Luca M. Bigatello, M.D.
Department of Anesthesia and
Massachusetts General Hospital,
Harvard Medical School,
HEMODINAMIC MONITORING IN TRAUMA
Patients who sustain major trauma may become
hemodynamically unstable at various times
during their course. Immediately following
a major traumatic injury, hypotension is
common, and its diagnosis must often be made
on simple clinical grounds, because time for
sophisticated hemodynamic monitoring is not
available. Fortunately, such diagnosis is
generally obvious: hemorrhage, pneumothorax,
and spinal shock are easily diagnosed by the
experienced clinician. Later in the
post-traumatic course, hypotension may
result from different reasons, including
hypovolemia, depression of myocardial
function, and vasodilation from inflammation
and sepsis. At this time, the clinical exam
may be insufficient to reach a satisfactory
diagnosis and institute the appropriate
therapy. Hence, the clinician must resolve
to use further monitoring. At this point,
the trauma patient is like any other
hemodynamically unstable, critically ill
patient in the intensive care unit (ICU).
The goal of hemodynamic monitoring is to
maintain adequate tissue perfusion. In
critically ill trauma victims, hypoperfusion
of vital organs may lead to multiple organ
systems dysfunction and death.
Classical hemodynamic monitoring is based on
the invasive measurement of systemic and
pulmonary vascular pressures and of cardiac
output. Although burdened with possible
flaws, central pressure monitoring is widely
used in the operating room and in the ICU.
Newer monitoring techniques are promising
but, for various reasons, have not yet
reached widespread acceptance, and they will
not be described in this lecture. The aim
of this lecture is to guide clinicians
through the interpretation of hemodynamic
data based on the application of classic
Why measure arterial blood pressure.
Regrettably, tissue perfusion (i.e.,
organ blood flow) cannot be directly
measured in clinical practice:
Organ Blood Flow = (arterial pressure -
venous pressure) / resistance
Assuming constant venous pressure and
constant resistance, measurement of arterial
blood pressure is the closest parameter we
have to blood flow. One can easily see how
crude this measurement is: by measuring the
blood pressure at the radial artery, we hope
to estimate the adequacy of blood flow to
the kidneys, brain, and coronary
circulation. However, physiology helps our
limited capacity: under normal
circumstances, organ blood flow is
maintained within normal range through ample
changes of blood pressure through
autoregulation. Unfortunately, in
pathological conditions such as trauma and
sepsis, autoregulation is significantly
impaired, and blood flow may become directly
dependent on perfusion pressure, which
therefore must be known.
Despite the limitations of peripheral blood
pressure measurement, maintaining a
reasonable value of arterial pressure is
associated with signs of adequate organ
function in most critically ill patients.
The following suggestions may enhance the
effectiveness of arterial blood pressure
The mean arterial pressure (MAP) is
the best physiological estimate of perfusion
pressure and is less subject to measurement
variability than the systolic pressure.
A MAP > 60 mm Hg is a reasonable target for
most patients. At times (chronic
hypertension, cerebral edema, spinal cord
ischemia, etc.), higher values are
necessary. Controversy exists on the
accuracy of clinical parameters of vital
organ function, such as urine
output and acid-base status, as early
indicators of tissue hypoperfusion.
However, no other proposed parameter, such
as serum lactate and gastric mucosal pH, has
yet been shown consistently to be superior.
Optimal blood flow through vital organs is
first achieved by maintaining an adequate
circulating volume. An increase in
blood pressure achieved using
vasoconstrictor agents in hypovolemic
patients does not provide adequate organ
perfusion and can be deleterious.
How to measure arterial blood pressure.
(generally automated) oscillometric blood
pressure measurement is no longer accurate
in the presence of rapidly changing blood
pressure, arrhythmias, hypotension and
hypertension. It should not be used in
hemodynamically unstable patients.
blood pressure measurement via a
catheter-transducer system is extremely
reliable if the system is properly set up,
and should be used whenever possible in
hemodynamically unstable patients.
Physiological approach to hypotension.
We will limit our discussion of hemodynamics
to the interpretation of hypotension, but
the general principles illustrated here
apply to hemodynamic monitoring in general.
We suggest a simple approach to the
diagnosis of hypotension, summarized in
This schema can be applied to clinical
practice using increasing levels of
monitoring. Table 2 shows a suggested
stepwise approach to the hemodynamic
monitoring of a hypotensive trauma patient.
In many cases, the diagnosis can be
suggested on clinical grounds. For
example, hypotension in a young patient
bleeding from a lower extremity crash injury
should be easily attributed to hypovolemia,
without the need of invasive monitoring.
In less obvious cases, it is reasonable to
“try” an intervention, and confirm or reject
the diagnosis post-hoc (“trial and
error”). For example, if our above
patient had also a history of coronary
artery disease, one should think of
myocardial dysfunction as a contributor to
the hypotension. Volume resuscitation could
still be a reasonable initial step.
As patients develop complex problems during
a prolonged ICU course, the etiology
of hypotension becomes be more and more
difficult to sort out, thus requiring
Example of a stepwise approach to the
hemodynamic monitoring of hypotensive trauma
Patient with sustained
Young, previously healthy patient
with lower extremity injury
65 y.o. patient with lower extremity
injury and a history of heart
“Trial & error”: volume, in a
Same patient, who did not respond to
a limited volume challenge
Arterial line + central monitoring
According to central monitoring
Same patient, hypotensive a week
later in the ICU
Arterial line + central monitoring
According to central monitoring
Central venous pressure (CVP)
monitoring provides a useful estimate of the
volume status of the systemic circulation
and (see below the discussion of
interpretation of CVP). The main
limitations of CVP monitoring are that
a) it does not allow measurement of
cardiac output, and b) it does not
provide reliable information on the status
of the pulmonary circulation in the presence
of left ventricular dysfunction.
Pulmonary artery (PA)
pressure monitoring with a PA
catheter allows to measure (CO) and stroke
volume (SV), PA pressure and PA occlusion
pressure (PAOP) and hence to separately
assess the performance of the right and the
left ventricle (RV and LV).
Central pressure measurements are often used
to estimate volumes,
i.e., the CVP estimates the volume of
the systemic circulation and the PAOP
estimates the volume of the pulmonary
circulation. As long as the postulate that
central pressures accurately reflect volumes
holds true, the characteristic hemodynamic
findings of hypotensive patients are
straightforward, as summarized in Table 3.
Central pressures and cardiac output changes
The following decision tree may guide
in the interpretation of hemodynamic data
obtained with invasive monitoring in a
hypotensive trauma patient.
Make a working diagnosis based on the
relationship between pressures (CVP and PAOP)
and cardiac output (CO or SV)
as summarized in Table 3. We assume at this
point that the CVP and the PAOP are adequate
estimates of the RV and LV end-diastolic
volumes respectively and that the right (CVP)
and left (PAOP) side of the circulation are
equally affected by the cause of
Revise our basic assumption
that CVP » volume of the right side of the
circulation and that PAOP » volume of the
left side of the circulation.
Unfortunately, this assumption is often
flawed. Knowledge of the basic physiology
underlying the pressure/volume relationship
in the central circulation is required to
accurately interpret central vascular
pressure data. Our basic assumption can be
altered under three main circumstances:
When the volume/pressure relationship (compliance)
of the RV or LV is abnormal, as it may
happen with concentric LV hypertrophy (LVH)
from hypertensive cardiomyopathy and aortic
stenosis. In this case, the measured PAOP
overestimates the LV end-diastolic volume.
When the pressure measurement does not
estimate the actual transmural pressure
across a cardiac chamber. An increase of
intrathoracic pressure gets transmitted to
the blood vessel where the tip of our
catheter is lodged, and increases the
measured vascular pressure without any
actual increase in circulating volume.
Common causes of increased intrathoracic
pressure that mislead the interpretation of
CVP and PAOP include PEEP, autoPEEP and
increased intra-abdominal pressure. The
fraction of pressure transmitted through the
blood vessel depends on a number of factors,
including the compliance of the anatomical
structures involved and the tension of the
blood vessel wall. A reasonable idea of the
amount of pressure transmitted can be
derived by considering the values of
compliance of the lung and of the chest
wall. For example, transmission of
auto-PEEP in a patient with COPD (compliant
lungs) may be substantial, while
transmission of applied PEEP in a patient
with ARDS (stiff lungs) may be minimal.
c. Mitral stenosis.
Valvular heart disease may affect the
interpretation of hemodynamic monitoring in
many ways, and yet invasive monitoring may
be crucial in the interpretation of
hypotension in patients with valvular
defects. With significant mitral stenosis,
the PAOP may not correctly estimate the LV
end diastolic pressure because of inadequate
LV filling time. Hence, a high PAOP may be
recorded when the LV is still underfilled.
d. Ventricular interaction.
RV volume overload from pulmonary
hypertension and/or RV congestive failure
may dilate the RV to a degree sufficient to
move the interventricular septum towards the
LV and limit its filling. Thus, the LV
pressure- and hence the PAOP- will increase
despite a lower volume of blood in the LV.
It is important to note that in all the
above situations, the pressures measured are
indeed correct, rather than
measurement errors. A high PAOP in the
presence of severe concentric LVH or mitral
stenosis is an accurate reflection of the
high pressure in the left atrium and, as
such, can result in acute pulmonary edema.
However, the LV may still be underfilled.
This example underscores both the difficulty
and the possible benefit of the correct
interpretation of invasive hemodynamic
monitoring in complex circumstances such as
valvular heart disease.
Look at the history.
The hemodynamic values evaluated at each
discrete point in time have to be put in the
patient’s context. Although any properly
obtained hemodynamic profile should be
interpreted as the reflection of a specific
moment in time, looking at previous numbers
as well as at all other relevant clinical
variables improves the accuracy of our
4. Separating RV and LV.
The CVP and PAOP may change independently,
because they measure two separate entities.
The CVP measures a pressure in the systemic
circulation, and the PAOP in the pulmonary
circulation. To better understand this
point, let’s examine the effect of a
hypothetical episode of acute, isolated LV
dysfunction from, e.g., ischemia.
The decreased LV contractility causes a
decreased stroke volume (SV), and a few less
mls of blood enter the systemic
circulation. This decrease of SV is so
minimal in respect to the size of the venous
reservoir that has no discernible effect on
the venous return to the RV. Thus, the RV
continues to eject an approximately normal
SV, which will be “accommodated” by the
dysfunctional LV by increasing the LV
end-diastolic pressure (~PAOP). At steady
state, the SV of the two ventricles will be
again equal and close to normal. Figure 1
summarizes graphically these events:
Isolated LV failure
LV failure + compensated RV failure
Isolated RV failure
RV failure + volume infusion
Interpretation of the CVP.
The following discussion is designed to
assist in the interpretation of the CVP when
the measurement of the CO is not available.
Venous return and CO are
described by these two curves:
In this graph., the starting CVP is 4 cmH2O.
If the CVP increases to 8 cmH2O,
the new value can occur at a variety of CO
values, as shown by the dotted vertical
line, with different physiological
implications. The two possible extremes are
that the CVP has increased only due to an
increase in volume (new venous return curve)
or that it has increased only due to a
decrease in contractility (new Starling
curve). Clearly, a combination of both
phenomena is possible. The same thinking
process can be illustrated for a decrease in
CVP. Hence, an isolated CVP value can
represent very different hemodynamic
conditions, and without a CO measurement, we
have to use clinical equivalents to
interpret the change in CVP. In a
reasonably stable patient, changes in MAP
should parallel changes in CO. An increase
in CVP will be likely due to an increased
circulating volume if the MAP also
increases. An increase in CVP will be
likely due to a decreased contractility if
the MAP decreases. In an unstable patient,
measurement of the CO may be necessary.
10. Magder S. Clinical usefulness of
respiratory variations in arterial pressure.
Am J Respir Crit Care Med 2004;169:151-55