Download CARDIOVASCULAR INTERACTIONS: AN INTERACTIVE

T E A C H I N G
W I T H
T E C H N O L O G Y
CARDIOVASCULAR INTERACTIONS:
AN INTERACTIVE TUTORIAL AND MATHEMATICAL MODEL
Carl F. Rothe1 and John M. Gersting2
1
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis,
Indiana 46202; and 2Department of Computer Science, University of Hawaii at Hilo, Hilo, Hawaii 96720
T
ADV PHYSIOL EDUC 26: 98 –109, 2002;
10.1152/advan.00031.2001.
Key words: simulation; heart; circulation; preload; afterload; contractility; Emax;
capacitance; resistance
True education is much more than retrieval and memorization of mere information. Our goal with the Cardiovascular Interactions project (CVI) has been to
develop a tool for “meaningful learning,” as described by Michael (7). With this approach, we expect the learner to understand cardiovascular interactions well enough to predict and explain responses
to disturbances by reasoning through the series
of cause-and-effect relationships of the system. A
reasonably complex conceptual model of the human
cardiovascular system that adequately fits reality requires a set of equations and parameters that can
be manipulated and solved with computer simulation. If the results of parameter changes do not
meet expectations, then the learner needs to explore
their conceptual model for inadequacies or find and
define the error in the equations of the mathematical
model.
1043 - 4046 / 02 – $5.00 – COPYRIGHT © 2002 THE AMERICAN PHYSIOLOGICAL SOCIETY
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he maintenance of an adequate cardiac output and systemic arterial blood
pressure is a complex process with intricacies that are often difficult to
understand. Cardiovascular Interactions is an active learning tool that
demonstrates the interactions between the functions of the heart and peripheral
circulation. This learning package consists of a Lab Book, a Model, and an Information file. The Lab Book is an interactive tutorial for exploring the relative influences
of parameter changes on the cardiovascular system under normal, stressful, or
pathophysiological conditions. The learners are guided to predict the direction and
relative magnitude of changes of key variables in the cardiovascular system, evaluate
the accuracy of their predictions, and describe the cause-and-effect mechanisms
involved. Consequences of heart failure, hemorrhage, exercise, and changes in
intrathoracic pressure can be explored. The results obtained in the Lab Book are
based on a five-compartment mathematical Model, which reflects our current understanding of the basic control of the cardiovascular system. The Model was
designed to be complex enough to be realistic, yet not so complex as to be
overwhelming. An Information File contains definitions and descriptions of classical physiology about key concepts, including figures, and a detailed description of
the Model. Hypertext tags embedded in the Lab Book are used to access the
Information File. The Cardiovascular Interactions learning package was designed to
run from its CD and so does not need to be installed.
T E A C H I N G
W I T H
Learning goal. The tutorial was developed to demonstrate and clarify the interactions between the functions of the heart and peripheral circulation in the
development and control of an adequate cardiac output and systemic arterial blood pressure. With the
help of this project, we expect the learner to grasp
how the individual components and underlying relationships are integrated, under the control of mechanical feedback mechanisms, into a self-correcting system that maintains functional integrity in the face of
challenges such as moderate stress or pathological
conditions. As Grodins et al. (6) stated in 1954: “The
essence of physiology is regulation. It is this concern
with ‘purposeful’ system responses which distinguishes physiology from biophysics and biochemistry.” This Cardiovascular Interactions project is about
“integrative physiology” at the total body level. The
five-compartment mathematical Model thus demonstrates the concept that mechanical feedback mechanisms (such as redistribution of blood volume within
the system and the vigor of cardiac contraction) control the cardiovascular system to reduce the susceptibility to disturbances that could cause deviations
from optimal function. The two facets of the vigor of
cardiac contraction revealed and emphasized with the
Model, are 1) the magnitude of preload (the enddiastolic volume that is the basis of the Frank-Starling
Law of the Heart) and 2) the magnitude of afterload
[the end-systolic pressure that, with the slope of endsystolic pressure-volume relationship (Emax), determines the end-systolic volume]. [These definitions are
not universally accepted (8).]
T E C H N O L O G Y
concept and the conservation of mass principle to
integrate heart function with that of the peripheral
vasculature.
Important topics covered to help the learner and
professor:
Explain the difference between Emax (related to
afterload, i.e., ventricular end-systolic pressure)
and the Frank-Starling Law of the Heart (related
to preload, i.e., ventricular end-diastolic volume) as major determinants of the vigor of cardiac
contraction.
●
Explain how a change in each characterizing parameter of the cardiovascular system, such as resistance, compliance, total stressed volume, vigor of
cardiac contraction, heart rate, or intrathoracic
pressure modifies cardiovascular function.
●
Explain why changes in blood volume distribution and vascular capacitance are important parts
of the inherent, hydraulic mechanisms for cardiovascular homeostasis.
●
Discover which parameter changes are most effective for providing compensation for heart failure,
vigorous exercise, or hemorrhage.
●
Understand why a venous resistance, which provides a difference between central venous and peripheral venous pressures, is necessary for explaining the coupling between the heart and peripheral
vasculature.
●
Predict conditions under which venous return
does not equal cardiac output and in what direction and why not.
●
Explain why the ventricular ejection fraction, although useful, is not a fully adequate measure of
cardiac contractility.
Learners targeted. The CVI project was designed for
freshman medical and biomedical graduate students
and senior bioengineering students. However, others,
including professors, physicians, and other health
care professionals as well as “continuing education”
students should find it helpful. From the biomedical
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The learning package is designed for those who have
a minimal working knowledge of both the structure
of the cardiovascular system and the underlying basic
physical principles, such as the concepts of 1) flow
related to pressure gradient and resistance, 2)
stressed volume related to distending pressure and
compliance, and 3) change in stressed volume computed as the integral of inflow minus outflow from a
compartment. These concepts, and many others, accessed by clicking on keywords in the Lab Book, are
reviewed, if needed, in the Information File. Davis
and Gore (3) have provided a simulation application
to describe the determinants of cardiac function. Our
study integrates the function of both ventricles with
the peripheral circulation. Carroll (1) discusses pressure-flow relationships in detail. Our study uses that
●
T E A C H I N G
W I T H
education textbooks and literature, teachers and professors of physiology will likely benefit from it also.
Unfortunately, the interactive concepts about the cardiovascular system are so complex and intertwined
that even professors or physicians cannot quickly and
easily grasp a clear and functional understanding of
the physiology of the system. Because diseases influence various parts of the system to varying degrees,
the therapies to be used depend on the choice of
which parameters need to be restored or enhanced to
attain adequate cardiac function for pumping blood to
the tissues.
T E C H N O L O G Y
2) strategies based on five fundamental equations for
predicting the effect of a change in the value of a
variable, given the change in the other variable
and the value of the governing parameter; applied
to each compartment, these equations make up
the simulation model.
3) a mini-physiology textbook (with figures, mostly
from Ref. 14) that defines and explains many basic
concepts of the cardiovascular system;
What’s new and valuable about this project? We
hope that professors developing course material may
find the tools used in this project worthy of adopting.
5) a detailed description of the model;
The tutorial Lab Book includes:
6) references to some of the relevant physiology literature and citations justifying the parameter values used; and
1) coding with hypertext tags to move data from the
model to the tutorial and for jumps from the tutorial to the Information File for definitions and descriptions of key concepts;
7) a button to jump to the Index for instant jumps to
the topic of interest.
2) a column for predictions and a site for answers to
provocative questions;
Audio-Video Interleaved (*.avi) files provide a succinct instructional description of the Main Menu, the
Model, the Lab Book, and saving the Lab Book to a
floppy disk.
3) conversion of the model results to percent of control and transfer of them from the model to a
column in the tutorial to ease the comparison of
the learner’s predictions to the results of the simulation;
With the goals of being accurate, inclusive, easy to
use, and concise, the development of the Tutorial and
Information File has been very intellectually challenging and time consuming.
4) a table of contents for both the tutorial Lab Book
and the Information File for quick jumps to the
topic of interest;
MODEL
The layout of the mathematical Model is shown in Fig.
1. The Model includes a left heart, arterial bed, venous
bed, right heart, and lung bed. This layout display can
be printed during a run to show the data and the
magnitude of parameter(s) changed at that time in
the “experiment.” The Model display (Fig. 2) provides
the data for the tutorial and shows the parameter
values currently in use. This example shows left ventricular failure. There are 27 variables displayed to
represent a typical adult human and 15 parameters
that can be changed. A plot of the time course of
changes in mean systemic arterial blood pressure,
5) provision for copying the Lab Book on the CD to
the learner’s own copy on a floppy disk that can
be retrieved for future additions of results of experiments and printed, if desired.
Details about architecture and design of the hypertext
coding used are provided in Gersting and Rothe (4).
The Information File includes:
1) instructions and help for using the project;
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4) a discussion of each of the 17 experimental modules
(See Table 1) in terms of evidence available and
cause-and-effect consequences; answers to the questions asked in each “experiment” are also provided;
T E A C H I N G
W I T H
T E C H N O L O G Y
cardiac output, and venous return, during the development of ventricular failure, are shown at 60-ms
intervals in Fig. 3.
Each of the three vascular compartments are simulated by the following:
1. The rate of outflow from a vascular compartment equals the outflow pressure gradient divided
by the outflow resistance—the resistance concept;
The five-compartment Model (Fig. 1) has no parallel
paths, no pulmonary vein compartment, and no transcapillary fluid shifts. These were compromises to minimize complexity and confusion and yet provide the
essentials for accurate understanding. The pulmonary
arterial, pulmonary capillary, and pulmonary venous
beds were lumped into one compartment, with the
pulmonary venous resistance set to represent the sum
of the outflow resistances of all three. Transcapillary
fluid shifts can be simulated.
2. The pressure in a compartment equals the distended volume divided by the vascular compliance—the compliance concept; and
3. The change in distended volume equals the integral of (inflow minus outflow)—the conserva-
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FIG. 1.
Layout of model, with control values of parameters and variables. This screen shows absolute, rather than
%control parameter values. It can be displayed or printed at any time during an “experiment.” As defined in
the legend at the bottom left, parameters, for example, are shown in boxes with a yellow background,
variables with a white background. See text for definitions of abbreviations.
T E A C H I N G
W I T H
T E C H N O L O G Y
1) cardiac output (CO) ⫽ HR ⫻ SV ⫽ HR ⫻ (EDV ⫺
ESV)
tion of mass principle. This integral is solved
numerically as a difference-differential equation
2) venous return (VR; into the ventricles) ⫽ K2 ⫻
(Pv ⫺ EDP)/Rv
Vt ⫽ Vt⫺1 ⫹ (Fin ⫺ Fout) ⌬t
where Vt is the volume at the current time (t), Vt⫺1 is
the volume at the previous time interval, Fin is the
inflow, which is the same as the outflow from the
upstream compartment, Fout is the outflow into the
downstream compartment, and ⌬t is the step size
(e.g., 0.001 min). If outflow from a compartment is
not identical to inflow, then the volume in the compartment will change.
where HR is heart rate, SV is stroke volume, EDV and
ESV are ventricular end-diastolic and end-systolic volumes, respectively, Pv is the peripheral venous
pressure, EDP is the end-diastolic ventricular pressure, and Rv is the venous outflow resistance. K2
is a factor “impeding” inflow when diastolic filling time is curtailed at high heart rates. K2 is 1.000
between a heart rate of 0 to ⬃125 beats/min. It then
Each of the two ventricles are simulated by:
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FIG. 2.
Model display during left ventricular failure (Emax reduced to 14% of normal).
Note warnings in magenta: “Patient hypotensive” and “Left EDV > 175 ml.”
(%normal values are shown in Fig. 4, data column 3).
T E A C H I N G
W I T H
T E C H N O L O G Y
declines to ⬃0.5 at 200 beats/min, and is 0 at 250
beats/min.
duration of diastole minus that of systole) is seriously limited at high heart rates. The relationship
between heart rate and cardiac output is complex.
Quality data are not readily available to quantify
the relationship, because an increased heart rate is
usually associated with exercise or stress. These
disturbances induce a reflex increase in sympathetic nervous system activity that increases heart
rate and also increases cardiac contractility and
causes venous and arterial constriction. Pacing the
heart (i.e., stimulation of the right atrium at various time intervals) changes the heart rate but does
not provide useful data if the cardiovascular reflexes are intact, because these reflexes tend to
nullify any heart rate effects on cardiac output by
changing other cardiovascular parameters.
EDV is the complex result of interacting factors influencing the preload of the heart and is a major determinant of cardiac output and the work done by the
heart during each beat. For each ventricle, the EDV is
determined by several factors, including:
1) EDP, the internal pressure at the end of the filling
phase. It is computed as: EDP ⫽ EDV/compliance
during diastole, and is the downstream pressure
influencing the rate of inflow from the veins;
2) intrathoracic pressure (Pit), the pressure in the
chest outside the heart. It is a factor determining
the ventricular distending pressure: Pdistend ⫽
EDP ⫺ Pit;
ESV of each ventricle is determined by:
3) ventricular compliance (C), the ease of ventricular
distention during diastole;
1) the cardiac contractility, represented by Emax, and
4) diastolic filling time limits the amount of filling at
high heart rates, because the time for filling (the
2) the ventricular (end-systolic) pressure, which is
the afterload on the heart.
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FIG. 3.
Data plotted during development of sudden left ventricular weakening (Emax 14% of normal). Note the initial decrease of cardiac
output to 0 (heavy red line) and then the recovery. As a consequence of the decreased cardiac output, arterial pressure (blue
line) decreases (but not to 0) and then increases as the right
ventricle continues pumping. The venous return (magenta line)
decreases to asymptote with the cardiac output.
T E A C H I N G
W I T H
TABLE 1
Experiments for study of Cardiovascular Interactions
cussed in the Information File, that the mean systemic
arterial pressure (Psa) adequately represents the endsystolic-pressure (ESP). Emax is the slope of the ESPVR:
Emax ⫽ ESP/(ESV ⫺ V0), and V0 is the ESV extrapolated to zero generated pressure.
Basic physiology
200% of normal
50% of normal
200% of normal
50% of normal
50% of normal
500% of normal
500% of normal
As the Model is run, blood volume progressively redistributes between the compartments to 1) meet the
constraints set by the equations and parameters and
2) reach a steady equilibrium state such that the flows
through each compartment are equal. (Data are displayed at 0.1-min intervals after each 100 iterations.)
The redistribution of blood volume between the various compartments explains, in large measure, why
the system is inherently self-correcting in response to
various disturbances. The control data (at time ⫽ 0)
are shown in the Layout screen (Fig. 1). Subsequent
changes in variable values depend on the magnitude
of changes of parameters, including total or unstressed blood volume. With a Pentium CPU chip
with 32-bit registers and double precision, the error is
less than a nanoliter, with a total normal blood volume of 5,000 ml. The model runs at least 100 times
faster than clock time. Blood volume changes caused
by hemorrhage or transfusions are made at the venous
compartment, which contains ⬎75% of the total unstressed volume. The concepts of stressed and unstressed volumes and mean circulatory filling pressure
(12) are discussed in the Information File.
500 ml
Pathophysiology and stress
11. Left heart failure via Emax
12. Congestive left heart failure
13. Congestive right and left
heart failure compared
14. Intrathoracic pressure (Pit)
15. Hemorrhage
Suggest effective compensatory
changes to mimic fluid shifts
and reflex control of the
cardiovascular system following
hemorrhage.
16. Hypertension with arteriosclerosis
17. Exercise
Explore and describe effective
compensatory changes that act
to maintain arterial blood pressure
while providing a cardiac output of
several times normal during vigorous
skeletal muscle exercise.
18. Experimental test bed. {to use the
Model without the tutorial}
15% of normal
Blood volume
⫹750 ml
from ⫺4 to 0 mmHg
Blood volume
⫺1500 ml
Ra ⫽ 150% of normal
Ca ⫽ 50% of normal
Ra ⫽ 20% of normal
Although the Model does not include provision for
transcapillary fluid shifts, changing total blood volume simulates such fluid shifts. Similarly, changing
appropriate parameters simulates autonomic reflex
compensation or drug action. Although details of the
pattern of arterial pressure during each cardiac cycle
are not included, values for systemic arterial systolic
and diastolic pressures are computed and displayed.
Ra, arterial resistance; Ca, arterial compliance; Emax, slope of endsystolic pressure-volume relationship.
The ventricle contracts to eject blood until the arterial
back pressure (force) matches the contractile force
generated by the heart muscle. At this time, ejection
stops. The end-systolic pressure-to-volume relationship (ESPVR) determining the ESV is
In a stand-alone mode, the Model (Fig. 2) and the plot
of model data (Fig. 3), along with the windows for
changing parameters, can be used to demonstrate
various responses during a lecture.
ESV ⫽ (ESP/Emax) ⫹ V0
LAB BOOK
The Lab Book provides a tutorial in which the
learner explores details about the interactions between various parameters and variables. A list of the
where ESV is the ventricular volume and ESP is the
ventricular pressure at about the time of maximum
ventricular elastance [P(t)/V(t)]. We assume, as dis-
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1. Arterial resistance (vasoconstriction)
2. Arterial resistance (vasodilation)
3. Venous resistance (venoconstriction)
4. Venous compliance
5. Arterial compliance
6. Left ventricular contractility
7. Right ventricular contractility
8. Heart rate on stroke volume
and cardiac output
(normal, 18, 48, 144, 216 beats/min)
9. Unstressed blood volume, venous
10. Venous-return: cardiac-output
relationship
T E C H N O L O G Y
T E A C H I N G
W I T H
INFORMATION FILE
17 experimental modules (Table 1) is available in the
Lab Book by clicking the “Show Table of Contents”
button and then clicking the desired experiment.
have the computer retrieve a set of normal values
for a Lab Book data table, and
●
then predict the influence of a change in a parameter value;
●
have the computer change a parameter the specified amount and run the model until flows leaving
each of the five compartments are equal (during the
run, data of the three important variables are graphically displayed);
●
have the computer retrieve the set of resulting data
from the model display into the Lab Book;
●
have the system compute percent of normal for
each of the model variables; and
●
have the computer retrieve the percent of normal
data for the Lab Book.
●
The learners then are asked to compare their predictions to the values developed by the Model and
give explanations for major discrepancies.
●
Finally, the learners are asked a series of questions
to elicit thoughtful explanations of mechanisms involved.
Hypertext links connect the Lab Book with the relevant sections of the Information File. A dynamic table
of contents (for both the Information file and the Lab
Book file) helps the learner navigate quickly to relevant sections of each. In addition an index to items in
the Information File is readily available, including a
list of abbreviations used.
Because this learning project is complex, an effort has
been made to minimize learner frustration with the
user interface by including a set of four audio-visual
clips (*.avi files) on the CD. These clips demonstrate
the mechanics of how to use the project effectively.
They may be played with a multimedia player and are
a highly recommended time saver for the learner who
has no readily available consultant.
Suggestions for use of the project. The CVI project
can be used by a single person, but from experience
with the pencil-and-paper version (11) and Michael’s
(7) definition of effective learning, the most effective
approach is to ask two to at most four students to
“experiment” and learn together. The Lab Book
should be saved to a named file on the learner’s
computer or floppy disk to save the predictions and
answers for subsequent use. This file can then be
retrieved for additional studies or corrections at a
By clicking on a hypertext tag labeled “Discussion” of
the results, an analysis of each experiment is displayed in the Information File in terms of chains of
cause-and-effect consequences. Answers to the questions are also provided for comparison to the learner’s
answers.
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An extensive Information File of ⬃100 pages with 14
figures provides 1) an introduction about the purpose
of the learning project, 2) the objectives, 3) detailed
instructions, 4) suggested strategies for predicting
responses, 5) a physiology section, which defines and
explains the major cardiovascular concepts and includes textbook-type figures [see Rothe and Friedman
(13)], 6) a discussion of the results of each module
and sample answers keyed to the questions at the end
of each experimental module, 7) a detailed description of the Model with the equations used plus documentation for parameter values used, the rationale
for choosing parameter values, and the assumptions
governing the model, 8) a parameter sensitivity analysis matrix, which is an important part of a mathematical model, and 9) a bibliography section providing citations to some of the relevant physiology and
references supporting the choice of normal variable
and parameter values.
The primary objective of the tutorial is for the learner
to be able to explain the influences and mechanisms
involved in response to changes of the parameters
listed in Table 1. Of particular importance are the
changes in 1) cardiac output, 2) mean systemic arterial pressure, and 3) blood volume distribution. The
Lab Book (example shown in Fig. 4) provides an
interactive learning environment for the learner(s)
who are asked to:
●
T E C H N O L O G Y
T E A C H I N G
W I T H
T E C H N O L O G Y
later date. The saved file can be printed or submitted
to the instructor. The key elements in the meaningful
learning process include:
2) comparisons between the predictions and the
Model results,
3) deciding what “experimental evidence” is needed
to understand the system, and
1) discussion to specify the predictions to be made,
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FIG. 4.
Data table in the Lab Book for left ventricular failure (Experiment 11, Emax 15% of normal). The
learner’s “predict” (i.e., predicted change in response to a parameter change) is expressed as a
percentage of normal for comparison with the “%Normal” in data column 3. In response to the
large reduction in left ventricular contractility, note the large increase in left ventricular ESV and
pressure. The cardiac output and arterial blood pressure decrease relatively less, because the right
heart continues pumping, thereby causing the compensatory increase in left ventricular EDV (the
Frank-Starling mechanism).
T E A C H I N G
W I T H
4) development of cause-and-effect chains of logic to
explain the results.
T E C H N O L O G Y
Bennet-Tec ALLText software, we developed a functioning Lab Book that used an interactive hypertext
format. The concept was presented at the ComputerBased Resources in Teaching and Research session of
the Experimental Biology meeting in 1999, and a
functioning version running from a CD was displayed
at the Experimental Biology 2000 meeting.
The discussion of each experiment in the Information
File is designed to reinforce (or help correct) the
learner’s progress in learning about the cardiovascular
interactions.
The Model provides a summarization of over 32 years
of research support by National Institutes of Health
Grant HL-07723 titled: “Reflex Control of Vascular
Capacitance” (see for example Refs. 12, 13, 15).
Are classroom faculty needed? The present selfpaced CVI project does not need the on-site presence
of a faculty member. However, our experience at the
Indiana University School of Medicine at Indianapolis
with the pencil-and-paper version of the CVI package
in the 1980s demonstrated that a knowledgeable faculty member present in the room with six to eight
computers and groups with two to four students each
was helpful. After a few years, however, the lack of
faculty with a working knowledge of cardiovascular
physiology led to the computer projects being assigned (we had about five) to the students to do in
their “free time.” No faculty member was present, and
there were no specific cardiovascular interactions
questions on the examinations. There is no good
substitute for a live, knowledgeable, friendly, computer-skilled faculty member. Without a faculty member
present, and without having specific questions on
exams related to the computer labs, the students soon
learned that the computer labs were optional and so
quit using them. Use of computer-assisted instruction
in our curriculum was thus abandoned.
Please note that these simulated experiments do not
provide real data. Only well designed experiments
with living subjects can provide the basic knowledge
needed to substantiate the equations and parameters
employed.
History of development of CVI project. Mechanical models have been used to help learners understand the cardiovascular system (15), but they are
limited. One of the first detailed mathematical analyses of cardiac and blood vessel hemodynamics was by
Grodins (5). However, it involved the solution of
complex algebraic equations and provided no dynamic patterns. Coleman, et al. (2) in 1974 pioneered
an alternative approach based on numerical integration, which was subsequently used for our cardiovascular simulation (9). This was combined with a paperand-pencil tutorial to help our medical and graduate
learners understand the overall function of the cardiovascular system. The model was implemented on a
group of personal computers with the support of an
IBM grant to the Department of Physiology. (The
PCs had 256 kilobytes of RAM and a 2-MHz CPU.) A
description and evaluation of the project was published (10).
The questions in the Lab Book and the Information
File are designed to encourage and help the student,
but there is no substitute for related questions on the
examinations to encourage students to use the
project. If these questions cover important concepts,
then the use of the self-paced project (and similar
ones) can be assessed and, if positive, justify their use.
Because of the subsequent availability of much more
powerful computers and computer software, the possibility of converting the pencil-and-paper tutorial
into a Windows-based package was explored. Using
Microsoft Visual Studios (version 5 and then 6) and
The reality of current medical school funding and
priorities and the press of limited scheduled time for
students justifies the attempt to use a learning environment that is “asynchronous” (i.e., “distributed
learning,” “distance education”). Continuing educa-
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Each experiment will require 10 –30 minutes to complete. The instructor may want to assign only a few
experiments if time is limited. For example, assign
Experiments 1, 3, 8, 11, 12, 14, and 17 as described in
Table 1. Using the “explore” version of the Lab Book
(instead of saving their own copy of the Lab Book
with predictions and answers to questions) provides a
quick review or update of understanding of the cardiovascular system.
T E A C H I N G
W I T H
tion for physicians and other professionals also benefits from the use of modern information technology
approaches. It is not easily accomplished, quickly
done, or inexpensive. Furthermore, packages put together by computer experts without major direction
and help from people skilled in both the discipline
and teaching will be a waste of time and money.
T E C H N O L O G Y
on the computer. The authors own the copyright to
the project but grant permission to reproduce and
distribute copies of this work for not-for-profit educational purposes. For a Cardiovascular Interactions
CD, please send an e-mail request to the author
([email protected]). It is also available as a supplement to this article at Advances in Physiology Education Online (URL: http://advan.physiology.org/cgi/
content/full/26/2/98/DC1).
In summary, this Cardiovascular Interactions project
was designed to help the learner gain a comprehensive understanding of the quantitative aspects of cardiovascular dynamics in a manner that is relatively
easy to use. It also provides much relevant background information in a readily accessible format.
We are grateful for the comments and helpful suggestions of many
students. The critique and encouragement of colleagues, including
James Randall, Glenn Bohlen, Judith Tanner, Phillip Andrew, and
Thomas Lloyd, are gratefully acknowledged.
The model and tutorial were developed in Microsoft Visual Basic
(versions 5 and 6). It includes hypertext and data links using
ALLText 4 HT/Pro (Bennet-Tec Information Systems, Jericho, NY).
Computer screen images were captured with HyperSnap for the
figures for this paper, and Hypercam was used to capture the action
from the computer screen and saved to AVI [audio-video interleaved movie files (http://www.Hyperionics.com)].
In the 1980s, two half-day sessions involving three to
four students with each computer and a 16-page paper-and-pencil lab book provided an effective learning
experience. About 80% of the 98 medical and graduate students of the 1985 class who responded to a
survey agreed or strongly agreed that the cardiovascular simulation package was helpful. Only about half
were satisfied with the printed instructional material,
however (10). In January 2001, 87 freshman medical
students returned a survey evaluating their experience with the project. Although over 75% felt that
their understanding was improved, most considered
the project difficult to use in the form then available.
Many useful suggestions were made. Unfortunately,
not all of the students who used the project attended
the 15-minute demonstration, nor did they use the
video clips then available. The presentation of the
project was radically revised, including a major revision of the Lab Book, a strong recommendation to use
the audio-video clips, and a more familiar and clearer
method for saving the Lab Book on a floppy and
retrieving it for later use.
This project was displayed in early development form at Experimental Biology 1999 and 2000.
Address for CD requests and other correspondence: C. F. Rothe,
Dept. of Physiology (Med. Science, Rm. 374), Indiana Univ. School
of Medicine, 635 Barnhill Dr., Indianapolis, IN 46202 (E-mail:
[email protected]).
Received 26 July 2001; accepted in final form 26 February 2002
References
1. Carroll RG. Cardiovascular pressure-flow relationships: what
should be taught? Adv Physiol Educ 25: 80 – 86, 2001.
2. Coleman TG, Manning RD Jr, Norman RA Jr, and Guyton
AC. Control of cardiac output by regional blood flow distribution. Ann Biomed Eng 2: 149 –163, 1974.
3. Davis MJ and Gore RW. Determinants of cardiac function:
simulation of dynamic cardiac pump for physiology instruction. Adv Physiol Educ 25: 13–35, 2001.
4. Gersting JM and Rothe CF. Cardiovascular interactions tutorial: architecture and design. J Med Syst 26: 29 –38, 2002.
5. Grodins FS. Integrative cardiovascular physiology: a mathematical synthesis of cardiac and blood vessel hemodynamics.
Quart Rev Biol 34: 93–116, 1959.
6. Grodins FS, Gray JS, Schroeder KR, Norins AL, and Jones
RW. Respiratory responses to CO2 inhalation. J Appl Physiol 7:
283, 1954.
Availability. A CD with the Model, Lab Book, Information File, and audio-video clips is available from the
author (C. F. Rothe) for a nominal fee to cover the
cost of reproduction, handling, and postage. The
project can be run from the CD without installing it
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Assessment of the learning project. Evaluating the
quality of a learning tool is a challenge. Surveys are
helpful but are not definitive. Pre- and posttesting are
feasible (7), but simple multiple-choice questions
about the interactive aspects of the system are difficult to develop. A statistically valid assessment would
require random assignment of students to the project
or to the lecture-only, animal lab, or research paperwriting formats. In the current climate in American
medical schools with their emphasis on molecular biology and the proliferation of many other important subjects that crowd the curriculum, this is rarely feasible.
T E A C H I N G
W I T H
7. Michael J. In pursuit of meaningful learning. Adv Physiol Educ
25: 145–158, 2001.
8. Norton JM. Toward consistent definitions for preload and
afterload. Adv Physiol Educ 25: 53– 61, 2001.
9. Rothe CF. A computer model of the cardiovascular system for
effective learning. Physiologist 23: 49 –53, 1980.
10. Rothe CF. Cardiovascular interactions—a simulation package
to help learning. Computers in Life Sci Educ 4: 49 –53, 1987.
11. Rothe CF. Mean circulatory filling pressure: its meaning and
measurement. J Appl Physiol 74: 499 –509, 1993.
12. Rothe CF. Venous system: Physiology of the capacitance system. Handbook of Physiology. The Cardiovascular System.
T E C H N O L O G Y
Bethesda, MD: Am. Physiol. Soc., 1983, sec. 2, vol. III, pt. 1,
chap. 13, p. 397– 452.
13. Rothe CF and Friedman JJ. Cardiodynamics and control of
the cardiovascular system. In: Physiology, edited by EE Selkurt.
Boston, MA: Little-Brown, 1984, 5th ed. chap. 15 and 17, pp.
261–277, 291–311.
14. Rothe CF and Maass-Moreno R. Active and passive liver
microvascular responses from angiotensin, endothelin, norepinephrine and vasopressin. Am J Physiol Heart Circ Physiol
279: H1147–H1156, 2000.
15. Rothe CF and Selkurt EE. A model of the cardiovascular system
for effective teaching. J Appl Physiol 17: 156–158, 1962.
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