Hemodynamic monitoring in the mechanically ventilated patient

Sheldon Magder
McGill University Health Centre, Montreal, Quebec,
Canada
Correspondence to Sheldon Magder, Royal Victoria
Hospital, 687 Pine Av W, Canada H3A 1A1
E-mail: sheldon.magder@muhc.mcgill.ca
Current Opinion in Critical Care 2011,
17:36–42
Purpose of review
Interactions between the heart and lungs are magnified in patients undergoing
mechanical ventilation and the consequences of these interactions always need to be
considered when managing ventilated patients. In patients with normal lungs and normal
cardiovascular function monitoring needs are minimal, but when oxygenation and
cardiac function are compromised careful assessment of the consequences of changes
in ventilator settings needs to be considered to ensure that adequate oxygen delivery is
maintained.
Recent findings
Primary determinants of heart–lung interactions are first reviewed and then approaches
to the use of simple hemodynamic measurements such as respiratory variations in
central venous and pulmonary artery occlusion, or arterial pressure are described for
assessing oxygen delivery, volume responsiveness as well as indicators of ventilatory
mechanics.
Summary
Use of simple measurements available during routine monitoring can be very helpful to
the informed clinician for optimizing hemodynamic performance as well as patient
ventilator interactions.

Keywords
arterial pressure, central venous pressure, heart–lung interaction, pleural pressure,
preload

Curr Opin Crit Care 17:36–42

ß 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins
1070-5295

discuss how the information from dynamic variations

Introduction
Maintenance of life requires the delivery of oxygen (O2)
to tissues and removal of the waste products of metab-
olism. The cardiovascular and respiratory systems are
intimately linked in these processes and must be func-
tioning adequately to maintain steady state physiological
conditions. Apart from being functionally linked, the
heart resides in the thorax and the right and left ventricles
are in series with the lungs so that ventilatory processes
have direct effects on cardiovascular performance and
cardiac function has direct effects on ventilatory function
[1]. The importance of these interactions becomes
greater when the respiratory system fails and ventilation
is supported by mechanical ventilation for the mechan-
ism of lung inflation changes from an increase in trans-
pulmonary pressure due to a fall in pleural pressure, to an
increase in transpulmonary pressure due to an increase in
alveolar pressure. The author will first outline briefly
some key physiological points in heart–lung interaction.
Next the author will discuss what needs to be known
about blood flow and ventilation to ensure adequate
delivery of O2 and removal of waste and what tools are
available to perform this task. Finally, the author will
1070-5295 ß 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins
in hemodynamic signals can be used to evaluate cardi-
ovascular function and give insights into pulmonary
mechanics.
Basic physiology of heart–lung interaction
Cardiac output is determined by the interaction of pump
function and return function [2,3,4] (Fig. 1). Pump
function is given by the Frank-Starling relationship
which determines the cardiac output for a given preload
at a given heart rate, afterload and contractility [2]. The
preload for the heart as a whole is the right atrial pressure
(Pra) which normally is the same as the central venous
pressure (CVP). Return function describes the force that
determines the return of blood to the heart from the large
peripheral reservoir, which under resting condition con-
tains approximately 70% of the blood volume. The
behavior of this reservoir region has been compared to
that of a bathtub [2,5]. Emptying of the reservoir is
determined by the blood volume that stretches the walls
of small venules and veins (equivalent to the height of
water in the bathtub above the drain), the compliance
(stretchiness) of these vessels (equivalent to the surface
DOI:10.1097/MCC.0b013e32834272c1

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 Hemodynamic monitoring in the mechanically ventilated patient Magder 37
Figure 1 Graphical solution of the interaction of venous return
curve (upper left) and cardiac function curve (upper right) define
the ‘working’ cardiac output, venous return and right atrial
pressure (Pra) values
Venous return Cardiac function
Pra
Pra
Working values
Q ¼ flow.
to height relationship in a bathtub) and the resistance
draining this region (equivalent to the hydraulic resist-
ance in the drain of the bathtub). A key point is that not
all volume in the vasculature stretches the vascular walls;
the bathtub equivalent in the body has the opening on
the side of the tub instead of at the bottom. The volume
that stretches the walls of the vessels, which is the
equivalent to the volume of water above the opening
in a bathtub, is called stressed volume, and the volume
below the opening unstressed volume. Only stressed
volume contributes to the return of blood to the heart
and normally about 30% of vascular volume is stressed
[5]. The relationship of total volume (stressed and
unstressed) to pressure is called capacitance [5,6]. Impor-
tantly, unstressed volume can be converted into stressed
volume by contraction of smooth muscle in vascular walls;
this is called a decrease in capacitance. Cardiac function
and venous return can be plotted together because they
both have flow on the Y-axis and Pra on the X-axis (Fig. 1)
and this provides a graphical solution for their interaction.
When these two functions intersect gives the working
cardiac output, working Pra and working venous return
[3].
One more concept needs to be understood before
explaining the effect of ventilation on cardiac output.
Vascular pressures obtained with the usual fluid-filled
catheters are made relative to an external reference [7].
First the transducer is opened to air so that changes in
pressure are made relative to the surrounding atmos-
pheric pressure, which is called zero for the purpose of
the measurement. Second the transducer must be leveled
at an agreed-upon physical position because the mass of
fluid in the fluid-filled measuring device adds a pressure
to the transducer, which is dependent upon the position
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
of the transducer relative to the region being measured.
The pressure that accounts for stretching of vascular
structures is called transmural pressure and is equal to
the pressure inside a vessel minus the pressure outside
the vessel of interest. When vascular structures are not in
the chest, the pressure outside the vessel is atmospheric
pressure which was used to zero the transducer. However,
this is not true for vascular structures in the chest for they
are surrounded by pleural pressure and pleural pressure
changes relative to atmospheric pressure during the
ventilation cycle. During spontaneous inspiratory efforts
pleural pressure becomes negative relative to atmos-
pheric pressure, which means that the pressure in the
heart decreases relative to atmosphere too. This is the
equivalent of lowering the heart relative to the rest of the
body and increases the pressure gradient for the return of
blood to the heart. On the contrary, on the left side of the
heart, the lower surrounding pressure relative to atmos-
phere must be overcome by the ejecting heart, which
means the afterload on the left ventricle is increased
during ejection. The opposite occurs with positive pres-
sure breathing. A positive pressure breath raises the
pressure in the heart relative to the rest of the body
and thereby decreases the return of blood to the right
heart. It also lowers the afterload on the left ventricle
during the ejection phase. The normal gradient for
venous return from the venous reservoir to the heart is
only in the range of 4–8 mmHg, which means that even
small increases in pleural pressure can significantly alter
the gradient for venous return and this process generally
dominates the effect of inspiration on the heart. Two
processes can compensate for the decreased gradient for
venous return when pleural pressure is positive. One is an
increase in blood volume. Clinically this occurs by the
physician giving a bolus of intravenous of fluid, but also
occurs over time by salt retaining mechanisms in the
kidney. The second is contraction of venous capacitance
vessels and the conversion of unstressed volume into
stressed volume [8–11]. This process can increase stressed
volume by 10–15 ml/kg and happen almost immediately;
it is the body’s way of producing an auto-transfusion.
Importantly, removal of venous tone can remove this
effective volume almost immediately.
The second major factor affecting cardiac output is
related to lung inflation. For lung inflation to occur
alveolar pressure must increase relative to pleural pres-
sure. Whereas the heart is surrounded by pleural pres-
sure, pulmonary vessels situated between alveolae are
surrounded by alveolar pressure and these vessels are
compressed by lung inflation. This effect is trivial when
pulmonary venous pressure is greater than alveolar pres-
sure because the blood in vessels is not easily compres-
sible. However, when alveolar pressure is greater than the
downstream pulmonary venous pressure, the soft-walled
veins collapse with lung inflation creating West zone II
 38 Respiratory system
[12]. When this occurs alveolar pressure becomes the
downstream pressure for pulmonary flow and the load on
the right ventricle goes up with lung inflation. If the lung
is in West zone II the load on the heart increases 1 : 1 with
the increase in alveolar pressure. Because vessel collapse
occurs downstream from the venous compliant region of
the lung, West zone II conditions will also result in back-
up of blood in the pulmonary vessels and can contribute
to increased lung water.
Factors affecting oxygen delivery and
monitoring implications
As stated in the Introduction section, the primary objec-
tive of the cardio-pulmonary systems is to maintain
adequate oxygen to tissues and remove waste. The
amount of oxygen delivered to tissues is determined
by the hemoglobin concentration [Hb], saturation of
the hemoglobin, and cardiac output:
DO2 ¼ ½Hb  saturation  K  cardiac output: (1)
K is a constant for the amount of O2 carried by each gram of
hemoglobin (Hb). The significance of this equation is that
a proportional change in any component has the same
effect on DO2. For example, if application of positive end-
expiratory pressure (PEEP) increases arterial O2 by about
10% from a saturation of 90–100%, but decreases cardiac
output by 10% from 5 to 4.5 l/min, DO2 does not change.
Thus it is important to know whether the maneuver used
to increase O2 saturation did not decrease cardiac output
and consideration of O2 delivery needs to be a central part
of monitoring mechanically ventilated patients.
Monitoring
The approach should begin as always with basic exam-
ination of the patient, and this is likely adequate in the
large proportion of patients. If the patient is easily rou-
sable, has well perfused extremities and functioning
kidneys, tissue perfusion is likely adequate and little
more is needed. Other simple guides are the base excess
and lactate. More careful monitoring is necessary when a
patient is heavily sedated and high levels of airway
pressure and PEEP are needed.
The first hemodynamic parameter to consider monitoring
is blood pressure and this should preferably be done
continuously with an arterial catheter which also allows
regular blood sampling, although noninvasive automated
devices can often be adequate. If blood pressure
decreases with a change in ventilator settings it is quite
likely that there is also a decrease in cardiac output and
signs of decreased tissue oxygenation need to be fol-
lowed. The direct relationship of a drop in blood pressure
to the change in ventilator settings can be assessed easily
by restoring the original ventilator settings. Despite the
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ready accessibility of blood pressure measurements, it is
important to appreciate the limitations of the measure-
ment. Lack of a fall in blood pressure with an increase in
positive pressure does not mean that cardiac output did
not fall for neuro-humeral reflexes can quickly increase
systemic vascular resistance and maintain or even
increase blood pressure when cardiac output falls. A fall
in blood pressure is thus fairly specific, but not sensitive
for detecting a fall in cardiac output.
The next simple hemodynamic parameter to follow is the
CVP which even can be assessed from the jugular veins in
most patients without a central line [13,14]. In a recent
meta-analysis that has received a lot of attention, Marik
et al. [15] argued that CVP does not indicate blood
volume and that CVP does not indicate whether or not
a patient will be volume responsive. These points are true
but from the basic physiology it makes no sense even to
ask these questions in the first place. The key point to
remember is that cardiac output is determined by
the interaction of cardiac function and return function.
Normal upright individuals have a very low CVP with a
normal blood volume and normal cardiac output, but the
same CVP can occur in someone with a low cardiac output
and hemorrhagic shock. On the contrary, a high CVP can
occur in someone with a normal cardiac output but fluid
overloaded as well as in someone with markedly depres-
sed cardiac function and a normal blood volume. Further-
more, CVP tells you nothing about the unstressed volume
which is the largest fraction of blood volume. Thus CVP
must be interpreted in the context of the overall hemo-
dynamic status and cardiac output and, yes, it is not
directly related to blood volume. Marik et al.’s second
criticism is also true; a specific CVP value does not
indicate whether or not a patient will be volume respon-
sive. However, the best way to use a single CVP value is
in the negative sense. A high CVP indicates that it is
unlikely that a patient will be fluid responsive. It has been
proposed that patients with a CVP greater than 10–12
(when referenced to 5 cm below the sternal angle) likely
will not respond to further volume loading [16]. There are
a number of exceptions to this general rule and an
important one relates to mechanical ventilation and the
concept of transmural pressure which is discussed next.
Thus the approach to use of the CVP first should be to ask
whether the patient needs hemodynamic optimization
based on clinical and biochemical exams. The next
question is will a volume bolus improve the hemody-
namics. The final question is then is the CVP in a range in
which it is still likely that cardiac output will increase
when CVP is increased by the change in volume.
As already discussed, the pressure that is important for
the preload of the heart is the transmural pressure across
the ventricular walls with the outside pressure being
pleural pressure. When pleural pressure is increased,
 Hemodynamic monitoring in the mechanically ventilated patient Magder 39

the transmural pressure of the heart is less than the
apparent value on the monitor. As a general rule, when
the lungs are normal, a little less than half of the airway
pressure is applied to the pleural space. When lungs are
diseased the fraction is smaller. As an example in some-
one on 20 cmH2O of PEEP and who has moderately
diseased lungs, the pleural pressure likely is increased
by around 8 cmH2O or close to 7 mmHg relative to
atmospheric pressure. This would mean that a CVP of
15 mmHg relative to atmospheric pressure only gives an
actually 8 mmHg distension force on the ventricular wall.
However, the capillaries in the periphery at the same
level of the heart are exposed to the 15 mmHg pressure
and another 4–8 mmHg to account for the resistance drop
from the periphery to the heart, which brings the value in
these vessels to 19–23 mmHg; this is in the range in
which net increased fluid filtration into the interstitial
space is expected. In capillaries on the dorsal surface of
the patients, another 7 cm on average must be added [16]
to account for the hydrostatic pressure added relative to
the heart and this brings the pressure to around 26–
30 mmHg in these vessels. Thus even though a high
cardiac filling pressure might increase cardiac output in a
patient with high PEEP, the price to be paid is increased
transudation of plasma fluid into the interstitial space.
When PEEP values are high and PaO2/FiO2 low and
arterial O2 saturation is low, measurement of cardiac
output provides important information for the manage-
ment for, as already discussed, it ultimately is not arterial
saturation that is important but rather delivery of oxygen
to tissues. When there is a large pulmonary shunt, a low
cardiac output also can impact on arterial O2. This occurs
because mixed venous O2 saturation falls with a decrease
in cardiac output so that shunted venous blood to the
arterial side has a greater impact on arterial O2 content.
Measurement of central or mixed venous O2 content is
useful in these cases and when very low, can indicate
that increasing cardiac output will increase arterial
oxygenation.
Diagnostic uses of ventilatory variation in
vascular pressure waves
Respiratory variations in central venous pressure
When pleural pressure falls with a spontaneous inspi-
ration the pressure in the heart also falls relative to
atmospheric pressure if there is no change in cardiac
volume and in the graphic representation, the cardiac
function curve moves to the left of the venous return
curve (Fig. 2). This includes spontaneous efforts that
trigger mechanical breaths in all demand modes. When
the heart is functioning on the ascending portion of the
cardiac function curve, CVP falls relative to atmosphere
and output from the right heart increases (Fig. 2a). How-
ever, when the heart is functioning on the flat part of the

Figure 2 Interaction of venous return and cardiac function curves with respiratory variations

(a) Shows that a spontaneous, negative (ve) pressure breath moves the cardiac function curve to the left of the cardiac function curve (symbols are
the same as in Fig. 1). When the venous return curve intersects the ascending part of the cardiac function curve a breath decreases Pra and increases
right-sided output (left upper) but when the venous return curve intersects the flat part of the cardiac function curve, there is no change in Q. (b) Shows
the changes with positive pressure breaths. In this case inspiration moves the cardiac function curve to the right. When the venous return curve
intersects the flat part of the cardiac function curve, positive pressure is expected to decrease Q (left lower) but when it intersects the flat part of the
curve there is potentially no change in Q or Pra until the cardiac function curve is shifted sufficiently to the right (lower right). These predictions are
weaker than those for predicting fluid responsiveness in (a) because of reflex adjustments to cardiac and return functions.

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 40 Respiratory system

Figure 3 Examples of respiratory patterns in hemodynamic tracings

(a) Shows respiratory variations in pulmonary artery occlusion pressure (Ppao) with spontaneous inspiratory efforts. The line marks the appropriate
place to make the measurement. (b) Shows examples of Ppao and CVP with positive pressure breaths and no spontaneous effort. (c) shows an
example of a spontaneous effort with a marked active expiration which increases the pressures throughout expiration. The lines at the bottom indicate
inspiration. The line on the CVP tracing suggests an appropriate place for the measurement; although it is early in expiration, it occurs before the major
push. The fall in CVP with the onset of inspiraton does not necessarily indicate fluid responsiveness in this case because it is due to release of a positive
pressure. (d) Shows an example of active expiration when the effort decreases throughout the expiratory phase. The value at end-expiration in the
middle breath is lower than the other two because the breath is longer and there is more time for expiration. In this example, even after the active
expiration there still seems to be a fall in CVP suggesting fluid responsiveness.

cardiac function curve, there is no change in CVP or right
heart output (Fig. 2b). Thus the ventilatory pattern of
CVP gives an indication as to whether the heart is
functioning on the ascending or flat part of the cardiac
function curve [17]. An inspiratory fall in CVP indicates
that the heart is on the ascending portion of the cardiac
function curve and may or may not respond to volume
depending how close CVP is to the plateau, whereas lack
of an inspiratory fall indicates that the heart is functioning
on the flat part of the cardiac function curve and will not
respond to a volume infusion (Fig. 3). This test is most
useful in the negative; that is lack of an inspiratory fall in
CVP indicates that the cardiac output will not respond to
volume. There are a few caveats for the use of this test.
There must be an adequate inspiratory effort. An increase
in the ‘y’ descent does not constitute an inspiratory fall in
CVP; there needs to be a fall in the whole wave form
which is best assessed at the base of the ‘a’ wave. One
must be careful to not confuse the fall in CVP from the
release of an active expiration for an inspiratory fall in
CVP (Fig. 3). It also must be appreciated that the
inspiratory rise in CVP with a mechanical breath gives
no indication of volume responsiveness. Finally, as with
any test of volume responsiveness, it must be remem-
bered that evidence of volume responsiveness does not
mean that the patient needs volume; that is a clinical
decision.
Ventilatory patterns in CVP can also give an indication of
the potential for cardiac output to fall with increases in
PEEP although the predictive value is not as strong as is
the case for the assessment of volume responsiveness
[18]. Patients who have an inspiratory fall in CVP would
be expected to always have a fall in cardiac output with
PEEP (Fig. 2c), but this is not the case because reflex
adjustments in venous capacitance as well as ventricular
function can maintain cardiac output [19,20]. Patients
who have no inspiratory fall in CVP with PEEP should
not have a fall in cardiac output unless the increase in
PEEP is sufficient to move the cardiac function curve far
enough to the right so that the venous return curve again
intersects the ascending part of the cardiac function curve
in which case cardiac output will fall (Fig. 2d).
Respiratory variations in arterial pressure and stroke
volume
Currently very popular techniques for assessing volume
responsiveness are the assessment of respiratory vari-
ations in arterial pressure including systolic or pulse
pressure or stroke volume [21,22]. During the inspiratory
phase of an unassisted mechanical breath, the rise in
pleural pressure decreases the gradient for venous return,
decreases right heart filling and decreases right heart
output. At the same time, there is increased output from
the left heart because of increased filling of the left heart
as a consequence of emptying of pulmonary veins by the
inflating lungs and a decrease in left-sided afterload due
to the rise in cardiac pressure relative to atmosphere. The
consequence is a transient inspiratory rise in arterial
pressure. The decrease in right-sided output is passed

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 Hemodynamic monitoring in the mechanically ventilated patient Magder 41

to the left heart over a few beats so that output from the
left heart decreases during the expiratory phase. When
the heart is functioning on the flat part of the cardiac
function curve there is less of a fall in right heart output
during inspiration and more volume in the pulmonary
veins to sustain left heart filling in the expiratory phase.
Thus patients who have large decreases in arterial pres-
sure or stroke volume during expiration are expected to
have an increase in cardiac output with a volume bolus,
whereas those without should not. Although this pattern
should predict volume responsiveness when used in the
operating room in patients with no spontaneous inspira-
tory or expiratory ventilatory efforts, regular rhythm and
standard ventilator settings as originally described by
Perel [23], it is not effective in patients who have any
spontaneous ventilatory efforts, including inspiratory or
expiratory efforts because the patterns of right and left-
sided filling differ [22]. Ventilatory variations in arterial
pressure or stroke volume have also been shown not to be
predictive in patients with smaller tidal volumes,
increased West zone II conditions and in patients with
pulmonary hypertension [24,25,26].
increase in pleural pressure for the same reason. Changes
in pulmonary artery pressure can also be used but are a
little more awkward because of the larger excursions of
the pressure during the cardiac cycle. Changes in CVP are
less useful because the source of volume for the right
heart is outside the chest and does not vary with the
change in pleural pressure. In contrast, the source of
volume for the left heart varies in the same way as the
left atrial pressure with changes in pleural pressure. Large
negative swings in either CVP or pulmonary artery occlu-
sion pressure with triggering of the ventilator indicate
inadequate settings of the trigger threshold, increased air
way resistance or decreased lung compliance, or
increased inspiratory drive and ventilator settings need
to be adjusted or potentially increased sedation (Fig. 4).
A large increase in CVP with a mechanical breath
indicates that there was a large rise in pleural pressure
and this is suggestive of a decrease in thoracic wall
compliance. This can occur with edema in the chest wall,
the presence of large effusions or even with increased
abdominal pressure.

A common ventilatory pattern in CVP, especially in

Evaluation of respiratory function
The ventilatory patterns in CVP and pulmonary artery
occlusion pressure also can be used to assess ventilatory
function. Ventilatory variations in pulmonary artery
occlusion pressure give an indication of changes in
pleural pressure and match changes in esophageal pres-
sure with a small bias [27]. During spontaneous nega-
tive pressure inspiration the fall in pulmonary artery
occlusion pressure slightly underestimates the fall in
pleural pressure because there is some increased filling
of the left heart during lung inflation in most patients.
During positive pressure breaths, the increase in pulmon-
ary artery occlusion pressure slightly overestimates the
patients with spontaneous efforts, is active expiration.
This comes in two general patterns. In one pattern, the
patient forcefully exhales throughout expiration which
raises CVP relative to atmosphere and leads to an erro-
neous estimate of the cardiac filling pressures (Fig. 3d). In
this case, one must observe multiple cycles and take the
value at end-expiration which is in the longest breath and
lowest value. The second pattern occurs when the patient
increasingly contracts expiratory muscles during expira-
tion so that the cardiac filling pressures rise throughout
expiration (Fig. 3c). In these patients the use of the end-
expiratory value of CVP gives a very misleading estimate
of cardiac preload and a value closer to the beginning of

Figure 4 Example of pulmonary artery occlusion pressure (Ppao), a reflection of left atria pressure, and CVP in a patient on a pressure
support of 6 cmH2O

There is a marked inspiratory fall in Ppao of 28 mmHg which would indicate an even greater fall in pleural pressure which in cmH2O would be greater
than 38. The fall in pressure is also evident in the CVP but that is not always the case. The patient was post cardiac surgery and had a history of chronic
obstructive lung disease. Rhonchi were evident clinically. He was treated with bronchodilators before extubation; this resolved the large inspiratory
swings and he was successfully extubated.

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
 42 Respiratory system
expiration is likely more valid. This process can some-
times be eliminated by having the patient try to talk,
even when intubated for this decreases contractions of
expiratory muscles.
Conclusion
In the straightforward mechanically ventilated patient
simple observation of the patient with intermittent blood
pressure and pulse oximetry is likely sufficient. When
ventilatory management becomes more difficult, careful
hemodynamic monitoring with an assessment of cardiac
output becomes more important to ensure that venti-
latory settings do not decrease oxygen delivery while
trying to increase arterial saturation. Finally, a lot of
information can be obtained from CVP and arterial pres-
sure waveforms that can help guide management. These
signals are continuously available on the monitor and
readily available to the informed clinician.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
 of special interest
 of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (p. 81).
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A recent study showing that pulse pressure variations fail to predict fluid respon-
siveness in patients with pulmonary hypertension.
26 Magder S. Further cautions for the use of ventilatory-induced changes in
arterial pressures to predict volume responsiveness. Crit Care 2010; 14:197.
27 Bellemare P, Goldberg P, Magder S. Variations in pulmonary artery occlusion
 pressure to estimate changes in pleural pressure. Int Care Med 2007;
33:2004–2008.
This study demonstrates that respiratory changes in pulmonary artery occlusion
pressures give a good estimate of changes in pleural pressure when compared to
measurements by an esophageal balloon.