors in
Bach’s feet --creating edema?”
effect measure volume. You are right.”
Doc: “Yes --that is, if the lymphatics are
Kay: “So these volume receptors send
overwhelmed and can’t keep up with the
impulses to the vasomotor center which
influx.”
increases sympathetic outflow to the
Kay: “What keeps his feet and legs from
kidney?”
getting bigger and bigger from all that
fluid?”
21
Doc: “Yes --and sympathetic nerves con-
transporters to move them back into blood
strict both the afferent and efferent arteri-
in the proximal tubule.”
oles of glomeruli in his kidneys.”
Kay: “You mean like the transporters for
Kay: “Why not just clamp down on the
glucose and amino acids that are fil-
afferent arteriole to decrease filtration
tered and reabsorbed in the proximal tu-
at the glomeruli and minimize loss of flu-
bule?”
ids in the urine?”
Doc: “Yes --potentially toxic substances
Doc: “By clamping down on the efferent
that have been digested and absorbed into
arteriole as well, you increase the filtration
blood in the gut are filtered in the glomeruli
fraction, which enhances salt and water re-
and because these foreign substances
absorption in the proximal tubule.”
don’t have transporters in the proximal tu-
Kay: “We had this in class: The filtration
fraction is equal to the glomerular filtra-
bule are left behind in tubular fluid and are
excreted in a smaller than usual volume of
urine.”
tion rate divided by renal plasma flow.
Right?”
Kay: “So you are saying that when the
kidney is not getting its usual share of
Doc: “Yes, Kay --so if you clamp down on
both the afferent and the efferent arteriole
--that is increase two resistances in series
blood it still tries its best to get rid of
wastes.”
--the filtration fraction increases more than
Doc: “Yes, Kay --that’s the idea. That is
if you had only constricted the afferent arte-
why the kidney has these two resistances
riole.”
in series in the glomeruli. A clever way of
Kay: “Got it Doc. But why? Why filter
making it do its job more efficiently with a
lower rate of glomerular filtration. It’s not
relatively more plasma fluid only to reab-
just sympathetic stimulation that increases
sorb it again in the proximal tubule.
the filtration fraction, but also hormones
Seems like a waste of energy.”
such as angiotensin II and epinephrine.”
Doc: “But that’s how the kidney can still
Kay: “If the glomerular filtration rate is
get rid of waste products that are filtered
decreased, the concentration of urea
and --unlike salts-- do not have special
22
and creatinine in blood will increase.
where both BUN and creatinine rise propor-
Won’t it, Doc?”
tionally in blood.”
Doc: “Yes, if there is a significant decrease
Kay: “So do you think Mr. Bach has pre-
in renal perfusion or if there has been dam-
renal azotemia because his heart is fail-
age to the glomeruli. That is how we can
ing?”
tell that kidney function is reduced. But if
function is reduced because of decreased
perfusion, the concentration of urea will
rise more than the concentration of creatinine. That is, the ratio of BUN/creatinine
Doc: “No, not at this time. Although we
don’t know for sure without analyzing a
blood sample for urea and creatinine. He
has presumably compensated for the de-
will increase.
creased blood flow to his kidneys by retain-
Kay: “Is that important?”
diac output back to normal -- at least while
Doc: “That is how we can distinguish a reversible from an irreversible decrease in
ing more salt and water and raising his carhe is resting. So his renal blood flow is
now normal.”
glomerular filtration due to destruction and
Kay: “So it is only intermittently that his
loss of glomeruli.”
kidney go into this salt and water retain-
Kay: “I don’t understand why the con-
ing state?”
centration of urea rises more than the
Doc: “Yes, especially during the day when
concentration of creatinine with de-
gravity causes blood to pool in his legs.
creased renal blood flow.”
That’s when he retains more salt and wa-
Doc: “Creatinine is filtered by the glomeruli
ter.
and never reabsorbed by the nephron. By
Kay: “From the proximal tubule because
contrast, urea is filtered but also reab-
of the increased filtration fraction?”
sorbed from tubular fluid --more so when
the kidney is underperfused. Therefore, a
rise in the BUN/creatinine ratio in blood is
called pre-renal azotemia to distinguish
this reversible cause of diminished kidney
function from irreversible loss of glomeruli
Doc: “Yes, and from the collecting ducts
because of vasopressin and aldosterone.”
Kay: “Is this because more vasopressin
and aldosterone are released into the
23
circulation when low pressure barore-
Kay: “Yes, Doc. We learned that noc-
ceptors in the atria are stretched less
turia is a common symptom in patients
than usual?”
with congestive heart failure.”
Doc: “Yes --and even much more so
Doc: “It probably helps Mr. Bach breathe a
should high pressure baroreceptors in the
little easier than if this fluid ends up in his
carotid sinuses sense a drop in blood pres-
lungs at night.”
sure as they did, for example, when Mr.
Bach stood up and fainted.”
Kay: “Doc, his legs and feet looked awful. The swelling, the discoloration, no
Kay: “So Mr. Bach collects extra salt and
hair, and the ulcer.”
water as he walks around during the
day and deposits it in his feet and legs
as edema, and then at night gets rid of
it again?”
Doc: “True, this is from stasis dermatitis.
Edema increases the diffusion path for oxygen and nutrients -- a greater distance between capillaries and skin. Hair no longer
Doc: ”Yes --at night when this fluid leaves
grows. Red cells burst leaving behind iron
the legs and enters the circulation, the vol-
deposits which stain his skin.”
ume receptors in the atria are stretched
and they turn off vasopressin and aldosterone secretion.”
Kay: “And that ulcer on his ankle is not
going to heal unless he takes care of
himself.”
Kay: “Is that why Mr. Bach said that he
couldn’t sleep because he had to go to
the bathroom several times at night?”
Doc: “Yes he had nocturia --not only from
lack of vasopressin and aldosterone but
also because another hormone, the socalled atrial natriuretic peptide. This hor-
Doc: “You are right. He has to keep the
leg up high as much as possible to reduce
the swelling.”
Kay: “But he has no feeling in his feet.
And he was also pretty unsteady. No
warning, no pain when he bumps into
mone is released from atrial muscle cells
things and gets an abrasion or a cut
when they are stretched and it increases
which will then go unnoticed and fester.
salt excretion by the kidney.”
Why is this, Doc? Why can’t he feel his
feet?”
24
Doc: “He probably has peripheral neuritis
he had also acquired. That is why he
and perhaps something more serious that
should have been tested with the VDRL
is interfering not only with pain sensation
test for syphilis, which was not done at the
but also with balance and his position
time. And so his condition quietly pro-
sense.”
gressed to the final stage of tertiary syphilis, which is causing him problems now --
Kay: “Could peripheral neuritis be re-
decades later.”
sponsible for his orthostatic hypotension?”
Kay: “How do we know that he has tertiary syphilis without the VDRL test?”
Doc: “Possibly.”
Doc: “He has the Argyll-Robertson pupil
Kay: “Embarrassing -- when you asked
which is almost diagnostic for syphilis.”
this nice old man if he had syphilis.”
Kay: “You tested for that when you alDoc: “Yes, Kay --taking a sexual history is
awkward -- but important.”
most poked him in the eye?”
Doc: “Yes, his pupils were small, and they
Kay: “And when he started reminiscing
constricted to an even smaller size when I
about the girls in Munich a long time
moved my finger towards his nose. That’s
ago.”
expected --a normal accommodation re-
Doc: “Kay, it’s sometimes difficult not to appear impatient when taking a history. But
you have to be polite while keeping your
patient focussed on what is essential to
making a diagnosis.”
Kay: “Well, he admitted to having had
sponse. But they did not constrict when I
was shining a light into his eyes. That’s abnormal. That’s the Argyll-Robertson pupil.”
Kay: “Why did he have aortic insufficiency?”
gonorrhea, but he said nothing about
Doc: “Syphilis is caused by treponema
syphilis.”
pallidum -- a spirochete, a little worm-like
Doc: “His treatment for gonorrhea masked
the more serious venereal disease which
organism -- that gets into the vasa vasorum of the ascending aorta.”
25
Kay: “You mean the little blood vessels
Doc: “Right --that’s what one fears may
that supply the tissues in the wall of the
happen with aneurisms. But before this
aorta?”
happens the aneurism stretches the aortic
valve so that the leaflets no longer close
Doc: “Yes --and these little vessels get
tightly during diastole. Hence the back-
clogged up by the spirochete, so the wall
leak of blood which you heard as an early
of the aorta doesn’t get the nutrients it
diastolic decrescendo murmur.”
needs and is weakened. “
Kay: “So what are they going to do for
Kay: “Yes, but what does that have to do
him?”
with a leaky aortic valve?”
Doc: “He needs a thorough workup by a
Doc: “I’m coming to that. The weakened
cardiologist and a neurologist, including
wall of the ascending aorta bulges a little.
the VDRL test, which he didn’t get several
This increases it’s radius. As the radius in-
decades ago in the Army -- and a spinal
creases, so does wall tension.”
tap to examine his cerebrospinal fluid.”
Kay: “Oh, I know -- the Laplace equa-
Kay: “And he needs a new aortic valve
tion again, but now in a blood vessel
and penicillin shots.”
where wall tension equals pressure
times the radius. So an increase in the
radius of the aorta will increase its wall
tension?”
Doc: “And as wall tension increases, a few
more fibers in the wall rupture and the
Doc: “A new valve, yes, but no penicillin
--remember he is allergic to it. So they will
give him something else, like doxycycline
perhaps.”
Kay: “The neurologist can also see
aorta bulges a little more. And this, in turn,
what’s happening with his balance. He
increases tension which ruptures more fi-
didn’t know if his big toe was up or
bers and so forth.”
down when you moved it and he had his
his eyes closed.
Kay: “Like a weak spot in a tire --usually
ends in a blow-out?”
Doc: “And he didn’t have a knee jerk or vibration sense either.”
26
Kay: “No he couldn’t feel the vibrations
of your tuning fork. What does that
mean?”
Kay: “See you tomorrow.”
Doc: “Good night, Kay.”
Doc: “No proprioception, no position
sense! And he also had a positive Romberg’s sign.”
Kay: “That’s when he couldn’t keep his
balance with his eyes closed and feet together?”
Doc: “Yes, he had a broad leg stance because the nerves in the dorsal column of
his spinal cord have probably lost their insulation --are demyelinated.”
Kay: “But why did he have to close his
eyes.”
Doc: “Sight may compensate for the loss
of proprioception in his feet. That’s why
you have to test for balance with closed
eyes. He has tabes dorsalis --one of the
many complications of latent syphilis.”
Kay: “An awful disease. Good that we
can now treat it with antibiotics.”
Doc: “--if we catch it early.”
Kay: “I feel sorry for him.”
Doc: “I do too.”
27
2
Regulation of
Cardiac Output
Regulation of Cardiac Output
Lecture 3-1: Regulation of Cardiac Output
29
This section examines how left and right
ventricular output are regulated by enddiastolic filling volume, myocardial contractility, and heart rate.
1. Effect of CVP and PAWP
on Right and Left Ventricular
Output
Cardiac output by the right or left ventricles is equal to ventricular stroke volume
times heart rate (CO = SV x HR). Because
stroke volume increases as a function of
end-diastolic volume (Frank-Starling phenomenon), and end-diastolic volume is proportional to CVP (right ventricle) or PAWP
(left ventricle), cardiac output also increases as a function of CVP or PAWP
(Fig. 8-4, normal function curve at rest). Because cardiac output also changes as a
function of heart rate and myocardial contractility at any end-diastolic filling volume,
the normal (resting) cardiac function curve
is shifted upward when the heart is con-
Fig. 8-4. Cardiac Function Curves. Cardiac
output of the right or left ventricles has been
plotted as a function of the central venous
pressure (CVP) or pulmonary artery wedge
pressure (PAWP), respectively. The cardiac
output curve is shifted upward in conditions
that increase myocardial contractility and
(or) heart rate, provided that the increase in
heart rate is not excessive or prolonged. The
cardiac output curve is shifted downward in
conditions that decrease myocardial contractility and (or) heart rate.
tracting more powerfully and/or more rapidly. The normal function curve is shifted
downward when myocardial contractility is
ing) cardiac function curve include: para-
depressed and/or heart rate is abnor-
sympathetic stimulation (causing sino-
mally slow. Conditions that raise the nor-
atrial and atrio-nodal conduction blocks),
mal (resting) cardiac function curve in-
beta-1-adrenergic antagonists, calcium
clude: sympathetic stimulation, beta-1-
channel blockers, myocardial infarction,
adrenergic agonists, or cardiac glycosides.
valvular heart disease, atrial fibrillation, or
Conditions that decrease the normal (rest-
acidosis. It is important to bear in mind
30
that an increase in heart rate will only in-
is diseased or its normal function (contrac-
crease cardiac output up to a point, which
tility or heart rate) is otherwise depressed,
depends (among other factors) upon the
cardiac output is limited not by venous re-
level of conditioning and the duration of
turn but by the pumping capability of the
the tachycardia. Indeed, in patients with
right and left ventricles.
atrial fibrillation or hypertension decreasing
heart rate below 100 beats/min or decreasing the afterload by reducing blood pressure will shift the cardiac function curve upward.
We will return to these various function
curves a little later. For now let's focus on
the normal (resting) curve. At rest, cardiac
output is about 5 liters/min and the CVP is
about 5 mmHg and the PAWP about 10
mm Hg. According to the normal cardiac
function curve in Figure 8-4, when CVP
and PAWP double cardiac output increases almost two and one-half times.
So why does the heart actually pump
about 5 liters/min instead of 12 liters/min?
Only 5 liters of blood are returned to the
heart each minute, and the heart cannot
pump more blood than is being delivered
to it. If venous return were 12 liters/min,
then the heart would pump 12 liters/min
and do so without any additional stimulation (the heart would not have to shift to a
higher function curve). In other words, venous return regulates cardiac output for a
normally functioning heart. When the heart
31
3
Regulation of
Venous Return
Effect of Peripheral Resistance
on Cardiac Output
Lecture 3-2: Effect of Peripheral Resistance on Cardiac Output
33
The amount of blood that flows into the
Thus, in the normal heart, venous return de-
central veins and generates the filling pres-
termines cardiac output.
sure of the right ventricle (and subsequently [via the PAWP] of the left ventricle)
will depend upon the amount of blood that
flows from the capillary beds of the various
organs and tissues of the body. Blood flow
through these capillary beds depends, in
turn, upon the various autoregulatory
mechanisms that allow blood to enter organs and tissues. Thus, when tissues need
more blood to meet their metabolic needs,
vasodilator substances accumulate and
cause pre-capillary sphincters and metarterioles to relax. As more blood flows to tissues and organs, more is returned to the
heart and cardiac output increases, accordingly. Therefore, cardiac output is regulated by the sum of the individual metabolic needs of the tissues. When more
blood is needed, for instance, with exercise, skeletal muscle will take a larger fraction of the cardiac output, which it will rapidly return via low resistance channels to
the veins. The CVP will increase and fill the
1. Increased Venous Return
(and Cardiac Output) with
Shunts and Altered Metabolic States
Venous return and cardiac output are normally regulated by the metabolic needs
and functions of the various organs and tissues that make up the body. There are
times, however, when blood flow through
tissues is excessive, for example when tissue metabolism is abnormally increased
(e.g., hyperthyroidism) or when blood is bypassing capillary beds altogether by flowing via low resistance shunts between arteries and veins (e.g., Paget's disease). In
both instances, the total peripheral resistance is decreased without changing the
compliance of the capacitance vessels responsible for conducting blood back to the
heart. This increase in venous return results in increased cardiac output.
right ventricle more, so the right ventricle
Let us illustrate this with a simulation (Fig.
will pump more blood into the pulmonary
8-5) of experiments carried out by Guyton
artery. The PAWP, in turn, will increase and
and colleagues on anesthetized dogs.
fill the left ventricle more, so that the left
Catheters are inserted into a femoral artery
ventricle will pump more blood into the
and vein, and the ends are connected by a
aorta, from where the increased cardiac
three-way stopcock. When the stopcock is
output is delivered to exercising muscles.
closed, only 5 L/min of blood flows
34
ceptor reflex, resulting in movement of fluids from the interstitium to blood and retention of salt and water by the kidneys. By
this regulatory mechanism, blood flow to
tissues is soon reestablished. With the additional 5 L/min of blood flowing directly
from the femoral artery into the femoral
vein, venous return will increase to 10 L/
min. The cardiac output will now increase
to 10 L/min, not from sympathetic stimulation, but simply from the increase in the
end-diastolic ventricular volume that inFig.8-5. Effect of an Arterio-Venous Shunt on
Venous Return and Cardiac Output. A shunt
was created between the femoral artery and
vein in an anesthetized dog, and blood flow
through the shunt was regulated by a stopcock. When the stopcock was closed, venous
return and cardiac output was 5 L/min. When
the stopcock was opened, 5 L/min of blood
flowed through the shunt to the femoral vein,
which was added to the 5 L/min of blood already returning to the heart from various organs and tissues. Venous return and cardiac
output were thereby increased to 10 L/min.
creases the stroke volume by the FrankStarling mechanism. This experiment illustrates that cardiac output is regulated by
venous return.
There are a number of conditions that are
characterized by an increase in cardiac output where the high cardiac output state
can be ascribed to a primary decrease in
the total peripheral resistance (without a
change in venous compliance). This is
seen, for example, in patients with Paget's
disease, where extensive arterio-venous
through capillary beds of various organs
fistulae are formed in bone. Also, during
and tissues and is returned to the heart.
the third trimester of pregnancy venous re-
When the stopcock is first opened, 5 L/min
turn and cardiac output increase markedly
of blood flows through the shunt and none
as blood is shunted through low resis-
through the tissues. The sudden drop in to-
tance pathways in the placenta. For this
tal peripheral resistance causes a fall in
reason, young women with rheumatic val-
blood pressure, which activates the barore-
vular heart disease may not be aware of
their cardiac disability until they develop
35
signs and symptoms of congestive heart
a decrease in sympathetic outflow to the
failure in the late stages of pregnancy. Hy-
vascular system - cardiac output de-
perthyroidism also is often associated
creases because blood pools in the veins
with an increased cardiac output, partly be-
and is not returned to the heart.
cause the heart is stimulated to contract
an increase in tissue metabolism leads to
2. Effect of Gravity on Venous Return (and Cardiac
Output)
enhanced blood flow through capillary
Gravity is an important factor in venous re-
more and tissues and is returned to the
heart. When the forcefully, partly because
beds. Marked peripheral vasodilation is
seen in beriberi (thiamine deficiency),
when glucose metabolism cannot proceed
normally. This condition causes high cardiac output states and high output cardiac
failure when the heart cannot keep up with
the high venous return. (The heart also contracts less forcefully than normal in beri-
turn (Fig. 8-6). Blood in veins below the
level of the heart is subjected to gravity,
which pulls on the column of blood, distending vessels below the heart. Just look
at the veins in your hand, when your arm is
relaxed and hanging down by your side.
Now raise your arm and watch the veins in
your hand collapse as it passes the level of
beri.) We have already seen that severe
your heart. The veins above the heart,
anemia in the man in case 6 can lead to
such as those in the neck, are normally col-
an increase in cardiac output. In this situa-
lapsed when a person is sitting or stand-
tion cardiac output increases as tissues de-
ing. As blood flows with gravity from the
prived of oxygen vasodilate and return
head to the chest, it creates a partial vac-
more blood to the heart.
uum in the venous sinuses of the cranium
It must be emphasized that a decrease in
total peripheral resistance (e.g., by relaxation of arteriolar smooth muscle) will only
lead to an increase in venous return and in
cardiac output, provided that venous compliance is not also increased (e.g., by re-
that tends to siphon blood from arteries
into brain capillaries. The neurosurgeon
must be aware of this when operating on a
patient in the sitting position. If a vein in
the head or neck is cut, air may be sucked
into the heart, resulting in an air embolus.
laxation of venous smooth muscle). When
both arterioles and veins relax simultaneously - as occurs in neurogenic shock with
36
3. Importance of VenousCompliance, Valves, and
Skeletal Muscle in Facilitating Venous Return (and Cardiac Output)
The tendency for gravity to cause pooling
of blood in the legs is counteracted in
three major ways:
(1) Pooling of blood in the extremities upon
sudden standing minimized by the baroreceptor reflex, which increases sympathetic
outflow to the smooth muscle of veins, decreasing their compliance.
(2) The major veins have one-way valves
pointing toward the heart. These valves,
when competent, break up the long column of blood between heart and feet into
smaller sections, so that the hydrostatic
pressure is felt only over the distance between any two valves. This is not true, however, when valves become incompetent.
Then the full effect of gravity is transmitted
Fig. 8-6. Effect of Gravity on Venous Pressure
(A) The hydrostatic pressure of blood due to
gravity for a person standing quietly is shown
to be a positive value in veins below the heart
and a negative value in veins above the heart.
Accordingly, in a foot vein 80 cm below the
heart pressure will equal +80 cm of water,
whereas in a hand held 40 cm above the heart,
venous pressure will equal -40 cm of water. (B)
Venous pressures at the ankle are compared
for a person lying, standing quietly, or running.
Note that during running skeletal muscle contraction squeezes veins, which pumps blood
from the ankle against the force of gravity toward the heart.
to the walls and the veins bulge and become tortuous. This is particularly true for
superficial veins, such as the saphenous
veins are squeezed and blood is milked
veins in the legs, which lack support from
from one valve past the next toward the
surrounding musculature. Such incompe-
heart. Lack of muscle contraction - as for
tent veins are called varicose veins.
soldiers standing at attention - may lead to
(3) Most deep veins are surrounded by
skeletal muscle, and as muscles contract,
peripheral venous pooling and fainting, especially in hot weather.
37
4. Importance of Inspiration
on Venous Return (and Cardiac Output)
Another important factor aiding venous return is inspiration (Fig. 8-7). During inspiration the intrapleural (or intrathoracic) pres-
InspirationChest wall
A
4
Negative intrathoracic
pressure distends
pulmonary vessels and
decreases venous return
to the left atrium
3
Negative intrathoracic
pressure sucks venous
blood into right atrium
sure drops, becoming more subatmos-
Negative pressure
pheric and causing distention of the large
vessels in the chest. This tends to suck
more blood into the right atrium. Because
the downward movement of the diaphragm increases intra-abdominal pressure, vessels in the abdominal cavity are
compressed, which simultaneously forces
blood toward the heart. It is noteworthy
that some patients in hemorrhagic shock,
who suffer from a decreased venous return, are found to have intense constriction
of the abdominal muscles, which would
tend to facilitate venous return.
While a deep inspiration increases venous
return to the right ventricle, left ventricular
filling and cardiac output actually decrease. Indeed, this is why the second
Lung
5
Pulmonic valve closure
delayed (physiologic
splitting of second heart
sound)
Arteries
Diaphragm
Veins
Positive pressure
2
Positive intra-abdominal
pressure forces blood in
vena cava toward right
atrium
Tissues
1
Downward movement
of diaphragm on
inspiration increases
intra-abdominal pressure
Capillaries
B
Intrathoracic pressure
Right ventricular stroke volume
Thoracic blood volume
Left ventricular stroke volume
Inspiration
Expiration
Decreased
Increased
Increased
Decreased
Increased
Decreased
Decreased
Increased
Fig. 8-7. P. Eggena,
The Physiological Basis of Primary Care, Novateur Medmedia
Fig. 8-7. Effects of Respiration on Venous Return and Cardiac Output. (A) The sequence of
events (1) thru (5) occur during inspiration. (B)
Effects of inspiration and expiration on intrathoracic pressure, thoracic blood volume, and right
or left ventricular stroke volumes are listed.
the lungs, so less flows into the left ventricle, and, therefore, the left ventricular
stroke volume is diminished (Fig. 8-7).
heart sound is split on inspiration (physio-
As more blood enters the right atrium on
logical splitting of S2). Only on expiration
inspiration, the rhythm of the heart be-
does the extra blood (returned to the heart
comes irregular (sinus arrhythmia) due to
during the deep inspiration) increase left
a brief increase in the rate of depolariza-
ventricular output. The reason is that dis-
tion of the SA node. This is partly caused
tention of pulmonary vessels on inspiration
by stretching of SA nodal tissues and
allows more blood to pool (temporarily) in
partly by stimulation of the SA node by the
38
Bainbridge reflex. This reflex is initiated
life is not divided into inspiration and expi-
when the atrium is stretched. Afferent im-
ration but that there are relatively long peri-
pulses are carried over vagal fibers to the
ods of time between breathing in or out. It
medulla and result in decreased parasym-
is in these long intervals between breaths
pathetic and increased sympathetic stimu-
that intrathoracic pressure is normally
lation of the SA node and atrial muscle.
slightly subatmospheric (e.g.,-2 mmHg).
This reflex moves blood out of the atrium
This is also true for patients on positive
and into the ventricle.
pressure ventilators, unless the ventilator
While inspiration facilitates venous return
to the heart, an increased (positive) intra-
has been set for continuous positive airway pressure (CPAP).
thoracic pressure during a forced expira-
Important changes in venous return, car-
tion impedes venous return. This is why a
diac output, and blood pressure are ob-
trumpet player has a red face and dis-
served in breathholding and straining dur-
tended neck veins. Blood will not drain
ing the Valsalva maneuver (Fig.8-8). Dur-
from the neck and face into the right
ing the Valsalva maneuver, a person takes
atrium as long as these structures are com-
in a deep breath, then exhales forcefully
pressed. This is, in part, why patients with
against a closed glottis. This may increase
prolonged and repeated coughing spells
intrathoracic pressure, for example, from
may faint. The continued positive intratho-
-2 to +40 mmHg. Because the aorta and
racic pressure during the coughing epi-
large arteries in the chest are exposed to
sodes prevents venous return and dimin-
this additional 42 mmHg, blood pressure in
ishes cardiac output. Patients on positive
the brachial artery rises by an extra 42
pressure ventilators, especially when the
mmHg and then falls gradually, as venous
ventilator is set for PEEP (i.e., positive
return to the right and left ventricles de-
end-expiratory pressure), experience a
clines and cardiac output decreases. The
decrease in venous return and in cardiac
decrease in blood pressure initiates the ba-
output. It is, therefore, important to weigh
roreceptor reflex, which causes heart rate
the potential benefits of using PEEP (e.g.,
and peripheral vascular resistance to in-
increased arterial oxygen tension of blood)
crease. This results in a small increase in
against a diminished cardiac output and
blood pressure toward the end of the pe-
decreased delivery of oxygenated blood to
riod of straining, which is an inadequate
tissues. We sometimes seem to forget that
compensatory response. As the glottis sud39
as blood, waiting to enter the heart during
the straining phase, suddenly floods the
ventricles and markedly increases cardiac
output at a time when the total peripheral
resistance is still high from the vasoconstrictor response initiated toward the end
of the straining phase. The high blood pressure decreases heart rate (via the baroreceptor reflex) and decreases peripheral resistance with the result that blood pressure
slowly returns to its pre-straining level.
The Valvsalva maneuver (with adequate
blood pressure monitoring as in Figure 8-8)
is useful in testing the responsiveness of
the baroreceptor reflex (and the autonomic
Fig. 8-8. The Valsalva Maneuver. Intrathoracic
pressure (A), mean blood pressure (B), and
heart rate (C) are recorded before, during, and
after the straining phase of the Valsalva maneuver. At the first arrow (start) the subject
breathes in deeply and then expires forcefully
against a closed glottis. At the second arrow
(stop) the subject opens the glottis and relaxes
the abdominal muscles.
nervous system). However, for certain patients, such as those with a recent myocardial infarction, the Valsalva maneuver
places an inordinate strain on the heart
and should be avoided.
denly opens and the diaphragm relaxes, intrathoracic pressure returns to normal (i.e.,
-2 mm Hg), and brachial artery blood pressure falls precipitously. Within seconds,
however, blood pressure and pulse rate
shoot up to levels well beyond normal (i.e.,
the overshoot of the Valsalva maneuver)
40
Model of the Circulation
Lecture 3-3: Model of the Circulation
41
5. Effect of Plasma Volume
on Venous Return (and Cardiac Output)
by a series of ventricular escape beats
Finally, an important factor in regulating ve-
value of approximately 10 mmHg (middle
nous return is the extent to which the veins
are filled with blood. It is not just the blood
volume that is important, but the relationship between the amount of blood and the
compliance of the veins (e.g., their sympathetic tone), because it is ultimately the venous pressure that moves blood toward
the heart. This force, which is generated
by veins as they contract around the volume of blood they hold, is sometimes referred to as vis a tergo. Also contributing
to this force is the pressure transmitted
through the capillaries by blood pumped
into arteries. Of course the volume of
(note the large, wide QRS complexes). As
the heart stopped beating, the femoral artery blood pressure decreased to a basal
panel) and pulmonary artery pressure
equilibrated at a similar level, i.e., at about
the level of the PAWP (top panel). These
observations indicated that, in the absence
of the heart's pumping action, blood simply flows down its pressure gradient from
arteries into veins until all pressures in the
circulation are equal. This equilibrium pressure is called the mean circulatory filling
pressure. In the experiment in Fig.8-9, the
mean circulatory filling pressure is about
equal to the pulmonary artery wedge pressure, or about 10 mmHg (A).
blood and the pressure in veins changes
When the electrical stimulus was removed
constantly as blood flows continuously
from the vagus (B), systemic blood pres-
into veins from capillaries on one end and
sure returned over a period of five beats to
is pumped out by the right ventricle on the
normal (C). The sequence of events respon-
other end. Therefore, the resting recoil
sible for returning the dog's blood pres-
pressures of veins and arteries can only be
sure to normal is shown in human terms in
measured when no blood is flowing, i.e.,
Figure 8-10. In this model of the peripheral
when the heart has stopped. We observed
circulation, we will assume that the periph-
such resting recoil pressures upon stop-
eral vascular resistance is 20 mmHg/L/
ping the heart in an anesthetized dog (Fig.
min.
8-9). Stimulating the animal's right vagus
with an electrical impulse caused sinus arrest (note the absence of P waves on the
ECG tracing in the bottom panel), followed
During vagal stimulation at point A (Figs.
8-9, 8-10), cardiac output was 0 L/min and
systemic arterial and venous pressures
42
had equilibrated to a value of about 10
mmHg, i.e., the mean circulatory filling
pressure (MCFP). When vagal stimulation
was stopped (B), the heart resumed beating. The first beat moved some blood from
central veins into the aorta and large arteries, causing the CVP to drop from 10 mm
Hg to 9 mmHg and systemic mean arterial
pressure to rise from 10 mmHg to 29
mmHg. The greater increase in arterial
pressure as compared to the fall in CVP for
an equivalent blood volume change is explained by the much lower compliance of
arteries than veins. Although the left ventricle ejects a certain stroke volume into the
aorta during the first beat (B), only part of
this stroke volume moves through capillaries and veins and is eventually returned to
the heart. The other portion of the stroke
volume was used to prime the arterial
pump. In other words, the aorta and large
arteries had to be first stretched to a point
where the recoil pressure was sufficient to
move blood through a peripheral resis-
Fig. 8-9. Mean Systemic Filling Pressure
(MSFP). The right vagus nerve was stimulated in
an anesthetized dog. ECG as well as pulmonary artery pressure (with a Swan-Ganz catheter) and systemic arterial pressure (with a catheter in the femoral artery) were recorded simultaneously. Vagal
stimulation caused a sino-atrial block with an ideoventricular escape rhythm. Note that systemic arterial pressure fell to approximately 10 mmHg and pulmonary artery pressure reached a level that was
close to the wedge pressure (PAWP) (A). When vagal stimulation was stopped (B), systemic arterial
pressure returned to pre-stimulation values within 5
heart beats (C).
tance of 20 mmHg/L/min. We can calculate the amount of blood flow (the cardiac
output) that occurred during the first two
beats, where the average systemic mean
arterial pressure was 29 mmHg and the
CVP 9 mmHg, in the following way:
CO = (MSAP -CVP)/TPR
The cardiac output (CO) is equal to the difference between the mean systemic arterial pressure (MSAP) and central venous
pressure (CVP) divided by the total peripheral resistance (TPR, fixed at 20 mmHg/L/
min). Accordingly, during the first two heartbeats (B):
43
CO = (29 - 9) mmHg/20 (mmHg/ L/min)
= 1 L/min
In other words, when vagal stimulation
was stopped, blood started to move
around the circulation at a rate of 1 L/min
during the first two heart beats.
Five heart beats later (C), enough blood
had accumulated in the aorta and large arteries to increase the systemic mean arterial pressure to 105 mmHg, and the loss of
blood from the central veins had reduced
CVP to 5 mmHg. Now:
CO= (105 - 5) mmHg/ 20 (mmHg/ L/
min) = 5 L/min
In other words, once the large arteries had
been primed with their usual blood volume, blood again moved around the circulation at a rate of 5 L/min, which is the normal resting value for both cardiac output
Fig. 8-10. Model of the Circulation. The circulatory system is modeled after the experiment depicted in Figure 8-9. Assuming a total peripheral resistance of 20 mmHg/L/min, cardiac output (CO) is 0 L/min (A) when the systemic
mean arterial pressure (SMAP) and central venous pressure (CVP) are both 10 mmHg; CO is
1 L/min (B) when SMAP rises to 29 mmHg and
CVP falls to 9 mmHg; and CO is 5 L/min (C)
when SMAP rises to 105 mmHg and CVP falls
to 5 mmHg.
and venous return.
6. The Effects of CVP on
Venous Return
to be. We could make a graph that shows
Let us focus for a moment on the venous
heart is stopped, venous return falls to 0 L/
part of the model in Figure 8-10. For blood
min, and CVP rises to 10 mmHg (Fig. 8-
to flow from peripheral to central veins,
11,A, point A), which is the MCFP. As the
pressure must be higher in the periphery
heart starts beating (Figs. 8-9,B and 8-
than it is centrally. Thus, the greater the
10,B), the right ventricle removes blood
CVP, the smaller venous return would tend
from the central veins so that the CVP falls
the relationship between CVP and venous
return (Fig. 8-11). For example, when the
44
from 10 to 9 mmHg, and venous return increases to 1 L/min (Fig.8-11,A, point B).
Once the heart is beating normally (Figs. 89,C and 8-10,C), CVP decreases to 5
mmHg, and venous return increases to 5
L/min (8-11,A, point C).
In addition to the normal venous return
curve, other curves may be drawn to depict conditions in which the mean circulatory filling pressure is increased or decreased from normal (Fig. 8-11,A). For example, when the plasma volume is increased (hypervolemia) or the walls of the
venous capacitance vessels are tensed (venoconstriction), the CVP will increase at
any given level of venous return. This will
cause the venous return curve to shift to
the right. Such rightward shifts in the venous return curve are seen, for instance, in
patients with right ventricular failure
Fig. 8-11. Venous Return Curves. Venous return has been plotted as a function of central
venous pressure (CVP). (A) The normal venous return curve includes points A, B, and C
from Figures 8-9 and 8-10. The normal curve
is shifted to the right with an increase in the
mean circulatory filling pressure (MCFP) and
shifted to the left with a decrease in MCFP.
(B) The normal venous return curve is rotated
upward with arteriolar dilation and downward
with arteriolar constriction without a change in
MCFP.
or in patients who have been overtransfused with isotonic saline.
On the other hand, when the blood volume
is reduced (hypovolemia) or the capacitance vessels are relaxed (venodilation),
the CVP will be decreased at any given
level of venous return. This will cause the
venous return curve to shift to the left.
Such leftward parallel shifts in the venous
return curve are seen, for instance, in patients who have been hemorrhaging or in
patients with severe diarrhea who are volume depleted.
Venous return curves may not only be
shifted (in parallel), but also rotated upward or downward as the total peripheral
resistance is decreased or increased, respectively (Fig. 8-11,B). For example, an
increase in sympathetic outflow to arterioles will increase total peripheral resistance (arteriolar constriction) and will
45
cause the venous return curve to be rotated downward. On the other hand, a decrease in sympathetic outflow to arterioles
will decrease the total peripheral resistance (arteriolar dilation) and will cause the
venous return curve to rotate upward.
Note that sympathetic stimulation of arterioles produces opposite effects on venous
return than does sympathetic stimulation
of veins (see Fig. 8-11,A). Note also that
the MCFP is not influenced by constriction
or relaxation of arterioles. The reason for
this is as follows. If the arterioles were
more constricted when the heart was
stopped in the experiment in Figure 8-9,
systemic arterial blood pressure would
have declined more slowly, but would eventually have reached the same MCFP pressure of 10 mmHg. Similarly, if the arterioles
had been more dilated when the heart was
stopped, arterial pressure would have
fallen more rapidly, but the same MCFP
would be reached.
46
4
Graphic Analysis of
Cardiac Output and
Venous Return
Graphic Analysis of Cardiac
Output and Venous Return
Lecture 3-4: Graphic Analysis of Cardiac Output and Venous Return
48
situations. Because cardiac output must
equal venous return (at least over a short
time interval) a person's circulation will stabilize at the point of intersection between
venous return and cardiac output. At rest,
this point is at a CVP of about 5 mmHg (for
the right ventricle) or at a PAWP of 10
mmHg (for the left ventricle) when venous
return and cardiac output are 5 L/min.
Fig. 8-12. Cardiac Output and Venous Return Curves. Cardiac output and venous return curves from Figures 8-4 and 8-11A
have been combined into a single graph.
Note that cardiac output must equal venous
return (when measured for more than a few
beats), so that the circulation will stabilize at
points of intersection between the venous
return and cardiac output curves. That equilibrium point is normally at a cardiac output
(or venous return) of 5 L/min and a CVP of 5
mmHg (or PAWP of 10 mmHg).
1. Graphic Analysis of Exercise
Point A on the graph in Figure 8-13 represents a person at rest with a cardiac output of 5 liters/min and a CVP of 5 mmHg.
As he anticipates exertion, sympathetic
cholinergic nerves cause vasodilation in
skeletal muscle and a decrease in the total
peripheral resistance. This causes an increase in venous return and results in an
upward rotation of the venous return
We can now combine the curves for cardiac output and venous return as a function of CVP (or PAWP) into a single graph
(Fig. 8-12). Similar graphs have been employed by Guyton, who used right atrial
pressure as the independent variable, to
analyze the relationship between cardiac
output and venous return in a variety of
common physiological as well as clinical
curve. Note that the curve is rotated upward rather than shifted in parallel to the
left, so that the MCFP (i.e., the pressure
when cardiac output and venous return are
0 liters/min) has not changed. As a consequence of this decrease in total peripheral
resistance, and a relatively normal heart
cannot handle the excessive load (high
output failure). A good example of high
49
Fig. 8-13. Cardiac Function Curves during Exercise. Cardiac output and venous return have
been plotted as a function of CVP. Anticipation of
exercise decreases total peripheral resistance
and thereby causes upward rotation of the venous return curve to a new equilibrium point B.
Further dilation of muscle arterioles during exercise rotates the venous return curve further upward to point C. Sympathetic stimulation of the
heart increases myocardial contractility and heart
rate, causing an upward (and leftward) shift of
the cardiac output curve to the final equilibrium
point D. At point D, cardiac output and venous return are twice the resting values (A), with only a
minimal increase in PAWP (or CVP).
Fig. 8-14. High Cardiac Output Failure in Severe
Anemia.
Cardiac output and venous return have been plotted as a function of CVP (or PAWP) in a case of
severe anemia. As the anemia increases in severity, the total peripheral resistance progressively
decreases and the venous return curve rotates
upward and to the right, resulting in an increase
in cardiac output from A to B to C. The increase
in cardiac output is associated with a significant
increase in CVP and in PAWP, causing symptoms of peripheral edema and congestive heart
failure, respectively.
less than 7 gm/dL, his total peripheral resiscardiac output failure was a 95 year-old
man with severe anemia. Let us assume
that he was at point A in figure 8-14 when
he was not anemic. As his hemoglobin concentration gradually fell from 15 gm/dL to
tance gradually decreased, presumably
due to a combination of a diminished
blood viscosity and release of vasodilator
substances from hypoxic tissues. His cardiac output increased progressively from A
to B to C as his venous return curve ro50
tated upward. Unlike a young person with
a normal heart (Fig. 8-13), the 95 year old
man, whose heart had been driven excessively for months, was incapable of shifting
his cardiac output curve to a higher level.
As a consequence, his PAWP and CVP
were elevated and he had pulmonary and
peripheral edema, respectively.
2. Graphic Analysis of Shock
When tissues are inadequately perfused
with blood a person is said to be in shock.
Shock can result from diminished venous
return, i.e., circulatory shock, or from
pump failure, i.e., cardiogenic shock (Fig.
8-15). Note that in circulatory shock CVP
and PAWP are decreased; whereas, in cardiogenic shock these pressures are increased.
A. Circulatory Shock
Fig. 8-15. Circulatory and Cardiogenic Shock.
Cardiac output and venous return curves have
been plotted as a function of CVP or PAWP for
right or left ventricles, respectively. The fall in cardiac output in circulatory shock is caused by a
downward shift in the venous return curve,
whereas the fall in cardiac output in cardiogenic
shock is caused by a downward shift in the cardiac output curve.
Note that CVP (or PAWP) is low in circulatory
shock, but high in cardiogenic shock.
Circulatory shock may result from a decrease in blood volume (hypovolemic
shock), from loss of sympathetic vasomo-
had ruptured her spleen (Fig. 8-16). Inter-
tor tone (neurogenic shock), allergic reac-
nal hemorrhage resulted in a decreased
tions (anaphylactic shock), or from toxins
released in certain infections (septic
shock).
mean circulatory filling pressure and a shift
in the venous return curve to a lower level.
At this new equilibrium point (B), her cardiac output had decreased to about one-
Let us consider case where a young
half of normal, resulting in a decrease in
woman (Michelle in series 2, episode 1),
blood pressure. Within seconds the barore-
51
ceptor reflex increased heart rate and cardiac contractility, moving the equilibrium
point to a higher cardiac output curve, and
sympathetic stimulation decreased the
compliance of capacitance vessels, which
shifted the venous return curve upward
and to the right, resulting in a new equilibrium point C. This latter effect, however,
was offset by intense vasoconstriction (by
sympathetic nerves and high circulating
concentrations of epinephrine acting on
alpha-1- adrenergic receptors of vascular
smooth muscle) that caused the venous return curve now to rotate downward, resulting in a decrease in cardiac output to point
Fig. 8-16. Hemorrhagic Shock. Cardiac output
and venous return curves are plotted for a patient, Michelle, with internal bleeding from a
ruptured spleen. Initial blood loss resulted in a
downward depression of the venous return
curve and a shift in the equilibrium point from
A to B. Compensation occurred by sympathetic stimulation of the heart, making it contract more rapidly and more forcefully, and by
venoconstriction. This shifted the equilibrium
point from B to C, where both the venous return and cardiac output curves were raised.
Cardiac output fell subsequently, however,
from C to D, as sympathetic arteriolar constriction rotated the venous return curve downward. Michelle was admitted to the hospital in
this state of shock and was treated with intravenous 0.9% NaCl, which shifted the venous return curve upward and the equilibrium point
from D to E.
D. This was the price that had to be paid
to maintain blood pressure as high as possible in order to perfuse the most vital organs - the brain and the heart. In other
words, the reduction in cardiac output was
more than offset by the increase in total peripheral resistance, so that blood pressure
increased (BP = CO x TPR).
The intense vasoconstriction lowered capillary blood pressure, which facilitated reabsorption of fluids from the interstitium. As
this fluid was slowly added to plasma, the
venous return curve shifted to the right. To
continue to increase plasma volume and
venous return, isotonic saline (and later
whole blood) were infused intravenously in
the hospital, which moved cardiac output
52
to point E. As the plasma volume returned
to normal, the intense sympathetic outflow
was no longer needed, and her pulse
slowed and became fuller and her color returned as the compensatory vasoconstriction of skin vessels subsided.
B. Cardiogenic Shock
When Mr. M first came to the hospital for
help, he was in a state of compensated
heart failure. His ECG showed evidence of
an inferior myocardial infarction, which he
had suffered several years earlier. The
curves in Figure 8-17 reconstruct the sequence of events that took place immediately following the heart attack.
As his left ventricle was injured as a result
of the coronary occlusion, his cardiac output curve decreased and he stabilized at a
new equilibrium point B, where cardiac output was reduced and pulmonary artery
wedge pressure increased. The fall in
blood pressure resulted, perhaps, in a
Fig. 8-17. Compensated Heart Failure. Cardiac output and venous return curves for Mr.
M. Following a myocardial infarction, cardiac
output dropped to a lower function curve and
the equilibrium point moved from A to B. Compensation occurred by venoconstriction and
mobilization of fluids from the interstitium, shifting the equilibrium to point C. Increased sympathetic stimulation of the heart, in turn, raised
cardiac output to a higher function curve so
that complete compensation (normal cardiac
output at rest) was obtained at point D. At
point D the PAWP is elevated above normal,
and the cardiac reserve is diminished.
short spell of dizziness or fainting, and certainly in a feeling of weakness. Within seconds, however, the baroreceptor reflex initiated the compensatory responses, which
we have already considered in hemorrhagic shock. Briefly, sympathetic outflow
tenses capacitance vessels, which shifts
the venous return curve to the right (point
C). This action, aimed at increasing cardiac
output, is reserve, which he lost and which
he needed when he had to exert himself.
He was not normal in another important respect. His pulmonary artery wedge pressure was significantly higher than normal.
The difference between this pressure and
53
a pulmonary artery wedge pressure of
about 27 mmHg is a safety margin for
avoiding pulmonary edema.
Mr. M was in a precarious situation without
an adequate cardiac reserve when his atria
started to fibrillate and his ventricles contracted irregularly at about 130 beats/min.
Because of the reduced stroke volume per
beat, his cardiac output curve fell and he
arrived at point C in Figure 8-18. Note that
this curve spells trouble. It is so flat that
even at its highest point it does not reach
a minimum cardiac output for sustaining
tissue metabolism at rest (about 5 L/min).
Although the heart is once again bombarded with sympathetic stimuli, it has
been stimulated for too long and norepinephrine receptors have been downregulated. The kidney, however, attempts
to compensate for the reduced cardiac output by retaining more salt and water (this is
mediated, as usual, by sympathetic stimuli, vasopressin, and aldosterone). Although renal compensation usually works
well with a normal or near-normal heart,
this strategy becomes counterproductive
in a heart with a flat cardiac output curve.
Fig. 8-18. Decompensated Heart Failure.
Cardiac output and venous return curves are
shown for Mr. M after he had compensated
for a myocardial infarct (Fig. 8-17,D). He
then develops atrial fibrillation and moves to
a lower cardiac function curve and a new
equilibrium point C. His heart is incapable of
compensating by moving to a higher cardiac
function curve with sympathetic stimulation,
but his kidneys function normally and retain
more salt and water, causing the venous return curve to shift progressively to the right
from C to F to G.
Note that the cardiac output curve is flat, so
that these shifts in the venous return curve
do not increase cardiac output to the minimum requirement of 5 L/min (at rest). Moreover, as PAWP exceeds a value of about 27
mmHg, pulmonary edema develops.
As days pass, the retained salt and water
shifts the venous return curve progressively to the right from point C to E to F to
G. Not only is the increased venous return
not increasing cardiac output, but the pul-
monary artery wedge pressure is continuously rising and the lungs are being progressively flooded with more and more
54
edema fluid. In addition, the ventricular
angiotensin-converting enzyme inhibi-
chambers are becoming progressively
tors (e.g.,ramipril), aldosterone antago-
more dilated, causing wall tension to rise
nists (e.g.,spironolactone), and beta-
according to the Laplace equation (T = P x
adrenergic blockers (e.g.,metoprolol, carv-
R/2). This means that the heart must now
edilol).
generate a greater than normal contractile
force to overcome wall tension to eject a
normal stroke volume.
Decompensated heart failure, as Mr. M
had on his second visit to the hospital is a
medical emergency requiring immediate intervention. Treatment included measures
aimed at moving the venous return curve
back to the left. This was accomplished by
decreasing the preload on the heart by administering intravenous furosemide. In addition, carvedilol was administered to improve cardiac function and reduce the afterload which moved the cardiac output
curve to a higher level.
Activation of the sympathetic nervous system and the renin-angiotensin-aldosterone
system are essential in increasing cardiac
output acutely following myocardial injury.
However, the long term effects of these
two systems results in remodeling, hypertrophy, and apoptosis of the myocardium
which results in a decrease in cardiac output. Indeed, clinical trials have shown that
mortality from congestive heart failure is
significantly reduced with the use of
55
5
Review
Interactive Questions
57
This is Mr. Bach.
Chief Complaint: He
fainted on standing
up and is bleeding
from a cut on his forehead.
His pupils are small
and constrict even
more as you move
your finger towards
his eyes, but not
when you shine a
light into them.
You hear an early diastolic decrescendo
murmur.
His neck veins are
distended 15 cm
above his sternal angle.
You hear wet rales on
auscultation.
His BP is 160/60
mmHg and he has a
Corrigan Pulse.
He cannot stand with
his feet together and
eyes closed. Can’t
feel if you move his
big toe up or down.
Can’t feel vibrations
of your tuning fork.
Swelling, discoloration, no hair, foot ulcer.
1
2
3
4
5
6
7
8
58
Case: Essay/Small
Group Questions
59
1. How does the Baroreceptor Reflex
keep you from fainting when you stand
up?
2. Define Orthostatic Hypotension. What
may cause it?
3. Why did Mr. Bach have a Corrigan
Pulse?
4. Draw the changes in intraventricular,
atrial and aortic pressures during a cardiac cycle for a healthy person and for
Mr. Bach who has aortic insufficiency.
5. To the graph above (4) add the murmurs of aortic insufficiency and the Austin Flint murmur and explain their origins.
6. Why are diastolic murmurs not as loud
as systolic murmurs?
7. Why does aortic insufficiency cause left
heart failure?
8. What ECG changes would you expect
to see in ventricular hypertrophy?
11. Why does left heart failure eventually
lead to right heart failure?
12. What are the signs and symptoms of
right heart failure?
13. Draw cardiac output and venous return
curves for Mr. Bach and explain how he
compensated for his aortic insufficiency.
14. Why do patients with congestive heart
failure complain of nocturia?
15. Why is the renal filtration fraction increased when cardiac output declines?
16. How do kidneys retain more salt and
water in congestive heart failure?
17. What causes pre-renal azotemia?
18. How do you test for the Argyll Robertson pupil?
19. What is tabes dorsalis?
20. How can you diagnose a defect in proprioception?
9. Why did Mr. Bach have congestive heart
failure and what are the signs and symptoms of this condition?
10.What causes dyspnea and why did Mr.
Bach have dyspnea on exertion?
60
Lecture: Essay/Small
Group Questions
61
Cardiac Function Curves
Cardiac Output/Venous Return Plots
1. What is the relationship between cardiac
9. Draw cardiac output/venous return plots
output and ventricular filling pressure?
2. Name conditions that increase or decrease the cardiac output.
3. Name high cardiac output states that
for a person who is exercising, hemorrhaging, or suffering an acute myocardial infarct.
10.
are caused by a decreased in total peripheral vascular resistance.
Venous Return
4. How does gravity affect venous return?
5. How does inspiration facilitate venous
return?
6. Why does the use of PEEP (positiveend-expiratory pressure) on a ventilator decrease cardiac output?
7. What is the mean systemic filling pressure?
Venous Return Curves
8. How is the venous return curve shifted
with plasma volume changes or with
changes in venous and arteriolar muscle
tone.
62
True/False Quiz
63
Directions: An answer is “True” (A) when the complete
statement(s) is (are) correct. Otherwise the answer is
“False” (B).
Question 1 of 10
Cardiac Output is determined by Venous Return.
A.
B.
Check Answer
64
6
More Episodes in iBooks
Physiology as a Country Doc
Series 1. Cardiac Physiology as a Country Doc
by Patrick Eggena, M.D.
Episode 1. Electrophysiology
Episode 2. The EKG
Episode 3. Heart Attack
Episode 4. Irregular Beats
Episode 5. Excitation-Contraction
Episode 6. The Heart as a Pump
Episode 7. Murmurs and Gallops
Series 2. Circulatory Physiology as a Country Doc
Episode 1. Hemodynamics
Episode 2. Regulation of the Circulation
Episode 3. Cardiac Output and Venous Return