J Med Philos-1989-Coulson-109-46

RICHARD L. COULSON, PAUL J. FELTOVICH, AND RAND J.
SPIRO
FOUNDATIONS OF A MISUNDERSTANDING OF THE

ULTRASTRUCTURAL BASIS OFMYOCARDIAL
FAILURE: A RECIPROCATION NETWORK
OF OVERSIMPLIFICATIONS*
Key Words: mental models, knowledge representation, reductionism, myocardium, heart failure, physiology.
A fallacious explanation of the syndrome of congestive heart

failure is widely invoked. While this misconception has a seductive plausibility, it is contraindicated by currently available
evidence. Although appropriate accounts of heart failure exist
(e.g., Katz, 1977), the incorrect explanation is to be found among
clinicians, basic scientists, and students. In this paper, pertinent
physiological principles are reviewed, and the nature of the
misconception is described. Then the internal structure of the
misconception is explicated, and factors that contribute to its
Richard L. Coubon, Ph.D., Professor of Physiology, Department of Physiology, Southern
Illinois University School of Medicine, Carbondale, Illinois, 62901, U.S.A. (for correspondence and reprint requests).
Paul J. Feltovich, Ph.D., Associate Professor of Medical Education, Department of
Medical Education, Southern Illinois University School of Medicine, Springfield, Illinois
62708, U.S.A.
Rand ]. Spiro, Ph.D., Department of Educational Psychology, University of Illinois,
Champaign, Illinois 61280, U.S.A.
The Journal of Medicine and Philosophy 14:109-146,1989.

1989 Kluwer Academic Publishers. Printed in the Netherlands.
Downloaded from http://jmp.oxfordjournals.org/ at University of Pittsburgh on February 20, 2014
ABSTRACT. A misconception regarding the ultrastructural basis of myocardial

failure has been observed in laboratory studies involving medical students and
practicing physicians, in medical textbooks, and in clinical instruction of
students. This misconception attributes heart failure to overextension of individual cardiac muscle fibres and their sarcomeres, resulting in a mechanically
based decline in contractile force production. The basis of the misconception is a
set of component misconceptions which interact in reciprocally supportive ways.
The interlocking nature of the component misunderstandings strengthens the
overall misconception, making it difficult to undermine. A contributor to many
aspects of the faulty account of heart failure is a tendency toward oversimplification of complex phenomena in learning, instruction, and scientific research.
Implications for medical education are considered.
110
Richard L. Coulson et ah
BACKGROUND: PERTINENT PHYSIOLOGICAL PRINCIPLES
Playing central roles in the misconception are the length-tension

relationship (L-T) of skeletal muscle, its instantiation to cardiac
muscle, the Frank-Starling (cardiac function) curve (F-S), the
contractile activation process, and cardiac hypertrophy. These are
well known principles of physiology which are discussed in turn.
Length-Tension Relationship
A general principle centrally involved in the misconception is the

length-tension relationship of skeletal muscle originally described
by Fick (Fick, 1882) and Blix (Blix, 1892) in the late 1800's. This is
the relationship which describes the force generated by a contracting muscle with respect to the length of the muscle. The measurements are made in a laboratory situation with muscles isolated
from animals. Gordon, Huxley, and Julian (Gordon, et ah, 1966)
provided the classical description (see Figure 1) which forms the
basis for modern muscle physiology. Part of this relationship has
an eminently supportable explanation consistent with the Sliding
Filament Theory (Huxley and Hanson, 1954; Huxley and Niedergerke, 1958) of muscle contraction (Huxley, 1957; Huxley and
Simmons, 1971). Functional anatomy supports the account of the
plateau of the curve (Figure 1) between about 2.0 and 2.2 nm
sarcomere length (Huxley and Hanson, 1954). The notion that
there will be no change in the number of heavy meromyosin
heads (Pollack, 1983) in a suitable position to react mechano-
development and persistence are addressed. It is shown that the

misconception can be characterized as a reciprocating cognitive
network of component misconceptions. It is argued that converging influences, attributable to cognitive processes of the learner,
some instructional practices, and some practices of scientific
research, jointly promote the acquisition and maintenance of the
misconception. A tendency toward oversimplification of complex
phenomena is a pervading characteristic of the misconception
network itself, as well as of the cognitive, instructional, and
laboratory influences that promote and support it. Implications
for medical education (and for instruction and cognition more
generally) are considered.
Misunderstanding the Basis of Heart Failure
111
100-
F
0
R
C
20-]
E
0-
1.5
2.0
2.5
3.0
3.5
4.0
SARCOMERE LENGTH CMICRONS)
Fig. 1. Skeletal Length-Tension Relationship.

The figure is redrawn from the classic work of Gordon, Huxley, and Julian (1966)
in which the measurements were obtained from frog skeletal muscle. The plateau
between 2.0 and 2.25 jim corresponds to the sarcomere lengths over which there
is no change in the potential number of sites at which force-generating chemical
reactions may occur. Since the muscle was maximally activated (turned on) there
was no change in the force generated at these lengths. At longer lengths (> 2.25
jim) the degree of overlap between the filaments which react to generate force
decreases and the force declines. If the muscle is stretched far enough, the
reactive filaments do not overlap at all and no force can be generated. The
famous "Sliding Filament Theory" never addressed the issues of the declining
force at lengths less than 2.0 \im, although the force drops towards zero at about
the length where the ends of the sarcomere would sharply abut the ends of the
central thick filaments. There is now considerable evidence that activation of the
contractile system declines at these short (< 2.0 \im) lengths.
chemically with actin active sites (Potter and Gergely, 1975) over
this range of length is supported by experimental observations
over the past thirty years (Martinosi, 1984; Pollack, 1983; Potter
and Gergely, 1975). Similarly, the anatomical evidence supports
an explanation for the decline in force on the right hand side of
p
E
R 80C
E
N
T
60H
M
A
X
I
M 40A
L
112
Richard L. Coulson et a\.
100p
E
R
C
E
N
T
80-1
F
0
R
C
E
20-
010
I.5
2.0
2.5
3.0
3.5
4.0
Fig. 2. Length-Tension Relationship of Cardiac Muscle.

The figure is drawn from data provided by the work of TerKeurs et ah (1980) and
is superimposed upon the diagram of Fig, 1. Partly because of a dense network of
structural latticework (Spotnitz and Sonnenblick, 1976) in cardiac cells, sarcomeres cannot be stretched to lengths greater than 2.3 or 2.4 urn. Since the
central thick filaments of cardiac sarcomeres are about 0.1 ^m longer than those
of skeletal muscle all functional lengths are longer than for skeletal muscle.
Accordingly, the skeletal relationship has been offset from the left by this amount
for purposes of functional comparison (Allen, et ah, 1977). Experimental efforts to
enhance activation of the cardiac contractile mechanism were used in obtaining
the cardiac muscle data and, still, it can be seen that the force at sarcomere
lengths greater than 2.0 ^m does not attain the potential force delineated by the
degree of overlap of the cardiac contractile filaments. The actual forces generated
in cardiac muscle in the life situation are only about 20-30% of those shown in
the figure. Thus, force in the heart muscle in the life situation never reaches the
limits imposed by the maximum potential decreed by overlap of the contractile
filaments. The amount of force generated is always regulated by the degree of
activation. Because of the structural latticework (Spotnitz and Sonnenblick, 1976),
and still not understood other (Huntsman et ah, 1983) considerations, sarcomere
lengths longer than 2.3 or 2.4 ^im are never attained in life; even when sarcomere
lengths are measured from hearts in severe failure they do not exceed this length.
60-j
M
A
X
I
M 40A
L
113
Investigation of Cardiac Muscle
Investigation of isolated mammalian cardiac papillary muscle in

the 1960's (Sonnenblick et al, 1967; Sonnenblick, 1968) indicated
that a similar length-tension relationship as had been described
for skeletal muscle formed the basis for cardiac muscle function.
This was difficult to confirm, because the long refractory period of
the cardiac sarcolemma, following the initiation of an action
potential, prevented maximally activated tetanic contractions in
which maximal force could be generated. Over the last twenty
years a variety of experimental techniques have accumulated
evidence in support of the view that the cardiac papillary muscle
has the potential for a length-tension relationship similar in some
aspects to that of skeletal muscle (Allen et al, 1977) (see Figure 2).
These techniques include light diffraction for accurate
measurement of cardiac sarcomere length (Gordon and Pollack,
1980; TerKeurs et al, 1980), mechanically (Fabiato and Fabiato,
1975) and chemically (Winegrad, 1982) skinned cardiac muscle
fibres which permit chemical (Gibbs and Loiselle, 1978; Maughn et
al, 1978) activation of the sarcomere, and pharmacologically
induced tetanic contractions (Cooper, 1976; Gibbs and Loiselle,
1978). Similarity between the skeletal and cardiac striated muscle
appears thoroughly engrained in the conventional wisdom of the
medical community. Most physiology textbook discussions of
cardiac muscle mechanics are prefaced by a review or a reference
to a review of skeletal muscle mechanics.
the curve (Figure 1). Progressive lengthening of the sarcomere

beyond 2.2 jim (the descending limb) is believed to disinterdigitate progressively the myosin and actin filaments, thereby
reducing the possible number of force-generating reactions
between myosin heads and actin active sites (Pollack, 1983). These
phenomena are among the most thoroughly entrenched concepts
in physiology. There is no similar explanation, based upon the
Sliding Filament Theory or the Cross Bridge Theory, for the
length-tension relationship at sarcomere lengths of less than 2.0
\ixn (the ascending limb). There is, however, accumulating
evidence that the degree of muscle cell activation is modulated
over this range of length (Allen et ah, 1977; Endo, 1973) and that
this modulation accounts for the ascending limb (left hand side) of
the length-tension relationship.
114
Richard L. Coulson et al.
Frank-Starling Relationship
The long-standing empirical observations of Frank (Frank, 1895)

and Starling (Starling, 1918), summarized by Starling's law of the
heart, are well established in the knowledge base of physic: an
increase in the volume of blood filling the ventricle during diastole leads to a more energetic ensuing systole of the ventricle (see
Figure 3).
Contractile Activation
Research of the past twenty years (Ebashi et al., 1969; Potter and
Gergely, 1975; Weber and Murray, 1973) has begun to elucidate
mechanisms of variable activation involving the C a ^ ion
(Martinosi, 1984), the calcium ATPase pump (Martinosi, 1984),
and the troponin-tropomyosin system of the actin filament
(Ebashi et al., 1969; Weber and Murray, 1973) which may explain
both the Frank-Starling relationship of the heart (Coulson, 1982)
and the ascending limb of the length-tension relationship in
physiological terms (Jewell, 1977).
Muscle Hypertrophy
The process of cardiac hypertrophy (the growth of heart muscle

cells rather than the addition of new ones) occurs whenever the
heart muscle experiences abnormally high levels of stress. The
However, while isolated skeletal and cardiac muscles do reflect

similarities, there are notable operational differences. Under
operational conditions, skeletal muscles are totally activated by
the stimulus action of nerves to produce tetanic contractions.
Skeletal muscle regulates the amount of force it generates by
recruiting varying numbers of motor units (groups of muscle cells
controlled by the same nerve). Thus, skeletal muscle force is
controlled by the number of recruited muscle cells (fibres), all of
which are completely activated (turned on). In contrast, the entire
muscle mass of the heart is spontaneously activated by special
pacemaker cells in the atrium of the heart, and the cells or fibres
twitch, never achieving the total activation of a tetanic contraction.
Thus, heart muscle force (in contrast to skeletal) is controlled by
regulation of the degree to which all cells are activated.
115
100/
80-
/
/
60-
;
\
/
2 *
,'
25 L/MIN
_ ^ _
'5 L/MIN
-"
0"
^
"
1.5
"
2.0
2.5
' I
3.0
3.5
' I
4.0
Fig. 3. Frank-Starling Relationship of the Heart Transposed to

the Domain of the Length-Tension Relationship.
The figure is drawn from calculations of left ventricular wall stress (force per
cross-sectional area) from a spherical model of the heart in a resting individual.
The model was assumed to have an end-diastolic volume of 97 ml and a stroke
volume of 70 ml, producing the indicated 5 L/min cardiac output at enddiastolic sarcomere lengths ranging from 2.0 ^m at the endocardium to 2.26 urn
at the epicardium. The heart rate was just over 71 beats/min. The model
ventricle had an end-diastolic radius of 2.85 cm and wall thickness of 1.5 cm. The
second, higher curve, corresponds to the same ventricle under conditions of
maximal exercise where the end-diastolic volume has increased to 165 ml and the
stroke volume has doubled to 140 ml, producing the indicated 25 L/min cardiac
output at end-diastolic sarcomere lengths ranging from 2.38 urn at the endocardium to 2.4 |im at the epicardium. The heart rate was just under 179 beats/min.
Mechanical shell stress theory would predict that the actual stress (muscle force)
would be somewhat higher than the average indicated in the figure at the
endocardial surface and somewhat lower at the epicardial surface due to the
distribution of forces across what is physically referred to as a thick walled
chamber. Thin walled, or LaPlacian, theory predicts the converse, but both
approaches agree roughly on the averages which are illustrated in the figure. The
highly activated length-tension curves from cardiac trabeculae muscle of Fig. 2
and frog skeletal muscle of Fig. 1 are superimposed with broken lines for
purposes of comparison. Note the rather poor correspondence between the
length-tension relationships of functioning heart and the stylized, experimentally
determined ones obtained from isolated tissues in the laboratory.
40-
116
THE INAPPROPRIATE ACCOUNT OF HEART FAILURE
The inappropriate explanation of heart failure can be summarized

as follows:
As the heart gets weak from a variety of sources, including myopathy and
coronary ischemia, the dwindling force of contraction is augmented by
compensation employing the Frank-Starling mechanism, which is the intact
heart's version of the muscle length-tension relationship. As diastolic
overfilling of the ventricle progresses following weakened contractions, the
sarcomeres of the ventricular muscle are stretched to long lengths, disengaging the actin and myosin filaments. At these long sarcomere lengths, on the
descending limb of the length-tension curve of muscle, the force declines,
leading to progressively weaker contractions, more overfilling of the ventricle
in diastole, and, hence, cardiac failure.
This characterization is a synthesis of descriptions of heart failure

provided by medical student subjects in our laboratory. The
descriptions were given in oral response to a fixed set of openended questions about the functioning of the heart and cardiovascular system. The synthesis also conforms to accounts offered by
some physicians and medical texts. Some descriptions given by
the students portray more of the facets of the characterization than
others or portray each facet in greater or less detail. However, the
key ingredients in these descriptions are that the Frank-Starling
mechanism is a direct reflection of the ascending limb of the
hypertrophic adaptation process intervenes when diastolic

sarcomere lengths approach and exceed their usual diastolic
length (about 2.1 urn), adding sarcomeres in series until the
resultant lengths are again below this level. This is the volume
overload hypertrophic adaptation process (Spotnitz and
Sonnenblick, 1976). In addition, sarcomeres are added in parallel,
exerting a restoration effect toward normal wall thickness. When
active systolic stresses higher than those which are compatible
with the basal level of contractility persist for any prolonged
length of time (more than about six hours - Nair et ah, 1968), the
pressure overload hypertrophic adaptation intervenes, adding
sarcomeres in parallel until the force per sarcomere is again
normalized and the wall thickness has increased so that nominal
wall stress has been restorted (Spotnitz and Sonnenblick, 1976).
117
length-tension relationship, and that heart failure results from the

overstretching of individual myocardial sarcomeres. Examples of
discussions of heart failure are given below to illustrate some of
the ways that the synthetic account is instantiated, and to show
the presence of the key facets across subjects with a wide range of
medical experience and in a textbook account. The first is from a
second year medical student:
The second description is from an established cardiac physician

and includes the key mechanism along with another one
(involving the law of Laplace):
What the Frank-Starling relationship indicated was that, ah, this, ah, matter
of, ah, a muscle fibre being stretched, there comes a point at which, ah, the
stretching is no longer productive, and therefore, we tend to talk about the,
ah, healthy part of the curve, that's one phrase which is used commonly,
which is the physiological, ah, range that, ah, as one stretches the muscle fibre,
it will contract more forcefully. However, a point is reached, ah, which is socalled plateau point, where stretching the muscle fibre a little bit more is
tolerated but does not result in any increased, ah, contraction and force of
contraction. And then, if one stretches <the muscle fibre> a little bit further
than that, we then go on to what is referred to as the down-slope of the curve,
where actually the ability to contract is decreased. The concept we have is that
there is a point at which the left ventricle can be so dilated that it is no longer
functioning. We think this probably is due to, so this is one reason for it. The
other we think is simply what we mentioned much earlier on in terms of the
physical property of the radius is, that when the ventricle is more dilated, ah,
Okay, discuss factors which cause the muscle contraction to be inadequate (in
heart failure). Okay, this takes me back to the Frank-Starling mechanism,
where there's a volume overload on the heart, and this, urn, leads to, um, the
muscle cell spindles to be spread apart so there's very little overlap between
the actin and the myosin, and, ah, the way I conceptualize this is with the
cross fibres as sort of like little guys rowing, or else people pulling on a tug of
rope, and, ah, with less overlap they're able to, ah, develop less tension, and
the entire muscle, muscle fibre itself, the heart is able to, is not able to do its
job as effectively... I like to think of the Frank-Starling as falling over the edge
of where, with, as the further the muscle cell gets stretched, the less it's able to
do its job effectively... I use the sort of the, conceptualize the number of
rowers or people pulling on a tug of rope to explain that with increasing
stretching of each cell they are less able to pull and shorten. And also, in the
Frank-Starling mechanism, where it's gone over the edge of where more
lengthening of the cell doesn't help with tension.
118
because of the law of LaPlace, more energy has to be, more force has to be
generated, ah, to achieve the same wall tension. So that there are two reasons
why a certain degree of dilation of the, of the ventricle is, is functional and
achieves increased cardiac output, but there is a point reached beyond which,
ah, function actually declines, and this is what is referred to as a failing
ventricle where cardiac output is falling.
Dilatation of the heart is also a factor that can decrease cardiac efficiency. The
force of contraction of a muscle (including cardiac muscle) depends on the
initial length of the muscle sarcomeres. When the sarcomere is initially
stretched, this is associated with a more forceful contraction. The optimum
sarcomere length is 2.2 pm. At this length the overlapping between the actin
and myosin filaments are ideally situated to allow the cross-bridges between
them to pull the actin filaments inward during contraction. When the
sarcomeres stretch beyond this point, the actin and myosin filaments do not
overlap so much and the cross-bridges cannot pull the actin filaments inward
adequately. As a result, the force of muscle contraction decreases. This is the
structural basis for Starling's law of muscle contraction.
In our laboratory, similar explanations of heart failure as

resulting, exclusively or in part (interspersed with other
mechanisms), from mechanical overstretching of muscle fibre
were given by students from two medical schools (one state, one
private) and by established cardiac physicians. For example, in the
state medical school where the bulk of our investigation has been
conducted, such explanations were offered (shortly after completion of the most pertinent sections of their curriculum) by eighteen
of twenty-eight (64%) first- and second-year medical student
subjects (1st yr.: 7 of 14, 50%; 2nd yr.: 11 of 14, 79%). (This sample
of 14 volunteer students from each class represented 20% of each
total class of 70 students). These proportions of students to whom
this explanation of heart failure is attributed should be considered
conservative, because we have only counted instances where the
explanation was clearly offered. Other subjects may have actually
held this view, but an explicit statement was not elicited by our
procedure. We have also observed this kind of explanation offered
to students by faculty during clinical teaching exercises. The
account appears to be pervasive, and it seems to be inherently
plausible. Unfortunately, the account is inconsistent with the
A third account which is particularly reflective of the synthesized

characterization is offered by a respected and reasonably current
(1982) textbook of clinical cardiology (Goldberger, 1982):
119
available evidence. Before proceeding to a more appropriate view

of heart failure, the major components of this common misconception are considered in more detail.
The Major Components of the Misconception
If you stretch any muscle excessively it's not going to be able to contract
because you've pulled the actin and myosin completely apart, so that it can't
form any cross-bridges and it can't contract, or, if you have a muscle that's too
contracted to begin with, it can't contract anymore because the actin and
myosin are pushed up against each other already, and there's no room for
them to slide any further. (Medical student discussing the length-tension
relationship).
2. The isolated cardiac muscle exhibits a length-tension relationship similar in all respects to the stylized skeletal muscle lengthtension relationship.
Direct statements of this correspondence are generally not
made; the correspondence probably has the status of a tacit
presupposition, as evidenced by the following statement by a
second year medical student, who describes the classical skeletal
muscle length-tension relationship in his discussion of the cardiac
function curve (also see the earlier textbook account, which more
overtly equates the two L-T curves in its parenthetical statement):
A number of salient aspects characterize this account of myocardial failure by a Mechanical Ultrastructural Mechanism (MUM); in
order to be tenable, several conceptual components appear to be
inherent in this "understanding" of the processes involved. These
components are listed together with quotes from subjects which
indicate their belief in each. (All quotes are from different subjects).
1. The entire length-tension relationship, both descending and
ascending limbs, has its functional basis in the highly mechanical
Sliding Filament Theory of contraction. On the descending limb,
declining forces are generated because of disengagement through
stretching of actin and myosin filaments. Optimal forces are
generalized at the plateau lengths of the relationship because of
optimal engagement. Suboptimal forces arise on the ascending
limb, because actin and myosin filaments are "smashed up"
against each other.
120
3. The cardiac length-tension relationship (equated with the

skeletal) is the underlying phenomenon accounting for the FrankStarling relationship between cardiac function and ventricular
filling.
Starling's law states that, as end-diastolic volume increases, the corresponding
cardiac output at systole also increases. This occurs up to a point where the
length of the fibres is too long and, therefore, tension at systole decreases,
causing a decrease in cardiac output. The decrease in contractile force
corresponds with the length of myosin fibres (sic: myofibrils) being in contact
with actin... as the length of contact between the fibres comes to a point
where it starts to decrease because the cardiac muscle fibre is pulled to the
length which is too long. That situation corresponds with the decrease in
tension, after a certain point is reached in the cardiac function curve. (Medical
student discussing the Frank-Starling relationship).
4. Since the classical length-tension relationship of muscle would

predict decreasing force of contraction at sarcomere lengths
corresponding to those on its descending limb, the heart is expected to fail when diastolic overfilling stretches cardiac sarcomeres to lengths corresponding to those on the descending
limbs of their individual length-tension relationships.
Okay, the length-tension relationship of the muscle fibre... the length-tension
curve, is a curve that relates to the sarcomere of the muscle fibre; as tension
increases, your length is going to increase (sic, backwards: for the active
relationship being discussed, an increase in length results in an increase in
tension). There's a plateau, and then it drops towards the end... The cardiac
function curve or the Frank-Starling relationship is what I was just talking
about, the cardiac function curve goes up and then plateaus out... I'm just
thinking of a curve in my mind where I see there's a certain level beyond
which, when it drops down, it puts you into congestive heart failure. (Medical
student discussing heart failure).
Previously I was discussing the length-tension relationship and bringing into

focus the idea that it is the length of contact between actin and myosin fibres
(sic: actin and myosin compose filaments within fibres) which up to a certain
point, as the length increases, will have a corresponding increase in tension
upon contraction of that muscle fibre. However, after a certain point the
length of actin-myosin contact decreases, because the muscle fibre is stretched
beyond a certain point. As a result, tension after that point decreases as the
fibre gets stretched and pulled past a certain length... This is responsible for
the fact that, as end-diastolic volume is increased, ah, and there is a corresponding increase in ah, contractile force and stroke volume at systole.
(Medical student discussing the basis for the Frank-Starling relationship).
121
APPROPRIATE INTERPRETATIONS OF PRINCIPLES

RELATED TO HEART FAILURE
Although the foregoing view of cardiac muscle function and heart

failure has a seductive plausibility, it has almost no substantiation.
Several important conclusions can be drawn from the current
scientific evidence which contribute to an explanation of heart
failure opposed to the Mechanical Ultrastructural Mechanism
commonly proffered. These conclusions correspond directly to the
four major components addressed in the previous section.
1. The Sliding Filament Theory (Huxley and Hanson, 1954),
which accounts well for the plateau and descending limb of the
skeletal muscle length-tension relationship, does not account at all
for the ascending limb. There is increasing evidence that variable
activation (Allen et ah, 1977; Fabiato and Fabiato, 1975; Jewell,
1977) substantially accounts for the ascending limb of the lengthtension relationship. While this activational modulation varies
with length, it is a matter of progressively energizing the contractile mechanism with increasing length, and it is not a matter of
anatomic variation in potential actin-myosin interaction sites, or of
overt anatomically based mechanical obstruction (e.g.,
"smashing" of actin filaments from opposing ends of the sarcomere).
2. The cardiac sarcomere (the subcellar force generating organelle), when directly chemically activated in the laboratory,
demonstrates a length-tension relationship similar, but not identical, to that of skeletal muscle (Fabiato and Fabiato, 1975).
However, the heart is composed of intact cells which can only
"twitch" with a long electrical refractory period, precluding
maximal activation. The actual force developed by cardiac muscle
fibres (intact cells) is always less than the potential delineated by
the maximally activated skeletal length-tension relationship (see
Figure 2). Furthermore, since length-dependent modulation of the
activation system determines the amount of cross-bridge interaction between actin and myosin filaments, the ascending limb of
the cardiac muscle length-tension relationship (under the muscle's
natural constraints of "twitch" activation) continues to rise and
plateau at lengths which physically correspond to the descending
limb of the fully activated skeletal length-tension curve, and there
is no corresponding cardiac descending limb.
3. The length-tension relationship of cardiac muscle does not
122
account well for the Frank-Starling mechanism for two reasons.

First, under the erroneous assumption (held by students) that the
cardiac length-tension relationship is identical to the classical
skeletal one (see Figure 1), for the account to work there would
have to exist conditions of end-diastolic volume corresponding to
sarcomere lengths on the ascending limb of the L-T. In life, any
volume small enough to accomodate this requirement would be
too small to produce a life-sized stroke volume. If the initial
sarcomere length were any less than 2.0 (im, no more than 20%
shortening could occur before the sarcomere had reached its
shortest possible length of 1.6 jxm. The shortening necessary to
produce the smallest stroke volume compatible with life is about
35%. Further, a relaxed ventricle, rendered open and empty in the
laboratory, already is at sarcomere lengths longer than 2.0 \im.
Hence, any ventricular diastolic volume starts at least at sarcomere lengths corresponding to the plateau of the L-T. Any
enhancement of performance associated with larger diastolic
volumes stretches the sarcomeres to lengths corresponding to the
plateau of the L-T. Second, even if the correct cardiac lengthtension relationship is considered (see Figure 2), where the
appearance of compatibility between ascending limb sarcomere
lengths and substantial ventricular volume exists, a further
consideration precludes the use of the L-T as an explanation for
the Frank-Starling relationship. The actual forces generated by
ventricles are much less than those demonstrated in the cardiac LT. This is due to sub-maximal activation. According to available
evidence, it is length-dependent variable activation which accounts for the Frank-Starling mechanism in large part. This
involves the calcium activating system of excitation-contraction
coupling: the calcium binding troponin-tropomyosin complex; the
sarcoplasmic reticulum cisternae; and ATPase ion pumps. All of
these factors lead to the augmented force of contraction by the
heart muscle as its fibres are extended in length by increasing
blood volume in the ventricles. While the length-dependent
activation system may be accompanied by alterations in the
degree of myofilament overlap, it is an independent process and
probably not a result of variations in myofilament overlap. Figure
3 illustrates examples of functional translations of Frank-Starling
curves of the intact ventricle to the domain of the sarcomere
length-tension relationship, and shows the generally poor correspondence between the two kinds of curves.
123
4. The mechanisms that lead to the decreased contractility

which characterizes heart failure remain controversial in some
particulars, but likely involve some combination of damaged
sarcomeres, disturbances of the activation system, altered activity
of ion pumps, and probably many yet undiscovered defects of
muscle chemistry (Nair et ah, 1968). Despite some areas of controversy in the account of heart failure, it is clear that overextension of muscle fibres and their sarcomeres, with loss of force as
would occur on the descending limb of the classical length-tension
curve, cannot be part of the explanation. Under the usually prevailing condition of submaximal activation, Starling mechanism
compensation permits the cardiac muscle to function effectively at
lengths (greater than about 2.2 p i ) corresponding to those on the
descending limb of the maximally activated skeletal lengthtension relationship (Figure 2) (Fabiato and Fabiato, 1975). Furthermore, structural elements of cardiac muscle which contribute
mechanical stiffness, such as collagenous matrices among the
fibres (Spotnitz and Sonnenblick, 1976) and, possibly, active
stiffness generated by actin-myosin interaction, lead to "the
existence of a maximal attainable sarcomere (TerKeurs et ah, 1980)
or segment length" (Huntsman et ah, 1983), a kind of "wall" which
precludes stretching the cardiac muscle to sarcomere lengths
beyond about 2.4 p i , even in the laboratory. In life, sarcomere
lengths longer than 2.3-2.5 p i are never found, even in the
pathology of heart failure. Hence, the basic premise which is
invoked in explanation of heart failure, i.e., that overextension of
the sarcomere disinterdigitates the contractile filaments resulting
in decreased force, never holds to any significant extent in the
intact heart. In point of fact, even within laboratory preparations,
where cardiac sarcomere length-tension relations are determined,
the fibres are irreversibly damaged when sarcomeres are stretched
to lengths beyond about 2.3-2.5 p i .
These four appropriate interpretations relate directly to the four
component misconceptions in the previous section (see The Major
Components of the Misconception). In addition to the misunderstandings which are included within the four misconceptions
(and which have been addressed), there are yet two phenomena
which contribute to the overall misconception of heart failure (the
MUM account) by their neglect within the account. If adequately
dealt with, these would likely mitigate against the development of
the observed misunderstanding.
124
The Effect of Variable Activation
The Effect of Hypertrophy on Size
Dilatation of the ventricle is inappropriately assumed to maintain

cardiac sarcomeres at extended lengths when this is only true in
situations of acute dilatation, and even then sarcomeres are not
extended to lengths which exceed those attainable in health. In the
chronic state of stress where heart failure usually ensues, hypertrophic compensation has normalized both length and, to a
substantial degree, stress on constituent sarcomeres, so that their
lengths are normal. Further, because of geometric considerations,
the chronically dilated ventricle can accommodate much more
increase in volume per unit of muscle stretch than is possible in a
heart of normal size.
These two phenomena (activation and hypertrophy) contribute
to the misunderstanding, principally by their inadequate incorporation within the account. They are germane to a more appropriate understanding, and their relative neglect perturbs
reasoning in complex ways, as will be discussed later.
To many expert cardiovascular physicians this discussion of the
principles pertinent to heart failure will have seemed unwarranted, since it restates what should be well known articles of
physiology. In fact, the main textbook used in the first year
cardiovascular course taken by our medical student subjects who
demonstrated the misconception contains a contemporary and
appropriate description of heart failure (Katz, 1977). The fact that
The ascending limb of the length-tension relationship is inappropriately mapped onto the Frank-Starling or cardiac function
relationship. This belies the fact that because cardiac muscle is
submaximally (twitch) activated, a large range of forces are
possible through variable activation at almost any given sarcomere length. The major part of the cardiac function curve occurs
at sarcomere lengths which correspond to the plateau (2.0 to 2.3
\im) and to that very small fraction of the descending limb of the
maximally activated skeletal length-tension relationship (from 2.3
to 2.5 pm) which can be achieved by cardiac sarcomeres. Because
of variable activation, even at sarcomere lengths between 2.3 and
2.5 |im the force generated by cardiac muscle rises rather than
falls.
125
the students could still manifest the misconception, despite direct

exposure to appropriate accounts, suggests that there is a complex
basis for the acquisition and maintenance of the misconception. A
detailed analysis of that complex basis is presented in the next
section.
GENESIS AND MAINTENANCE OF THE MISCONCEPTION
We have seen a pattern of misunderstanding of various concepts

associated with cardiac failure. The compounding of those misconceptions results in a commonly held but inappropriate interpretation of cardiac failure itself (the MUM account). Examination of
this web of mutually reinforcing misunderstandings reveals a
common element that has implications extending beyond learning
and instruction in the cardiovascular system to medical education
and education more generally. That common element is a
pervasive (yet frequently unnoticed) tendency to oversimplify
complex concepts. We call this tendency the Reductive Bias (see
also, Wimsatt, 1980; expositions of biases in judgment and decision making that are in some ways similar to, but not the same as,
the conceptual biases we address, can be found in Elstein, in press,
and in Kahneman et al., 1982). Potential implications of this bias,
extrapolating from the cardiac findings we have discussed, are
many undetected misunderstandings of complex biomedical
concepts and concerns about the prudence of some well established practices in education.
In what follows, we first illustrate the operation of the Reductive Bias in the component misunderstandings of the basis of
myocardial failure, discussing cognitive contributions on the part
of the learner, as well as contributions from instruction and
biomedical research. The misconception of heart failure is then
characterized as a reciprocating network of the component
misconceptions, a network in which the components interact with
each other and reinforce each other in various ways. Then we
discuss how the various forms of the Reductive Bias likewise
reinforce each other and reflect a general reductive "world view".
Following this, we discuss further the partial origin of the Reductive Bias and sources of its strength in common educational
practices. Finally, we discuss a potential remedy for this tendency
toward oversimplification in cognition and instruction.
126
The Role of the Reductive Bias in the Misunderstandings
In this section and the next, we provide a scenario for the development of the misconception of the basis of heart failure (the MUM)
and for the maintenance of this misconception. In developing this
account, we are guided by what appear to be two basic tenets of
the misconception: (i) an in vitro, skeletal phenomenon (the L-T) is
ultimately mapped in the misconception to an in vivo, cardiac one
(cardiac failure). These two phenomena, one skeletal and created
in the laboratory and the other cardiac and occurring in a natural
context, are two "anchor points7' of the overall web of misconception and must be connected in any account; (ii) within this mapping, physiological activational properties and morphological
aspects of compensatory hypertrophy in cardiac muscle are
relatively neglected.
The four misconceptions given earlier in the paper (see The
Main Components of the Misconception) appear to be the links
which tie together the two anchor points and provide for the
neglect of activation and the effects of hypertrophic adaptation.
Briefly recapitulating, these major contributors to the overall
misconception are: 1) that the length-tension (L-T) relationship in
skeletal muscle is accounted for exclusively by anatomical factors
(the Sliding Filament Theory); 2) that the L-T relationship of the
cardiac muscle cell is the same as that for skeletal muscle; 3) that
the Frank-Starling relationship is the collective counterpart of the
L-T relationship for individual cardiac cells; and 4) that cardiac
failure is attributed to cardiac cells being collectively stretched to
the descending limb of the L-T curve. We now illustrate the
possible role of various forms of the Reductive Bias within each of
the Four Misconceptions
First Misconception: The Whole Length-Tension Curve has an Anatomical Basis.
A. When students (and others) discuss the "length-tension
relationship", they most likely mean the L-T relationship for
isolated skeletal muscle. There are several reasons why this
particular L-T relationship should have special status (as compared to other length-tension curves). First, it is a classic teaching
example and most students are exposed to it. Second, it was the
first L-T relationship demonstrated and the only one for nearly 60
}
|
127
years. Third, even quality expositions of cardiac muscle function

in the literature take the skeletal muscle function as a prototype.
The plateau and descending limb of this length-tension curve
can be accounted for by the anatomical/mechanical Sliding
Filament Theory. Despite the fact that the ascending limb (short
lengths) has a more complex explanation involving physiological
activational processes, the entire curve is taken to have an anatomical basis.
Several influences probably contribute to the application of this

reduction in the present instance. One is a tendency of the
scientific enterprise to strive for unformity and, hence, elegance of
explanation (Occam's razor; see also Wiser and Carey, 1983).
When the Sliding Filament Theory was originally proposed by
Huxley (Huxley, 1957) as an account for the L-T relationship, the
application was restricted to the plateau and descending limb.
There followed a vigorous (albeit ultimately unsuccessful) effort
among the scientific community to extend the account to the
ascending limb. This striving for "good form" and consistency in
scientific explanation reinforces a similar tendency in human
cognition (Abelson et al., 1968; Koffka, 1935), and it is conceivable
that the latter may even be one contributor to the former. Yet a
third influence may lie in the procedures that were employed in
establishing the length-tension relationship for skeletal muscle
itself. The active tension developed by a muscle fibre is a function
of both activational processes and potential sites for sarcomere
binding related to anatomy. In establishing both the skeletal and
cardiac L-T curves, activational processes were controlled to
maximal levels, thereby further de-emphasizing the role of
activation. This third influence suggests its more general reductive
counterpart, as follows.
B. The degree of activation is a third "variable" which
moderates tension developed by muscle fibre at particular
lengths. Hence, the dynamics of muscle contraction are multidimensional. It is common experimental and teaching technique
Reductive Bias 1 (Uniformity of explanation). The whole of a system is like

some known part of the system. One explanation is better than many
explanations. Uniformity of explanation throughout the range of application
of a functional relationship is preferred to a plurality of explanations.
128
to address multidimensional phenomena by investigating relationships among subsets of the operative variables. The strategy is to
build from lower dimensionality to an ultimate understanding of
phenomena in their full dimensionality. The attribution of the
entire length-tension dynamic to length, colored as it is by ignoring the variable nature of activation (i.e., controlling it at one of its
values), suggests that this reassembly often does not occur.
C. Once the activational basis for the ascending limb of the L-T
was recognized, why was it the anatomical influence that was
overextended to the entire relationship rather than the activational
component? A likely reason is that the anatomical account is
much easier to teach and learn than the biochemical physiological
components, for a number of reasons. First, the anatomically
based Sliding Filament Theory is less complicated. It involves only
a few key elements (e.g., invariant filament lengths; shortening
occurs by relative filament translation) and, especially when
misinterpreted, is linear - the more potential binding sites the
more tension produced. In contrast, the process of activation
involves numerous interacting subcellular components and
processes (e.g., Ca4* release sites, binding proteins, ion pumps)
and the effects are nonuniform (e.g., activation works qualitatively
differently at different levels of anatomical extension). Second, as
we have seen, neat, easily envisioned, and cognitively productive
analogies are readily available to aid anatomical understanding
(for example, rowing crews and tug-of-war). Finally, details of the
physiological activational accounts are less well understood and
are more controversial in their particulars. Options and controversy are not as easy to handle in teaching and are not conducive to elegant structuring by the learner. (Anecdotal lore is
widespread among medical school teachers to the effect that
medical school students dislike competing or controversial
accounts).
Reductive Bias 3 (Teach toward the simple). If more than one concept is
involved in understanding a process, the harder concepts (e.g., those that are
non-mechanical, non-linear, multidimensionally interacting, or less well
Reductive Bias 2 (Reduction of simultaneously considered dimensions). In

multidimensional phenomena, concentrate in turn on the effects of subsets of
the total dimensional space, with the faith that the full multidimensionality
can and will be reassembled.
129
established) are neglected. Either they are not taught, or if taught, they are
presented cursorily, with less vigorous justification and without full modeling.
K
/
Reductive Bias 4 (Confirmation bias). Evidence is sought to support beliefs that

are already held.
Reductive Bias 5 (Tangential importations of evidence). Desired oversimplifications are bolstered by the importation of superficially related but logically
irrelevant evidence from elsewhere.
So, a confluence of oversimplifications leads to the misconception

that the full scope of the L-T relationship has an anatomical basis
in the Sliding Filament Theory.
D. According to Reductive Bias 3, there is a tendency for the

more difficult aspects of the L-T relationship either to be ignored
or to be treated superficially. How can concepts be neglected, just
because they are pedagogically difficult? One way is by independently bolstering the simplification. Here, additional support
comes from the proliferation of other findings related to the
Sliding Filament Theory. An example is the observed similarity in
ultrastructural morphology of the cardiac striated muscle to that
of skeletal muscle, which in the case of skeletal muscle supported
the sliding filament account for its descending limb. The greater
the frequency of empirical findings (however partial or qualified
they may be) supporting anatomical accounts of L-T relationships,
the more likely one is to accept an exclusively anatomical account
of the complete L-T relationship. Conversely, since the state of
knowledge with respect to the role of physiological activation
processes in the L-T relationship is not nearly so advanced,
attention to that aspect is not forced.
Of course, the fact that the morphological basis supporting the
sliding filament account of the right side of the length-tension
relationship for skeletal muscle is replicated for heart muscle, has
no logical bearing on the extension of the right side account to the
left side, within skeletal or cardiac muscle. However, the important factors operating here are not logical, but psychological.
People use as evidence that which is most likely to support the
conclusions they already want to draw (Festinger, 1957; Lord et ah,
1979).
130
Richard L Coulson et al.
Second Misconception: The Length-Tension Relationship for Cardiac Muscle is the Same as for Skeletal Muscle.
Reductive Bias 6 (Homogeneity of components). Explanations that account for

one component of a system will account for other components of a similar
type.
B. Evidence does now exist that skeletal and (a type of) cardiac
muscle produce similar but not identical length-tension relationships. The demonstration of a length-tension relationship for
cardiac muscle comparable to that of skeletal muscle bolsters what
had previously been an unsupported step in the chain of misconceptions. This superficial support also has the negative effect of
reinforcing other missteps in the argument that depend on cardiac
muscle being like skeletal muscle (see Reductive Bias 5). If some
aspects of cardiac muscle function are like those for skeletal
muscle (e.g., potential for the generation of tension increases [to a
point] as function of length, and there are anatomical accounts for
parts of both curves), then it is easier to transport other attributes
from the skeletal to the cardiac muscle domains. These
overextensions might include overattributions of activational
similarity, e.g., that cardiac, like skeletal muscle, functions at full
activation.
Reductive Bias 7 (Extension of attributes). If A is like B with regard to X, then A
will be like B with regard to Y, Z, and so on.
A particularly poignant example of this kind of overextension

pertains to the "descending limb" of the cardiac muscle lengthtension relationship itself. Since cardiac muscle only achieves
lengths corresponding to a small fraction of the descending limb
of the skeletal muscle L-T curve, and even there the potential for
tension is still rising, a descending limb (beyond 2.3-2.5 jim) for
cardiac muscle is a hypothetical extrapolation (a literal extension);
A. The (overgeneralized) anatomical account of the lengthtension relationship in skeletal muscle is ultimately transported to
cardiac muscle. Prior to 1959 there was not even evidence that
skeletal and cardiac cells generated comparable maximally
activated length-tension curves. When the overextension in
reasoning was made prior to this time, it was probably supported
by a tacit presupposition that "all muscles are alike".
131
the descending limb for cardiac muscle would be like that for
skeletal muscle if there were a descending limb for cardiac muscle
- which there isn't.
'
W
L
j5
Reductive Bias 8 (Experimental orchestration). Configure experimental

situations to maximize transfer of existing methodologies and to enhance the
likelihood of hypothesized outcomes.
f.
D. Furthermore, one thing that ultimately makes possible the

line of reasoning that concludes that myocardial fibres fail collectively for anatomical reasons, is the assumption that the way
isolated entities function is representative of the way they function in the context of other entities. Support for such a belief is
provided by the analytic research strategy under consideration,
which bolsters the idea that the way isolated preparations function in the laboratory in the same way that they function in vivo.
Behavior of isolated preparations studied in the laboratory may be
fundamentally different from their intact function in natural
contexts.
The danger is that the researchers' strategy will spread to the
consumers of that research (teachers and students in the medical
education system) and become something more than a research
strategy: an assumption about the nature of the world. The world
C. It is worth noting the ways that medical research strategies

are implicated in the chain of oversimplification-based misinterpretation. For example, even though evidence was eventually
assembled that cardiac and skeletal muscles exhibit similar lengthtension relationships, this was achieved only through great effort
at reducing inherent differences in the two kinds of muscle. First,
the particular kind of cardiac muscle chosen for study, papillary,
was the type most like skeletal muscle in various pertinent aspects
(e.g., anatomic linearity; relatively well delineated end-points
conducive to mounting in preparations). Second, means were
found to forcibly maximally activate the cardiac muscle to
artificially induce tetanic contractions, contrary to the muscle's
more normal constraints of "twitch" activation (Cooper, 1976,
Gibbs and Loiselle, 1978). Thus, ecological invalidity was built
into the laboratory demonstration of the cardiac L-T relationship,
partly for reasons of procedural convenience, and perhaps partly
to enhance the possibility of demonstrating the anticipated effect.
132
Reductive Bias 9 (Atomization and Extirpation). Context does not matter. If

something works under idealized conditions in the laboratory, separated from
context, it will work in more complex and dynamic natural situations.
Properties and dynamic operation of materials in isolation faithfully reflect
properties and dynamics in fuller contexts of operation. Parts are microcosms
of the whole.
So, cardiac muscle is like skeletal muscle, and, since isolated

skeletal muscle loses tension and "fails" for anatomical reasons (if
stretched too far, it pushes the L-T curve into its descending limb),
cardiac muscle also loses tension and fails for that reason.
Third Misconception: The Frank-Starling Relationship is a Collective
Length-Tension Relationship.
A. The Frank-Starling relationship is treated as a collective in
vivo counterpart of the length-tension relationship of isolated
cardiac muscle (equated with the classical skeletal L-T). In essence,
this involves attributing to intact cardiac muscle in its natural
context the characteristics which individual fibres display in
isolation. The functioning of a collection of fibres is additively
adduced from properties of the isolated fibres that compose the
collection. The possibility of emergent properties is ignored. In
part, this may be attributable to a kind of "converse" to Reductive
Bias 9, involving the presumption of insulation from synergistic
effects.
Reductive Bias 10 (Insulation from synergism). The whole is equal to the sum
of its parts. Complex phenomena are simple combinatory assemblages of their
elements. The heart will behave like isolated cardiac muscle preparations.
is made up of parts, and characteristics of parts will remain the

same whether studied in isolation or within functioning context.
So all one needs to do is study the parts, or particular aspects of
the parts, and infer the rest. Given the general predisposition to
simple accounts we have proposed, this view would be primed
for acceptance. Add to this the credibility of eminent researchers
and much of scientific tradition that seems to support the
metaphysical assumption of analytic simplicity, and it is not
surprising that this assumption permeates much of biomedical
learning and instruction. Why would all those researchers value
research with isolated preparations if it lacked ecological validity,
if that was not the way the world was organized?
133
Reductive Bias 11 (Analogy treated as isomorphism). Analogy is interpreted

more strictly than it should be. Relations that bear superficial similarity are
treated as being the same relations, based on the same underlying
mechanisms.
Interestingly, an analogical correspondence between muscle

activation in the L-T base domain and cardiac contractility in the F-S
y
I
I
j
&
domain could also be made and would be most helpful in fostering a more appropriate understanding of heart failure. However,
it is just this correspondence that appears to be underutilized in
favor of a mechanical, anatomical account. This is perhaps not
surprising, since the activational component of L-T is often
systematically controlled out (held at maximal value) in laboratory
demonstrations (see earlier discussions). Students and others may
not think to represent an analogue of activation in the F-S domain,
because they do not recognize that it exists in the base (L-T)
domain.
B. At least two influences would seem to contribute to the

operation of Reductive Bias 10 (as well as Reductive Bias 9) in the
present instance. First, although collective, in vivo cardiac function
is not the same as isolated cell function, similarities do exist which
make the two situations appear analogous. Analogy involves the
mapping of entities and (especially) relations among them in a
"base domain" to entities and relations in another domain, the
"target domain" (Gentner, 1983). Points of slippage in the
mapping must be recognized, because analogous domains are not
identical. With the L-T relationship as base domain and the FrankStarling relationship (F-S) as target domain, several correspondences exist which promote and support the analogy. For example, length (L-T) is similar to ventricular volume (F-S), and
tension (L-T) is similar to ventricular pressure which produces
cardiac output (F-S). Also similar are the general shapes of the two
curves representing the fundamental relationships in the two
domains. A danger in analogy, and what appears to be happening
in the faulty reasoning chain, is that the dissimilarities can be lost
in the superficial similarities. For example, volume is not length,
and the details of the geometric relationship between them
underscore the difference between the range of sarcomere lengths
achieved within a length-tension curve and the relatively
restricted dynamic ranges that can be operative in a heart (see
Figure 3).
134
Fourth Misconception: Cardiac Failure Results from Overstretching

Sarcomere Filaments.
The set of applications of the Reductive Bias, taken together,
supports the overall misinterpretation of cardiac failure as having
an anatomical basis that it could not, in view of current understanding, actually have. Physiological, activational processes
which are, in fact, most germane tend to be de-emphasized.
A. In addition, there may be yet another Reductive Bias in
operation which serves to bolster and reinforce the overall interpretation. It is related to the fact that the failing heart frequently is
enlarged, a classical sign of failure. The question is the causal
direction - does the heart fail because it gets big, or, more accurately, does it get big because it fails? The additional reduction
involves glossing over the many details of causal mechanism
involved in a correlation, enabling simpler but erroneous causal
attributions (e.g., that the overstretch of the heart causes the
failure).
A second contributor to overextension of in vitro muscle function to in vivo heart function may involve a chain of analogies. The
first step involves the correspondence between isolated and intact
(in vivo) skeletal muscle. Whole skeletal muscle does better reflect
individual L-T characteristics, largely because skeletal muscle
naturally functions at maximal activation. It is another small step
from isolated skeletal muscle to cardiac papillary muscle which
resembles skeletal muscle in some, but not other, pertinent ways.
Then, since isolated and collective skeletal muscle operation are
similar, and since isolated papillary muscle is like isolated skeletal
muscle in some ways, it is only another small step to generalize
from papillary muscle to more general cardiac muscle. Like the
parlor game of "Russian Scandal", each analogical step introduces
only relatively small losses in correspondence, but the loss across
the whole chain is great.
So, if the entire skeletal length-tension curve has an anatomical
basis in Sliding Filament Theory, the cardiac L-T curve is the same
as that for skeletal fibre, and the Frank-Starling cardiac function
relationship is just a generalized restatement of the L-T relationship, then it would follow that heart failure has an anatomical
basis in an "overstretch" of its individual sarcomeres.
135
Reductive Bias 12 (Attributing directional causal status to correlation). The

causal mechanisms underlying correlational relationships are glossed over,
promoting fallacious causal attributions.
B. Contrary to the basic tenet of this misconception is the fact

that when the heart gets "big" the sarcomeres become shortened
to unstressed lengths. This is a result of the hypertrophic adaptation process which, we have argued, is generally neglected in the
overall account of heart failure. Why do students not incorporate
these processes into a more appropriate understanding? This
neglect appears to be a particularly good example of the application of Reductive Bias 10, Insulation from Synergism. The growth
processes that lead to normalization of sarcomere lengths in
response to stress (including increased volume) are clearly
properties of in vivo heart muscle and have no counterpart in the
isolated muscle dynamics which contribute so heavily to the
MUM account. A particularly pertinent set of dynamics is neglected in an attempt to assemble whole heart function from
information about the isolated behavior of some of its pieces,
ignoring synergistic effects.
Mutual and Circular Reinforcement of the Component Misconceptions
Four intermediate, or "stepping-stone", misconceptions which

serve to link the skeletal length-tension relationship to the ul-
Furthermore, we suspect that the "bigness" of hearts in failure

serves as a cognitive cue both for eliciting and supporting a
mechanical overstretching argument for heart failure. Would
students so widely engage a sarcomere elongation argument to
account for an in vivo skeletal muscle that has somehow "failed",
i.e., is failing to develop normal force? We suspect that they would
not (even though intact skeletal muscle is one step closer to the
classic length-tension curve) because an "overstretch" of such
muscle is so clearly constrained by bone attachments. In contrast,
the potential for "bigness" and overstretch seems relatively unconstrained in the heart. A concomitant "bigness" does exist in heart
failure, and we speculate that its effect cognitively spreads back
(Anderson, 1983), via the semantic closeness of the ideas of
"enlargement" and "long length", to further elicit and bolster
notions of failure based on the extension of fibres.
136
First, ideas embedded within the misconception bolster and feed back
on each other in complicated ways. One way is global, through the
influence of pervasive colorations provided by some major themes

that thread through the account, producing theme-related spreading activation (Anderson, 1983). An example is the theme of "size"
and attention to size. Size is a dominant aspect in the lengthtension relationship through the salient property of length, in the
Frank-Starling relationship through volume, and in the largeness
of the failing heart. This recurrence of the theme of size helps to
interlock the components of the misconception, lending credence
to the component misconceptions themselves and to the overall
misconception synergistically. This is ironic, in that if "size" in its
relationship to activational and hypertrophic processes were
understood better, the notion of size could serve to enervate
rather than strengthen the entire network of misunderstandings.
In addition to these global thematic effects, some sets of ideas
are intertwined and reciprocally bolster each other in circuitous
timate misconception of heart failure (the MUM account) have

been presented. The ways that the hypertrophic adaptation
process and activational dynamics of cardiac muscle become deemphasized in this linkage have also been indicated. Each misconception has been tied to certain ways of thinking (the Reductive
Biases) which serve to generate and support each misconception.
The manner of exposition we have used has conveyed a sense of
"syllogism" - that the mistaken ideas largely flow from one to
another to an end point. This exposition no doubt captures some
realities of the situation, but even within the exposition elements
of multi-directionality began to emerge - most specifically in the
reciprocating effects of "big hearts" in failure, i.e., misconceptions
that reinforce the notion that the heart fails due to overstretching
are themselves bolstered by that conclusion.
We now turn to a discussion of this view of the overall misconception (an idea) as a tangled web or reciprocating network of
component ideas, a network that is closely coupled to the influences that produce and maintain it. It is this multifaceted, weblike nature that we believe contributes to the tenacity of the
misconception. Such a structure, involving widely distributed and
mutually supportive components and influences, may account for
why our students continued to hold the misconception despite
exposure to more appropriate accounts. This web-like nature
manifests itself in various ways.
ways. For example, the belief that cardiac muscle is like skeletal
muscle makes it easier to believe that cardiac muscle has a descending limb within its length-tension curve. In turn, the neglect
of activational factors within muscle function leaves an anatomical
mechanism as the only plausible means for providing an account
for cardiac failure. Within a mechanical account, the most
plausible way to account for loss of "strength" in a muscle is
through disinterdigitation of its filaments. This further disposes
one toward believing that a descending limb exists for cardiac
muscle. Thus multiply bolstered, belief in the existence of a (nonexistent) cardiac descending limb, in turn, is a keystone in the
entire Mechanical Ultrastructural Mechanism account of heart
failure.
Another example is in the constellation of ideas surrounding
what is, in essence, the belief that the Frank-Starling relationship
(at least the "healthy part" and, hence, normal heart function) has
its basis in the ascending limb of the length-tension curve. This
belief appears to be supported through a web of reciprocating
confluences. Because the cardiac L-T has a left-side similar to that
of the skeletal L-T, it is easy to think that the Frank-Starling
relationship is a manifestation of the length-tension relationship,
because in both situations "longer is stronger"; that is, as expressed by many of our subjects, "up to a point" greater muscle
size produces more "force". Also, since anatomy explains well the
descending limb and top of the skeletal L-T relationship, it is easy
to believe that it explains the ascending limb. If one thinks that
anatomy explains the left side, then activational explanations for
the L-T are not needed anywhere. Since the Frank-Starling relationship looks like a left-side L-T relationship, it is easy to believe it is
one. If activational explanations for the left side of the L-T are not
needed, then they are not needed for the Frank-Starling relationship. Further, the microstructural differences in sarcomere lengths
achievable in both situations (L-T and F-S) are opaque and, hence,
are susceptible to mental construal to support belief. The overall
result of this complex pattern of reciprocation is a belief that
normal heart function, as reflected in the Frank-Starling relationship, is a matter of creeping down (or up) the left side of the
length-tension curve; in fact, most of the Frank-Starling
phenomenon occurs at sarcomere lengths on and near the plateau.
If it is believed that normal heart function is a matter of traversing
the left side of the L-T, then it is a simple logical jump to the MUM
137
138
account, that is, that failure is a matter of "falling over the top", to
a descending limb.
A second reason why our "syllogistic" exposition is an oversimplified
portrayal is that the steps of reasoning among the misconceptions are
Third, the reductive ways of thinking, the Reductive Biases which

contribute to producing the misconceptions, also reinforce each other.
This reinforcement appears to be involved, for example, in the

general neglect of physiological activational properties of muscle
in the faulty MUM account. The tendency to seek elegant and
uniform explanation (Reductive Bias 1 - RBI), which disposes
toward a single mechanical account for the L-T, is reinforced by
laboratory demonstrations of the length-tension relationship
which hold the activational component constant (RB2). The
appropriateness of holding activation at maximal levels is
bolstered by the particular kind of muscle, skeletal, involved in
the demonstration (RB9). Extrapolations to the cardiac domain are
accomplished via papillary muscle (RB6). Since papillary muscle
is like skeletal muscle in some ways, it is easier to assume that
activational properties are similar in the two kinds of muscle
(RB7) and, hence, that variable activation is not important.
Fourth, even though for purposes of exposition each Reductive Bias
has been tied to a single misconception, each one actually applies in
many places across the network of misconceptions. Consider some
examples. The relatively simple anatomic view of heart failure

may be bolstered by wanting it to be that way; if Reductive Bias 1,
Uniformity of Explanation, operates at the level of the lengthtension relationship, why not at the level of heart failure itself? It
would be handy and cognitively efficient if it too had a simple
mechanical account (especially one that correlates well with
classic, practically assessable clinical signs). In this view, the same
reductive bias operates on the conclusion (as well as the premises)
of an argument, and in so doing, contributes further support to
the premises that are supposed to establish the conclusion.
multi-directional. In our exposition, we have shown how the faulty

understanding of heart failure could progress from an inititial
focus on the (misconceived) length-tension relationship, the first
step in the reasoning chain. But a person may also begin at the
end of the chain, by thinking about heart failure. In trying to
decipher a possible cause, the big heart associated with failure
makes it easy to step backwards and to find a plausible basis for
failure in the right side of the length-tension curve.
139
1. Motives. Dispositions to want to see things as simple (e.g.,

RBI).
2. Beliefs. A metaphysical presupposition that complex things
can be decomposed or treated in their partial aspects and still
retain their essential nature (e.g., RB9).
3. Manipulation operators. A set of ways of manipulating the
environment to constrain it to reflect simplicity (e.g., RB2).
4. Evidence operators. A set of ways of interpreting evidence to
enable it to conform to oversimplified belief (e.g., RB5).
Taken together, the set of reductive biases reflect a way of thinking about complex things - a reductive "world view". This world
view involves wanting and believing phenomena ultimately to be
simple, and configuring the world to appear that way.
Reductive Bias 13. (Configure toward desired simple view). Spuriously bolster
all components of a chain of argument that support the desired simple
conclusion to the argument. Configure the environment to assure result.
To summarize, the development, structure, and maintenance of

the Mechanical Ultrastructural Mechanism as a misconception of
heart failure embody a set of entangled influences that elicit and
support each other in complex, non-linear ways. Some of the
influences that foster and maintain the web are cognitive (what is
easy to do in the mind), some are educational (what is easy to do
in conveying subject matter), and still others are in some norms
and practices of science (what is easily controllable in the
Another example pertains to Reduction of Simultaneously Considered Dimensions (RB2), as well as to aspects of RB3, Teach
Toward the Simple. These biases are manifest in two-dimensional
textbook presentations of the L-T curve (as opposed to multidimensional surfaces) with activation held at one value, in similar
two-dimensional presentations of the Frank-Starling relationship
with the contractile dimension not represented, and in research
demonstrations of both of these phenomena.
That the reductive biases apply in many places and reinforce
each other is an indication that they reflect a general way of
thinking. The set of reductions we have enumerated fall into four
discernible groups (with, of course, some overlap), all related to
some aspect of simplifications:
140
laboratory). The misconception itself is a network. Running

through and underlying this web of mutually and circularly
supporting misconceptions is a pervasive predisposition in
instruction, learning, and research towards simplicity and
simplification.
The Reductive Bias and Medical Education
We have seen a variety of manifestations of the Reductive Bias.

These manifestations are characterized by a tendency to portray
things simply. This tendency is common in the educational
(instructional and learning) process. Sometimes it is satisfied by
imputing too much uniformity to a concept, sometimes by overgeneralizing behavior of an entity in isolation to its behavior in the
ecological context of other entities, sometimes by overextending
by analogy information about one entity to superficially similar
entities, sometimes by presuming more well-formed regularity of
a concept than is warranted, sometimes by assuming that
prototype examples (e.g., "textbook" cases or "classical" rules of
clinical data interpretation) are more characteristic of complex
realities than they actually are (Feltovich et ah, 1984) and so on.
The Reductive Bias is an insidious educational phenomenon for
several reasons (Spiro et ah, 1987). First, it comes in many forms.
Second, its operation tends not to be noticed: as in the unconscious first principles or thematic biases found to govern scientific
inquiry (Holton, 1973), the Reductive Bias tends to involve unquestioned axiomatic presuppositions governing teaching and learning. Third, there are many tacit incentives in education to simplify
complex topics of instruction: it makes things easier for teachers to
teach (and to be liked by their students), easier for textbook
writers, easier for students to take notes, prepare for exams, and
attain a satisfying (but false) sense of understanding, and easier
for exam constructors and graders. Fourth, the Reductive Bias has
wide potential scope of application: many biomedical science
concepts are characterized by complexity, and many contexts of
knowledge application or clinical practice are complex and illstructured. This makes learning difficult and encourages various
forms of simplification in instruction.
It should be understood that the Reductive Bias is not meant to
refer to the legitimate incorporation of simplification strategies
within instructional sequences. Approaches that employ carefully
141
Addressing the Problem of Educational Oversimplification
All that we have said may elicit agreement, yet draw the response,
"But what can be done about it?" We believe that there are directions to take which may offer help, and that in any case there is
something that should surely be done.
There has been a revolution in cognitive and instructional
theory in the last ten years (Glaser, 1978, 1982; Spiro et ah, 1980).
Much of it has been spurred by the recognition that useful approaches to a psychology of cognition and instruction must deal
with the fuller complexities of human thinking and subject
matters as they exist in substantial domains of practice and
directed, incremental introduction of complexity (i.e., approaches

that move from the simple to the complex) can be effective and are
often necessary (Glaser, 1984). However, under certain conditions,
such approaches are susceptible to hazards of the sort illustrated
in this paper. First, oversimplified initial versions of a concept can
yield a fake sense of understanding, aborting the pursuit of
deeper understanding. The more complex and multifaceted the
concept, the more acute this problem can become, because partial
misunderstandings can reinforce each other. Second, instructional
attempts to challenge and change a student's oversimplified
conception, in order to raise it to a higher level of sophistication,
may fail. Discrepancies with the simpler, cognitively satisfying
model will be minimized by the student, so that the student's
model can be retained. Discrepant aspects of the concept may go
unnoticed or, if noticed, may be filtered toward the model already
held. Attempts to make local adjustments in this model will
override fundamental reformulations. Third, educational
strategies that address complex concepts by focusing on their
simpler components (with the hope of building toward assembly)
may encounter yet another kind of problem. It is the inherent
nature of some concepts that their components are inextricable
from their organic functional context (as in the phenomenon of
heart failure). Such concepts involve synergistic properties or
interactions among numerous variables. For concepts of this sort,
any decomposition is a fundamental misrepresentation. The
components cannot be made to "add-up" to the whole, and there
is no instructional alternative but to find means to convey the
irreducible complexity in a tractable way.
142
NOTE
* This research was supported by a grant from the Josiah Macy, Jrv Foundation,
Grant No. B8S2001. The paper does not necessarily reflect the views of the
Foundation.
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RICHARD L. COULSON, PAUL J. FELTOVICH, AND RAND J.

FOUNDATIONS OF A MISUNDERSTANDING OF THE

A fallacious explanation of the syndrome of congestive heart

The Journal of Medicine and Philosophy 14:109-146,1989.

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ABSTRACT. A misconception regarding the ultrastructural basis of myocardial

BACKGROUND: PERTINENT PHYSIOLOGICAL PRINCIPLES

Playing central roles in the misconception are the length-tension

A general principle centrally involved in the misconception is the

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development and persistence are addressed. It is shown that the

Misunderstanding the Basis of Heart Failure

SARCOMERE LENGTH CMICRONS)

Fig. 1. Skeletal Length-Tension Relationship.

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Richard L. Coulson et a\.

SARCOMERE LENGTH CMICRONS)

Fig. 2. Length-Tension Relationship of Cardiac Muscle.

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Misunderstanding the Basis of Heart Failure

Investigation of Cardiac Muscle

Investigation of isolated mammalian cardiac papillary muscle in

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the curve (Figure 1). Progressive lengthening of the sarcomere

Richard L. Coulson et al.

The long-standing empirical observations of Frank (Frank, 1895)

The process of cardiac hypertrophy (the growth of heart muscle

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However, while isolated skeletal and cardiac muscles do reflect

Misunderstanding the Basis of Heart Failure

SARCOMERE LENGTH CMICRONS)

Fig. 3. Frank-Starling Relationship of the Heart Transposed to

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THE INAPPROPRIATE ACCOUNT OF HEART FAILURE

The inappropriate explanation of heart failure can be summarized

This characterization is a synthesis of descriptions of heart failure

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hypertrophic adaptation process intervenes when diastolic

Misunderstanding the Basis of Heart Failure

length-tension relationship, and that heart failure results from the

The second description is from an established cardiac physician

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Richard L. Coulson et al.

In our laboratory, similar explanations of heart failure as

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A third account which is particularly reflective of the synthesized

Misunderstanding the Basis of Heart Failure

available evidence. Before proceeding to a more appropriate view

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Richard L. Coulson et a\.

3. The cardiac length-tension relationship (equated with the

4. Since the classical length-tension relationship of muscle would

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Previously I was discussing the length-tension relationship and bringing into

Misunderstanding the Basis of Heart Failure

APPROPRIATE INTERPRETATIONS OF PRINCIPLES

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Although the foregoing view of cardiac muscle function and heart

Richard L. Coulson et al.

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account well for the Frank-Starling mechanism for two reasons.

Misunderstanding the Basis of Heart Failure

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