Hemodynamic Monitoring Chapter 6 121
Chapter 6
Hemodynamic Monitoring
Michael R. Pinsky, MD, CM, Dr h.c., FCCP, MCCM
Key words: hemodynamic monitoring,
cardiovascular function, minimally invasive,
monitoring, pulmonary artery catheter, shock,
thermodilution
Disclosures: The author has consulted for and received
honoraria/speaking fees from Edwards Hfesciences, LiDCO
Ltd., and Cheetah Medical. He holds stock options in UDC°
Ltd. and Cheetah. He has received or applied for patents
6776764 and 11/388661. This work was supported in part by
NIH grant HL67181.
The purposes of hemodynamic monitoring arc to
characterize the cardiovascular state of the individual,
identify cardiovascular insufficiency and its most probable
causes, and monitor response to targeted therapies aimed
at restoring cardiovascular sufficiency.'2 The previous
chapters outlined the various forms of circulatory shock. It
is within this physiological framework that interpretation
of data derived from hemodynamic monitoring arises.
Circulatory shock and systemic hypotension are medical
emergencies, because if sustained, even for a short time,
they will result in end-organ dysfunction and increased
morbidity and mortality. The basic tenet of resuscitation
is to provide adequate oxygen (O.) delivery (DO,) to
meet metabolic demand and reverse any existing tissue
hypoperfusion. Accordingly, the choice of monitoring
technique must be individualized for each patient. In
general, noninvasive continuous monitoring, if available
and accurate, is preferred to invasive intermittent
monitoring. In reality, some degree of invasiveness
of monitoring is often required to accurately assess
the physiological data in a continuous fashion in the
monitoring and management of the critically ill patient.
The principal hemodynamic monitoring biomarkers
discussed in this chapter are arterial pressure, central
venous pressure, pulmonary artery pressure and its
occlusion pressure, estimates of cardiac output (CO), and
the various ways of assessing oxygenation. Like all vascular
monitoring using catheters connected to
electronic pressure transducers, hemodynamic monitoring
122 Chapter 6 I Comprehensive Critical Care: Adult
requires an open tubing system without obstruction
at the tip (often due to blood clots), elimination of
air bubbles in the tubing that dampen the signal, and
hydrostatic zeroing to the isoshcstic point (5 cm below
the ma nubrium sterni) in order to measure dynamic and
mean pressure and arterial pressure-derived estimates of
CO. However, unlike other vascular pressure measures,
arterial pressure has large pressure swings associated with
rapid acceleration and deceleration, and these demand
that stiff and short tubing be used to connect the intra-
arterial catheter to the pressure transducer.' The technical
aspects of measuring pressures and pressure-derived CO
are beyond the scope of this chapter. Similarly, measures
of CO by indicator dilution require complete indicator
mixing, no early recirculation (eg, intracardiac shunts), and
an appropriate sensor. All commercially available indicator
dilution devices have sufficiently accurate sensors, so most
measurement errors come from incomplete indication
mixing or early recirculation artifacts.
ARTERIAL BLOOD PRESSURE
Arterial blood pressure is the primary force driving blood
into the tissues. Thus, hypotension is a medical emergency
because it not only causes tissue hypoperfu.sion but also
effectively abolishes normal autoregulation of blood flow
distribution. Furthermore, owing to haroreceptor feedback
and the increased use of 13-adrenergic blocking agents,
often neither tachycardia nor hypotension occurs in shock
until the final terminal stages.'
Blood pressure varies phasically with each heartbeat.
Systolic pressure is the maximum pressure during
ventricular ejection, and diastolic pressure is the lowest
pressure in the blood vessels between heartbeats during
ventricular filling as the stored arterial blood runs off
into the periphery.The systolic to diastolic pressure
difference is called the pulse pressure and is determined
by left ventricular (LV) stroke volume, central arterial
capacitance, and to a certain extent the rate of LV
ejection. Since the arterial circuit is elastic and
functions as both a capacitor for the ejected blood and an
outflow resistor to prevent rapid decreases in arterial
pressure in
diastole, both systolic and diastolic pressures vary across
the vascular tree, Systolic pressure usually increases from
central to peripheral sites whereas diastolic pressure
decreases slightly. Mean arterial pressure (MAP),
estimated as the sum of diastolic pressure plus one-third
of the pulse pressure, is the primary driving pressure
for cerebral and peripheral organ perfusion. Coronary
perfusion is primarily determined by diastolic arterial
pressure because cardiac contraction during systole
otherwise stops intramyocarc.lial blood flow. Importantly,
MAP throughout the large to medium-sized arteries is
constant because these central arteries have almost no
measurable resistance.
Noninvasive Measures of Arterial
Pressure
The most common way of measuring arterial pressure
is with a sphygmomanometer.' This is often automated
using an oscillatory algorithm that senses flow. There is
a fundamental distinction between the automatic blood
pressure measures (eg, Dynamat) and auscultation-defined
measures of blood pressure using Korotkoff sounds. In
an unstable patient, one should not rely on noninvasive
automatic measures of blood pressure, because the
oscillatory sensing algorithm degrades, but rather should
measure blood pressure manually using a stethoscope•
Sphygmomanometric measurements of blood pressure
often give slightly higher systolic pressure and lower
diastolic pressure than those reported from simultaneous
direct measurement using an intra-arterial catheter. This
is because with cuff inflation the reflected pressure waves
summate, increasing systolic pressure, whereas the ischemic
vasodilation downstream from the occluded cuff decreases
cuff-opening diastolic pressure.
Invasive Measures of Arterial Pressure
Intra-arterial catheterization is the reference method
for blood pressure measurement and should be used
in all hemodynamically unstable patients in whom
accurate and continuous measures of arterial pressure are
required:The reason for this statement, which may be at
odds with prior recommendations:4 is that intra-arterial
catheterization provides instantaneous measures of MAP.

arterial pulse pressure, pulse pressure variation, and CO
with newer transducer technologies, The arterial catheter
allows easily repeated blood sampling for chemistries
and blood gas analysis. The most frequently used site for
arterial catheterization is the radial artery, Femoral artery
catheterization is also used and can be easier to perform
in hypotensive patients, although it is associated with more
complications when the catheter is left in place, Still, in the
profoundly vasoconstricted patient, radial arterial pressure
can underestimate central arterial pressure measured more
proximally."
Arterial Pressure Targets
Once one measures arterial pressure, the major question is
the target range of pressures to be maintained in order to
sustain organ perfusion without excessively increasing LV
afterload. Hypotension decreases organ perfusion pressure
and blood flow, stimulating a sympathetic response to
increase vasomotor tone, heart rate, and contractility. The
change in local vasomotor tone in response to decreased
arterial pressure forms the basis of autoregulation to
maintain constant blood flow. Cardiac output is important
to sustain an adequate and changing blood flow to match
changes in vasomotor tone such that arterial pressure
to the organ remains optimal. Since CO is proportional
to metabolic demand, which itself can vary 3-fold in a
matter of minutes, there is essentially no normal CO in the
critically ill patient. However, as MAP decreases below
65 nun Hg in a previously nonhypertensive patient, organ
perfusion becomes compromised.Thus, a reasonable
arterial pressure target is a MAP between 90 and 6() mm
Hg,'" although the optimal MAP will vary depending
on the underlying cause of hernodynamic instability."
To assess the adequacy of MAP to sustain peripheral
perfusion, the bedside clinician needs to assess additional
measures of organ perfusion, such as mixed venous 02
saturation (Svo2), central venous 0, saturation (Scvo,),
lactic acid levels, urine output, capillary blood flow, or
gastric mucosal Pco,.Thc first 2 of these parameters are
discussed further subsequently. Finally, cerebral perfusion
is a function of MAP relative to intracrkmial pressure. Thus,
in the setting of neurotrauma cerebral perfusion pressure
must be measured. As a general rule one should target a
Hernodynamic Monitoring Chapter 6 123
MAP of 90 mm Hg for traumatic brain injury': and a MAP
greater than 65 min Fig for other forms of shock.
CENTRAL VENOUS PRESSURE
Although central venous access is often used as a secure
venous access site for infusion of fluids and vasoactive
drugs as well as sampling of blood for various things
including Scvo,, its use in assessing intravascular volume
status is poor. Central venous pressure (CVP) is not a
measure of central blood volume nor can its values be
used to determine whether a patient will be volume
responsive.'3.1' Still, dynamic decreases in CVP of greater
than 2 mm Hg during spontaneous inspiration appear
to identify those patients who arc volume responsive
independent of the absolute CVP value.'5 CVP is the back
pressure to systemic venous return., thus, high CVP values
(>12 mm Hg) indicate a larger than normal mean systemic
pressure allowing an adequate perfusion pressure gradient
to sustain venous return.'6 However, CVP in and of itself
does not reflect blood volume status. From the perspective
of patient safety, the insertion of a central venous catheter
using ultrasound guidance for internal jugular vein
insertion has also become part of standard care and has
markedly reduced complications."
Noninvasive Measures of CVP
Central venous pressure can he estimated noninvasively
by inspection of jugular venous pulsation. With the patient
sitting at 450, the height of the jugular venous distention
(JVD) above the sternal angle (itself about 5 cm above the
center of the right atrium) can be used to estimate CVP'8
Potentially, this approach is most useful in documenting
sustained increases in NU" on phasic increases in WO
with spontaneous inspiration, suggesting cor pulmonale or
pulmonary hypertension, and periodic cannon waves seen
in atrial fibrillation,
Invasive Measures of CVP
Although CV? is usually measured from the internal
jugular or suhclavian vein via an indwelling catheter, it can
be estimated from a femoral venous site as long as there
124 Chapter 6 Comprehensive Critical Care: Adult
is no intra-abdominal hypertension (ie, intra-abdominal
pressure <12 mm Hg). Using the femoral site for a central
venous catheter is also associated with a greater incidence
of complication0 The effects of the respiratory cycle on all
intrathoracic vascular pressures must be considered when
examining a continuous CVP measurement. To minimize
the pressure artifact induced by respiratory pressure
changes, all intrathoracic vascular pressures should he
measured at end-expiration. In the dyspneic patient or a
patient who is fighting the ventilator, determination of end-
expiration can be very difficult, if not impossible. Extreme
caution needs to be used when estimating CVP under
these conditions.
PULMONARY ARTERY PRESSURE
AND PULMONARY ARTERY
OCCLUSION PRESSURE
Bedside balloon flotation insertion of a pulmonary artery
catheter and subsequent measurement of right atrial.
pulmonary arterial, and pulmonary artery occlusion
pressure (Ppao) plus CO and mixed venous 0, saturation
defined hemodynamic monitoring in critical care for more
than 40 years.21 Pulmonary artery pressure is measured
from the tip of a nonoccluded pulmonary artery catheter
once this catheter has been floated past the pulmonic
valves into the main pulmonary arteries. Mean pulmonary
artery pressure measures can be calculated similarly to
MAR as described previously, with the proviso that they
are measured at end-expiration. Thus, one can measure
pulmonary artery systolic, diastolic, and mean pressures.
Mean pulmonary artery pressure is usually used to
assess input pulmonary vascular pressure for calculating
pulmonary vascular resistance (PVR), whereas systolic
pulmonary artery pressure reflects the a fterload against
which the right ventricle ejects.
By balloon inflation and migration of the catheter tip into
a medium-sized pulmonary artery where it is occluded, one
can measure Ppao. Pulmonary artery occlusion pressure
is used most often to assess PVR. pulmonary edema,
intravascular volume status and LV preload, and LV
performance."-:1
Pulmonary Hypertension and
Pulmonary Vascular Resistance
Increased pulmonary arterial pressure impedes right
ventricular (RV) ejection, causing RV dilation and
a decreased CO. If pulmonary hypertension occurs
rapidly, as with massive pulmonary embolism or marked
hyperinflation, acute cor pulmonale and cardiovascular
collapse occur. Pulmonary hypertension can be due to
an increase in pulmonary vasomotor tone, pulmonary
vascular obstruction, or passive increases in Ppao due
to LV failure. The pulmonary circulation normally has a
low resistance, with pulmonary arterial diastolic pressure
only slightly higher than Ppao. By measuring pulmonary
artery pressure, Ppao, and CO, one can calculate PVR
as the ratio of the pressure gradient divided by flow:
(mean pulmonary artery pressure — Ppao)/C0. If
PVR is increased, then therapies to reduce pulmonary
artery pressure are needed (eg, 0„ inhaled nitric oxide,
intravenous pulmonary vasodilator therapy). Patients
with pulmonary hypertension who have increased PVR
that is not responsive to vasodilator therapy usually have
either vascular obstruction (eg, pulmonary embolism), or
vascular loss (eg, emphysema). If pulmonary hypertension
is associated with a normal PVR, then LV failure is its
probable cause.
Unfortunately, PVR is a poor measure of pulmonary
vasomotor tone, Pulmonary vascular pressure can
vary across lung regions because of lung distention,
structural damage, and acute inflammatory processes
(eg, hyperinflation. emphysema, pulmonary fibrosis.
pulmonary emboli, and acute lung injury). Thus. measuring
PVR cannot identify local injury or explain why PVR
is elevated. Furthermore. with nonhomogeneous lung
disease. pulmonary blood flow will preferentially go to
those regions with the lowest resistance, thus masking lung
abnormalities
Pulmonary Edema
Pulmonary edema can he caused by elevations of
pulmonary capillary pressure (hydrostatic or secondary
pulmonary edema), increased capillary or alveolar
epithelial permeability (primary pulmonary edema),

or a combination of both. If pulmonary capillary
pressure increases above 20 mm Hg, hydrostatic
vascular forces promote increased fluid flux across the
capillary membrane, flooding the alveoli. However, if
capillary or alveolar cell injury is present, as in acute
lung injury, alveolar flooding can occur at much lower
pulmonary capillary pressures. Clinicians usually use
Ppao as a surrogate of pulmonary capillary pressure,
and if pulmonary venous resistance is not increased, this
assumption is valid. Measures of absolute Ppao are used
to determine the cause of pulmonary edema. In the setting
of pulmonary edema, Ppao values less than about 18 rnm
Hg suggest capillary leak, whereas values greater than
this suggest heart failure. However, these are not hard
values. For example, transient severe LV dysfunction can
transiently increase Ppao during upper airway obstruction
with vigorous inspiratory efforts (inspiratory stridor,
obstructive sleep apnea), unstable angina (reversible
ischemia), and arrhythmias. Increased pulmonary capillary
pressure can occur when massive sympathetic discharge
increases pulmonary venous resistance (eg, intracerebral
hemorrhage and heroin overdose), which reverses quickly
while the pulmonary edema remains. Furthermore,
persistently elevated pulmonary capillary pressures can
coexist with normal Ppao values if pulmonary venous
resistance is increased and CO is also increased. as is often
the case in high altitude pulmonary edema and end-stage
acute lung injury.
Left Ventricular Preload and Volume
Status
Pulmonary artery occlusion pressure is often used
erroneously to assess intravascular volume status and
LV preload. Regrettably, neither absolute Ppao values
nor their change in response to fluid infusion trends
preload or volume responsiveness." The reasons for this
are multiple. First, although increases in LV end-diastolic
volume will increase CO in volume-responsive patients,
the relation between Ppao and LV end-diastolic volume
is curvilinear and may be very different among subjects
and within subjects as RV volumes, intrathoracic pressure,
and myocardial ischemia vary. Second, Ppao is not the
distending pressure for LV filling but is only an estimate
Hernodynarnic Monitoring I Chapter 6 125
of LV intraluminal pressure, whereas pericardial pressure
and LV diastolic compliance can vary widely and not
he indicated by this or other measures. Hyperinflation,
tamponade, and active inspiratory and expiratory muscle
activity can rapidly alter pericardial pressure. Myocardial
ischernia, arrhythmias, and acute RV dilation can alter LV
diastolic compliance and can occur over a few heartbeats.
Thus, it is not surprising that Ppao is a very poor predictor
of preload responsiveness. The use of Ppao as a measure of
LV end-diastolic volume and preload responsiveness is not
recommended.
Assessment of Left Ventricular
Performance
The assessment of LV performance is central to invasive
hemodynamic monitoring. The primary determinants of
LV performance are preload (LV end-diastolic volume),
afterload (LV wall stress, which is itself the product of
LV end-diastolic volume and diastolic arterial pressure),
heart rate, and contractility. Since LV end-diastolic volume
is a fundamental determinant of stroke volume and LV
stroke work. Ppao is often used as a surrogate for LV
end-diastolic volume and for the calculation of stroke
work, which is the product of the difference between
MAP to Ppao and stroke volurne.Thus, Ppao can be
used to construct Starling curves that plot Ppao versus
LV stroke work. With this approach. patients with heart
failure can be classified by their Ppao and cardiac index
values using a Ppao of 18 mm Hg and a cardiac index of
2.2 Uminim2 as cutoff values. Low cardiac indices and
high Ppao reflect heart failure, and low Ppao reflects
hypovoIemia, whereas high cardiac indices and high Ppao
reflect volume overloaded and low Ppao reflects increased
sympathetic tone.
These constructs are probably too simplistic, as many a
clinical study has documented. Still, in the patient without
lung or pericardial disease. tamponade, or pulmonary
embolism, the relation between Ppao and LV stroke work
can be used to assess LV performance.
126 Chapter 6 I Comprehensive Critical Care: Adult
CARDIAC OUTPUT
Shock reflects an inadequate DO, to meet the body's
metabolic demand, and CO is a primary determinant of
DO2, Indeed, except for extreme hypoxemia and anemia,
most of the increase in DO, that occurs with resuscitation
and normal biological adaptation is attributable to
increasing CO. A vast array of devices, both invasive and
noninvasive, are available that measure CO accurately
enough to drive clinical decision making.
Noninvasive Measures of Cardiac
Output
Cardiac output can be reliably measured noninvasively
using a variety of techniques including ultrasound,
plethysmographic pressure profile analysis, and
bioreactance. The most commonly used noninvasive
techniques arc ultrasound based and include
echocardiography, pulsed esophageal Doppler, and
continuous-wave suprastemal notch ultrasound.:`
Echocardiography
To conduct transthoracic echocardiographic analysis of
the aortic root flow, the clinician places the echo probe
along the short axis of the aorta using pulse Doppler to
measure the aortic value diameter and then positions the
probe from the suprastemal notch looking through the
aortic value to measure aortic velocity using continuous-
wave Doppler. Although this procedure requires training
and measures only a single point in time, it can reliably
estimate CO.'" The accuracy of the measure increases
with transesophageal echocardiography, but so does
its invasiveness. One can use changes in aortic flow
during positive pressure ventilation to predict volume
responsiveness, as described subsequently,=2:-4 Recent
consensus conferences of multiple professional societies
have stated that basic expertise in ultrasound techniques
should be a central part of all critical care medicine
training. However, since the transthoracic measures of CO
are highly dependent on the expertise of the operator and
cannot he measured continuously, this important method
will not be discussed further.
Esophageal Doppler Ultrasound
Esophageal Doppler ultrasound uses an esophageal
probe similar in size to a nasogastric tube to measure
descending aortic flow as it parallels the esophagus. A
Doppler transducer probe is inserted orally or nasally
to midthoracic level and rotated until the probe senses a
characteristic aortic velocity signal profile' This technique
can be taught to bedside nurses and can be used to drive
resuscitation algorithms to improve patient outcomes in
patients undergoing high-risk surgery.3° Several studies
have documented that esophageal Doppler estimates of
CO and its change can be made accurately after minimal
training.;' Similarly, dynamic increases in CO assessed by
esophageal Doppler in response to a passive leg-raising
test predict volume responsiveness.32 The only drawback
to this technology is that nasogastric insertion is difficult,
necessitating oral insertion, so this is not the preferred
technique in the awake nonintubated patient. However,
when compared with standard therapy in randomized
clinical trials, the use of esophageal Doppler ultrasound
to achieve targeted DO, levels in high-risk perioperative
patients resulted in decreased hospital length of stay and
decreased postoperative complications.'` Furthermore.
complications with the use of esophageal Doppler
measures are very rare.
Transcutaneous Doppler Ultrasound
This modification of the esophageal Doppler technique
uses a handheld probe placed at the suprastemal notch
with the transducer aimed downward at the aortic
valve. This technique is easy to learn and gives accurate
measures of IY stroke volume and CO.'u-1 However, like
echocardiographic techniques, transcutaneous ultrasound
cannot be used continuously. This accurate. noninvasive
device can be used as a decision support tool to identify
patients who are volume responsive and to calibrate
minimally invasive devices (discussed later). Potentially,
transcutaneous ultrasound will he most readily accepted in
the emergency department?'" during medical transport,'
and on the general medical floor to rapidly identify
cardiovascular instability." Still, no clinical trials have
been published using this promising technology to guide
resuscitation.

Thoracic Electrical Bioreactance
Thoracic electrical bioimpedance has been around
for decades and is accurate only in highly shielded
environments because electrical interference makes the
measures of CO unreliable." However, using the frequency
modulation component of the thoracic impedance signal
in a process called bioreactancc markedly eliminates this
artifact and increases the accuracy of the estimates of CO
and its change.4° Both bioimpedance and bioreactance rely
on a derivation of Ohm's law, which states that the flow of
an electrical current is equal to the voltage drop between
2 ends of a circuit, divided by the resistance or
impedance to current flow. Since most of current flow
through the thorax occurs in the aorta and versa cava,
changes in impedance reflect changes in volume and CO.
Validation studies comparing bioreactance and
pulmonary artery catheter thermodilution CO conclude
that bioreactance has acceptable accuracy.'" Furthermore,
the dynamic responsiveness of the bioreactance signal
allows it to he used in combination with a passive leg-
raising maneuver to assess fluid responsiveness. However,
although clinical trials using bioreactance technology to
guide resuscitation are ongoing, no clinical studies have
yet been published using this promising technology.
Invasive Measures of Cardiac Output
Thermodilution Using the Pulmonary
Artery Catheter
Invasive measurement of CO using the pulmonary
artery catheter remains the most common method used
clinically, although this trend is rapidly changing.42 The
pulmonary artery catheter has a thermistor located 4 cm
from the tip and a proximal port located 30 cm from the
tip. Cardiac output is measured by injecting cold fluid
through the proximal port. Under normal conditions, once
the pulmonary artery catheter is placed. the proximal
port resides at or above the right atrium such that
bolus injections of cold (thermal) fluid are mixed in the
contracting right ventricle. The thermistor records the
dynamic change in blood temperature.The thermodilution-
estimated CO is inversely proportional to the area under
the temperature versus time curve. Subsequently, a random
Hemodynamic Monitoring Chapter 6 1 27
thermal (heat) signal using an induction coil in the RV
region of the pulmonary artery catheter permits the
clinician to estimate CO continuously, albeit less accurately
measuring dynamic changes in flow." Importantly,
measures of stroke volume and CO when coupled with
other measured hemodynarnic variables allow for the
calculation of various important parameters, like LV stroke
work and both systemic DO, and consumption. Although
the clinical utility and outcome benefit of pulmonary
artery catheterization have been debated for many years:"
no study has used pulmonary artery catheter—specific
measures to drive resuscitation algorithms and compared
outcomes with those of other patients not having such
inforrnatione' Given the present climate in critical care
medicine, it is highly doubtful that such a study will be
undertaken.`'
Similar to the pulmonary artery catheter is the
transthoracic thermodilution method of estimating CO, the
only difference being that the measure of thermal change
is made in a central artery instead of the pulmonary artery.
This approach does not require pulmonary artery catheter
insertion but has a major limitation in that the arterial
sample needs to be of a flow-by sensor, since the thermal
signal must pass by the sensor to report its change, thus
requiring insertion of the thermistor probe into a femoral
artery.
Arterial Pulse Pressure Waveform Analysis
Pulse pressure waveform analysis is also referred to as
minimally invasive monitoring because it requires only
the insertion of an arterial catheter. Several commercially
available devices use proprietary algorithms that analyze
the arterial pressure waveform (or the pulse contour).47
Each estimates central arterial compliance differently, and
the techniques that require a standard external measure
of CO for their calibration are the most aceurate.48 Since
arterial compliance varies depending on the patient's
blood pressure, age, sex, and height, these devices usually
need to be recalibrated on a regular basis. The 2 common
reference standards for calibration are transthoracic
lithium dilution`' and thermodilution.'° Recent algorithms
have been developed that do not require external
128 Chapter 6 1 Comprehensive Critical Care: Adult
calibration with a CO reference standard.'' Recent head-
to-head comparisons of all the invasive and minimally
invasive devices demonstrated significant intradevice
variability,' suggesting that if one uses these devices. it
is hest to stick with only 1 or 2 devices and learn to use
them well rather than use several over time in the same
patient, A list of the available devices commonly used to
estimate CO is given in Table 1 on page 128. In general, a
minimally invasive device should be externally validated
using an independent means if possible, and this should be
done often if the cardiovascular tone of the patient varies
rapidly.
A central question in the resuscitation of hemodynamically
unstable patients is whether they need increased blood
flow to the tissues. A patient who is in circulatory shock
will need increased DO,. Accordingly, efforts to rapidly
increase blood flow are important to minimize tissue
ischernia and organ dysfunction.Traditionally, an increase
in CO of greater than 15% after a fluid challenge has
been considered the gold standard reflecting fluid
responsiveness. If CO does not increase in response to
fluid challenge. then the presumptive diagnosis of impaired
Table 1.
Commercially Available Devices to Estimate Cardiac Output at the Bedside
Noninvasive
Echocardiography
Transcutaneous ultrasound
Esophageal Doppler
Rioirrpedance
Bioreactance
Plethysmographic
Invasive
Minimally invasive (external calibration)
Minimally invasive (self-calibrating)
Pulmonary artery catheter
cardiac contractility is made and inotropes are given to
increase blood How. Importantly, there is no absolute CO
target that should he taken as optimal. The focus during
resuscitation from circulator shock should be a relative
change in CO in response to therapy and the associated
change in organ perfusion.
Over the past 15 years, numerous studies have validated
that either arterial pulse pressure or stroke volume,
referred to as pulse pressure variation (PPV)°.54 and
stroke volume variation (SVV),• respectively, induced
by positive pressure ventilation can accurately identify
patients who are volume responsive and those who are
not.' A threshold value of either PPV or SVV greater
than 15% defines volume responsiveness when patients
are ventilated with a tidal volume of 8 mlikg or more.
These parameters are not accurate during arrhythmias and
spontaneous breathing because of varying R-R intervals
and ventricular interdependence—induced changes in
LV diastolic compliance, respectively. In those cases, one
can perform a passive leg-raising maneuver and note
the transient increase in CO. Postural changes such as
passive leg raising have been used for many years to
Various manufacturers
USCOM (LJSCOM Ltd)
CardioO (Deltex Medical)
Bio2 (SonoSite)
NICOM (Cheetah Medical)
Nexfin (8MEYE)
PiCCO plus (Pulsion Ltd)
LiDCO plus (LiDCO Ltd)
FloTrac (Edwards Lifesciences)
LiDCO rapid (LiDCO Ltd)
Bolus thermodilution (Edwards Lifesciences) & Continuous
thermodilution

transiently increase venous return. The legs are raised to
300 above the chest and held for I minute, and the maximal
increase in CO is recordcd.This maneuver approximates
a 300-mL blood bolus in a 70-kg patient that persists for
approximately 2 to 3 minutes Changes in heart rate,
blood pressure, CVP, or CO are then observed after
passive leg raising (PLR).The dynamic increases in CO
induced by passive leg raising are as sensitive and specific
in predicting volume responsiveness as is PPV during
positive pressure mechanical ventilation using any of the
commercially available, minimally invasive monitoring
devices. Importantly, one cannot use the pulmonary
artery catheter because neither bolus nor continuous CO
measures by this device are rapid enough in their sensing
to detect these small and short-lived changes in CO.
OXYGENATION AND TISSUE
PERFUSION
Since there is no specific CO that is considered normal,
only one that is adequate or inadequate to meet the
metabolic demands of the body, other measures of
cardiovascular sufficiency need to he made to assess the
adequacy of blood flow. Importantly, maintenance of a
normal blood pressure does not equate to adequate tissue
blood flow because vasomotor tone varies to keep arterial
pressure in an acceptable range. Furthermore, targeting
a defined supranormal level of DO, does not ensure
adequate flow to meet metabolic demand.To assess the
adequacy of 02 delivery, one needs to measure arterial and
venous blood 0, saturations and surrogate measures of
tissue hypoxia, such as serum lactate levels and tissue 0,
saturation."' Pulmonary artery catheterization indentifies
true mixed venous 0 saturation (Svo 2), whereas Sevo2
taken via a central venous catheter mostly reflects the
degree of 0, extraction from the brain and the upper part
of the body.
Pulse Oximetry
Continuous monitoring of arterial blood 0 2 saturation
(Sao) using pulse oximetry is universally used in the ICU
although clinical data of its usefulness are lacking despite
Hemodynamic Monitoring F Chapter 6 129
impressive clinical trials attempting to demonstrate a
beneficial effect.'l The greatest utility of pulse oximetry
is in reducing the need for repetitive arterial blood
gas analysis. Pulse oximeters estimate Sao, saturation
by measuring the tissue light absorption at 2 specific
wavelengths, 660 nrn (red) and 940 run (infrared).
The
absorption ratios, based on calibration against known Sao,
values, allow for the continuous measurement of Sao,.
Importantly, nonphasic 02 absorption also occurs, so the
devices presume that dynamic changes in the density of
absorption must reflect the arterial pulse, hence the name
pulse oximetry. Accordingly, if no arterial pulsatility is seen
from the plethysmographic waveform, Sao, cannot be
calculated using these devices. Since they actually measure
the pulsed 0, saturation, they arc referred to as pulse 0,
saturation (Spa,), which in practice approximates Sao2
wel1,62
Detection of Hypoxemia
The most commonly used application of Spa, is the
detection of hypoxemia.6' Hypoxernia is usually defined
as a Spa, less than 90%. Titration of Fio2 and other
ventilatory maneuvers to keep Spa, greater than 90% is
a common goal in most critically ill patients. However,
there is little additional benefit in increasing Spot
above 95% because of the shape of the oxyhemoglobin
dissociation curve limits 02-carrying capacity. Taking the
usually stated 95% confidence limits of ±4%, an oximeter
reading of 95% could represent a Pao, between 60 mm
Hg (Sao2 > 91 %) and 160 mm Hg (Sao, > 99%). Thus,
decisions on ventilatory therapy should not be determined
solely by Spa, values.
Detection of Volume Responsiveness
Another novel use of pulse oximetry is the
plethysmographic waveform analysis. Variation in
plethysmographic density from beat to beat reflects
paired variations in arterial pulse pressure, thus making
plethysmographic variability another method of assessing
volume responsiveness in the ventilator-dependent patient,
as discussed earlier.mm
130 Chapter 6 Comprehensive Critical Care: Adult
Venous Oximetry and the Physiology
of Svo 2 and Scvo 2
DO2 describes whole-body 02 supply without
reference to blood flow distribution or 0, uptake. DO, is
equal to the product of CO and arterial 0, content (Can,).
Arterial 0, content is the sum of 0, bound to hemoglobin
(Hb) (product of lib concentration Sao,) and dissolved
02 (No,). The formula is Cao, = Hb x 1.36 x Sao, x Pao: x
0.0031. Thus, dissolved 0, in the plasma has minimal effect
on overall Cao,.
Clinically DO2 only has relevance to 0: demand estimate
,
by whole-body 0, consumption (VO:). Since VO, must
equal the difference in DO, and the amount of 0,
remaining in mixed venous blood, VO, can be expressed by
the Fick principle as the product of CO and
arteriovenous 0, content difference (Cao2 - Cvo,): VO, =
CO (Can, -Cvo,), where mixed venous 0, content (Cvo,)
like Cao,
is Cvo, = Hb x 1.36 x Svo, x Pao, x 0.0031. By simple
algebraic transposition, Cvo, = Can, - (V0„/C0). Thus.
Cvo, reflects the relationship between whole-body VO,
and CO under conditions of a constant Cao,. Importantly.
Svo2 is the most important factor to determine Cvo, since,
like in arterial blood, the dissolved 0, can be neglected and
Hb is usually constant over short time intervals. Thus, Svc),
correlates well with the 0, supply-to-demand ratio f6
Trending Svo2 and Scvo2 to Assess
Circulatory Sufficiency
A decrease in Svo, and Scvo, usually represents an
increased metabolic stress. Factors that decrease Svo,
include low CO or anemia (decreasing DO,), exercise
(increasing VO,), and hypoxemia. In the sedated patient
not actively bleeding and in whom Sao, is greater than
90%, Svo, and CO covary Importantly, the normal
cardiovascular response of increasing VO, (exercise) is
to increase 0, extraction and CO.Thus, Svc), normally
decreases during exercise despite increasing
Therefore, a decrease in Svc), or Scvo, does not necessarily
mean that tissue hypoxia occurs. Only if Svc), decreases
less than 50% can one he sure some degree of tissue
hypoxia has occurred." Conversely, a normal Svo, (eg,
>72% saturation) does not ensure that some vascular
beds are not underperfused. In summary, Svo, can
decrease, suggesting increasing cardiovascular stress
due to a decrease in DO2 (eg, anemia, hypoxia,
hypovolemia, or heart failure) or increased VO, (eg, fever,
pain, stress, shivering).
Since central venous catheterization is commonly
performed for a variety of reasons in critically ill patients,
direct access to central venous blood is also commonly
available in most critically ill patients. Thus, Sevo2 is often
used as a surrogate for Svo2. Since most central venous
catheters have their distal tip in the superior vena cava,
Scvo2 reflects the venous blood of the upper body but
neglects venous drainage from the lower body (ie, intra-
abdominal organs). Accordingly, Scvo, is usually lower
than Svo, by 2% to 3% because the lower body extracts
less 0, than the upper body, making inferior vena caval 0,
saturation higher.` The primary cause of the lower inferior
vena caval 0, extraction is the oxidative phosphorylation
blood flow (eg, renal blood flow, portal flow, hepatic blood
flow). Importantly, however, Svo, and Scvo2 change in
parallel when the ratio of whole-body 02 supply and
0, demand is altered.' Still, the difference between the
absolute values of Scvo, and Svo: changes under conditions
of shock. In septic shock, for example, Scvo2 often exceeds
Svc), by as much as 8%, and the opposite can occur with
hypovolemic and cardiogenic shock. During cardiogenic
or hypovolemic shock. mesenteric and renal blood flow
decreases, which for the same level of metabolic demand
increases local 0, extraction.' In septic shock. splanchnic
0, consumption increases, thus increasing local 0,
extraction despite increased CO." Thus, Scvo, cannot be
used as surrogate for Svo, under conditions of circulatory
shock. As a rule, if Scvo, is less than 65% then inadequate
DO, probably exists, but if Scvo, is greater than 70% it has
no prognostic utility.''•"
Near-Infrared Spectroscopy to
Measure Tissue 0 2 Saturation
Near-infrared spectroscopy (NIRS) is a noninvasive
technique capable of continuous measurement that uses
the varying light absorption properties of deoxygenated
and oxygenated blood to determine tissue 0,

saturation (Sto2).Near-infrared light (680-800 nm) is
largely transparent to biological tissue and is absorbed
primarily by Hb, and absorption is minimally affected
by skin blood flow, The Sto2 signal primarily reflects
oxygenation in the small end-vessels and, unlike pulse
oxirnetry, approximates the venous 0, saturation.
Although different devices have different tissue
penetration levels and sensitivities to changes in lib
concentrations, several studies showed that Sto, can
vary independently of Spa, and Scvo,. Regional Sto2
measurements can detect occult regional hypoxia even
when Svo2 and vital signs have normalized, making
it a valuable tool in the assessment of compartment
syndromes."' Tissue 0, saturation values greater than
85% also reflect resuscitation adequacy, whereas in trauma
patients persistent Sto, values less than 60% reflect a
poor outcome.73 Dynamic Sto, measurements using brief
vessel occlusion challenges, referred to as a vascular
occlusion test, can define initial blood flow distribution: a
decreased deoxygenating slope suggests misdistribution
of microcirculatory flow whereas a reduced reoxygenation
slope suggests inadequate CO," This dynamic technique
has been used to assess circulatory sufficiency in patients
with trauma and sepsis and during weaning from
mechanical ventilation.
FUNCTIONAL FIEMODYNAMIC
MONITORING
The primary utility of hemodynamic monitoring is to
identify cardiovascular instability, help determine causal
factors, and guide therapy.8° A fundamental assumption
underpinning these methods is that the rapid identification
of tissue hypoperfusion and its correction will improve
patient outcomes. Functional hcmodynamic monitoring
uses defined physiological perturbations to stress the
cardiovascular system and reveal resultant changes in
arterial pressure and C0.8' These methods include the
assessment of volume responsiveness and the detection of
occult tissue hypoperfusion.
Hemodynamic Monitoring I Chapter 6 131
Preload Responsiveness
The use of positive pressure breathing-induced PPV
and SVV (discussed earlier) and passive leg-raising-
induced changes in C0s2 accurately predicts volume
responsiveness. Similarly, one can measure inferior vena
caval diameter decreases during inspiration," superior
vena caval decreases during inspiration,"' and aortic flow
velocity changes and plethysmographic pulse oximetry
change to predict volume responsiveness. Using a simple
SVV minimization can markedly reduce intra-operative
protocol hospital length of stay.a7
Occult Circulatory Shock
Examining the changes in Sto2 deoxygenation and
reoxygenation during a vascular occlusion test reveals
misdistribution of blood flow and occult circulatory shock,
respectively, and the Sic, changes induced by a vascular
occlusion test!"
Goal-Directed Therapy
Initial studies suggested that the nonspecific
increase in DO, to supranormal levels in critically ill
patients
improved survival' Subsequent studies using aggressive
resuscitation to increase DO, to supranormal levels in
patients with existing organ failure to document survival
benefit reported that if anything this procedure increased
mortality.'" In essence, the benefit of increased flow
cannot he realized by already dead tissues.' '`'5 However,
early aggressive resuscitation driven by hemodynamic
monitoring if done before the onset of organ injury
uniformly improves survival, whether done as early
goal-directed therapy in septic patients presenting to
an emergency department,%." and as preoptimization
therapy for high-risk surgical patients,"'w but less so in
postoptimization therapy for postoperative patients with
difficult intraoperative courses," suggesting that early
aggressive resuscitation is most useful in the intraoperative
arena but still shows benefit in the ICU, although to a
lesser degree.
132 Chapter 6 I Comprehensive Critical Care: Adult
SUMMARY
Hemodynamic monitoring is done to determine whether
a subject is physiologically stable, to determine whether
blood flow to the periphery is adequate to meet metabolic
demands, to diagnose specific causes of circulatory
shock, to determine specific therapies. and to indicate
when cardiorespiratory sufficiency has been
reestablished. Using our knowledge of cardiorespiratory
physiological changes, disease pathophysiological factors,
and the strengths and limitations of device
measurement, the bedside caregiver now has an extremely
powerful array of monitoring devices to accomplish these
goals. However,
no hemodynamic monitoring device will improve outcome
unless coupled with a treatment that itself improves
outcome at What is primarily missing now is a field theory
of global cardiorespiratory performance and validated
management protocols of sufficient generalizability to be
universally applied. Until that time arrives, the need for
well-trained bedside applied physiologists in the guise of
intensivists will remain a health care priority.
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