EMERGING TECHNOLOGY REVIEW
Gerard R. Manecke, Jr, MD
The Heart: Pressure-Propulsion Pump or Organ of Impedance?
Branko Furst, MD, FFARCSI
H EMODYNAMIC MONITORING and support of circu-
lation are at the center of acute intervention-based
specialties such as anesthesiology and critical care. In spite of
the general assumption that the understanding of basic and
clinical hemodynamics is relatively complete, clinicians often
invoke a number of reasons to explain away the discrepancies
between the commonly used mental model of circulation and
various pathophysiologic states. A cursory review of the
literature on treatment modalities of various hemodynamic
states over the past several decades suggests that this mental
model has undergone a steady revision. For example, contrary
to expectations, the results of a 2012 intra-aortic balloon pump
(IABP)-Shock II randomized, open-label multicenter trial found
no difference in 30-day mortality (40%) in patients with acute
myocardial infarction associated with cardiogenic shock and
treated with combined pharmacologic therapy, percutaneous
intervention and IABP, or with pharmacologic therapy and
percutaneous intervention only.1 Results of the recently pub-
lished follow-up study confirmed the original outcomes.2 On
the basis of previously reported meta-analyses and conflicting
evidence from data registries, joint American College of
Cardiology and American Heart Association, together with
the European Society of Cardiology, downgraded the class of
recommendation for IABP use from class IB (should be used)
to IIbB (may/can be used).3
In the wake of these findings, some have questioned the
recommendations of potentially harmful adjunct therapies,
namely, the use of intra-aortic balloon pumps, in this high-
risk group of patients based on “pathophysiologic assumptions
and expert opinions” rather than on randomized clinical trials.4
Moreover, in the editorial to this landmark study, O’Connor
and Rogers submitted that “the results of the IABP-SHOCK II
trial parallel those from many recent outcome trials that have
challenged the understanding of the management of acute and
chronic heart failure, including those regarding the use of
pulmonary artery catheters and the role of revascularization in
ischemic cardiomyopathy.”5
Similarly, the emerging modalities in pharmacologic therapy
of acute and chronic heart failure further question the funda-
mental understanding of the circulation. Most notable is a shift
from the use of potent sympathomimetic amines (epinephrine,
isoproterenol, and dopamine) in the 1960s and 1970s,6,7 to a
widespread use of vasodilators (dobutamine and milrinone). On
the contrary, the use of inotropes (dobutamine and milrinone)
currently is reserved for the treatment of a minority of patients
with severe systolic dysfunction who do not tolerate vasodilators
due to hypotension.8 Data from the ADHERE registry showed
that fewer than 3% of acute heart failure patients (from a group
of 150,000) had a systolic BP of o90 mmHg,9 and of
Journal of Cardiothoracic and Vascular Anesthesia, Vol ], No ] (Month), 2015: pp ]]]–]]]
Section Editor
approximately 14% of those who were treated with inotropes,
19% had higher mortality compared with non-inotrope-treated
patients (14%).10 Practice guidelines of the Heart Failure Society
of America (HFSA), the American College of Cardiology
Foundation/American Heart Association (ACCF/AHA), as well
as the European Society of Cardiology (ESA) therefore recom-
mend the use of vasodilators and deemphasize the use of
inotropes in the management of acute heart failure syndromes.11
It is of note that, from the range of available inotropes,
dobutamine and milrinone are chosen for their significant
vasodilatory effect. In addition, the use of ß-blockers is
recommended universally in all patients with stable mild,
moderate, and severe heart failure with ischemic or non-
ischemic cardiomyopathy and reduced LV ejection fraction.12
The question naturally arises as to whether or not the above-
mentioned treatment modalities and recommendations arose
from poorly designed trials or whether or not the understanding
of pathophysiologic mechanisms involved is in need of
“renewed growth and development.”5
A number of other examples challenge the understanding of
the basic tenets of circulation, such as the curious phenomenon
of increase in cardiac output during aortic cross-clamp by up to
25% in a controlled experimental setting13 and, in some
patients, during aortic surgery.14 The Fontan repair used for
surgical correction of various hypoplastic right and left heart
syndromes (HLHS) presents a yet-to-be explained hemody-
namic paradox which, in the absence of the right heart
complex, the single, often weakened, ventricle supposedly
pumps the blood through systemic and pulmonary circula-
tions.15 There are a large amount of conflicting data from
exercise physiology in which the concept of a muscle pump has
been evoked in order to explain the greatly increased systemic
blood flows that exceed theoretical limits of the heart’s
pumping capacity. Review of literature suggests that increased
cardiac outputs can neither be ascribed to the heart (on account
of a greatly shortened diastole that precludes adequate filling)
nor to contracting muscles.16
From the Department of Anesthesiology, Albany Medical College,
Albany, NY.
Address reprint requests to Branko Furst, MD, Department of
Anesthesiology, Albany Medical College, 47 New Scotland Avenue,
MC-131, Albany, NY 12208. E-mail: furstb@mail.amc.edu
© 2015 The Authors. Published by Elsevier Inc. All rights reserved.
1053-0770/2601-0001$36.00/0
http://dx.doi.org/10.1053/j.jvca.2015.02.022
Key words: blood circulation, pressure-propulsion model, impe-
dance model, cardiac output control, nonequilibrium, systems
1
2 FURST
From the physiologic perspective, the heart is considered to
be a dual pump, driving the blood through pulmonary and
systemic circuits arranged in series. In the course of an average
life span of 75 years, the heart, weighing around 350 grams,
pumps 400 million liters of blood (the amount that fills a lake
1 km long, 40 m wide and 10 m deep)17 through a system of
conduits with the total length of about 100,000 km. Consider-
ing the fact that the diameter of the red blood cells frequently
exceeds the width of the capillary beds, the heart as a pump
truly performs a prodigious task.
The idea that the heart is a pump providing the total
mechanical energy for blood’s propulsion has dominated the
field of cardiovascular physiology for well over a century. A
detailed discussion of the history of the propulsion pressure
circulation model is beyond the scope of this article,18 but even
a cursory look at the leading medical journals in the 1850’s
showed that there was a lively debate among the proponents of
the heart-centered circulation model who supported the view
that the heart is the “motor” of the circulation, and those who
maintained that the “capillary power,” or the force from behind
(vis á tergo), played a principal role in blood’s propulsion.19 It
should be noted parenthetically that the classic concept, vis á
tergo, goes back to antique medicine when it played only a
secondary role to vis á fronte, or “force from the front,” which
referred to suction forces (vacuum) working locally, (eg,
ventricular diastolic suction) and at a distance, akin to
gravity.20 By the 1950s, these concepts still were mentioned
in physiologic texts for historic interests 21–23 but, largely bereft
of their original meaning, slowly acquired a new identity. The
force from behind now assumes the dominant role as pressure
generated by ventricular contraction, pushing the blood through
the capillary beds back to the atria. A portion of this force is
stored in vessel walls as elastic energy and is represented in the
concept of the mean systemic pressure (Pms). The force from
the front, on the other hand, became a generic term for a host of
phenomena ranging from ventricular diastolic suction and/or
respiratory pump, which facilitate filling of the heart, to a range
of factors that impede venous return.22 The latter became the
mainstay of Guyton’s venous return model of circulation
discussed in the following section.
Over time, the pressure-propulsion (PP) model has become
deeply engrained in the collective subconscious and, with few
exceptions, virtually has remained unchallenged. It is suggested
that in the light of rapidly accumulating growth of information
obtained with the help of in-vivo experimental and clinical
imaging modalities, the number of discrepancies between the
observed phenomena and the constraints imposed by the
existent circulation model is likely to increase. It is the purpose
of this article to present some of the recently collected evidence
against the commonly accepted PP model of circulation and to
propose the conceptual framework for a new, more complete
understanding of the circulatory phenomena.
In the first part of the article a brief historic outline and the
salient features of Guyton’s venous return (VR) model of
circulation are discussed as well as the reason for its incon-
gruence with the left ventricular (LV) model of circulation.
Attention then is turned to the heart and to ways in which its
mechano-energetic function compares to a standard hydraulic
pump. Work on isolated heart preparations demonstrates that
the heart is unable to maintain constant pressures or flow in
face of the changing loading conditions and suggests that it is a
rather inefficient pressure-propulsion pump. It is proposed that
the heart functions by interrupting the flow of blood already in
motion; that is, as an impedance pump, whose mechanical
action can be compared to a hydraulic ram. It is further
suggested that in place of the mechanistic PP model, the
biologic model of circulation be adopted in which the blood is
a self-moving agent driven by the metabolic demands of the
tissues. The evidence in support of this model comes from
observations of the embryonic circulation, through comparative
anatomy and from phenomenology of the mature circulation. It
is then shown that the conceptual framework for the PP model
is rooted in the principles of a thermodynamically closed
system, which, according to current understanding, no longer
adequately describes the biologic phenomena in general and, as
proposed in this article, the circulatory system in particular.
Finally, the phenomenon of autonomous blood movement is
discussed in the context of open-systems biology.
WHAT CONTROLS CARDIAC OUTPUT?
In spite of the general assumption that the heart provides the
total mechanical energy for blood propulsion, the experimental
observations have polarized basic scientists and clinicians into
2 opposing views concerning the control of cardiac output
(CO). While proponents of Guyton’s VR model contend that
the peripheral circulation plays the dominant role in control of
CO, adherents of the LV model ascribe this role, by default, to
the heart.24–27 Since the ultimate source for blood propulsion in
both models can be traced to the hydrodynamic equivalent of
Ohm’s law (where the power source for the circulating blood
clearly originates in the pump, ie, the heart), those seemingly
opposing views differ only on the surface but not in essence. It
is apparent that this central issue in cardiovascular physiology
will not be resolved until the fundamental question (“What
makes the blood go around?”)25 is considered not only in the
light of the conventional model but also from the observed
circulatory phenomena themselves.
GUYTON’S VENOUS RETURN MODEL
Between the 1950s and 1970s, Arthur Guyton and cow-
orkers developed a circulation model that has, in due course,
become almost universally accepted. At the core of the model
is the idea that venous circulation plays a central role in control
of CO. The starting point for the VR model was a number of
observations that convinced Guyton and his collaborators that
cardiac output largely was unaffected by the activity of the
heart.28 For example, artificial pacing of the heart at rates up to
4 times above baseline in animals29 and humans30,31 did not
cause an increase in CO. Similarly, experiments on dogs, in
which the right heart was replaced by a bypass pump, showed
that CO could be maintained at the baseline level only when
the pump output matched the autonomous rate of venous
return. The increase in pump flows above the baseline would
result in collapse of the great veins without change in CO.32
Significant to Guyton’s model is the division of the
circulatory system into 2 parts. The first consists of the heart
and lung and the second of the entire systemic circulation.
HEART: PROPULSION OR IMPEDENCE? 3

Both parts were, in turn, investigated separately. The heart-lung
segment was examined on the isolated heart preparation and in
an intact animal under a variety of experimental settings. The
isolated systemic circulation, on the other hand, was studied by
replacing the heart with a bypass pump, and on intact animals
by measuring pressure and flow at different points while
stressing the circulation.33
The other key component of the model is the role of elastic
recoil pressure within the vessels that supplies potential
energy to the circulating blood. This pseudostatic pressure,
technically known as Pms, is defined as the equilibrium
pressure generated by the elastic recoil of the vessels during
no-flow state. Its value represents the filling of the vessels and
is, according to the theory, the principal force for driving the
circulation.34 As the heart begins to pump, it transfers the
blood from the highly compliant venous into the poorly
compliant arterial limb of the circuit where the pressure
increases with each increment in pump flow. Concomitantly,
on the venous side, the right atrial pressure (Pra) begins to
decrease until it reaches zero when the veins collapse and the
flow ceases (Fig 1). According to the model, the right atrial
pressure plays a dual role; viewed from the heart, Pra
determines the degree of filling of the right heart and regulates
its output according to the degree of its filling (Starling’s law).
In respect to the blood returning to the heart (ie, venous
return), the positive value of Pra acts as an impedance to
venous return by exerting back pressure. Therefore, any value
of Pra smaller than Pms allows for the flow of venous blood in
accordance with the pressure gradient.
In a simple analogy, the model has been compared to the
flow of water from a bathtub (venous compartment) in which
the rate of emptying is determined by the height of water in the
tub (Pms) and the physical characteristics of the drain pipe, (ie,
its resistance and downstream pressure [pressure difference
between the Pms and Pra]). Importantly, the outflow from the
tub does not depend on the force of stream issuing from the tap
filling the tub, as represented by the action of the heart in
generating arterial pressure.25
Guyton skillfully demonstrated the dual role of Pra in
control of cardiac output by a composite diagram in which
cardiac function and venous return curves are shown on the
same coordinates. Guyton, moreover, maintained that venous
return and cardiac function curves are complementary to each
other and that the crossing of the 2 in the equilibrium point
represents their solutions (Fig 2).
The value of Guyton’s emphasis on the role of peripheral
circulation in the overall approach to studying the cardiovas-
cular system has undoubtedly set the stage for progressive
growth in knowledge about control of cardiac output. His
unique graphic representations of dividing the circulation into
systemic and cardiac segments (comprising of the heart and
pulmonary circulations) has made it possible to visualize
changes in hemodynamic variables in normal and pathologic
conditions. They became a valuable tool in the hands of
clinicians and educators and have been reproduced in virtually
every text of basic and clinical hemodynamics. However, for
reasons mentioned below, this model remains incomplete.
CRITIQUE OF GUYTON’S MODEL
Critics of the VR circulation model contend that the pivotal
role played by the right atrium as back pressure in Guyton’s
analysis is exactly its most controversial point.35 At the core of
the argument is the fact that simultaneous depiction of “cardiac

Fig 1. Normal venous return curves obtained on 14 open-chest, anesthetized, areflex dogs during right-heart bypass experiments. Venous
return reaches a maximum value and remains on a plateau at Pra less than
2 to
4 mmHg due to progressive collapse of the great veins and
the right atrium. Decrease in pump flow causes a steady rise in Pra and results in decrease in venous return (sloped segment of the curve) until
it reaches zero value, defined as the Pms. Note that points for construction of each curve were obtained during brief periods when Pra was kept
at a desired level. Pra, right atrial pressure; Pms, mean systemic pressure. Adapted with permission.99
4 FURST
function” and “venous return” curves on the same diagram
presupposes that the 2 sets of experiments were performed on
the same preparation, whereas they were obtained in two
different sets of experiments.36
Levy repeated the above-mentioned Guyton’s right-heart
bypass experiment on a dog with arrested circulation in which
the heart had been replaced by a bypass pump. He showed that
over the range of pump flows from zero to maximal, the Pra
progressively declined with a concomitant rise in arterial
pressure, thus demonstrating a reciprocal relation between the
two.37 In the graphic representation of the experiment, Levy
expressly stated that under conditions of this experiment, the
venous return is clearly the dependent variable (Fig 3). He
further argued that in a plot with joint representation of cardiac
and vascular function curves, one of the curves necessarily is
depicted backwards, giving the erroneous impression that Pra
controls CO as back pressure rather than the bypass pump. It
has, moreover, been pointed out that Guyton and coworkers
recorded venous return curves and cardiac function curves at
steady states where, for each point on the graph, the flow of the
pump was adjusted manually (Fig 1). As such, the relationships
do not record venous return in dynamic states, blur distinction
between dependent and independent variables, and confuse
mathematic abstraction with reality.36 It also should be
mentioned that the method by which these experiments were
performed by Guyton and Levy, namely, on animal prepara-
tions with arrested hearts and abolished vasomotor reflexes, is
essentially not compatible with life.38 In this sense, the
circulatory system of a nearly deceased experimental animal
does approach a mechanical system subject to pressures and
flows as demonstrated in Levy’s experiment, and it is super-
fluous to talk of Pms as the driving force for venous return. For
methodologic difficulties with stopping the circulation and the
Fig 2. Guyton’s combined plot of “normal cardiac output” and
“normal venous return” curves crossing at a single level of Pra and
flow, the “equilibrium point,” to show independent properties of the
heart and vasculature. According to critics, such graphic representa-
tion implies that 1 of the functions necessarily is plotted backwards.
Pra, right atrial pressure. Adapted with permission.22
Fig 3. The changes in the Pa and Pv produced by alterations in Q
in canine right-heart bypass preparation with abolished cardiovas-
cular reflexes. Stepwise changes in Q were produced by altering the
rate at which blood was pumped mechanically from the right atrium
to the pulmonary artery. Note reciprocity between Q and Pv; the
preparation essentially behaves like a closed-loop hydraulic system.
Pa, arterial pressure; Pv, central venous pressure; Q, systemic flow.
Adapted with permission.37 Promotional and commercial use of the
material in print, digital or mobile device format is prohibited
without the permission from the publisher Lippincott Williams &
Wilkins.
measurement of mean systemic pressure, the reader is referred
to reference 39.
In conclusion, it can be argued that for all its inconsistencies
with the pressure-propulsion model, Guyton’s concept of right
atrial pressure as an impedance to venous return finds its
validation in numerous experimental and clinical studies. The
intersection point of the cardiac and vascular function curves in
his graphic analysis (Fig 2) is an ingenious attempt to represent
dependence of the pulmonary and systemic circulations on
right atrial pressure. However, by considering the heart and the
pulmonary circulation as a single unit, rather than, in analogy
with the systemic venous return, treating it independently as
pulmonary arterial return, the real function of the pulmonary
circulation and of the left heart complex had been obscured.40
LEFT VENTRICULAR MODEL OF CIRCULATION
Implicit in the LV circulation model is the idea that, in
addition to impelling the blood, the heart is also the chief
regulator of cardiac output. The model further assumes that the
circulation is a closed system of vessels in which the pressure
gradient between the aorta and the right atrium determines the
flow and where, during a steady state, the outputs of the left
and right hearts are closely matched in accordance with the law
of conservation of energy and matter.
The understanding of the physical laws governing the flow
of fluids through hydraulic systems as described by Hagen-
Poiseuille in the 19th century was the starting point for
quantification of flow-related phenomena in biologic systems.
The law describes the relation between pressure drop and
volume flow in a rigid tube under steady conditions with
laminar flow,
8mLQ
ΔP¼ ðEq:1Þ
πr 4
where: ΔP is the pressure gradient along the tube, L is the
length of tube, μ is the dynamic viscosity, Q is the volume flow
HEART: PROPULSION OR IMPEDENCE?
rate, r is the radius, and π is the mathematic constant. However,
since the physical dimensions of the circulatory system are not
known, a simplified relation of variables in the form of Ohm’s
law for fluids has been adopted:41
Pao
Pra¼CO  Rp ðEq:2Þ
where the pressure gradient (Pao-Pra) is the difference between
the mean aortic and right atrial pressures, the flow is cardiac
output (CO), and (Rp) is the peripheral resistance.41 Assuming
a zero value for right atrial pressure the equation can be re-
written as:
Rp ¼ Pao=CO ðEq:3Þ
By analogy, the pressure difference between the right ventricle
and left atrium is used to calculate resistance of the pulmonary
circulation. It should be noted that pulmonary capillary
wedge pressure (PCWP) is used as a surrogate for left atrial
pressure.
The integration of the above concepts with the emerging
technology of pulmonary artery pressure measurement in the
1970s ushered in a new era in the understanding of normal
hemodynamics and of various pathophysiologic states. Simul-
taneous measurement of CO and right and left ventricular
filling pressures with the use of Swan-Ganz catheters became
an essential tool in the hands of sapient practitioners to observe
trends and manipulate CO in terms of preload, afterload, and
contractility. The presence of such a relationship may undoubt-
edly be applicable in a laboratory setting where the heart of an
experimental animal has been replaced by a bypass pump and
vascular reflexes have been abolished, as demonstrated in
Levy’s experiment cited above.37 The problem arises when a
causal relationship among flow, pressure and resistance in a
closed hydraulic system of known dimensions (where the
source of pressure is unambiguous, and the flow and resistance
are independently verifiable) is applied to a highly dynamic
circulatory system. The difficulty of applying the concept of
resistance to complex hemodynamic states recently has been
reviewed.42 The issue has been summarized eloquently by
Fishman:
The idea of resistance is unambiguous when applied to rigid
tubes perfused by homogenous fluid flowing in a laminar
stream…complexities are introduced when these concepts
are extended to the pulmonary (as well as to systemic)
circulation: the vascular bed is a non-linear, viscoelastic,
frequency-dependent system, perfused by a complicated
non-Newtonian fluid; moreover, the flow is pulsatile, so that
the inertial factors, reflected waves, pulse-wave velocity,
and interconversions of energy become relevant consider-
ations…as a result of many active and passive influences
that may affect the relationship between the pressure
gradient and flow, the term “resistance” is bereft of its
original physical meaning: instead of representing a fixed
attribute of a blood vessel, it has assumed physiologic
meaning as a product of a set of circumstances.43 (Used by
permission of the American Physiological Society)
Critics of the LV model ascribe its relative success to the
erroneous assumption on the part of some practitioners that the
right atrial pressure (and, in turn, RV filling pressure) is an
5
index of circulatory volume, whereas it should be considered
an impedance to venous return, as defined in Guyton’s
circulation model.44,45 Accordingly, the LV model of circu-
lation provides only limited information about the state of
organ perfusion in various hyperdynamic or low-output states.
For example, cardiac output can increase several-fold during
aerobic exercise, with a drop in peripheral resistance to one-
third without significant changes in blood pressure. Similarly,
in patients with septic shock, cardiac output can be more than
double, with increase in vascular resistance in non-reactive
vascular beds, such as the skin, and decreases in the brain, heart
and the skeletal muscle with the overall resistance unchanged.
It hardly is surprising that a number of studies have failed to
demonstrate a significant correlation between CO and ventric-
ular filling pressures (CVP and PCWP) in a variety of
physiologic and pathologic circulatory states.46–50 Collectively,
they demonstrate the weakness of the current circulation model
and call for its revision. While it is intuitively obvious that
during normal, steady-state conditions flow through the sys-
temic and pulmonary circulations must be equal; the assump-
tion, however, that this distribution is governed by pressure
gradients alone is certainly an oversimplification.
QUANTIFICATION OF THE VENTRICULAR PUMP
The notion that the heart is a pump has prompted
researchers to characterize its mechano-energetic principles
and compare it to a standard mechanical pump. The perform-
ance characteristic of a hydraulic pump typically is defined by a
pump function graph that is obtained by measuring pressures
while changing the resistance of the outflow tube at constant
levels of inflow. The flow at which the pump operates at a
particular steady state is said to be the working point of the
pump (Fig 4). As is evident from the graph, an inverse
relationship exists between flow and pressure generated by
the pump when operating at constant power.
To exclude the effects of neurogenic and humoral control
mechanisms, Elzinga and coworkers carried out a number of
studies in which the pumping capacity of the left ventricle in an
Fig 4. Pump-function diagram for a fluid pump. The pump can
operate at any point within the confines of its function curve. The
working point of a pump denotes the maximal flow (B) the pump can
generate at a given pressure (A). The pump is said to be a pressure
source when it generates a range of flows at the same pressure and
a flow source when a constant flow is generated irrespective of
pressure. The “working point” of this particular pump is between the
2 limits.
6 FURST

isolated cat heart was compared to a mechanical pump and

tested against a hydraulic impedance as represented by a model
arterial tree, the 3-element Windkessel. (Lumped parameter
models assume that circuit parameters [capacitance, resistance
and impedance] that occur along the length of the arterial tree,
are summed into single capacitance and resistance, which can be
independently controlled.) The model has been used extensively
to study pressure-volume relationships of the ventricle and has
given results that closely match in vivo studies.51 The exper-
imental setup allowed for control of heart rate, ventricular filling,
and contractility. The heart was ejecting against variable aortic
loads (as determined by the investigators) by changing the
resistance and compliance of the model arterial tree. The results
of experiments were represented as mean aortic pressures, at
which the heart was working, versus flow (Fig 5). In similarity to
a mechanical pump operating at constant power, when ejecting
at increasing arterial loads (mean aortic pressure), the left
ventricle generates smaller stroke volumes until it reaches the
state of isovolumic contraction when no blood is expelled. It is
evident from the graph that, in the absence of increased
contractility, the heart’s output changes significantly with load-
ing conditions; its output decreases when pumping against
higher pressures and vice versa. Thus, the ventricle is neither a
“flow source” (ie, it cannot maintain the same flow [stroke
volume] under different [aortic] loads) nor a “pressure source”
(ie, it cannot maintain pressure independently of the load).52,53
Similar performance was shown for the right ventricle.54 Fig 6. Left ventricular pump function graph of the isolated feline
It is a remarkable finding, confirmed by experiments on the left ventricle (top) with its related external power (middle panel) and
isolated hearts, anesthetized cats,55 and humans,56 that the heart external efficiency (lower panel). Power output of the heart is
measured at different arterial loads while ventricular filling, heart
transfers the blood to the aorta with optimal power (calculated rate, and contractility are kept constant. The ventricle ejects with
from pressure and flow) and efficiency (expressed as the ratio optimal power (the product of pressure and flow) at the physiologic
of external work and myocardial oxygen consumption) arterial load that represents 58% of maximum cardiac output at zero
(Fig 6).55 The control mechanism of this matching principle pressure (middle panel) and with optimal efficiency at 69% of
maximum cardiac output. Vertical lines demonstrate a close connec-
remains unknown and cannot readily is explained by the
tion between the heart’s working point (arrow) and its optimal
power and efficiency. Adapted with permission.52 Promotional and
commercial use of the material in print, digital or mobile device
format is prohibited without the permission from the publisher
Lippincott Williams & Wilkins.

current knowledge of cardiovascular control. Since both power

Fig 5. Pump function graph of the isolated cat heart paced at a
fixed rate of 120 beats per minute. The lower curve shows ventricular
output under control conditions, and the upper during increased
contractility. Note that under different loading conditions, the heart
neither generates the same pressure nor flow (ie, it is neither flow
nor pressure source but has a working point between the 2 limits).
CO, cardiac output; SV, stroke volume. With kind permission from
Springer Science and Business Media.100
and efficiency have their maximum at some intermediate value
of cardiac output, any value smaller than optimum would have
to be registered twice (ie, at a smaller and at a higher output)
(Fig 6).52 Given the fact that in most mammals the arterial
pressure is about the same, this value can be achieved at
multiple settings. However, there is only 1 setting (working
point) at which the heart “chooses” to operate.57
An alternative way to determine ventricular performance
can be obtained by simultaneous recording of ventricular
pressure and volume during a series of cardiac contractions.58
Similarly to the ventricular pump function graph, the end-
systolic pressure-volume relationship (ESPVR) is obtained
when the aortic pressure is varied over several beats and the
family of end-systolic points is joined with a line (Fig 7). The
slope of the line corresponds to maximal ventricular elastance
(Emax) for each ventricular contraction. (Elastance is defined
as a change in pressure for a corresponding change in volume.)
It has been confirmed in numerous experiments that during a
HEART: PROPULSION OR IMPEDENCE? 7

Fig 7. Ventricular pressure-volume relationships. (A) When the ventricle contracts against increasing load, a series of P-V loops are
generated whose left upper corner falls on a straight line with a slope of Emax. (B) Time-varying elastance model of left ventricular contraction.
Ventricular performance of a single beat can be characterized in terms of elastance, which increases towards maximum (Emax) during end-
systole and decreases with relaxation in diastole. (C) The PVA of a single beat represents the total mechanical energy, which the ventricle
expends during EW and during PE. P, pressure; V, volume; V0, unstressed ventricular volume; ED, end-diastolic volume; ES, end-systolic volume;
E(t), time-varying elastance; P-V, pressure volume; Emax, maximal elastance; PVA, pressure-volume area; EW, ejection; PE, isovolumic
contraction. Adapted with permission.58

stable contractile state, the slope of the ESPVR line represents
a sensitive, load-independent index of contractility and that the
left ventricular oxygen consumption per beat corresponds
linearly to the systolic pressure-volume area (PVA).59 It is of
note that for a given contractile state, the oxygen consumption
per beat is independent of heart rate and of the type of
contraction, whether ejecting or isometric (ie, when the aorta is
occluded), and therefore, of cardiac output.59
However, this linear increase between myocardial oxygen
consumption and mechanical load occurs in the absence of
measurable changes in high-energy phosphates, ATP, and
phosphocreatinine.60 This surprising metabolic stability para-
dox61 continues to be one of the enigmas of myocardial
energetics.62,63 In comparison with the striated muscle, the
non-beating myocardium exhibits about a ten-fold-higher
metabolic rate, 30% of which is dissipated as heat. During
contraction, the metabolic rate increases 3 to 4 times, with
some 70% of consumed energy converted into heat. This
accounts for a surprisingly low myocardial energetic efficiency
(the ratio of the heart’s external work and consumed oxygen) in
the range of 10% to 15%.64,65
It is apparent from the previous discussion that in comparison
with mechanical pumps engineered to maintain either constant
pressure or flow under varying loading conditions, the heart is a
rather poorly “designed” pressure-propulsion pump, or could it
be that the heart, in fact, functions according to sound mechano-
energetic principles emulated by a different type of pump? It is
proposed that such a pump is the hydraulic ram.
THE HEART AS AN ORGAN OF IMPEDANCE
At the beginning of the 20th century, Steiner proposed a
radically different circulation model by suggesting that rather
than being an inert fluid propelled by the heart, the blood has
autonomous movement that is closely linked to metabolic
activity of the tissues. He further suggested that the heart
creates pressure by rhythmically interrupting the flow of blood
and, thus, primarily functions as an organ of impedance whose
mechanical function conceptually can be compared to a
hydraulic ram.66 By all accounts, this theory was way ahead
of its time and largely went unnoticed. (As discussed below,
the first ideas about physics of the open systems appeared in
the 1930s.) Over the years, sporadic studies appeared, mostly in
German, such as a paper by Havlicek, who drew a mechanical
and morphologic analogy between the heart and the hydraulic
ram and even constructed a physiologic model of a hydraulic
ram.67 In the 1970s and 1980s, Manteuffel-Szoege, a cardiac
surgeon, published a number of observational studies of the
embryonic circulation and of patients in deep hypothermic
arrest and made the following remark:
Is it really true that the heart works like a pump? A pump
sucks in fluid from a reservoir, which is a hydrostatic
system and not a hydrodynamic one. In the circulation, on
the other hand, not only is blood ejected from the heart, but
it flows into the heart. The heart is a mechanism inserted
into the blood circuit, and so it is a very peculiar kind of
pump.68
The impetus for his work came from work by Thompson
who studied the effect of artificial ventilation on the blood
circulation in asphyxiated dogs in which it was demonstrated
that residual circulation persisted for up to 1 hour after the heart
had stopped.69 Repeat experiments showed that even in the
absence of mechanical ventilation, significant movement of the
blood continued in the asphyxiated animals for up to 2 hours.70
On the basis of his work and existing evidence, Manteuffel-
Szoege concluded that the blood possesses its own kinetic
energy, which is intricately bound with the thermal conditions,
(ie, metabolic state of the subject). 68
The hydraulic ram is a cyclical pump that converts kinetic
energy of flowing water into pressure. The ingenious design of
the pump allows the water to perform work on itself, thus
obviating the need of additional external power for its operation
(Fig 8.1). It is apparent that the hydraulic ram bears more than a
casual resemblance to the isolated heart preparation, which is
also “driven” by the inflowing blood (Fig 8.2). The reservoir
represents the atrium, and the combination of drive pipe (A)
8 FURST

Fig 8. Components and working cycle of a hydraulic ram. (1). Water from the reservoir accelerates with the force of gravity along the drive pipe
(A) and escapes via the loaded spill valve (B). As the water flow reaches some critical velocity the spill valve (B) is suddenly closed, creating a back
surge (water hammer) that opens the delivery valve (C) and forces the water into the pressure vessel (Windkessel) (D). Increased pressure in the
vessel (D) forces water up the delivery pipe (E) and closes the delivery valve (C). The flow of water is once more redirected along the drive pipe (A)
where it escapes via the opened waste valve (B), completing the cycle. Note similarity with the simple model of the isolated heart preparation; see
text for explanation. With kind permission from Springer Science and Business Media.75 (2). Isolated left heart preparation. Blood flowing from the
venous reservoir enters the left atrium (LA) at a pressure determined by the height of the reservoir relative to that of the atrium (preload). The left
ventricle (LV), when stimulated to contract, ejects the blood through the aorta (AO) into a tube; the height of the aortic outlet constitutes the
ejection pressure (afterload). Note conceptual resemblance to the hydraulic ram. Adapted with permission.101 Promotional and commercial use of
the material in print, digital or mobile device format is prohibited without the permission from the publisher Lippincott Williams & Wilkins.

and pressure vessel (D) represent the ventricle. The spill valve
(B) corresponds to the A-V valve, the delivery valve (C) to the
semilunar valve, and, finally, the delivery pipe (E) stands for
the aorta/pulmonary artery. For the sake of simplicity, the
ram’s operation will be compared to the function of the right
heart. The blood accelerates from the right atrium (reservoir)
into the right ventricle (combined compartments of drive pipe
A and pressure vessel D) where it suddenly decelerates upon
closure of the tricuspid valve (spill-valve B). A steep rise in
ventricular pressure opens the pulmonic valve (delivery valve
C) and impels the blood into the pulmonary artery (delivery
pipe E). Like the heart, the ram only ejects a portion of its
ventricular volume, and the pressure recordings of a model ram
closely resemble ventricular pressures.68
Morphologic features of the right ventricle with a thin,
highly compliant wall and a long, curving outflow tract,
suggest that its ram-like function is optimized for generation
of low pressures. The opposite is the case with the left ventricle
where a short, acutely-angled outflow tract (the angle between
the long ventricular axis and the left ventricular outflow tract
being less than 45º), and a thick, poorly compliant wall is
“designed” to generate high pressures. It is noteworthy that, in
a recent editorial, the function of the RV has been compared to
a hydraulic ram.71
It is significant that within given design constraints and
experimental settings, the ram always operates at optimal
power and efficiency since both are derived from the hydraulic
energy of the driving flow.72 This is not unlike the heart,
which, as mentioned, also works at (hitherto unexplained)
optimal power and efficiency. Thus, the missing link to
understanding the isolated heart’s remarkable energetic stability
and optimal matching of its work to the prevailing state of the
arterial system can be explained by comparing its function to a
hydraulic ram.73
It is suggested that a number of other circulatory phenom-
ena, such as the ones listed in the introduction, become
HEART: PROPULSION OR IMPEDENCE? 9

Fig 9. Comparative circulatory systems in fish, amphibians, mammals, and birds. In fish’s single-circuit circulation the gill and systemic
circulations are placed in series. The heart has a single atrium and a single ventricle placed in the venous limb of the circuit. In addition to
systemic, the amphibians also have a rudimentary lung circulation (bottom-heavy lemniscate) and a new heart chamber, the left atrium, which
receives oxygenated blood from the primitive lung. Systemic and pulmonary circulation are placed in parallel and are served by a single
ventricle. Complete adaptation to air respiration in mammals is associated with development of a new heart chamber, the left ventricle. The
pulmonary and systemic circulations again are placed in series with a pulmonary-to-systemic flow ratio of 1:1 (balanced lemniscate). With
adaptation to life in the air, the cardiorespiratory system in birds reaches a new level of development and surpasses the mammalian in
efficiency, (top-heavy lemniscate). In comparison to mammals, the birds have higher metabolic rates (physiologic hyperthermia and
hypertension) and aerobic capacity. With kind permission from Springer Science and Business Media.75

intelligible in light of the proposed model. For example,
beyond helping to maintain pressure by the weakened heart
in patients with acute myocardial infarction, application of the
aortic balloon pump would not be expected to increase CO. In
addition to jeopardizing myocardial perfusion, the use of potent
vasoconstrictors, such as norepinephrine and epinephrine, will
further compromise the flow of the autonomously moving
blood and contribute to an adverse outcome in patients with
acute cardiogenic shock or other types of heart failure, all of
which benefit at some level by the use of vasodilators.
Similarly, the use of ß-blockers and vasodilators in a failing
heart can improve hemodynamics in spite of reducing its
inotropic state and pressure gradients, respectively.
The ram-like function of the heart, moreover, can explain
the inimical intervention of aortic occlusion. Should the heart
function as a pressure-propulsion pump, occlusion of the
pump’s outflow would be expected to result in loss of arterial
pressure and cardiovascular collapse. On the contrary, studies
in dog models have shown that CO can increase from 20% to
40% during occlusion of the thoracic aorta.13,74 Finally, the
greatly increased COs that far exceed the theoretical pumping
capacity of the heart during aerobic exercise can be understood
as the acceleration of blood flow in response to increased
metabolic demands. For extended discussion of the above and
for other examples, see reference 75.
BIOLOGIC MODEL OF CIRCULATION
Some of the best evidence in support of the new circulation
model comes from the emerging field of embryonic hemody-
namics. It could be argued that the minute scale of early
embryonic circulation is far removed from the conditions (ie,
pressures and flows) prevailing in the mature circulation.
According to the proposed model, the forces for the circulating
blood arise at the interface between the blood and the tissues
(ie, at the level of the microcirculation). The movement of
blood is, therefore, the primary phenomenon and is inextricably
linked with the metabolic demands of the tissues (tissue and
organ autoregulation), irrespective of the size of the organism.
(For example, the flows in zebrafish embryo heart measuring
the width of human hair are in the range of 0.5 cm/s. When
adjusted for size, these flows exert a surprisingly large shear
wall stress of about 75 Dyn/cm2, which is about half of that in
the adult human aorta.) The comparative (evolutionary) model
of circulation shows that the arterial circulation in lower
vertebrates is preceded by a low-pressure venous circulation.
With transition from water to land, the species undergo a
profound change in physiology as they adapt to life in gravity
and atmospheric pressure. A change from gill to lung respira-
tion is tied closely with remodeling of the heart (ie, the
emergence of the left-heart complex), and increased refinement
of the reno-adrenal system, as the pressurized arterial circu-
lation increasingly gains in importance (Fig 9). It has been
suggested that the existence of pressure in the arterial compart-
ment in warm-blooded vertebrates does not primarily serve
blood propulsion but plays a different evolutionary role. Its
magnitude depends on species, activity, posture, and a host of
neurohumoral mechanisms and environmental factors.76
The heart, the system of vessels, and the blood are the first
functional organs to develop in the vertebrate embryo. They
originate from the common mesodermal progenitors. Morpho-
logic features of early embryonic hearts are almost identical
across the vertebrate classes. The heart’s primordium is a
capillary-sized tube which, in due course, undergoes a series of
complex transformations (collectively known as looping)
10
Fig 10. A comparison of the classic PP and biologic models of
circulation. A defining feature of both PP models is that the pressure
gradient created by the heart is the source of blood propulsion. In
Guyton’s VR model, CO predominantly is regulated by the circuit
parameters (ie, elastic and resistive properties of the blood vessels
and blood volume). The Pra plays a dual role; viewed from the heart,
increased Pra promotes ventricular filling, thereby increasing CO.
Viewed from the circulation, increased Pra exerts back pressure,
impedes venous return, and reduces CO. The LV model assumes that
the CO is limited by the pump’s output and is proportional to the
gradient between the mean aortic and Pra and inversely proportional
to Rp. The blood is considered an inert, incompressible fluid, and the
amount pumped into the arterial side of the circuit is equal to the
amount of blood returning at the venous side. The biologic model
assumes the existence of dynamic tension between the source of
oxygen in the lung and its sink in the metabolically active tissues.
The blood, a liquid self-moving organ, bridges this tension and plays
a dual role by procuring oxygen and nutrients to the peripheral
tissues and also to itself. The forces for blood propulsion thus
originate at the level of the microcirculation. The heart plays a
secondary role and exerts a negative feedback to the metabolic
demands of the tissues by rhythmic interruption of the blood flow.
Its ram-like function maintains pressure in the systemic and pul-
monary arterial compartments and carries the rhythm of life. PP,
pressure-propulsion; VR, venous return; LV, left ventricular; CO,
cardiac output; Pra, right atrial pressures; Rp, peripheral resistance.
before it reaches the stage of a 2-chambered organ consisting of
a single atrium and a ventricle. At this early stage, the heart
contains no valves.
It traditionally has been assumed that the valveless embryo
heart impels the blood by means of peristaltic contractions
originating at the venous inflow and propagating along its
length in analogy with the propulsive action of hollow organs
such as the esophagus or the gut. This long-held view has been
overturned by recent observations that demonstrated that the
blood traverses the heart’s lumen at a rate that exceeds the
velocity of the peristaltic wave,77 leaving the question of the
mechanism of blood propulsion wide open.78 It has, therefore,
been proposed that the embryonic heart functions as an organ
of impedance and generates pressure by rhythmic interruption
of the flow.79
Additional evidence supporting the heart’s flow interrupting
function is the presence of diastolic vortices in the embryonic
heart chambers. It increasingly is recognized that intracardiac
blood flow patterns play a key epigenetic role in the heart’s
FURST
embryonic morphogenesis.80,81 In fact, the final form of the
vertebrate heart invariably assumes a vortex-like structure. It
further has been proposed that, at least in the case of adult
hearts, diastolic vortex flows perform an important energy
dissipation function. By trapping kinetic energy of the
inflowing blood and dissipating it as heat, diastolic vortices
facilitate filling at lower intracavitary pressures,82 thereby
confirming the primary function of the heart as an organ of
impedance.
IS THE CIRCULATION A CLOSED SYSTEM?
The question arises as to whether or not the circulatory
system indeed functions according to the principles of a
mechano-energetically closed system? It still was assumed by
19th century biologists that the life of organisms was inex-
plicable within the confines of physicochemical laws postulated
by the emerging new science of thermodynamics. Life suppos-
edly was sustained by a vitalistic factor governed by a set of
laws that essentially are different from the laws of inorganic
nature. This outlook was to change with the arrival of a new
generation of physiologists who made it their task to free
organic sciences of vitalistic ideas and, in the words of one of
the fathers of modern physiology, Carl Ludwig, “…to con-
stitute physiology on chemico-physical foundation and give it
equal scientific rank with physics.”83 Moreover, Du Bois-
Reymond, Ludwig’s collaborator, boldly proclaimed that “the
more one advances in the knowledge of physiology, the more
one will have reasons for ceasing to believe that the phenomena
of life are essentially different from physical phenomena.”83 As
revolutionary as these statements sound, they were conceived
within the framework of the Newtonian (deterministic) frame
of reference that, in spite of tremendous advances in techno-
logic and analytic methods, necessarily lead to a reductionist
view in physiology.84 The assumption implicit in the PP model,
that energetically the circulation is a closed system where
classical laws of conservation of mass and energy apply, is
only an extension of this paradigm.
This view was changed radically in the middle of the 20th
century with the advent of physics of open systems introduced
by Prigogine and others, according to which closed or isolated
systems are only a special case of time-dependent, irreversible
processes.85 Von Bertalanffy, one of the pioneers of the open-
system biology, pointed to a profound difference between the
open and closed systems in physics and biology. The main-
tenance of a constant inner environment (ie, of invariable form,
growth, and reproduction), is said to constitute a time-depend-
ent, self-emergent property of an organism. Homeostasis and
numerous feedback controls known to exist in organisms all
presuppose the theory of open systems.86 Only on transition
from steady state to equilibrium does an organism succumb to
its environment, leading to illness, death, and disintegration
of form.
According to the second law of thermodynamics, a closed
system must attain a time-independent equilibrium state with
maximum entropy (wasted heat) and minimum free energy
(potential energy that could do more useful work). A chemical
reaction where, at equilibrium, the final concentration of
products depends on the initial conditions is an example of
HEART: PROPULSION OR IMPEDENCE?
such a system. Living structures, on the other hand, are capable
of just the opposite. Unlike in the closed systems in which
useful energy continuously degrades into heat (entropy), a
steady state is maintained in organisms through continuous
exchange of substrate and energy with the environment under
nonequilibrium conditions.86
It is evident from the foregoing discussion that the PP model
of circulation is construed on the principles of the closed
system. For example, in his core text, Guyton explicitly stated
how “special attempts have been made to remove all time-
dependent factors in the construction of the curves in this
book.”22 This similarly applies to models based on electric
analogs offered by some of his critics.36 Considered mecha-
nistically, autonomous movement of the blood represents a
violation of the second law of thermodynamics, which states
that perpetual motion (machine) is impossible; such behavior,
however, is predicted when an organism is considered a far-
from-equilibrium, living system.
A long-recognized self-regulating form principle of the
cardiovascular system originally was proposed in 1913 by
Hess and formulated by Murray (1926). Murray’s law of
optimal cardiovascular design predicts that there is a functional
relationship between the vessel radius and the volumetric flow
rate and that the energy required to maintain blood flow and
vasculature is minimal.87 It has been confirmed experimentally
that a blood vessel responds to increase in flow by automatic
adjustment of its diameter until the flow is stabilized at a new
rate. Similarly, in a set of vessels in parallel, an optimal
relationship is established during maximal flow between their
radius and conductance.88 Increased sheer stress on the vessel’s
wall triggers the release of nitric oxide, a potent vasodilator,
and a number of other flow-modulating factors by the
endothelial cells. In the long term, increased shear stress
stimulates endothelial cell proliferation, which results in adjust-
ment of the vessel diameter to increased mean flow rate.88 The
endothelial cells literally will “sense” and respond to a set of
flow “instructions” directly in accordance with their specific
locations in the vascular system. They can be considered a
prime example of a self-regulating structure.
WHAT MOVES THE BLOOD?
The ability of vascular beds to sustain the metabolic
demands of the tissues is known as tissue and organ autor-
egulation and is based on metabolic, myogenic, and endothelial
processes. As mentioned, a number of factors have been
identified that contribute to changes in vascular tone, such as
intraluminal pressure (myogenic response), local metabolite
concentrations, and the effect of shear stress on endothelial
lining. Their common denominator is the maintenance of
optimal flow across the capillary beds, often at minimal
pressure gradient.89,90
There is growing evidence that local biochemical and
mechanical factors, in conjunction with red blood cells (RBCs),
play a far more direct role in tissue metabolism than previously
assumed. Ellsworth and others have shown that, in addition to
convective flow and diffusive oxygen transfer, erythrocyte
oxygen content is critical for the maintenance of tissue oxygen
supply. It has been demonstrated that erythrocytes release ATP
11
as they perfuse a region of tissue with a low oxygen saturation
(SpO2) and, in turn, stimulate the production of endothelium-
derived relaxing factors, including nitric oxide (NO-). Thus, the
erythrocytes act as tissue oxygen sensors and suppliers and
have emerged as the key regulators of tissue perfusion.91,92
Significantly, the pivotal role of the erythrocytes in supplying
oxygen to the metabolically active systemic vascular beds is
complemented by the opposite effect in the pulmonary vessels.
In contrast to the systemic vascular smooth muscle, which
reacts to hypoxemia with vasodilation and increased blood
flow, pulmonary vessels constrict in response to low levels of
inspired oxygen. This important regulatory mechanism matches
pulmonary ventilation with perfusion by diverting blood away
from hypoxic lung regions. Nitric oxide, a potent vasodilator, is
produced continuously by the pulmonary vascular and respira-
tory epithelium and acts as an inhibitor of pulmonary hypoxic
vasoconstriction. Its powerful vasodilating activity is counter-
acted through irreversible binding to RBC hemoglobin.93 In
light of existing evidence, the RBCs increasingly are consid-
ered an important regulator of blood flow not only in systemic
but also in pulmonary microvascular beds. It is estimated, for
example, that the RBC-induced production of NO- by vascular
endothelium accounts for 25% to 30% of basal human blood
flow.94 It has been proposed that the RBC-induced endothelial
release of NO- is the common denominator in various forms of
distributive and cardiogenic shock,95 and the microcirculation
aptly has been called “the motor of sepsis.”96
A number of other conditions can be listed in which this
motor becomes unmasked and goes into overdrive though for a
different pathophysiologic reason. Congenital heart defects
with large, nonrestrictive communication between the systemic
and pulmonary circulations at the level of the heart or the great
vessels such as ASD, VDS, and PDA, share a number of
similarities. Because of the anatomic defect, the heart is unable
to separate the systemic and pulmonary circulations and
maintain them at their normal ratios of 1:1. The short-
circuited pulmonary circulation becomes subject to accelerated
flows that far exceed the flows through the systemic circulation,
a condition known as Eisenmenger syndrome. Pulmonary-to-
systemic blood flow ratios as high as 5:1 have been reported.97
Left uncorrected, they invariably lead to increased pulmonary
resistance and equalization pressures between the pulmonary
and systemic circulations and end with the patient’s demise.
Hyperdynamic circulation with disturbed balance between
the pulmonary and systemic circulations also can be observed
in the case of systemic arteriovenous fistulas. While smaller
fistulas present with a range of peculiar phenomena such as
flow reversal in the feeding arteries and arterializations of
proximal fistula veins, large-volume fistula flows, on the other
hand, result in high-output heart failure or lead to an increase in
pulmonary vascular resistance and pulmonary hypertension.
For a more detailed account of the above conditions, see
reference 40.
Since, according to the proposed model, the pressure
sustained by the heart in the arterial vascular compartment,
though essential for maintenance of normal physiology, can no
longer be assumed to be the primary cause of blood’s move-
ment, the question arises as to how the circulation can be
understood not only locally, where it is self-regulated, but also
12
at the level of the entire organism. Phenomenologic evidence
suggests that a “dynamic tension” exists between the lung, as
the supplier of oxygen, and the peripheral tissues, where it is
consumed. This far-from-equilibrium state is bridged by the
blood which, as a fluid organ with its own oxygen and
metabolic demands, circulates between the two. (Here, a crude
analogy can be drawn between the blood’s movement and the
coil rotating between 2 poles of the magnetic field.) In this
context, the heart, as a feedback organ of impedance, regulates
and maintains the balance between the pulmonary and systemic
circulations in accordance with global metabolic demands.
In summary, an attempt has been made to review some of the
inconsistencies of the widely accepted pressure-propulsion
circulation model that fails to explain an increasing number of
observed circulatory phenomena and has, in due course, become
increasingly complex and even self-contradictory. The model is
construed on the basis of a closed hydraulic system functioning
at a quasi-equilibrium state in which blood, an inert fluid, is
propelled around the circuit by the pressure gradient created by
the heart. Experimental and phenomenologic evidence suggest
the opposite, namely that the blood possesses autonomous
movement sustained by the metabolic demands of the tissues
at the level of microcirculation. The heart plays a crucial role by
maintaining the pressure in the pulmonary and systemic arterial
circulations through rhythmic interruption of flow. It functions as
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