10
26
Chapter Title
Principles of Invasive Cardiovascular
Monitoring
CHAPTER AUTHOR
MATTHEW R. TIMLIN AND KENNETH A. SCHENKMAN
PEARLS
• To gain basic knowledge of the development of the eye.
• To develop essential understanding how abnormalities at
P Evarious
A R L Sstages of development can arrest or hamper normal
formation of the ocular structures and visual pathways.
• Hemodynamic monitoring refers to measurement of the func-
tional characteristics of the heart and circulatory system that
affect the perfusion of tissues with oxygenated blood.
• Hemodynamic monitoring can be performed invasively or
noninvasively and can be used for diagnosis, surveillance, or
titration of therapy.
• The central venous waveform is composed of three waves
(a, c, and v) and two wave descents (x and y).
Role of Invasive Hemodynamic Monitoring
Since William Harvey’s observation in the early 1600s that the
heart pumps blood in a continuous circuit, the function of the
circulatory system has been the subject of intense scrutiny. Hemo-
dynamic monitoring refers to measurement of the functional char-
acteristics of the heart and circulatory system that affect the perfu-
sion of tissues with oxygenated blood in order to maintain
homeostasis and to remove byproducts of metabolism. Several dif-
ferent types of invasive hemodynamic monitoring can be used
concurrently to guide management. The goal of hemodynamic
monitoring is to provide accurate diagnoses and to guide additional
interventions to deliver improved care to the critically ill patient.
In his 1733 report “Statical essays: containing haemastaticks;
or, an account of some hydraulick and hydrostatical experiments
made on the blood and blood-vessels of animals,” Hales1 de-
scribed early experiments in horses in which he used tubular
devices inserted directly into arteries to measure intravascular
pressures. Fig. 26.1 depicts Hales and an assistant in the process
of these early experiments. This figure also illustrates a simple
method for inferring arterial versus venous placement of a vascu-
lar catheter, which can also give a quick bedside estimate of
central venous pressure.
Frequently in the pediatric intensive care unit (PICU), nonin-
vasive assessments of hemodynamics are supplemented by inva-
sive hemodynamic measures that require entrance into the intra-
vascular space. Such invasive hemodynamic measurements include
placement of central venous catheters (CVCs), arterial catheters,
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• To acquire adequate information about normal anatomy of
the eye and related structures and develop a strong foundation
for the understanding of common ocular problems and their
consequences.
• The arterial waveform has three components: rapid upstroke,
dicrotic notch, and runoff.
• Pulse pressure variation has excellent specificity as an indicator
of fluid responsiveness in many critically ill patients.
• Cardiac output can be calculated using the Fick method or
measured directly via thermodilution.
• A pulmonary artery catheter can be used to measure cardiac
output and indices of oxygen delivery and extraction.
and pulmonary artery catheters (PACs). Invasive hemodynamic
monitoring can provide the skilled intensivist with a plethora of
valuable information but should still be integrated with all patient
data rather than viewed in isolation. Successful use of invasive
hemodynamic measurements necessitates skills to obtain these
measures safely with attention to the risks imposed on the patient.
As with any technology, the use of invasive hemodynamic moni-
toring is in evolution, and it is incumbent on the clinician to be
familiar with developments as they arise.
This chapter aims to be a practical guide to the use of hemo-
dynamic monitoring in the PICU. It reviews general principles
of measurement and discusses the three main types of invasive
hemodynamic monitoring: CVC, arterial catheter, and PAC. It
addresses the indications and controversies, interpretation of
waveforms, and potential complications and also reviews cardiac
output (CO) monitoring and calculation of oxygen consumption
and delivery. New techniques coupling invasive monitoring with
noninvasive devices are also discussed. The specific techniques
for gaining access to make these measurements are detailed in
Chapter 14, which covers invasive procedures.
Indications for Invasive Hemodynamic
Measurements
The three main indications for invasive hemodynamic monitoring
are diagnosis, surveillance, and titration of therapy. Diagnosis may
include the differentiation of septic shock (through assessment of
227
228 S E C T I O N I V  Pediatric Critical Care: Cardiovascular
•  Fig. 26.1  ​Clinician and an assistant measuring the blood pressure of a
horse. (From Pickering G. Systemic arterial hypertension. In: Fishman AP,
Dickinson WR, eds. Circulation of the Blood: Men and Ideas. New York:
Oxford University Press; 1964.)
factors such as diminished right heart filling pressures or preload
and decreased systemic vascular resistance) from cardiogenic
shock (characterized by elevated left heart pressures and after-
load). Surveillance implies observation over time. The purpose of
surveillance may be to assess the stability of a patient at risk for
adverse changes or to determine the response to therapy. Invasive
measurements performed for diagnostic purposes often are con-
tinued for surveillance. Titration of therapy is often based on
information gleaned from invasive measurements.
Principles of Measurement
Intensive care clinicians rely on a wide variety of measurement
systems to assess patient clinical status and response to therapy.
However, not all clinicians have a good understanding of how
physiologic variables are measured and, consequently, may not be
able to troubleshoot monitoring systems or recognize when infor-
mation obtained is inaccurate. A detailed discussion of monitor-
ing is beyond the scope of this chapter, but a basic understanding
of the principles of measurement is helpful in deciding which
measurements to trust and how to assess a monitoring system for
accuracy. Detailed descriptions of monitoring systems are pro-
vided elsewhere.2–4
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1-Fundamental
Harmonic amplitudes
2
4 3
6 5
1+2+3+4+5+6
Pressure
Carotid artery pressure
Average
Time
pressure
•  Fig. 26.2  ​Fourier
series representation of an arterial pressure tracing.
Bottom, High-fidelity carotid artery pressure tracing and the sum of the
first six harmonics of its Fourier series representation. Despite the few
terms used in the synthesis, the close fit of the two curves is evident. Top,
Individual harmonic components labeled with their harmonic number.
(From Cobbold RSC. Transducers for Biomedical Measurements: Princi-
ples and Applications. New York: John Wiley & Sons; 1974.)
Signal Analysis
Measurements generally are made directly by comparison with
known standards or indirectly by use of a calibration system. De-
termination of length or weight usually is made by direct com-
parison with a standard ruler or standard mass. Most invasive
measurements in the ICU are made indirectly, thereby requiring
use of a calibration system. Thus, understanding the basis for
calibration of a system is important to determine the validity of
the measurement.
Measurement systems detect and transform signals so that they
can be presented in an interpretable way to the user. Signals can
be characterized as static or dynamic. Slowly changing signals,
such as body temperature, can be thought of as static. Hemody-
namic measurements change from moment to moment and thus
are dynamic. Physiologic signals may be periodic; for example,
arterial pressure is periodic because it varies with the cardiac cycle.
Complex periodic signals, such as an arterial pressure waveform,
can be described mathematically as the sum of a series of simpler
waveforms, called a Fourier series. Alternatively, the arterial tracing
can be thought of as a sum of simpler waveforms, sine waves, and
cosine waves. Fig. 26.2 depicts an arterial pressure waveform as the
sum of the first six terms in the Fourier series. The sum of the first
six terms in the series forms a waveform similar to the original trac-
ing. Adding terms from the Fourier series, or higher harmonics,
results in an increasingly better representation of the actual wave-
form. In general, to reproduce a pressure tracing without loss of
significant characteristics for clinical use, the measurement system
must have an accurate frequency response to approximately
10 times the fundamental frequency (first 10 harmonics).
 CHAPTER 26  Principles of Invasive Cardiovascular Monitoring
The sampling rate of a measurement system determines how
often a physiologic value is measured. For body temperature,
sampling every few minutes might be sufficient, but for arterial
pressure measurement, a higher rate is necessary. This principle
may seem obvious; however, as an example of the importance of
sampling rate, consider the number of points needed to define a
circle. If three equidistant points are placed on a circle, a triangle
is described, not a circle. Similarly, four points describe a square.
If the number of points (sampling rate) is increased, the circle is
described more completely. For a sine wave, the minimum fre-
quency of sampling needed to preserve the waveform is twice the
frequency. This mathematical minimum is known as the Nyquist
frequency.4 For complex waveforms, such as arterial pressure tracings,
the sampling rate must be at least twice the highest frequency
component in the waveform.
Measurement Systems
Hemodynamic monitoring in the clinical setting usually uses a
fluid-coupled system in which changes in pressure are transmitted
via a column of (ideally incompressible) fluid in an (ideally in-
compressible) tube to a mechanical transducer. The mechanical
transducer, usually a displaceable screen diaphragm, converts a
change in pressure to an electrical signal, which can be processed
and displayed. In laboratory settings, vascular pressures can be
measured by a transducer at the point of interest rather than re-
motely, as in the clinical setting. Measuring pressure at the point
of interest—directly in the aorta, for example—decreases loss of
signal integrity because of the measurement system. Most clinical
pressure measuring systems have sufficient fidelity for clinical
purposes. However, compliance, resistance, or impedance in the
pressure tubing can result in damping or alteration of the re-
corded signal. Care should be taken to ensure that the length of
the tubing is not overly long, as this can lead to resonance of the
physiologic signal. Similarly, the narrower the tubing used in the
system, the more resonant it will be. The presence of bubbles in
the fluid can further damp the recorded signal.
Errors in Measurement
The ideal measurement system determines the actual or “true”
value for the measured variable. However, determination of a true
value may be difficult. Every measurement system is subject to
various errors. Errors in measurement can be classified as either
systematic or random. Systematic errors occur in a predictable
manner and are reproduced with repeated measures. Bias in a
measurement system—for example, a baseline offset—results in a
systematic error. Random errors are unpredictable and do not
recur predictably with repeated measures.
Accuracy of a measurement is defined by the difference between
the measured and true values, divided by the true value. Precision is
defined by the reproducibility of the measurement; thus, a more
precise system yields more similar values for repeated measures un-
der the same conditions than does a less precise system. Imprecision
can be thought of as a representation of random errors, whereas bias
can be thought of as a representation of systematic errors.
Calibration
Many measurement systems are linear, that is, based on an as-
sumption that the relationship between the inputs and outputs
from a measurement device can be fitted to a straight line. This
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229
assumption allows a system to be calibrated under two conditions,
with the rest of the values falling on the line defined by those two
points. Actual nonlinearity of the system adversely affects the
measurements.
Calibration is a process in which the reading, or output of a
device, is adjusted to match a known input value. For example, an
electronic pressure transducer may be calibrated against a mercury
manometer. If the input to the device is zero, the output should
be adjusted so that the reading also is set to zero. This “zeroing”
reduces any baseline offset, thus reducing systematic errors in
subsequent readings. The system then is calibrated to a nonzero
value, for example, 100 mm Hg pressure, and the system gain is
adjusted to read this value as well.
Frequency Response
The ability of a measurement system to accurately measure an os-
cillating signal, such as arterial blood pressure, is dependent on the
system’s frequency response. The system can either overestimate or
underestimate the true amplitude of a signal. If the system is over-
damped, the value reported underestimates the amplitude, and
waveform characteristics may be lost. Resonance in the system may
result in overestimation of the amplitude. Measurement of arterial
systolic pressure—the amplitude of the arterial waveform—may
be inaccurate because of overdamping, and important waveform
characteristics may be lost if the frequency response of the mea-
surement system is poor.
Impedance
Impedance is the ratio of the change in blood flow along a vessel
to the change in the pressure in the vessel. Impedance has both
resistive and reactive components. In a pulsatile system such as the
cardiovascular system, resistance alone does not fully describe the
impediment or impedance to forward flow of blood. The caliber,
length, and arrangement of the blood vessels and the mechanical
properties of the blood (such as its rheology and viscosity) deter-
mine resistance in the blood vessels. Reactance includes compli-
ance of the vessels and inertia of the blood and thus is a dynamic
component of impedance. This is important because the pulsatile
nature of the cardiovascular system is dynamic.
When blood is propelled through a vessel at a branch point, a
reflected pressure wave back toward the heart increases the imped-
ance of the system. The major sites of wave reflection from vessel
branching are from vessels approximately 1 mm in diameter.2 Thus,
these small vessels contribute significantly to overall impedance.
Fig. 26.3 shows the relationships between pressure and flow velocity
with distance along the length of the aorta. Because blood pressure
increases with distance from the heart and flow velocity decreases
with distance, the impedance increases toward the peripheral vascu-
lature. Hemodynamic measuring systems are essentially physical
extensions of the vascular system; thus, the configuration and char-
acteristics of the tubing and transducer system can alter the overall
effect of impedance.
Invasive Techniques
Central Venous Catheters
Indications
Indications for CVC placement in pediatric patients include as-
sessment of central venous pressure (CVP), monitoring of large
230 S E C T I O N I V  Pediatric Critical Care: Cardiovascular
fluid shifts between the intravascular and extravascular spaces, infu-
sion of vasoactive substances, monitoring central venous oxygen
saturation, and infusion of hyperosmolar fluids and/or irritants.5–7
Interpretation of Waveforms
CVP is ideally a measure of right atrial pressure, although it may
be measured in the inferior or superior vena cava (SVC). It is a
measure of preload—the force or load on the right ventricle dur-
ing relaxation or filling. CVP is measured at the end of diastole,
just prior to ejection. Final filling of the right ventricle occurs at
the end of atrial contraction. When the tricuspid valve is open
during diastole, the right atrium and right ventricle form a con-
tinuous column; therefore, right atrial pressure reflects right ven-
tricular end-diastolic pressure. CVP is used to measure filling
pressure or preload and is an indicator of volume status; however,
it is influenced by a variety of physiologic phenomena. It is com-
monly used in patients with hypovolemic or septic shock in
whom volume resuscitation is desirable prior to institution of
vasopressor therapy. In patients with decreased right ventricular
function or pulmonary hypertension, an increased CVP well be-
yond normal limits may be observed and further fluid resuscita-
tion may contribute to the development of congestive heart fail-
ure. Increases in positive end-expiratory pressure can decrease
preload despite an increased CVP. Finally, increases in extrathoracic
pressure, such as that caused by increased abdominal distension,
can increase CVP.
260
Pressure (cm H2O)
220
180
140
Ascending Thoracic Abdominal Abdominal Femoral
90 aorta aorta aorta aorta
middle distal
Flow
Velocity (cm/sec)
50 velocity
0
30
• Fig. 26.3  ​Pressure pulses and flow velocity at various points in the sys-
temic arterial circulation. Data were obtained from dogs and are similar to
measurements made in humans. The data indicate that both peak and
pulse pressure increase with distance from the heart, whereas oscillation
in flow velocity shows a progressive decrease. Consequently, impedance
(discussed in the text) must increase toward the periphery.
• Fig. 26.5  ​Cannon a waves are enlarged a waves seen when the right atrium is ejecting against a closed
tricuspid valve. These waves are typically seen when atrioventricular discordance occurs, such as during
junctional ectopic or ventricular tachycardia or heart block.
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It is important to keep in mind that CVP as an absolute num-
ber does not necessarily indicate fluid status due to its many
physiologic determinants (stressed venous volume, venous com-
pliance, venous resistance, right heart function, and sympathetic
tone, among others). At the extremes (i.e., ,6–8 or .12–15 mm
Hg), CVP has satisfactory performance as an indicator of fluid
responsiveness.8 Additionally, the change in CVP (or its staying
the same) during therapeutic interventions or diagnostic maneu-
vers has been shown to perform better9 than the absolute number.
As with most widely available measurements, the widespread
availability of CVP at the bedside has many limitations but, when
integrated into other data, frequently provides important infor-
mation.
The CVP waveform is divided into three components: a, c, and
v waves (Fig. 26.4). Each component can be correlated with a
specific portion of the electrocardiogram (ECG) tracing. The a wave
occurs with atrial contraction and is seen after the P wave of the
electrocardiogram during the PR interval. Thus, the mean value
of the a wave approximates right ventricular end-diastolic pres-
sure. Cannon a waves (Fig. 26.5), which are enlarged a waves seen
when the right atrium is ejecting against a closed tricuspid valve,
may be seen when atrioventricular discordance occurs (i.e., during
junctional ectopic tachycardia, ventricular tachycardia, or heart
A A C
C V V
X Y X Y
•  Fig. 26.4  ​Central venous pressure (A) tracing with corresponding elec-
trocardiogram (ECG). The a wave is produced by atrial contraction and
occurs after the P wave of the ECG during the PR interval. The c wave
(C) is produced by closure of the tricuspid valve and takes place early in
systole at the end of the QRS complex in the RST junction. The v wave
(V) is caused by rapid filling of the right atrium late in systole before open-
ing of the tricuspid valve and is seen between the T and P waves of the
ECG. The x descent (X) reflects the decrease in pressure in the right atrium
after the a wave as the tricuspid valve is pulled away from the right atrium
by the right ventricle as it contracts during systole. The y descent (Y) is the
decrease in right atrial pressure that occurs after the v wave as the tricus-
pid valve opens and blood moves from the right atrium into the right
ventricle.
 CHAPTER 26  Principles of Invasive Cardiovascular Monitoring
block). The c wave occurs in early systole with closure of the tri-
cuspid valve and is seen at the end of the QRS complex in the
RST junction. The v wave occurs during filling of the right atrium
in late systole before opening of the tricuspid valve and is seen
between the T and P waves of the ECG. The v wave is increased
in the setting of tricuspid regurgitation. The x descent is the de-
crease in pressure after the a wave, reflecting atrial relaxation. The
y descent is the decrease in pressure that occurs after the v wave as
the tricuspid valve opens and passive filling of the right ventricle
occurs.
Mixed Venous Oxygen Saturation
Mixed venous oxygen saturation (Svo2) can be measured inter-
mittently by blood sampling from a CVC or continuously by
using a specially designed CVC. Such catheters typically have two
to three lumens and have the same capabilities of standard CVCs,
with the additional potential for spectrophotometric monitoring.
The Svo2 catheters use reflection spectrophotometry and are able
to read hemoglobin oxygen saturation continuously. The reflected
light is dependent on the oxygenated and deoxygenated hemoglo-
bin concentration in the circulating blood.10
Svo2 measurement may be used to inform the practitioner of
the relationship between oxygen delivery and consumption and is
often used as a surrogate for cardiac index (CI). Rivers et al.11
showed that when continuous Svo2 monitoring was used to guide
resuscitation and hemodynamic support in patients with severe
sepsis and septic shock, survival rates improved. Guidelines set
forth by the American College of Critical Care Medicine/Pediat-
ric Advanced Life Support have recommended goal-directed
therapy with a target Svo2 of 70% or more in children and ado-
lescents who are in septic shock.7 Rivers’ findings have subse-
quently not been replicated, and continuous monitoring of Svo2
has not been shown to improve patient outcomes in large well-
conducted studies.12–14 However, since Rivers’ initial report on
goal-directed therapy, there have been sustained improvements in
sepsis mortality15 that have coincided with an increase in aware-
ness of the importance of monitoring end-organ perfusion. This
has led to the development of many new noninvasive techniques
for perfusion monitoring.16
When placing CVCs for monitoring, the catheter should be
placed such that the tip taking measurements is at the cavoatrial
junction. Svo2 measurements obtained from the inferior vena
cava exhibit greater variability because of fluctuations in splanch-
nic oxygen utilization and thus are less reliable. Svo2 measure-
ments from the right atrium contain coronary sinus blood and are
more desaturated because of the high oxygen extraction rate of the
myocardium. Studies in critically ill children have evaluated Svo2
measurements obtained in the pulmonary artery and SVC. Con-
cordance analysis showed appropriate agreement in the measure-
ments between these two sampling sites.17 This finding has clini-
cal importance because the use of PACs has declined and CVC
use has been increasing.18,19
Arterial Pressure Catheters
Indications
The transition to direct monitoring of arterial blood pressure
dates back to the mid-1950s when two separate studies compared
invasive arterial measurements and noninvasive or cuff measure-
ments in healthy adults.20,21 Van Bergen et al.21 noted a frequent
difference between direct and indirect measurements, with indi-
rect measurements increasingly lower than direct measurements as
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231
the systemic blood pressure increased. The greatest disparity was
found in young hypertensive patients. Similarly, Cohn and
Luria22 observed that invasive arterial pressures were significantly
greater than cuff pressures and emphasized the importance of di-
rect measurements of systemic arterial pressure when caring for
patients with hypotension and shock. Continuous direct moni-
toring of arterial blood pressure should be considered when treat-
ing patients who require more than minimal vasopressor therapy.
Indications for arterial catheterization include continuous
monitoring of systemic arterial blood pressure, frequent blood
sampling, and withdrawal of blood during exchange transfu-
sions.23 The procedural information regarding site selection and
procedural techniques for placing arterial lines is covered else-
where in this text.
Interpretation of Waveforms
The arterial waveform has three main components: (1) a rapid
upstroke and downslope that correlates with systolic ejection,
(2) a dicrotic notch that correlates with closure of the aortic valve,
and (3) a smooth runoff that correlates with diastole. The dicrotic
notch or incisura is decreased in situations of hyperdynamic CO in
which left ventricular output and stroke volume (SV) are increased,
pulse pressure is widened, and diastolic blood pressure (DBP) is in-
creased (e.g., surgical systemic-to-pulmonary shunts, patent ductus
arteriosus, aortic regurgitation, anemia, fever, sepsis, hypovolemia,
exercise). Conversely, cardiac tamponade and severe aortic stenosis
can narrow the pulse pressure and are associated with a deflection
(anacrotic notch) on the ascending limb of the waveform.24
Systolic pressures measured in the periphery typically are
greater than those measured more centrally because of pulse ampli-
fication of pressure waves reflected back from arterial branch
points24,25 (see Fig. 26.3). More peripheral sites, such as the radial
artery, have greater systolic blood pressure (SBP) and lower DBP
than more central sites and thus taller and narrower waveforms
with greater pulse pressures (difference between SBP and DBP).
Important to note is that the mean arterial pressure (MAP, in
Eq. 26.1) represents the area under the waveform curve. It has
traditionally been felt that the overall magnitude of the reading re-
mains the same regardless of the location of the tracing. However,
some evidence exists that, among critically ill adults, MAP readings
from radial artery catheters are consistently lower than those from
femoral artery catheters by up to approximately 5 mm Hg.26–29
 MAP 2 DBP 1 (SBP 2 DBP)/3 Eq. 26.1
The appearance of the arterial waveform also provides clinical
information to the observer. Pulsus alternans (Fig. 26.6A) is ob-
served when regular variations occur in the amplitude of the peak
systolic pressure during sinus rhythm. This phenomenon can be
seen in patients with severe left ventricular failure. Pulsus para-
doxus (Fig. 26.6B) demonstrates an exaggerated decrease in the
systolic pressure (.10 mm Hg) during the inspiratory phase of
the respiratory cycle. This phenomenon can be observed in pa-
tients with pericarditis, pulmonary hyperinflation, and decreased
intravascular volume.
The physiology that leads to pulsus paradoxus in pathologic
states may also be used to assess for fluid responsiveness in intu-
bated patients by measuring their pulse pressure variation (PPV). A
number of studies have shown that, in intubated patients without
spontaneous breathing, substantial (.12%–13%) PPV between
cardiac cycles during insufflation and expiration have excellent
performance in predicting fluid responsiveness.30–33 Many modern
232 S E C T I O N I V  Pediatric Critical Care: Cardiovascular

monitors can now analyze PPV automatically and report the
number to the clinician directly.34 The physiology of cardiopul-
monary interactions that underlie this is discussed at length in
Chapter 32. Briefly, during insufflation of a sufficiently large
tidal volume (at least 8 mL/kg ideal body weight) right ven-
tricular preload falls dramatically, resulting in a decreased
left ventricular preload after a delay of a few cardiac cycles
(Fig. 26.7).
Pulmonary Artery Catheters
History and Controversy
In 1847, Claude Bernard described a method for measuring intra-
cardiac pressures in animals by inserting a glass tube in the
Pulsus alternans
A contrast dye during the procedure.39,40
Pulsus paradoxus
Inspiration
B
•  Fig. 26.6  ​(A)
Pulsus alternans occurs with left ventricular failure and is
characterized by regular variations in the peak amplitude of systolic pres-
sure during sinus rhythm. (B) Pulsus paradoxus is characterized by an
exaggerated decrease in the systolic blood pressure during inhalation. It
is commonly seen in conditions marked by great swings in intrathoracic
pressure, such as in status asthmaticus, or when there are changes in
cardiac function, as in pericarditis. In severe hypovolemia, pulsus para-
doxus also can be observed as a result of a decrease in preload. (Modified
from McGee S. Evidence-Based Physical Diagnosis. Philadelphia: Elsevier;
2018.)
heart.35 However, the true pioneers of cardiac catheterization were
two other Frenchmen: Jean Baptiste Auguste Chaveau, at that
time a veterinarian interested in the relationship between the dy-
namic motion of the heart and heart sounds, and Etienne-Jules
Marey, a physician interested in the physiology of the circulation.
In the early 1860s, using techniques adapted from Bernard’s
work, Chaveau and Marey inserted a double-lumen catheter into
the right atrium of a horse to record phasic changes in intracardiac
pressures as they simultaneously recorded the apical impulse.35–38
Right heart catheterization was not considered a safe practice
in humans until the early 20th century. In 1929, Werner Forss-
man, a German surgeon, secretly performed a right heart cathe-
terization on himself. In direct contradiction to his supervisor’s
instructions, Forssman inserted a urinary catheter into his own
left antecubital vein and then the remainder of the way to his
right atrium under fluoroscopic guidance with the aid of a mirror.
Forssman performed right heart catheterizations on himself a to-
tal of nine additional times without adverse consequences and
expanded his findings by demonstrating the feasibility of injecting
In the early 1940s, Andres Cournand and Dickinson Richards,
working at Bellevue Hospital in New York, continued Forssman’s
work. They performed right heart catheterization in healthy hu-
mans and in those with cardiac failure.40–43 In 1956, Forssman,
Cournand, and Richards won the Nobel Prize in Physiology or
Medicine for their discoveries relating to heart catheterization and
pathologic changes in the circulatory system. They were the first
investigators to measure pulmonary capillary wedge pressures us-
ing cardiac catheterization.44,45
In 1953, Lategola and Rahn46 performed experiments in dogs
in which they were the first to use a self-guiding balloon-tipped
catheter to measure pressures in the pulmonary circulation.
Seventeen years later, Swan et al.47 at the University of California,
Los Angeles, used this technique to assess right heart pressures in

RV
Preload
RV LV LV
Pleural Ejection Preload Ejection
RV
pressure
Afterload

LV
Transpulmonary Afterload
pressure LV
Ejection
LV
Preload

PPMax

PPMin

•  Fig 26.7  ​Mechanisms of heart-lung interactions that lead to pulse pressure variation. Top line, Airway
pressure tracing. Bottom line, Arterial pressure tracing. LV, Left ventricle; PP, pulse pressure; RV, right
ventricle. (Figure based on data from Teboul JL, Monnet X, Chemla D, Michard F. Arterial pulse pressure
variation with mechanical ventilation. Am J Respir Crit Care Med. 2019;199:22–31.)

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 CHAPTER 26  Principles of Invasive Cardiovascular Monitoring
humans. In doing so, they brought this methodology to the bed-
side, where it is still used today.
In the 50 years since Swan and Ganz added balloon flotation
and thermodilution to the PAC, its use has been controversial.
The literature is rife with studies reporting salutary effects of placing
them, studies showing no effect, and studies showing harm.48–53
Due to this controversy and the significant risks attendant to its
use, the PAC has fallen out of favor; its routine use today is rare
outside of specific clinical scenarios discussed later.
With regard to pediatric patients, the Pulmonary Artery Cath-
eter Consensus Conference, based on a consensus of expert opin-
ions, concluded that the PAC was useful for clarifying cardiopul-
monary physiology in critically ill infants and children with
pulmonary hypertension; shock refractory to fluid resuscitation
and/or low-to-moderate doses of vasoactive medications; severe
respiratory failure requiring high mean airway pressures; and, on
rare occasions, multiple organ failure. They found no data indicat-
ing that PAC use increases mortality in children; however, they
also failed to find any controlled trials that demonstrated a benefit
of PAC use. The panel recommended PAC use for selected patients
and called for randomized controlled trials, a registry of PAC use,
and studies to assess the impact of PAC use on cost and duration
of ICU/hospital stay.54 A further review of current studies55 dem-
onstrated level B and level C evidence for most indications.
Indications
Although controversial, current indications for PAC use in chil-
dren include septic shock unresponsive to fluid resuscitation and
vasopressor support,56–58 refractory shock following severe burn
injuries,59 congenital heart disease (CHD),58 pulmonary hyper-
tension,60,61 multiple organ failure,62 liver transplantation,63 and
respiratory failure requiring high mean airway pressures.58,64
Capabilities of PACs include determination of CVP, pulmo-
nary artery pressure, and pulmonary artery occlusion pressure
(PAOP), also referred to as pulmonary capillary wedge pressure.
PAOP is a measurement of left atrial pressure and left ventricular
end-diastolic pressure (when the mitral valve is open). PACs are
also used to assess CO, Svo2, oxygen delivery (Do2) and con-
sumption (Vo2), and pulmonary vascular resistance (PVR) and
systemic vascular resistance (SVR). The PAC is the only bedside
tool that can examine the function of the right and left ventricles
separately aside from echocardiography, which provides signifi-
cantly less precise assessments. PACs are used to establish diagno-
ses, guide response to therapy, and assess the determinants of
oxygen delivery. PACs are especially helpful in cases of discordant
ventricular function.
One of the most common uses of the PAC in infants and chil-
dren is monitoring pulmonary pressures during and after repair of
CHD. In addition to flow-directed, balloon-tipped PACs, trans-
thoracic left atrial catheters are often used in these patients.65 Use
of PACs has altered the management of children with CHD by
identifying residual anatomic defects and diagnosing pulmonary
hypertensive crisis.66,67 The ability to monitor PAP provides the
means to titrate response to inhaled nitric oxide and other pul-
monary vasodilators.68,69 The lack of response to inhaled nitric
oxide may suggest a residual structural anomaly in postoperative
patients and indicate the need for interventional cardiac catheter-
ization and/or surgical repair.69 In addition to monitoring for
pulmonary hypertensive crisis, PACs can be used to assess the
effects of changes in concentration of inspired CO2 on mean
pulmonary artery pressure (MPAP), pulmonary vascular resis-
tance index (PVRI), and CI.70
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233
Monitoring Techniques with the Pulmonary
Artery Catheter
The functional features of the PAC are several. Its use as a method
of indicator thermodilution, measurement of cardiac output,
monitoring, and blood sampling is well documented. Fig. 26.8
demonstrates the expected waveforms as the catheter passes
through the cardiovascular system. Technical concepts are impor-
tant for understanding the calculations needed for optimum use.
See Table 26.1 for a summary of the hemodynamic parameters
that can be derived from a PAC.
Catheter Placement
PACs typically contain the following ports (see Fig. 26.8). The
proximal port is located 15 cm from the tip in 5 Fr catheters and
30 cm from the tip in larger catheters. It opens into or near the
right atrium. The proximal port provides access for infusion of
fluid or drugs, injection of cold saline solution as indicator
(thermodilution method), CVP monitoring, and blood sam-
pling. In infants or small children, PAC placement may result in
improper location of the proximal port before the right atrium
such that the port lies inside the sheath or outside the body.
Therefore, it is essential to verify not only the placement of the
distal tip in the pulmonary artery but also the location of the
proximal port.
The distal port opens at the tip of the catheter. It is used for
monitoring PAP and PAOP, blood sampling of mixed venous
blood gases, and infusion of fluids. By monitoring pressure
continuously through this port during catheter placement, the
location of the tip can be determined from the characteristic
pressure tracings shown in Fig. 26.8. After placement, PAP
should be monitored continuously in order to identify inad-
vertent migration into the pulmonary capillary bed or
“wedged” position. It is important to allow the catheter tip to
“float” into the wedged position only when actively measuring
PAOP in order to minimize risk of pulmonary artery infarct or
rupture.
The balloon inflation port inflates the balloon, which is located
1 cm proximal to the catheter tip. The balloon is inflated for flow-
directed catheter placement and PAOP monitoring.
The thermistor is located just proximal to the balloon and con-
nects to a bedside computer to measure changes in the temperature
of pulmonary artery blood. The oximeter uses a fiberoptic-based
sensor to continuously measure the Svo2.
Larger catheters also may have cardiac pacing ports. An adult-
sized catheter is available for continuous CO determination when
coupled with an appropriate bedside computer.
Indirectly Measured Variables
Measurements from PACs include directly and indirectly mea-
sured or derived variables. Directly measured variables include
CVP, MAP, MPAP, PAOP, CO, arterial oxygen saturation (Sao2),
and Svo2. Derived parameters include CI, PVR, SVR, PVRI, and
systemic vascular resistance index (SVRI), as well as SV (in mL/
beat) and stroke volume index (SVI; in mL/beat per m2). Stroke
index (SI), or SVI, normally is 30 to 60 mL/m2.71,72
 SV 5 CO/HR Eq. 26.2
SVI
 5 SV/BSA Eq. 26.3
234 S E C T I O N I V  Pediatric Critical Care: Cardiovascular

SvO2 %
Proximal port 100

80
60
Distal port 40
20
0
Thermistor Balloon inflation port 0 15 30 45 60
connector Time min
Oximeter
connector

W
ed
ge
po
sit
um

Pulm
tri

ion
l
tric
a
ht

en

ona
ig
R
tv
40

ry a
gh
Ri

rtery
30
mm Hg

20

10

• Fig. 26.8  ​Components and functional features of a thermodilution flow-directed pulmonary artery cath-
eter. The flexible multilumen catheter with the balloon at the distal tip inflated is in the wedge position. The
proximal ends of the five lumens are labeled. The distal port is connected to a pressure measurement
system for catheter insertion and subsequent monitoring. When the distal tip is within the central venous
circulation, the balloon is inflated to enhance flow direction of the tip through the right atrium into the right
ventricle and then to the pulmonary artery. Recorded pressures (bottom) correspond to these locations,
confirming the course of the catheter. The last tracing on the right corresponds to the “wedge” position,
commonly reflecting pressure transmitted from the left atrium via the pulmonary veins and capillaries.
Upper right panel shows an example of a continuous Svo2 (venous oxygen saturation) tracing from the
fiberoptic monitor available on adult-size catheters.  (Modified from Daily EK, Tilkian AG. Hemodynamic
monitoring. In: Tilkian AG, Daily EK, eds. Cardiovascular Procedures, Diagnostic Techniques and Thera-
peutic Procedures. St. Louis: Mosby; 1986.)

Left ventricular stroke work index (LVSWI) and right ventricular

stroke work index (RVSWI) normally are 56 6 6 and 0.5 6
0.06 gm-m/m2, respectively.71,72 Note that all values are for pedi-
atric patients unless otherwise indicated.
 LVSWI 5 SI 3 MAP 3 0.0136
 RVSWI 5 SI 3 MAP 3 0.0136
Measurement of Cardiac Output
CO is the volume of blood pumped by the heart each minute, or
SV multiplied by the number of ejections per minute or HR (CO 5
HR 3 SV) and often is expressed as CI, which is CO divided by
the body surface area (BSA) in square meters. The normal range
for infants and children is approximately 3.3 to 6 L/min/m2.71,72
Two methods for calculating CO are discussed here: the Fick
method and thermodilution.
Fick Method
In 1870, Adolph Fick was the first to study the relationship be-
tween blood flow and gas exchange in the lungs using a mathematic
model.73 Fick hypothesized that the amount of oxygen extracted by
the body from the blood must equal the amount of oxygen taken
Eq. 26.4 up by the lungs during breathing. Fick also reasoned that the flow
of blood through the lungs must equal the CO to the remainder of
Eq. 26.5 the body in the absence of a shunt. If the amount of oxygen con-
sumed by the body and the amount of oxygen extracted by the
body from the blood can be determined, then the CO can be de-
termined. In Fick’s time, oxygen consumption was measured using
a basal metabolism spirometer, and the oxygen content in arterial
and venous blood was measured using a rudimentary method.73
Although Fick’s method remains the gold standard, it is rarely used
in the ICU because it is less practical than the more commonly used
thermodilution method described in the next section. However,
Fick’s method is commonly used in the cardiac catheterization
laboratory because the required data are easily measured in this
setting, although oxygen consumption is often estimated.

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 CHAPTER 26  Principles of Invasive Cardiovascular Monitoring 235

TABLE
26.1 Hemodynamic Parameters

Parameter Formula Normal Range Units

Cardiac index CI 5 CO/BSA 3.5–5.5 L/min/m2
Stroke index SI 5 CI/heart rate 3 1000 30–60 mL/m2
Arterial-mixed venous O2 content difference avDo2 5 Cao2 – Cvo2 30–55 mL/L
O2 delivery Do2 5 CI 3 O2 620 6 50 mL/min/m2
O2 consumption Vo2 5 CI 3 avDo2 120–200 mL/min/m2
O2 extraction ratio ERO2 5 avDo2/Cao2 0.26 6 0.02
Arterial oxygen content (1.34 3 Hb 3 Sao2) 1 (Pao2 3 0.003) mL/L
Venous oxygen content (1.34 3 Hb 3 Svo2) 1 (Pvo2 3 0.003) mL/L
Fick principle VO2 5 CO 3 (Cao2 – Cvo2)
Systemic vascular resistance index SVRI 5 80 3 (MAP – CVP)/CI 800–1600 dyne • s/cm5/m2
Pulmonary vascular resistance index PVRI 5 80 3 (MPAP – PAOP)/CI 80–200 dyne • s/cm5/m2
LV stroke work index LVSWI 5 SI 3 MAP 3 0.0136 56 6 6 gm-m/m2
RV stroke work index RVSWI 5 SI 3 MPAP 3 0.0136 0.5 6 0.06 gm-m/m2

avDo2, Arterial-mixed venous content difference; BSA, body surface area in m2; Cao2, O2 content of systemic arterial blood in mL/L; CI, cardiac index; CO, cardiac output; Cvo2, O2 content of mixed
venous blood in mL/L; CVP, central venous pressure in mm Hg; DO2, oxygen delivery; ERO2, O2 extraction ratio; Hb, hemoglobin; LVSWI, left ventricular stroke index; MAP, mean systemic arterial
pressure in mm Hg; 80 is the conversion factor used for the units in the table; MPAP, mean pulmonary arterial pressure in mm Hg; PAWP, pulmonary artery wedge pressure in mm Hg, which is
approximately equal to the left atrial pressure under many circumstances; Pvo,2, partial oxygen pressure in mixed venous blood; PVRI, pulmonary vascular resistance index; RVSWI, right ventricular
stroke work index; SI, stroke index; Svo2, venous oxygen saturation; SVRI, systemic vascular resistance index; Vo2, oxygen consumption.
Modified from Katz RW, Pollack MM, Weibley RE. Pulmonary artery catheterization in pediatric intensive care. In: L.A. Barness, ed. Advances in Pediatrics. Chicago: Year–Book; 1984.

As noted previously, Fick’s equation is based on the assump-
tion that the amount of oxygen extracted by the body from the
blood equals the amount of oxygen taken up from the lungs
during breathing.
The oxygen content of blood is generally expressed in millili-
ters of O2 per deciliter of blood. The difference in oxygen content
of arterial blood (Cao2) and venous blood (Cvo2) is termed the
arterial-mixed venous oxygen content difference (avDo2). By multi-
plying the avDo2 by the amount of blood pumped through the
lungs or body (CO) we can calculate the oxygen consumption.
Note that CO is generally expressed in L/min. Therefore, we must
multiply the avDo2 by 10 to convert it to milliliters of O2 per liter
of blood if we are to perform the calculation using CO in L/min.
The oxygen content of the blood is a function of the hemoglo-
bin (Hb) concentration of blood in g/dL, the Sao2 or Svo2 ex-
pressed in decimal form, and the arterial or venous partial pres-
sure of arterial oxygen (Pao2 or Pvo2) expressed in mm Hg. The
oxygen-carrying capacity of adult Hb is 1.34 mL O2/g Hb, and
the Bunsen solubility coefficient of O2 in plasma at 37°C equals
0.003 mL/mm Hg per dL. A true Svo2 is measured in the pulmo-
nary artery; however, in the presence of an intracardiac left-
to-right Svo2 shunt, Svo2 should be measured in the SVC.
 2 5 (1.34 3 Hb 3 Sao2) 1 (Pao2 3 0.003)
Cao
 2 5 (1.34 3 Hb 3 Svo2) 1 (Pvo2 3 0.003)
Cvo
As noted earlier, the amount of oxygen extracted (consumed)
by the body from the blood equals avDo2 multiplied by the
amount of blood that flows through the lungs (QP). Assuming
QP equals the flow of blood through the systemic circulation
(QS), then QP is a measure of CO. (Note that pulmonary and
systemic blood flows cannot be assumed to be identical in chil-
dren with CHD with single-ventricle physiology or those with
anatomic shunts.)
 2 extraction 5 10 3 (Cao2 – Cvo2) 3 CO
O Eq. 26.9
The amount of oxygen taken up by the lungs equals the
amount of oxygen consumed by the body. According to Fick,
the amount of oxygen extracted by the body from the blood
(Eq. 26.10) equals oxygen consumption (Vo2).
 3 (Cao2 – Cvo2) 3 CO 5 VO2 in L/min
10 Eq. 26.10
CO
 5 VO2/[10 3 (Cao2 – Cvo2)] Eq. 26.11
As noted in Eqs. 26.6 and 26.7, the amount of dissolved
oxygen in blood (Pao2 or Pvo2) contributes an almost negligible
amount to the oxygen content and can be left out (unless very
Eq. 26.6 high) for ease of computation. By rearranging Eq. 26.11, a rough
estimate of CO can be calculated rather easily at the bedside with-
Eq. 26.7 out use of a PAC:

 avDo2 5 Cao2 – Cvo2 Eq. 26.8 CO

 5 VO2/(1.34 3 Hb 3 (Sao2 – Svo2) 3 10) Eq. 26.12

The avDo2 is the difference between Cao2 and Cvo2 and normally Oxygen consumption can be measured using the metabolic
ranges from 2.8 to 7.8 mL/dL in children.72 cart or taken from standardized tables.17 Hb concentration can be

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236 S E C T I O N I V  Pediatric Critical Care: Cardiovascular
measured directly. Sao2 can be taken from the pulse oximeter.
Svo2 can be measured by the oximeter at the distal end of the PAC
or determined from a venous blood gas sample from a catheter in
the internal jugular or subclavian vein.
These data also can be used to calculate the intrapulmonary
shunt fraction, which is the fraction of blood that passes through
unventilated areas of lung:
Qs/Qt
 5 (Cpvo2 2 Cao2)/(Cpvo2 2 Cvo2) Eq. 26.13
where Cao2 is systemic arterial oxygen content and Cvo2 is mixed
venous oxygen content.
Cpvo2 is the theoretical oxygen content in a normal pulmo-
nary vein and can be estimated using the alveolar gas equation:
Cpvo
 2 5 1.34 3 Hb 3 Spvo2 1 Ppvo2 3 0.003 Eq. 26.14
where Spvo2 is pulmonary vein O2 saturation and Ppvo2 is pul-
monary vein po2.
For the normal lung, Ppvo2 can be estimated from the alveolar
air equation (Eq. 26.15), and Spvo2 is presumed to be 1.0:
Ppvo
 2 5 Pao2 5 (Pio2 2 Pwp) 2 Paco2/R Eq. 26.15
where Pao2 is alveolar partial pressure of oxygen, Pio2 is inspira-
tory pO2, Pwp is vapor pressure of water (47 mm Hg at 37°C),
Paco2 is arterial CO2, and R is respiratory quotient, which is
normally assumed to be 0.8.
The normal shunt fraction is 3% to 7%.
Thermodilution Method
In 1921, Stewart74 first described an indicator-dilution method
for measuring CO. Flow was calculated by measuring the change
in concentration of an indicator over time. The “ideal” indicator
is “stable, nontoxic, uniformly distributed, and does not leave the
system between sites of injection and detection. However, it
should be rapidly cleared in a single circulation time to prevent
recirculation interfering with measurement.”75
In 1953, Fegler76,77 demonstrated that a change in the heat
content of blood could be used as an indicator for CO measure-
ment. A bolus of cold liquid of a known temperature is injected
into or proximal to the right atrium. A thermistor near the PAC
tip in the pulmonary artery or a pulmonary artery branch mea-
sures a change in the temperature of the blood as the bolus passes
by the end of the catheter. A computer calculates the flow by in-
tegrating the change in temperature at the thermistor.
The first law of thermodynamics, the conservation of heat, is
the fundamental principle underlying thermodilution. Thermodi-
lution makes several assumptions: physiologic conditions must
remain constant during the period of observation; all heat ex-
change occurs between the indicator and the blood without heat
loss to the surrounding tissues; mixing of the injectate and blood
is complete upstream of the temperature measurement; and the
temperature sensor is sufficiently sensitive, accurate, and rapidly
responsive to depict accurately the change in temperature over
time.
Measurement of CO using the thermodilution method can be
understood by examining a modified version of the Stewart-
Hamilton equation.75 V1 is injectate volume (in mL); Tb is tem-
perature of the pulmonary artery at baseline (in degrees Celsius);
Ti is temperature of the injectate (in degrees Celsius); K1 is the
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density factor that equals the specific heat of the injectate multi-
plied by the specific gravity of the injectate, divided by the prod-
uct of the specific heat and specific gravity of blood; and K2 is a
constant that figures in the dead space of the catheter and the loss
of heat from the injectate as it moves through the catheter. The
denominator of the equation is the integral of the change in the
temperature of the blood (Tb) over time (t):
CO
 5 V1(Tb 2 Ti)K1K2/∫DTb(t)dt Eq. 26.16
The computer generates a CO curve with the area under the
curve inversely related to the magnitude of the CO. In settings of
low CO, less warm blood flows with the injectate, and the injec-
tate stays cooler. The difference between the injectate temperature
and that of the blood remains large, and the CO curve has a high
domed shape, with a slow return to baseline temperature. In situ-
ations of high CO, more pulmonary artery blood flows with the
injectate, and the temperature of the injectate approaches or
equals that of the blood more rapidly. In these situations, because
the difference between the final temperature of the injectate and
that of the blood is small, the CO curve rapidly returns to baseline
following a sharp spike from the cold injectate. In extreme low-
flow states, the change in temperature of the injectate resulting
from handling alone, before the injectate even enters the catheter
from the proximal port, may be greater than the change caused by
warming of the injectate by the flow of blood.
A correction factor is added to the equation to account for
warming of the injectate because of handling alone. However, the
correction factor may be inaccurate if the injection is too slow or
the syringe is held in the injector’s hands too long. Therefore, CO
readings should be made as quickly as possible and should be re-
peated until three successive readings are within 15% of each
other. Other sources of error include a falsely elevated CO be-
cause of inadvertent warming of the thermistor when it is up
against the wall of the pulmonary artery. The thermodilution
method generally should not be used in patients with an intracar-
diac shunt. However, if the shunt fraction is less than 10%, the
error likely is negligible.24
Measurements in the cardiac catheterization lab are frequently
considered the gold standard for CO determination, but the PAC
has clinical advantages for intermittent measurements at the bed-
side. It is important to keep in mind the shortcomings of the
PAC, including accuracy of measurements and risks to the pa-
tient. Stetz et al.78 evaluated PAC thermodilutional determination
of CO and found that a difference of 15% or less across three
measurements suggested acceptable precision. More recent fol-
low-up studies have found that this level of precision is infre-
quently achieved; for example, Dhingra et al.79 evaluated thermo-
dilutional PAC measurements against direct Fick calculations and
found a percentage of error of 62%. An animal model study80
found that PACs were only able to consistently detect CO
changes of at least 30%.
Calculation of Oxygen Delivery
and Consumption
Metabolic derangements, such as fever, sepsis, and shock, interfere
with DO2 to and VO2 by the tissues. Svo2 is a measure of the
oxygenation of blood returning to the heart. Svo2 can be mea-
sured continuously by a fiberoptic oximeter (see description of
PAC ports in the catheter placement section) and normally ranges

from 65% to 75%. The oxygen extraction ratio (ERO2) is avDo2
(see Eq. 26.8) divided by Cao 2 (Eq. 26.11) and usually is
approximately 25%71,72:
 ERO2 5 avDo2/Cao2
Do2 also can be expressed as the product of CI and Cao2 and Vo2
as the product of CI and avDo2. The normal value for Do2 is
620 6 50 mL/min per square meter. Vo2 typically ranges from
120 to 200 mL/min per square meter.71,72
 Do2 5 CI 3 Cao2
 Vo2 5 CI 3 avDo2
Interpretation of Waveforms
The waveforms corresponding to the right atrium and systemic
arterial blood pressure were discussed in previous sections. The
pressure in the right atrium ranges from approximately 3 to
12 mm Hg. As the PAC passes into the right ventricle, the
diastolic pressure drops to 0 to 10 mm Hg and the systolic
pressure increases to 13 to 42 mm Hg. As the catheter enters
the pulmonary artery, the diastolic pressure increases to 3 to
21 mm Hg while the systolic pressure remains relatively simi-
lar to that of the right ventricle, 11 to 36 mm Hg. Once the
catheter tip advances into the pulmonary capillary bed and the
pulmonary artery is occluded by the inflated balloon, the mea-
sured pressure decreases to 2 to 14 mm Hg.24 By recognizing
the changes in the various tracings, the movement of the cath-
eter tip can be followed through the chambers of the right
heart and into the pulmonary circulation without simultane-
ous imaging.
The waveforms are affected by the components of the respi-
ratory cycle. As expected, the effects of respiration differ dur-
ing unsupported breathing (negative pressure) versus mechan-
ical ventilation (positive pressure). During normal unsupported
ventilation, PAP decreases during inhalation and increases
during exhalation. In contrast, during mechanical ventilation,
PAP increases during inhalation and decreases during exhala-
tion. The cyclical changes induced by the respiratory cycle
cause the tracings to take on a sinusoidal pattern once the tip
of the catheter enters the thorax. The effects of respiration on
PAC determinations can be minimized by measuring pressures
at the end of expiration, when pleural pressures are closest
to zero.
Because CVP is a measure of preload or filling of the right
ventricle, it reflects changes in volume status, right ventricular
function, and pulmonary vascular tone. Similarly, PAOP mea-
sures filling pressures of the left atrium and ventricle. When the
pulmonary artery is occluded, the pressure from the left atrium is
transmitted back to the catheter tip. During diastole, when the
mitral valve is open and the aortic valve is closed, a continuous
fluid-filled column is formed from the catheter tip to the left
ventricle and PAOP is equivalent to the left ventricular end-
diastolic pressure. In patients with cardiogenic shock, an elevated
PAOP may reflect decreased function of the left ventricle. In this
situation, rather than providing further fluid resuscitation or pre-
load, increasing contractility or decreasing afterload may be pref-
erable. Afterload is the load that the heart must eject blood
against.
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CHAPTER 26  Principles of Invasive Cardiovascular Monitoring 237
According to Laplace’s law, ventricular wall stress (T) is pro-
portional to ventricular transluminal pressure (P 5 intraluminal
pressure – extraluminal pressure) and radius (r) and is inversely
related to twice the wall thickness (t):
Eq. 26.17
 T 5 P 3 r/2t Eq. 26.20
For a given pressure, wall stress is increased by an increase in
radius (ventricular dilation); therefore, volume administration
may increase ventricular diameter and, consequently, wall stress.
Similarly, during spontaneous breathing, the transluminal pres-
Eq. 26.18 sure and, consequently, the wall stress increase, whereas during
mechanical ventilation (positive pressure), the transluminal
Eq. 26.19 pressure and wall stress both decrease. Ventricular hypertrophy
increases wall thickness and therefore decreases wall stress.
Resistance
To understand resistance, returning to Ohm’s law is helpful:
voltage (V) varies directly with resistance (R) and current (I):
 V 5 IR Eq. 26.21
Rearranging Eq. 26.21 by substituting pressure for voltage and
flow for current gives Eq. 26.22:
 R 5 (Pin 2 Pout)/Q Eq. 26.22
where R is resistance, Pin is pressure going into a vessel, Pout is pres-
sure exiting the vessel, and Q is flow. According to Poiseuille’s law,
the resistance of flow through a tube varies directly with the viscos-
ity of the fluid and the length of the tube and is inversely propor-
tional to the radius to the fourth power multiplied by pi (π):
 R 5 8hl/pr4 Eq. 26.23
where h is viscosity, l is length, and r is radius. Unfortunately,
Poiseuille’s law assumes uniform viscosity, length, and radius,
none of which holds true in the case of pulmonary or systemic
circulation; however, the principles behind the law are valuable in
understanding the major determinants of resistance.
By substituting the appropriate values into Eq. 26.20, the formu-
las for SVR and PVR can be derived. CO is substituted for Qs and
Qp in the absence of a right-to-left or left-to-right shunt or single-
ventricle physiology. In the case of the equation for PVR (Eq. 26.25),
PAOP is substituted for pulmonary vein pressure in determining Pout:
 SVR 5 (MAP 2 CVP)/CO Eq. 26.24
 PVR 5 (MPAP 2 PAOP)/CO Eq. 26.25
SVR and PVR are measured in mm Hg 3 minute 3 L21 (or mm
Hg/L per min). These units also are referred to as hybrid resistance units
or Wood units after the cardiologist Paul Wood.21 By multiplying by
80, hybrid resistance units or Wood units can be converted to the
centimeter-gram-seconds (cgs) system, where resistance is measured as
dyne • s/cm5, also known as absolute resistance units.
PVR and SVR often are indexed for BSA (in m2). The SVRI
and PVRI are measured as dyne • s/m2 per cm5:
 SVRI 5 80 3 (MAP 2 CVP)/Cl Eq. 26.26
 PVRI 5 80 3 (MPAP 2 PAOP)/Cl Eq. 26.27
238 S E C T I O N I V  Pediatric Critical Care: Cardiovascular
SVRI usually is 800 to 1600 dyne • s/m2 per cm5 in children72,73
and 2180 6 210 in adults.81
Calculation of Intracardiac Shunt
If the oxygen saturations throughout the cardiopulmonary circu-
lation are known, derivation of the values for the ratio of pulmo-
nary to systemic blood flow or intracardiac shunt (Qp/Qs) is
possible:
 5 Vo2/(1.34 3 10 3 Hb[Spvo2 2 Spao2])
Qp Eq. 26.28
 5 Vo2/(1.34 3 10 3 Hb[Sao2 2 Svo2])
Qs Eq. 26.29
Qp/Qs
 5 (Sao2 2 Svo2)/(Spvo2 2 Spao2) Eq. 26.30
where Spvo2 is oxygen saturation in the pulmonary vein and
Spao2 is oxygen saturation in the pulmonary artery. In the ab-
sence of severe intrapulmonary shunt, Spvo2 approaches 98% to
100%. In a complete mixing lesion, Spao2 and Sao2 should be
equal by definition, enabling Sao2 to be substituted for Spao2.
Novel Monitoring Strategies
As PAC use has fallen dramatically and familiarity with it has
waned, providers have been replacing it with many innovative
techniques, often used in concert with one another, to obtain
similar information. Many of these investigations can be per-
formed noninvasively. Pulse wave Doppler (PWD) has shown
promise82 as an assessment of left ventricular function, as has
esophageal Doppler,83 although the latter requires a transesopha-
geal echocardiogram probe. Thermodilution from PACs may be
supplanted by lithium dilution and/or transpulmonary thermodi-
lution methods.84,85 Although the long-term utilization of such
techniques is not yet routine in children, the relative ease of use
or placement, often using in situ CVCs and arterial lines, in com-
parison with the PAC, and additional monitoring capabilities,
make them attractive.
Conclusions
Invasive hemodynamic monitoring provides the intensivist with
valuable information regarding the condition of critically ill chil-
dren. Correct interpretation of this information is important to
aid in the management of these patients, but these data must be
integrated with the rest of the patients’ assessments. When pieces
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of data conflict with one another, the invasive origin of one does
not necessarily suggest its superiority. New noninvasive monitor-
ing modalities are emerging that may eventually supplant the
need for these invasive measurements. Thus far, however, invasive
monitoring remains a cornerstone of pediatric critical care
medicine.
Key References
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Eskesen TG, Wetterslev M, Perner A. Systematic review including re-
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Marik PE, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterial
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The full reference list for this chapter is available at ExpertConsult.com.

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 e3

Abstract: Hemodynamic monitoring refers to measurement of the
functional characteristics of the heart and circulatory system that
affect the perfusion of tissues with oxygenated blood. Hemody-
namic monitoring can be performed invasively or noninvasively
and can be used for diagnosis, surveillance, or titration of therapy.
The central venous waveform is composed of three waves (a, c, and
v) and two wave descents (x and y). The arterial waveform has three
components: rapid upstroke, dicrotic notch, and runoff. Pulse
pressure variation has excellent specificity as an indicator of fluid
responsiveness in many critically ill patients. Cardiac output can be
calculated using the Fick method or measured directly via thermo-
dilution. A pulmonary artery catheter can be used to measure
cardiac output and indices of oxygen delivery and extraction.
Key words: pulmonary artery catheter, Swan-Ganz, arterial line,
central venous catheter, pulse pressure, hemodynamics

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