Functional hemodynamic monitoring

Mehrnaz Hadian and Michael R. Pinsky

Purpose of review Introduction

To assess the recent literature on effective use of
information received from hemodynamic monitoring.
Recent findings
Dynamic hemodynamic measures are more effective in
assessing cardiovascular status than static measures. In
this review, we will focus on the application of hemodynamic
monitoring to evaluate the effect of therapy.
Summary
A systematic approach to an effective resuscitation effort
can be incorporated into a protocolized cardiovascular
management algorithm, which, in turn, can improve
patient-centered outcomes and the cost of healthcare
systems, by faster and more effective response in order to
diagnose and treat hemodynamically unstable patients both
inside and outside of intensive care units.
Keywords
cardiovascular, clinical trials, hemodynamic monitoring,
preload responsiveness, pulse pressure variation, stroke
volume variation, volume responsiveness
Curr Opin Crit Care 13:318–323. ß 2007 Lippincott Williams & Wilkins.
Department of Critical Care Medicine, University of Pittsburgh Medical Center,
Pittsburgh, Pennsylvania, USA
Correspondence to Michael R. Pinsky, MD, 606 Scaife Hall, 3550 Terrace Street,
Pittsburgh, PA 15213, USA
Tel: +412 647 5387; fax: +412 647 8060; e-mail: pinskymr@upmc.edu
Current Opinion in Critical Care 2007, 13:318–323
Functional hemodynamic monitoring is that aspect of the
measure of cardiovascular variables, either alone or in
response to a physiologic perturbation, that defines a
pathophysiological state, drives therapy or identifies car-
diovascular insufficiency more accurately and often earlier
than possible by analysis of static hemodynamic variables.
Why hemodynamic monitoring?
Hemodynamic monitoring is a crucial part of care for the
hemodynamically unstable patient. The pattern of
hemodynamic variables often helps physicians to
differentiate different causes of hemodynamic instability
and to decide the appropriate therapeutic interventions
accordingly. With rapidly developing technology and
with improvement in our understanding of the
pathophysiology of diseases, the utility of hemodynamic
monitoring has changed significantly over time. One of
the main reasons for hemodynamic monitoring is to
detect an impending cardiovascular crisis before any
organ damage occurs, and also to allow clinicians to
monitor the response to therapy. No monitoring device
can improve patient-centered outcomes, however, unless
it is coupled with a treatment that itself improves out-
come. Thus, hemodynamic monitoring must be applied
within the context of therapeutic interventions proven to
be effective in reversing the identified disease process
[1].

Abbreviations
Hemodynamic monitoring must also be considered within
the context of time points of the disease process and the
CO cardiac output
CVP central venous pressure site at which monitoring takes place, which has a major
DO2 oxygen delivery impact on the type of monitoring and its risks, utility and
MAP mean arterial pressure
PAC pulmonary artery catheter efficacy. For example, monitoring outside the hospital and
PCO2 partial carbon dioxide tension emergency department is usually less invasive than in the
Ppao pulmonary artery occlusion pressure
ScvO2 central venous oxygen saturation operating room or intensive care unit. Or, from the time
SvO2 mixed venous oxygen saturation point perspective, a preoperative optimization of cardio-
vascular status [2] and early goal-directed therapy of septic
ß 2007 Lippincott Williams & Wilkins shock in the emergency department [3] reduces morbidity,
1070-5295
whereas applying the same monitoring and treatment in
unstable patients with existing shock-induced organ
damage has not been shown to improve outcome [4–6].

Static hemodynamic monitoring of single

variables
Although their utility as a single absolute hemodynamic
value is questionable, a few hemodynamic variables are
commonly measured at the bedside and their values are
used in clinical decision making. The most common
variables used in clinical settings are arterial blood pressure
318

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(ABP), heart rate (HR), central venous pressure (CVP),
pulmonary artery occlusion pressure (Ppao), cardiac output
(CO), mixed venous oxygen saturation (SvO2) and arterial
oxygen saturation (SaO2). The rationale for the use of
individual hemodynamic values in a clinical setting is
primarily based on the fact that threshold values have
been defined for some of these hemodynamic variables
and that specific constellations of specific values
reflect autonomic response to specific disease processes,
as analyzed by hemodynamic profile analysis. For
example, as a primary determinate of organ perfusion is
perfusion pressure, systemic hypotension to below a cer-
tain threshold [e.g. a mean arterial pressure (MAP) of
<65 mmHg] is clinically relevant, even though it is
possible for a patient with ‘normal’ MAP values to still
be in circulatory shock [7]. On the same note, an elevated
central venous pressure (i.e. >10 mmHg) indicates right
ventricular pressure overload, usually due to an expanded
effective circulating blood volume, even though this gives
no information about the exact cause of the disease
process. One can also argue that CO can only be
interpreted relative to metabolic demand of the patient.
As blood flow varies to match the metabolic requirements
of the body, there can be no such thing as normal CO or
oxygen delivery (DO2). Therefore, CO and DO2 are either
adequate or inadequate to meet the metabolic demands of
the body. Inadequate DO2 is presumed to occur if tissue
O2 extraction is markedly increased, as manifested by a
decrease in SvO2 below 70% [8].
Systemic arterial blood pressure
Arterial blood pressure can be measured intermittently
and noninvasively using a sphygmomanometer [9], or
continuously with an indwelling arterial catheter. Blood
pressure is not a single pressure value, but a range of
pressure values from systole to diastole. Therefore, in
noncardiac tissues, if the back pressure to venous outflow
is not elevated, MAP is the best approximation of the
organ perfusion pressure. Blood pressure is a regulated
variable through baroreceptor reflex arcs keeping it con-
stant despite changing CO, whereas CO varies with
changing tissue metabolic demands. Thus, a normal
blood pressure does not necessarily reflect hemodynamic
stability [7]. As different organs may vary markedly,
different intraorgan vascular resistances and global blood
flow may vary as baseline vasomotor tone varies, such as
would be the case in patients with essential hypertension;
there is no threshold blood pressure value that can define
adequate organ perfusion among organs, between
different patients, or in the same patient over time
[10]. Still, as arterial pressure is a primary determinant
of organ blood flow because increased intraorgan flow
only occurs because local vasodilation allows a high organ
input pressure to increase its local blood flow, one
should consider hypotension (MAP < 65 mmHg) as a
pathological state of organ hypoperfusion and loss of
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Functional hemodynamic monitoring Hadian and Pinsky 319
autoregulation of blood flow. The other application
of continuous arterial blood pressure monitoring is to
estimate beat-to-beat left ventricular stroke volume
and CO using an algorithmic analysis of arterial pulse
pressure [11] based on the patient’s age, sex, height
and weight, which are the determinants of arterial tone.
The overall accuracy of these techniques varies, based
on limited studies [12,13,14
]. Arterial pulse pressure,
however, is a much better estimate of stroke volume and
requires no additional calculations.
Central venous pressure
CVP (also called right atrial pressure) is the back pressure
to systemic venous return. It can be easily measured
through a central venous catheter placed in the neck
or chest. Studies [15–17] using echocardiographic
techniques have shown more than 36% superior vena
caval collapse during positive-pressure inspiration or
that complete inferior vena caval collapse identifies
individuals whose CVP is less than 10 mmHg. This
finding is of important but limited utility in the bedside
management of the critically ill patient. Jellinek et al. [18]
showed that if CVP is 10 mmHg or less, then cardiac
output will uniformly decrease in ventilated patients in
whom 10 cmH2O positive end-expiratory pressure is
given. If CVP is more than 10 mmHg, however, CO
may increase, remain the same or decrease. No threshold
value of CVP identifies patients whose CO will crease in
response to fluid challenge [19]. From a static variable
perspective, an elevated CVP only occurs in disease
processes, but the clinical utility of CVP as a guide for
diagnosing which disease is causing it or what the
individual patient’s response to treatment will be cannot
be identified from measures of CVP.
Hemodynamic values measured by pulmonary
artery catheter
The pulmonary artery catheter (PAC) is designed to
estimate left ventricular filling pressures by measuring
Ppao [20,21]. One can also measure the values of pul-
monary artery pressure (Ppa), CVP, SvO2, CO and right
ventricular ejection fraction. Ppao is the back pressure to
pulmonary blood flow, and it can be used to identify the
presence of a hydrostatic component to pulmonary
edema and to assess pulmonary vascular resistance. Ppao
values do not correlate with left ventricular end-diastolic
volume, however, and neither do they predict preload
responsiveness [22]. PAC can also be used to monitor
right ventricular end-diastolic volume which, in turn, can
be used in differentiating different causes of circulatory
shock, such as right-sided cardiac failure. For example,
if right ventricular end-diastolic volume increases as
CO decreases, then the patient has cor pulmonale [23].
As mentioned before, however, the utility of any
static single-point measurement in predicting preload
responsiveness or in improving outcome in unstable
 320 Cardiopulmonary monitoring
patients has not been demonstrated [24]. There have also
been studies [25

,26
] showing that cardiac filling
pressures are not appropriate values to predict
hemodynamic response to volume challenge.
CO can be calculated by measuring blood flow using
dilution techniques with a thermal [27] or lithium indicator
[13] via PAC or CVP. As mentioned before, because
CO is either adequate or inadequate to meet the meta-
bolic demands of the body, and because an accurate
measurement of CO is less important than accurate
documentation of trends in blood flow, these measures
may have profound clinical utility if the trends are
accurate and stable over time.
SvO2 measures may reflect better DO2 adequacy,
however. The normal value for SvO2 is 70–75%. Muscle
activity, anemia, hypoxemia and decreased CO all
independently decrease SvO2, whereas hyperdynamic
sepsis, hypothermia and muscle relaxation increase
SvO2. Although SvO2 above 70% does not necessarily
reflect adequate tissue oxygenation (e.g. in sepsis), a
persistently low SvO2 (<50%) is associated with tissue
ischemia [28]. Although central venous oxygen saturation
(ScvO2) and SvO2 are not equal, measures of ScvO2 tend
to track SvO2. Therefore, ScvO2 may be used to monitor
resuscitation efforts if special attention is paid to related
clinical variables [29].
Tissue partial carbon dioxide tension gap
The other potential hemodynamic monitoring value is
measurement of the gap between tissue partial carbon
dioxide tension (PCO2) and arterial PCO2. Tissue PCO2
reflects both local metabolism and regional blood
flow [30]. Thus, if blood flow decreases, then tissue
PCO2 will increase relative to arterial PCO2. Therefore,
measurement of this PCO2 gap could allow one to assess
whether tissue blood flow is effective. Examples
clinically relevant to this application are measures of
gastric [31] and sublingual [32,33] PCO2 gaps to identify
tissue hypoperfusion and guide resuscitation in critically
ill patients.
Hemodynamic profile analysis: grouping of
static variables
The relation between specific hemodynamic variables is
complex in health and even more complex in disease. A
solid understanding of the cardiovascular underpinnings
of blood flow homeostasis is required, however, to inter-
pret hemodynamic variables effectively. If disease causes
CO and DO2 to decrease, MAP decreases as well. This, in
turn, will result in increased sympathetic tone and heart
rate, which can increase MAP toward normal values by
reducing unstressed circulatory blood volume and
increased arterial vasomotor tone. Thus, hypotension
reflects failure of the sympathetic nervous system to
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Table 1 Hemodynamic profile analysis in different types of
circulatory shock
Type of shock MAP CO CVP Ppao SVR DO2
Hypovolemic #! # # # " #
Cardiogenic #! # " " " #
Obstructive # # " "! "! #
Distributive # " # # # "
MAP, mean arterial pressure; CO, cardiac output; CVP, central venous
pressure; Ppao, pulmonary artery occlusion pressure; SVR, systemic
vascular resistance; DO2, tissue oxygen delivery.
compensate for circulatory shock, while normotension
does not ensure hemodynamic stability [34–36].
Of the four categories of shock (Table 1), only
distributive shock states, following intravascular volume
resuscitation, are associated with an increased CO but
decreased vasomotor tone. In the nonresuscitated
subject, this presents as hypovolemic shock, but with fluid
resuscitation, blood pressure does not increase despite
an increase in CO, which is due to loss of vascular
responsiveness. Therefore, hemodynamic monitoring
can aid in determining the cause of circulatory shock.
Dynamic (functional) hemodynamic
monitoring: response to therapy
As most forms of circulatory shock reflect inadequate
tissue DO2, a primary goal of resuscitation is to increase
DO2. Thus, the primary functional question usually
asked of the hemodynamically unstable patient is
will CO increase with fluid resuscitation and, if so,
by how much? Physiologically speaking, this equates
to defining whether the patient is or is not preload
responsive. Unfortunately, although specific patterns of
hemodynamic values, as described above, reflect specific
types of disease, they do not predict individual patient
response to therapy.
Hemodynamic monitoring to evaluate the effect of
therapy is known as functional monitoring, because it
implies a therapeutic application [1]. As a rapid change in
trends of measured values in response to a specific
therapy has a greater clinical utility, the most common
type of functional monitoring is a therapeutic trial. In the
following discussion, we look at some of the important
and commonly used functional monitoring variables that
are currently validated.
The volume challenge
One of the methods in assessing preload responsiveness
is to rapidly give a small-volume bolus intravascularly and
evaluate the hemodynamic response by observing any
changes in arterial blood pressure, heart rate, CO, SvO2 or
other relevant measures. A patient is considered respon-
der to a volume challenge trial if there is an improvement
in circulatory status, such as increasing MAP and CO or a

decreasing heart rate. Other indicators of preload
responsiveness are increasing SvO2 or decreasing blood
lactate, which reflect improved effective blood flow.
A fluid challenge must be conducted within the
context of known or suspected tissue hypoperfusion
[37]. Importantly, a volume challenge is only a diagnostic
test to identify those who are preload responsive, and
it should not be considered as fluid resuscitation,
which itself needs to be continued until hypovolemia
is resolved [38]. If clinical evidence of hypoperfusion
persists, then volume responders should be given
additional fluid resuscitation with minimal risk for
worsening cor pulmonale or inducing pulmonary edema.
One of the primary disadvantages of this diagnostic
approach in hemodynamically unstable patients is that
it is only positive in half the hypotensive patients [39].
Thus, it will delay primary treatment in half the patients
who are not responders to volume challenge. This is of
special importance when a delayed appropriate therapy
can be associated with negative consequences on
patient survival. Furthermore, a volume challenge in a
nonresponder may even worsen or precipitate pulmonary
edema or cor pulmonale. Fortunately, there are several
validated alternative methods that mimic a reversible or
transient volume challenge without any volume actually
given to patients, which are discussed in the following
paragraphs.
Method used in positive pressure-ventilated
patients
Positive pressure ventilation cyclically alters the pressure
gradient for systemic venous return, proportionally alter-
ing right ventricular output on the next beat. After about
two to four beats, left ventricular filling and output are
also proportionally altered. Thus, in patients who are
preload responsive, positive pressure ventilation will
induce cyclical changes in left ventricular stroke volume.
As the forcing function is the tidal volume-induced
change in intrathoracic pressure, the greater the increase
in tidal volume for the same lung compliance, the greater
is the transient decrease in venous return and
subsequently greater decrease in left ventricular output
[40]. The degree of changes in either arterial pulse
pressure or systolic blood pressure in response to a series
of increasing tidal breaths quantifies the degree of
preload responsiveness [41,42
]. On the other hand,
when fixed tidal volume is delivered during positive
pressure ventilation, the degree of variations in systolic
pressure [43], pulse pressure [44,45,46

], left ventricular
stroke volume [47–50] and aortic flow [51–53] accurately
reflects preload responsiveness. A systolic pressure or a
pulse pressure variation of 13% or more in septic
patients’ breathing with a tidal volume of 8 ml/kg
is highly sensitive and specific for detecting preload
responsiveness [44].
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Functional hemodynamic monitoring Hadian and Pinsky 321
One can estimate left ventricular stroke volume based on
the arterial pressure pulse contour. As mentioned before,
stroke volume variation can be used in predicting preload
responsiveness [48,49,54]. Unfortunately, there are con-
troversial results regarding the accuracy of the pulse
contour algorithm used to calculate stroke volume on
commercially available devices, but studies are limited
[12,13,14
]. Thus, the extent to which these measures
accurately track the real stroke volume fluctuations is
unclear [55].
Finally, recent studies suggest that the pulse oximetry
plethysmographic waveform amplitude co-varies with
arterial pulse pressure [56–58]. Like pulse pressure vari-
ation (PPV), plethysmographic signal variation predicts
fluid responsiveness in hypotensive patients [58,59

,60].
If validated to predict preload responsiveness in the
broader group of hemodynamically unstable patients,
then such noninvasive techniques could expand the
application of this applied physiological approach at
the bedside.
Estimating preload responsiveness during
spontaneous breathing
During spontaneous inspiration, venous return normally
increases due to increase in negative intrathoracic pressure
[61]. A normal right ventricle pumps this increased blood
flow into the pulmonary circulation. Therefore, CVP will
decrease with decreasing intrathoracic pressure with each
spontaneous inspiratory effort. An inspiratory decrease in
CVP of more than 1 mmHg when intrathoracic pressure
decreases more than 2 mmHg has been shown to
accurately predict preload responsiveness, whereas those
patients whose CVP does not decrease in such setting do
not increase their CO in response to fluid challenge [62].
That this approach requires central venous catheterization
need not be mentioned. A change in inferior vena
cava diameter during positive pressure ventilation can
be also interpreted as CVP changes [63], but it requires
complex echocardiographical technology and has minimal
diagnostic utility at bedside. A simpler approach to
assessing preload responsiveness has been recently
validated using the changes in mean CO from before to
during a passive leg-raising (PLR) maneuver.
Passive leg-raising
PLR to 308 transiently increases venous return [64]
in patients who are preload responsive. As PLR only
transiently increases CO and blood pressure [65] in
responders, it is only a diagnostic test and cannot be
considered as a treatment for hypovolemia. The main
advantage of the PLR approach is that it is reversible and
easy to perform in patients breathing spontaneously
and with arrhythmias [66

]. It also can be repeated
many times to reassess preload responsiveness without
any risk of inducing pulmonary edema or cor pulmonale
 322 Cardiopulmonary monitoring
in potential nonresponders. One of the major limitations
of this technique is that in severely hypovolemic patients,
the blood volume mobilized by leg-raising which is
dependent on total blood volume could be small, which,
in turn, can show minimal to no increase in CO and
blood pressure, even in responders.
Conclusion
A systematic approach regarding functional hemodynamic
monitoring is the cornerstone of an effective resuscitation
effort. This approach can be incorporated in a protocolized
cardiovascular management algorithm based on functional
hemodynamic monitoring [67,68], which, in turn,
can improve patient-centered outcomes and cost of the
healthcare system, by faster and more effective response in
order to diagnose and treat hemodynamically unstable
patients, both inside and outside of intensive care
units.
Acknowledgements
This work was supported in part by the NIH grants HL67181, HL07820
and HL073198.
Potential conflict of interest: Michael R. Pinsky, MD, is the inventor of a
University of Pittsburgh-owned US Patent called ‘Use of aortic pulse
pressure and flow in bedside hemodynamic management’ that used the
approaches discussed in this study to drive its treatment algorithms.
There are no additional potential conflicts of interest.
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. 359).
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