Download Monitoring Arterial Blood Pressure: What You May Not Know

Monitoring Arterial Blood Pressure: What You May Not Know
Beate H. McGhee and Elizabeth J. Bridges
Crit Care Nurse 2002;22:60-79
© 2002 American Association of Critical-Care Nurses
Published online http://www.cconline.org
Personal use only. For copyright permission information:
http://ccn.aacnjournals.org/cgi/external_ref?link_type=PERMISSIONDIRECT
Subscription Information
http://ccn.aacnjournals.org/subscriptions/
Information for authors
http://ccn.aacnjournals.org/misc/ifora.shtml
Submit a manuscript
http://www.editorialmanager.com/ccn
Email alerts
http://ccn.aacnjournals.org/subscriptions/etoc.shtml
Critical Care Nurse is the official peer-reviewed clinical journal of the American
Association of Critical-Care Nurses, published bi-monthly by The InnoVision Group
101 Columbia, Aliso Viejo, CA 92656. Telephone: (800) 899-1712, (949) 362-2050,
ext. 532. Fax: (949) 362-2049. Copyright © 2002 by AACN. All rights reserved.
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
Monitoring Arterial
Blood Pressure:
What You May Not Know
Beate H. McGhee, BSN, MN, APN
Maj Elizabeth J. Bridges, USAF, NC
To receive CE
credit for this
article, visit the
American Association of CriticalCare Nurses’
Online
(AACN) Web site
at http://www.aacn
.org, click on
"Education" and select “Continuing
Education,” or call AACN’s Fax on
Demand at (800) 222-6329 and
request item No. 1152.
A
rterial
blood pressure (ABP)
is a basic
hemodyn a m i c
index often
utilized to
guide therapeutic interventions,
especially in critically ill patients.
Inaccurate ABP measuring creates a potential for misdiagnosis
Beate H. McGhee is an adult care
nurse practitioner and a recent
graduate of the master’s program in
the School of Nursing, University of
Washington, Seattle, Wash. Maj
Elizabeth J. Bridges has a doctoral
degree from the School of Nursing,
University of Washington, Seattle.
To purchase reprints, contact The InnoVision
Group, 101 Columbia, Aliso Viejo, CA 92656.
Phone, (800) 809-2273 or (949) 362-2050
(ext 532); fax, (949) 362-2049; e-mail,
[email protected].
and mismanagement. The results
of a recent pilot study1 at 2 university-affiliated hospitals suggested
a knowledge deficit in arterial
pressure monitoring and some of
the most basic aspects of hemodynamic monitoring. A total of
391 critical care nurses practicing
in various critical care specialties
were invited to participate in the
study. The response rate was
17.4% (n = 68). Most of the participants were between the ages of 30
and 39 years (56.1%) and had a
baccalaureate degree as their
basic (61.8%) and highest degree
in nursing (58.8%). Most participants had more than 4 years of
nursing experience (94.1%) and
critical care experience (83.9%),
and most did direct ABP monitoring at least once or twice each
week (97.1%). The participants
were asked to complete an 18-item,
criterion-referenced questionnaire on ABP physiology, technical aspects of ABP monitoring,
and ABP waveform interpretation
in selected pathophysiological
conditions. The mean score in
this pilot study was 36.7% (SD,
11.8%). Total scores ranged from
11.1% to 61.1%.
Literature on nurses’ knowledge of hemodynamic monitoring
is limited, but several studies, 2-5
published and unpublished, indicate a general knowledge deficit in
pulmonary artery pressure monitoring. Because of these research
findings, in this article, we focus
on areas of particular knowledge
deficit related to essential principles of hemodynamic monitoring
and ABP monitoring. We discuss
the physiology of ABP, physiological and pathophysiological factors
that affect ABP, and the arterial
pressure waveform and its interpretation in clinical situations
common in critical care patients.
ABP PHYSIOLOGY
The cardiovascular system has
3 types of pressures 6,7: hemodynamic, kinetic energy, and hydrostatic. Hemodynamic pressure is
the energy imparted to the blood
by contraction of the left ventricle.
This type of pressure is preserved
by the elastic properties of the
arterial system. Kinetic energy is
the energy associated with motion
and affects the pressure measured
during direct ABP monitoring.
Fluid density and gravity contribute to hydrostatic pressure,
which is the pressure a column of
fluid exerts on the container wall.
For example, in a column of fluid,
the pressure at a given level in the
container is proportional to the
60 CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
height of the fluid column above
that level. The pressure is highest
at the bottom of the column. In
the vascular system, hydrostatic
pressure is proportional to the
height of the column of blood
between the heart and the peripheral vasculature. In a standing
person, the pressure in the leg is
higher than the pressure in the
arm by the difference in hydrostatic pressure. In summary, arterial blood pressure represents the
force exerted by the blood per
unit area on the arterial wall6-8 and
is the sum of hemodynamic,
kinetic, and hydrostatic pressure.
The arterial tree starts with the
aorta and the major branches of
this vessel. The aorta and its
branches stretch to receive blood
from the left ventricle and recoil
to distribute the blood and to
maintain arterial pressure. Arteries and arterioles control blood
pressure through vasoconstriction or vasodilation. 6 Arterioles
are the primary sites that contribute to systemic vascular resistance (SVR). 6,9-11 In addition,
adrenergic control of the arterioles is a major determinant of
blood flow into the capillaries. In
the skin, for instance, blood can
be shunted from the capillary
beds to flow directly from arterioles into the venous system. 9
Arteriovenous shunting occurs in
shock states and helps to redirect
blood flow to vital organs. Arteriovenous shunting is one reason
measurements of blood pressure
alone are not a good indicator of
peripheral tissue perfusion.
Arterial pressure is measured at
its peak, which is the systolic blood
pressure (SBP), and at its trough,
which is the diastolic blood pressure (DBP). The SBP is determined
by the stroke volume, the velocity
of left ventricular ejection (an indi-
rect indicator of left ventricular
contractile force), systemic arterial
resistance, the distensibility of the
aortic and arterial walls, the viscosity of blood, and the left ventricular preload (end-diastolic
volume).11-13 The blood pressure in
the aorta during systole is a clinical
indicator of afterload (the sum of
the forces the left ventricle must
overcome to eject blood).14,15 The
diastolic pressure is affected by
blood viscosity, arterial distensibility, systemic resistance, and the
length of the cardiac cycle.11,16
Pulse pressure is the difference
between systolic and diastolic
pressure. A normal pulse pressure
in the brachial artery is approximately 40 mm Hg. An increased
pulse pressure may be the result of
increased stroke volume or ejection velocity and is common during fever, exercise, anemia, and
hyperthyroidism.11 Other causes of
increased pulse pressure include
bradycardia (increased stroke volume), aortic regurgitation, and
arterial stiffening, which is most
noticeable after the age of 50 to 60
years. 11,17-19 An acute decrease in
pulse pressure may indicate an
increase in vascular resistance,
decreased stroke volume, or
decreased intravascular volume.11-13
Systemic mean arterial pressure (MAP) is defined as the mean
perfusion pressure throughout the
cardiac cycle. MAP is sensed by
baroreceptors located in the
carotid sinuses and the arch of the
aorta. These receptors control arterial pressure mainly by adjusting
heart rate and arteriolar vessel
radius. MAP is also the basis for
autoregulation by some organ systems such as the kidney, heart, and
brain. Autoregulation is the automatic adaptation of the radius of
an arteriolar vessel in an organ to
maintain constant blood flow over
a wide range of mean pressures
(60-150 mm Hg) to protect functioning of the organ.7,20 MAP is the
product of SVR and cardiac output
(MAP=SVR×cardiac output).7,10
As indicated previously, a main
determinant of SVR is the radius of
arterial, and particularly arteriolar,
vessels. Changes in cardiac output
are related to heart rate and stroke
volume. Stroke volume, in turn, is
determined by several factors,
including heart rate, preload, afterload, cardiac contractility, and synergy of cardiac contraction (related
to ventricular dilatation, abnormalities in ventricular wall motion, and
ventricular arrhythmias).10,11 MAP is
generally closer to diastolic pressure because diastole represents
about two thirds of the cardiac
cycle when the mean heart rate is
close to 60/min. This relationship
is expressed in the well-known formulas MAP = DBP + (SBP -DBP)/3
and MAP = [SBP + (DBP x 2)]/3.
However, the proportion of
diastole in the cardiac cycle
changes with changes in heart
rate. In calculations of MAP for a
manually obtained ABP, these formulas must be used with caution,
because they provide a good estimate of MAP only when the heart
rate is close to 60/min. 10 Fortunately, MAP is provided by most
automatic ABP measuring devices
and direct ABP monitoring systems, each of which uses a systemspecific method to directly
determine MAP.
In summary, because of the
multiplicity of factors that contribute to ABP and the complexity
of their interrelationships, interpreting changes in arterial pressure and its components (SBP,
DBP, MAP, and pulse pressure) as
indicative of any single factor may
lead to an erroneous assessment
of a patient’s condition. When SBP
CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002 61
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
and DBP are measured using different (oscillometric or direct)
monitoring methods, the values
can differ significantly. When MAP
is measured using different monitoring methods, however, the values are very similar, because MAP
is little affected by the phenomenon of wave reflection.21-25 Wave
reflection and other factors that
affect measurement of SBP and
DBP are discussed later.
PRINCIPLES OF
HEMODYNAMIC
MONITORING
Three Conventions of
Cardiovascular Pressure
Measurement
For measurement of cardiovascular pressures, 3 conventions
are observed 6,7,20 : (1) Cardiovascular pressures are expressed
in millimeters of mercury, with
the exception of central venous
pressure, which may be measured
in millimeters of mercury or in
centimeters of water. For converting values in centimeters of water
to values in millimeters of mercury, the value given in centimeters of water is divided by the
factor 1.36. (2) Most cardiovascular pressures, such as ABP, central
venous pressure, and pulmonary
artery pressure, are referenced to
the heart or, more specifically, to
the atria, to eliminate hydrostatic
pressure. (3) All cardiovascular
pressure monitoring devices are
zeroed to ambient atmospheric
pressure, so that the actual pressure measured reflects the pressure above atmospheric pressure.
The Hemodynamic
Monitoring System
A hemodynamic monitoring
system contains 2 compartments:
the electronic system and the
fluid-filled tubing system. Al-
though clinicians have little control over the electronic components such as the monitor, correct
setup and maintenance of the
tubing system and the pressure
transducer are absolutely crucial
to avoid error. With an improperly
prepared or inadequately functioning monitoring system, not
only the actively measured hemodynamic indices but also any
derived variables will be erroneous, 26 potentially invalidating a
patient’s entire hemodynamic profile. Three procedural steps should
be followed to prepare the monitoring tubing system and ensure its
continued accuracy: priming of the
pressure tubing, leveling and zeroing, and dynamic response testing.
Priming of the Pressure Tubing.
The generation and recording of all
arterial waveforms (systemic arterial pressure and pulmonary artery
pressure) are based on the same
basic principles. The invasive
catheter provides access to the
arterial system being monitored
and is designed to pick up the pressure waves generated in the arterial
system by cardiac contractions.
The catheter is connected to the
fluid-filled tubing of the monitoring system. The fluid column in the
tubing system carries the mechanical signal created by the pressure
wave to the diaphragm of the electrical pressure transducer. The
transducer creates the link between
the fluid-filled tubing system and
the electronic system, and converts
the mechanical signal into an electrical signal. The electrical signal is
transmitted to the monitor and
then is amplified and displayed as
an analog waveform and digital
output.
Air as a medium transmits
mechanical impulses much differently than does fluid. Air bubbles in the tubing system are one
of the most frequent and important sources of error in hemodynamic monitoring. Air bubbles
most often blunt or damp propagation of the mechanical signal,
causing a damped analog waveform and erroneous pressure
readings.27 Even tiny air bubbles
only 1 mm in diameter can cause
serious waveform distortion. 28
Therefore, air-free priming of the
entire tubing system is one of the
most important steps to avoid
technical error.
Air-free priming starts with
removal of all air from the flush
solution to prevent air from going
into the solution as a result of the
pressure applied by the external
pressure cuff. Then, the entire
tubing system should be flushed.
Stopcocks, Luer-Lok interconnections, and the transducer are common locations of air entrapment27
and deserve special attention
throughout priming and use of the
catheter system. In order to maintain the air-free status after the
initial setup of the system, the following measures are important:
■ After opening the system for
blood sampling or zeroing, briefly
fast-flush the tubing system,
including the proximal access
stopcock or the air-fluid interface
stopcock.
■ Tighten all connections, and
ensure that the stopcocks are
closed to air.
■ Avoid adding stopcocks and
line extensions.
■ Keep the flush solution bag
adequately filled, and keep the
external pressure cuff at 300 mm Hg.
■ Periodically flick the tubing
system and flush the tubing system and stopcocks to eliminate
tiny air bubbles escaping the
flushing solution.
Leveling and Zeroing. The
arterial pressure monitoring sys-
62 CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
tem must be referenced to heart
level, technically the level of the
left atrium, and set at atmospheric pressure as the zero reference
point. These criteria can be met
through leveling and zeroing.
Leveling or referencing of the
catheter system is accomplished
by aligning the air-fluid interface
of the monitoring system (eg, the
stopcock on top of the transducer) with the external reference
point of the heart. The external
reference point of the heart is the
phlebostatic axis, which can be
located by finding the junction of
2 lines: a vertical line drawn out
from the fourth intercostal space
at the sternum and a horizontal
line drawn through the midpoint
of a line going from the anterior to
the posterior side of the chest.29,30
Where to level the air-fluid
interface is a matter of discussion.
The answer depends on which
vascular bed is to be monitored.
In most clinical situations, the
central arterial pressure is the
pressure of interest, because it is
a key determinant in cardiac and
cerebral perfusion. In order to
monitor central arterial pressure,
the monitoring system must be
leveled to the heart by using the
phlebostatic axis. Research indicates that the phlebostatic axis
most accurately reflects the level
of the atrium in both supine and
upright patients.29-31 The midaxillary line, which has also been
used as an external reference
point for the heart, is not accurate
in all chest configurations and
thus is not recommended.31 When
the monitoring system is referenced to the tip of the catheter,
then the transmural pressure of a
particular point in the arterial tree
is monitored and not central arterial pressure. Peripherally measured transmural pressure is
markedly increased by hydrostatic pressure unless the patient is
supine.32
Zeroing consists of 2 steps.
First, the air-fluid interface is
opened to atmospheric pressure.
Then the monitor’s zeroing function key or button is pressed.
Zeroing in this fashion has several
purposes. Zeroing electronically
establishes for the monitor atmospheric pressure as the atmospheric zero reference point. Zeroing
establishes the interface level as
the hydrostatic zero reference
point. Zeroing also eliminates zerodrift. Zero-drift is the potential, but
usually minimal, transducer offset
or distortion occurring over time.33
Two key practice objectives are
related to referencing and zeroing:
accuracy and consistency. In order
to ensure accuracy, leveling and
zeroing must be done whenever
the relationship between the airfluid interface and the reference
point is changed. The reason is
hydrostatic pressure. For every 1
cm the air-fluid interface is above
or below the actual level of the left
64 CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
atrium, 0.74 mm Hg of hydrostatic
pressure is subtracted or added to
the measured pressure. If the airfluid interface is placed 10 cm
below the phlebostatic axis, the
measured pressure will be an overestimation of the actual hemodynamic pressure by 7.4 mm Hg. This
example illustrates that though
accurate referencing and zeroing
are important for all hemodynamic
monitoring, they become even
more crucial when small hemodynamic pressures, such as pulmonary artery wedge pressure
(6-12 mm Hg) and central venous
pressure (2-6 mm Hg) are being
monitored. In these instances,
small offsets from the phlebostatic
axis and the zero reference point
can cause large errors34 and may
prompt inappropriate treatment.
In order to ensure consistency,
once the external reference point
has been selected, it should be
marked on the patient for easy
identification. Consistency allows
correct determination of trends in
a patient’s hemodynamic status.
Whether the same body position
must be used for consecutive
measurements may be debatable.
Although several studies on pulmonary artery pressure monitoring indicated no significant
changes in pulmonary artery
pressures related to certain bed
positions, according to a recent
research abstract, 35 ABP values
obtained with various bed positions differed even when the phlebostatic axis was used as the
external reference point. The statistical significance of differences
in ABP values for monitoring systems referenced to the phlebostatic axis was not addressed in
the abstract.
Dynamic Response Testing. In
order to determine if a hemodynamic monitoring system can
adequately reproduce a patient’s
cardiovascular pressures, the
dynamic response characteristics
of the catheter system must be
tested. Only when system accuracy, also termed fidelity, has been
confirmed, can the analog waveform be accepted as an accurate
reflection of a patient’s status.
The dynamic response of a
hemodynamic monitoring system
is defined by its natural frequency
and the damping coefficient. The
natural frequency indicates how
fast the pressure monitoring system vibrates when shock excited by
a signal such as the arterial pressure pulse or the pressure signal
caused by a fast-flush test. The
damping coefficient of a monitoring system is a measure of how
quickly the oscillations of a shockexcited system dampen and eventually come to rest.23,26,36
Dynamic response testing is a
3-step procedure: determining
natural frequency, determining
the amplitude ratio of 2 consecutive fast-flush oscillations (as an
indirect way of determining the
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
damping coefficient), and determining the dynamic response
characteristics of the monitoring
system (eg, optimal, adequate,
underdamped, overdamped, or
unacceptable). These steps are
summarized in Figure 1.
Dynamic response testing may
seem complicated at first. Clinical
experience has shown, however,
that with proper training, dynamic response testing can be performed in less than 2 minutes. A
few simple observations provide
almost as much information and
may serve as a close estimate. (1)
If the period between 2 oscillations of the fast-flush test is less
than 1.2 mm, then natural frequency will be at least 21, and the
system will most likely be adequate. If the period between 2
oscillations is 1 mm or less, then
the natural frequency is 25 or
higher, and the system will almost
always function properly with any
degree of damping. As a rule-ofthumb, the higher the natural frequency (or the smaller the
period), the better is the dynamic
response of the monitoring system. (2) The system is overdamped if the fast-flush produces
sluggish or no oscillations. If the
square wave shows undulations
or if ringing occurs after the
release of the fast-flush device, the
system is most likely underdamped. Overdamping and underdamping both indicate that the
dynamic response characteristics
of the monitoring system are
unsatisfactory.
Simple visual evaluation of the
arterial waveform, the square
waveform, and oscillations generated by the fast-flush has been
suggested as a suitable method
for determining the dynamic
response characteristics of a
monitoring system. However, the
square waveform and fast-flush
oscillations may look adequate
when the natural frequency and
amplitude ratio of the system
actually make the system inadequate (underdamped, overdamped, or unacceptable). Or, the
arterial waveform may look distorted because of physiological
variations, yet the dynamic response characteristics of the system assure a faithful recording of
the arterial pressure.36 When accuracy is needed for clinical decision
making, the ideal method of determining if the measured ABP, or
any other directly monitored
hemodynamic parameter, is true
is to determine the dynamic response characteristics of the monitoring system.26,36 Examples of the
importance of formally assessing
the response characteristics are
discussed in more detail later.
COMPONENTS OF
THE NORMAL ABP
WAVEFORM
Left ventricular contraction
creates a pressure pulse or pulse
wave. It is the pressure pulse that
a clinician feels when determining a patient’s pulse by palpation.
The pressure pulse is also what is
sensed by the intra-arterial
catheter. 34,35 The normal arterial
pressure waveform is shown in
Figure 2. The systolic upstroke or
anacrotic limb mainly reflects the
pressure pulse produced by left
ventricular contraction. The pressure pulse is followed slightly
later by the flow wave caused by
the actual displacement of blood
volume. The anacrotic shoulder,
that is, the rounded part at the top
of the waveform, reflects primarily volume displacement. 22,37 The
systolic pressure is measured at
the peak of the waveform. The
dicrotic (or downward) limb is
demarcated by the dicrotic notch,
representing closure of the aortic
valve and subsequent retrograde
flow. The location of the dicrotic
notch varies according to the timing of aortic closure in the cardiac
cycle. For example, aortic closure
is delayed in patients with hypovolemia. Consequently, the dicrotic notch occurs farther down on
the dicrotic limb in hypovolemic
patients. The dicrotic notch also
appears lower on the dicrotic
limb when arterial pressure is
measured at more distal sites in
the arterial tree (Figure 3). The
shape and proportion of the diastolic runoff wave that follows the
dicrotic notch changes with arterial compliance and heart rate.
Diastolic pressure is measured
just before the beginning of the
next systolic upstroke.
The analog waveform visible
on the monitor or recorded on a
strip chart is not only caused by
the forward pressure pulse but is
also a result of a phenomenon
known as wave reflection. Wave
reflection is related to the impedance of blood flow by the narrowing and bifurcation of the
arterial vessels; the impedance
leads to backward or retrograde
reflection of the pressure wave.23,38-40
In a manner similar to waves on
the beach, the forward or antegrade pressure waves and the
reflected waves collide. The combination of the 2 types of waves
increasingly augments the SBP
the farther down the blood pressure is measured in the arterial
circuit. In other words, the contribution of reflected waves to the
measured systolic pressure occurs
earlier in the periphery, particularly in the radial and dorsalis
pedis arteries (Figure 3), where
the measured SBP may be 20 to 25
mm Hg higher than central aortic
CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002 67
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
Fast flush
A1 = 7 mm
A2 =
3 mm
Period (t) = 1.2 mm
A
1. Determining natural frequency (Fn)
At the end of a waveform
a. Perform the fast-flush maneuver (square waveform test): pull and release the pigtail or compress and release
the button of the fast-flush device of the monitoring system.
b. Record the resulting square waveform and subsequent oscillations on calibrated strip chart paper.
c. Measure the distance (period, t, of 1 cycle) in millimeters between 2 oscillations. (One small box on the
calibrated strip chart paper equals 1 mm.)
d. Calculate Fn by using the formula
Fn = paper speed (mm/s)/t of 1 cycle (mm)
(The standard paper speed is 25 mm/s.)
Example: paper speed = 25 mm/s; t = 1 mm; Fn = (25 mm/s)/1 mm = 25 Hz
2. Determine the amplitude ratio
a. Measure the amplitude (A) in millimeters of 2 successive oscillations (A1, A2).
b. Calculate the amplitude ratio: divide A2 by A1 (A2/A1).
B
3. Determine the dynamic response characteristics
On the Fn-versus-amplitude ratio graph
a. Plot Fn along the x-axis (result of step 1)
b. Plot the amplitude ratio along the y-axis on the right (result of step 2)
c. Find the intersection of the 2 lines. Where the 2 lines intersect on the Fn-versus-amplitude ratio graph determines
if the system is able to correctly reproduce the hemodynamic waveform (adequate, optimal) or if the system is not
functioning at a desirable level (overdamped, underdamped, unacceptable).
Figure 1 The 3 steps of dynamic response testing. A, The fast-flush test. B, The frequency-versus-damping coefficient
graph.
A, Adapted from Bridges and Middleton,36 with permission. B, Reprinted from Gardner and Hollingsworth,28 with permission; adapted from Bridges and Middleton,36
with permission.
68 CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
Anacrotic limb
120
SOURCES OF
ARTIFACT AND
CHANGES IN
WAVEFORM
MORPHOLOGY:
RECOMMENDATIONS
FOR CLINICAL
PRACTICE
Dicrotic limb
Systolic=115 mm Hg
Pulse pressure
=35 mm Hg
97
80
Diastolic=80 mm Hg
Dicrotic notch
40
MAP=Area + Base
=97 mm Hg
0
BASE
Damping, Overdamping, and
Underdamping
Figure 2 The normal arterial pressure waveform.
MAP indicates mean arterial pressure.
Reprinted from Darovic,10 with permission.
pressure.22,23 Under normal conditions, 80% of the original wave is
thought to be reflected.22
Clinically, wave reflection plays
an important role in left ventricular workload and cardiac oxygen
consumption. In young adults
with elastic arteries, the reflected
wave returns to the heart during
the diastolic phase of the cardiac
cycle and thus augments coronary
artery perfusion. In elderly patients
or patients with stiff, atherosclerotic vessels, the reflected wave
returns to the heart during systole
and thus increases systolic pressure and left ventricular afterload.39
Central
aorta
Brachial
Radial
Femoral
Dorsalis
pedis
Figure 3 Changes of the arterial
pressure waveform configuration
throughout the arterial tree. Note
the increasing steepness and
amplitude of the systolic upstroke
and the changing location of the
dicrotic notch.
Reprinted from Gorny,8 with permission.
Pharmacological vasoconstriction
can similarly increase wave reflection and cardiac workload.23,39
The contribution of reflected
waves to the measured systolic
pressure is diminished during
hypovolemia, hypotension, the
Valsalva maneuver, and vasodilatation. 23 In pharmacologically
induced vasodilation, such as
occurs with nitroglycerin for
instance, peripherally measured
systolic pressure may not change
in proportion to the actual degree
of reduction in central aortic pressure.39,40 The effect of nitroglycerin
may be visible in the appearance
of reflected waves after the systolic
peak (Figure 4), but reduced aortic
pressure, afterload, and cardiac
work load may be more evident
through clinical improvement of
the patient. During shock with
vasoconstriction, wave reflection
can lead to the overestimation of
central aortic pressure, because
peripheral SBP may be 20 mm Hg
higher than aortic pressure. 36,39
Peripherally measured SBP could
in this situation provide a false
sense of security that the patient is
maintaining adequate perfusion
pressures. A slower systolic upstroke and a prominent diastolic
waveform with reflected waves
may be visual indicators of shock
with vasoconstriction39 (Figure 5).
A common scenario when
working with arterial catheters is
comparing the blood pressure
recorded by the arterial catheter
with the blood pressure obtained
manually or with an oscilloscope.
If a discrepancy occurs, the arterial
catheter is often said to be somehow “damped,” with the underlying understanding that pressure
readings obtained with the catheter cannot be trusted. Such an
interpretation may be premature
and probably disregards several
important facts. Differences exist
between (1) damping, overdamping, and underdamping; (2) overdamped and underdamped pressure waveforms caused by overdamped or underdamped monitoring systems and overdampedor underdamped-appearing
waveforms that reflect the true
physiological status of a patient;
and (3) blood pressures obtained
via direct versus indirect monitoring methods.
All hemodynamic monitoring
systems are damped. Damping is
desired, because without damping the vibrations of the system’s
fluid column caused by the arterial pressure pulse would go on
indefinitely and no accurate
waveform could be recorded.
Conversely, both overdamped
and underdamped systems exist,
and their recordings are indeed
erroneous. With an overdamped
system, the waveform loses its
characteristic landmarks and
CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002 69
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
Figure 4 Example of a waveform common in patients with hypertension
(arterial blood pressure, 192/84 mm Hg; pulse pressure, 108 mm Hg). Note
the narrow systolic tip, the position of the dicrotic notch (D), and the
reflected waves (R). A reflected wave like the first reflected wave after the
systolic upstroke may appear with the initiation of nitroglycerin therapy.40
Overall, the arterial waveform appears underdamped, but the dynamic
response characteristic is adequate, close to optimal. Natural frequency,
25/1 = 25 Hz; amplitude ratio, 3.5/8 = 0.44.
appears unnaturally smooth, with
a diminished or absent dicrotic
notch. Overdamping results in
falsely low systolic and falsely high
diastolic pressure readings 26
(Figures 6 and 7). An overdampedappearing (often simply called
damped) waveform can also be the
result of aortic stenosis, vasodilatation, or low cardiac output
states such as cardiogenic shock,
sepsis, or severe hypovolemia
(Figure 5). In order to determine if
the waveform is a result of an overdamped system or is an accurate
reflection of a patient’s status, the
dynamic response characteristics
must be tested.
Today’s commercially available catheter-transducer systems
tend to have a low natural frequency and consequently are
often underdamped. 22,36 Anecdotal reports of manufacturers of
an improved natural frequency
often do not hold up in clinical
practice. Typically, the natural
frequency of hemodynamic monitoring systems currently on the
market is less than 25 Hz. An
underdamped system will record
falsely high systolic pressures
(15-30 mm Hg) and falsely low
diastolic pressures26 (Figures 8-10).
Underdamping, most often in
the form of systolic overshoot
(the artificial exaggeration of systolic pressure), must be suspected in patients with hypertension,
atherosclerosis, vasoconstriction,
aortic regurgitation, or hyperdynamic states such as fever. 23 In
these conditions, typically a rapid
rise in the systolic slope occurs,
frequently exceeding the dynamic response characteristics of the
monitoring system. A heart rate
greater than 150/min may also
cause systolic overshoot, because
of the rapid succession of
impulses.26
The variable natural frequency
of available monitoring systems
explains why with different monitoring systems, different hemodynamic pressures can be measured
even though the patient’s condition has not changed.22 The often
observed discrepancies between
directly and indirectly obtained
SBP and DBP readings are also
partly caused by underdamping.22
Clinically, recognition of possibly overdamped and underdamped waveforms and an
awareness of physiological situations when each type of waveform may occur are important.
Then the question to be
answered is whether the cause of
the waveform is the patient’s
condition or the monitoring system. Practically, the intervention
for both overdamped and underdamped systems is the same:
maximizing natural frequency.
Techniques for Maximizing
Natural Frequency
Figure 5 Waveform in a patient in shock with vasoconstriction. Note slow
systolic upstroke and relatively high diastolic wave with reflection waves (R).
The waveform appears overdamped.
D indicates dicrotic notch.
As mentioned earlier, air bubbles are a main factor in waveform blunting or overdamping. In
addition to air bubbles, other factors may alter the natural frequency of a monitoring system
and distort the recorded signal.
These factors include narrow,
compliant, and long tubing; presence of additional stopcocks; and
loose connections. Translated into
practice, the monitoring system
70 CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
Figure 6 Overdamped waveform due to an overdamped monitoring system.
Note the absence of fast-flush oscillations.
should (1) be primed air-free, (2)
consist of wide-bore, high-pressure tubing with its length limited
to 122 cm (48 in), (3) not be
extended with tubing or added
stopcocks, and (4) have tightly
secured connections.27,36 In addition, the continuous flush bag
should be cleared of any air and
be maintained adequately filled,
and the external pressure cuff surrounding the flush solution bag
should be maintained at a pressure of 300 mm Hg. This practice
will not only prevent air from
going into the solution but also
help prevent catheter clotting.
Catheter clotting is a rare, but
possibly serious, complication of
intra-arterial monitoring. One of
the first indications of clotting may
be a waveform that looks overdamped. Whenever waveform
overdamping is observed, the
patient should be assessed
for signs and symptoms of hypotension or low cardiac output.
Then, the potential clot should
be removed by aspirating blood
from the distal stopcock before
performing any flushing maneuver
for the dynamic response test. 37
Fluids with viscosities higher than
the viscosity of normal isotonic
sodium chloride solution also lead
to overdamping of the hemodynamic waveform.23 For example,
blood in the arterial catheter (due
to blood backup or insufficient
flushing) should be cleared from
the system. As a general rule, the
catheter-tubing system and stopcocks should be flushed before any
hemodynamic measurement is
performed, especially when clinical decisions are to be made. The
Table summarizes the most
important recommendations for
Figure 7 Example of an overdamped-appearing waveform. The dynamic
response characteristic of the system gives an answer to the question, is the
waveform overdamped because of the monitoring system or is it a correct
reflection of the patient’s condition?
optimizing the natural frequency
of the monitoring system and
dynamic response testing.
In general, overdamping and
underdamping affect mostly SBP
and DBP. MAP is less sensitive to
these sources of waveform distortion and is therefore less dependent on the dynamic response
characteristics of the catheter system. 26 When all steps have been
taken to maximize the natural
frequency of a system, yet the
dynamic response test indicates
overdamping or underdamping,
then either MAP should be
followed or an alternative method
of monitoring (eg, oscillometric
blood pressure monitoring)
should be used.
End-Hole Artifact
The arterial catheter of the
ABP monitoring system points
upstream. The forward-flowing
blood contains kinetic energy.
When the flowing blood is suddenly stopped by the tip of the
catheter, the kinetic energy of the
blood is partially converted into
pressure. This converted pressure
may add 2 to 10 mm Hg to the
systolic pressure measured by an
intra-arterial monitoring system.23
The artificial augmentation of
directly monitored systolic pres-
Figure 8 Example of an
underdamped waveform. Natural
frequency, 25/1.5 = 16.7 Hz;
amplitude ratio, 7/14 = 0.5.
CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002 73
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
for hemodynamic pressure measurement is to use the analog
strip-chart recording.43,44
Respiratory Variation
Figure 9 Example of an underdamped waveform. Natural frequency, 25/2 =
12.5 Hz; amplitude ratio, 4/11 = 0.36. Note the normal-appearing fast-flush
oscillations.
sure by converted kinetic energy
is referred to as the end-hole artifact or the end-pressure product.
Movement Artifact
Motion of the tubing system
enhances the fluid oscillations of
the system. Although the clinical
significance of movement artifact
is not known, it is recommended
that extrinsic movement of the
tubing system be kept at an absolute minimum.10
Monitor Artifact
The differences (>5 mm Hg)
between the digital pressure output displayed on the monitor and
pressures directly read from analog
or strip chart recordings are potentially important.43 These differences
can lead to erroneous data collection and are especially notable in
patients with hypotension, hyper-
tension, dysrhythmias, or pulsus
paradoxus.43 The monitoring system cannot discriminate between
pressure readings during zeroing,
obtaining blood samples, and
fast-flushing and real arterial
pressure readings. Consequently,
all readings are incorporated into
pressure trends.43 Monitoring artifact (ie, monitoring noise caused
by movement of the patient and
disturbances in a monitoring system due to, for example, electrical
heating or cooling blankets) may
also be superimposed on the
patient’s pressure waveform.
Experienced clinicians can recognize and eliminate some of these
error sources and use a representative set of waveform tracings on
a calibrated strip-chart recording
to obtain the most valid assessment of a patient’s hemodynamic
status.43 Thus, the optimal method
Figure 10 Example of an overdamped-appearing waveform. However, the
dynamic response test places the system on the border between
underdamped and adequate. Natural frequency, 25/1.8 = 13.9 Hz; amplitude
ratio, 9/19 = 0.47.
Normal breathing leads to
changes in intrathoracic pressure,
which affect cardiac output and
systemic pressure. With spontaneous inspiration, intrathoracic
pressure decreases. The decreased pressure is recognizable
on the ABP tracing as a downward
displacement of the waveform
baseline. Concurrently, during inspiration, venous return to the
right side of the heart is increased,
augmenting right ventricular
stroke volume. The increase in
right ventricular stroke volume is
offset by increased pulmonary vascular compliance and blood pooling during inspiratory thoracic
expansion. Consequently, left ventricular stroke volume is decreased.
Heart rate and SVR both increase
as a compensatory reflex. The net
result of this chain of reflexes is the
phenomenon known as physiological pulsus paradoxus (a decrease
in ABP of usually <10 mm Hg during spontaneous, unassisted inspiration).45 An inspiratory decrease in
ABP greater than 10 mm Hg (pulsus paradoxus) may indicate cardiac tamponade or restrictive
pericarditis. Pulsus paradoxus also
occurs in patients with obstructive
lung disease, pulmonary embolism, and severe heart failure
and can be induced by mechanical
ventilation.46,47
During positive-pressure ventilation, the inspiratory increase in
intrathoracic pressure can be recognized in the upward displacement of the baseline of the arterial
pressure waveform. If a patient
receiving mechanical ventilation is
hypovolemic, the increase in
CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002 75
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
Recommendations for optimizing the natural frequency of the arterial pressure monitoring system and dynamic response
testing
Recommendations
Feature
Natural frequency of the monitoring
system23,27,41
System requirements
Use wide-bore, high-pressure tubing no longer than 122 cm (48 in)
Avoid tubing extensions and minimize stopcocks
Ensure that all connections are tightened
Eliminate air from the flush fluid and air bubbles from the tubing system
Keep continuous flush bag filled and keep external pressure cuff at 300 mm Hg
pressure
Clear access catheter and tubing system of any fluid other than isotonic sodium
chloride solution
Prevention of catheter clotting
Maintain continuous flush device as described
Use heparinized flush solution42
Prevention of catheter kinking
Keep cannulated extremity in a neutral or slightly extended position
Dynamic response test27,41
Implementation of test
Whenever the waveform seems overdamped or underdamped
Whenever physiological changes of the patient (increased heart rate,
vasoconstriction) place higher demands on the monitoring system
After opening the system
Before implementing interventions or changes of interventions
Whenever the accuracy of the arterial blood pressure measurement is in doubt
At least every 8-12 hours
intrathoracic pressure may lead to
artificial augmentation of directly
monitored SBP.
Current monitoring systems
determine the mean of pressure
readings at predetermined intervals. Respiratory artifact could lead
to erroneous digital output data.
The unpredictable effect of respiratory variation on arterial pressure
provides a strong argument for
reading and recording arterial pressure, like any other hemodynamic
index, at the end of expiration by
using a freeze-frame picture or,
best, a strip-chart recording.48,49
resulting in a high pulse pressure
waveform may be an overesti-
and late high systolic peak, often
mation of systolic pressure and
manifested as a narrow systolic
thereby central aortic pressure. As
peak in the peripheral ABP wave-
explained earlier, hypertension
form tracing.
39
In addition, the
and atherosclerosis place high
diastolic wave may be reduced or
demands on the monitoring sys-
disappear. Figures 4 and 11 show
tem. The arterial waveforms
peripheral ABP tracings typical in
shown in Figures 4 and 11 could
patients with hypertension or
also be the result of systolic over-
atherosclerosis. In each instance,
shoot due to inadequate dynamic
the small and narrow tip of the
response characteristics of the
10,38
39
Hypertension and
Atherosclerosis
Hypertension is due to agerelated arterial stiffening, atherosclerotic narrowing, or reninrelated vasoconstriction, all of
which increase the magnitude of
reflected waves. In these physiological conditions, reflected waves
fuse with the systolic upstroke,
Figure 11 Example of a waveform common in patients with hypertension
(arterial blood pressure, 150/45 mm Hg). Note steep systolic upstroke,
narrow systolic peak, diminished diastolic run-off wave, and relative decrease
in the diastolic proportion of the waveform due to a heart rate of 100/min.
The waveform appears underdamped.
76 CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
monitoring system. The result of
the dynamic response test provides
reassurance that the recorded ABP
tracing is correct.
MAP is measured as the area
under the pressure curve divided
by the width of the base of the
pressure curve (the time interval
of a single cardiac cycle) 10,37
(Figure 2). A small and narrow
systolic tip such as the ones in
Figures 4 and 11 adds relatively
little to the total area under the
pressure curve, whereas it can
add significantly to measured
SBP. Consequently, the measured
MAP is less affected by wave
reflection and the response characteristics of the monitoring system than is measured SBP. The
MAP remains relatively constant
when measured at different sites
throughout the arterial circuit,
whereas measured SBP and DBP
may differ.10 In general, MAP is a
more stable hemodynamic parameter and provides a more accurate interpretation of a patient’s
hemodynamic status.10,34,36,38
INDIRECT VERSUS
DIRECT ABP
MONITORING
A discussion of the various
methods of indirect ABP measurement and how they compare
with direct ABP monitoring is
beyond the scope of this article.
However, several key principles
should be emphasized in this
context. Direct ABP monitoring
measures pressure pulse, whereas
all indirect methods of ABP measurement are related to blood
flow. No absolute relationship
exists between these 2 phenomena because they follow different
laws of physics and physiology. In
low-flow conditions, such as
hypotension and vasoconstricted
states, indirect methods yield
lower pressure readings than does
direct ABP monitoring. 22,36 Conversely, if SVR is low, in patients
with sepsis for instance, the relatively high flow results in an indirect ABP reading that is higher
than the directly measured
ABP. 22,36 Factors such as underdamping, end-hole artifact, and
wave reflection contribute to
direct systolic pressure readings
that are often higher than indirectly obtained pressure values.
In other words, when obtaining
ABP readings by using different
measuring methods, different
results should be expected. More
specifically, a “good” correlation
between the oscilloscope and the
arterial pressure monitoring system is not a gauge for the proper
functioning of the pressure monitoring system. MAP, on the contrary, is closely approximated
when oscillometric and direct
measurements are compared.21-25,36
Although both the oscillometric and the direct ABP monitoring
methods are generally accurate in
clinical practice, direct ABP monitoring has a distinct advantage.
Direct ABP monitoring is the only
scientifically and clinically validated method that allows realtime and continuous monitoring
of a patient’s ABP. With stripchart recording, beat-to-beat
analysis of a patient’s ABP is possible. This feature may be of clinical relevance when evaluating the
effect of positive end-expiratory
pressure during mechanical ventilation or the effect of changing
stroke volume in atrial fibrillation
or other arrhythmias.
SUMMARY
Hemodynamic monitoring is a
costly procedure, both materially
and with regard to nursing time
involved to ensure proper functioning of the monitoring system
and correct interpretation of the
data obtained. Dynamic response
testing is the ideal method of confirming the ability of a monitoring
system to accurately reproduce
hemodynamic waveforms. MAP is
a stable hemodynamic parameter,
because it is least affected by monitoring method, catheter insertion
site, the dynamic response characteristics of the catheter system, and
wave reflection. MAP provides the
best estimate of central aortic pressure and is the main hemodynamic
parameter monitored by the neurohormonal system to control
blood pressure. The superior informational value of MAP provides
strong support for its preferred use
in clinical practice, especially when
use of vasoactive drugs is started or
the dosages of these drugs are
titrated.10,21 However, numerically
satisfactory ABP or MAP values are
not necessarily related to adequate
peripheral tissue perfusion and
organ system function. For optimal
management of patients, data
obtained from assessment tools
such as hemodynamic monitoring
devices must be integrated with
information gained from clinical
assessment of patients’ status. ✙
Acknowledgments
I (B.H.M.) am grateful to Maj Bridges for
sharing her expertise and for her help and
support in preparing this article.
References
1. McGhee BH, Woods SL. Critical care nurses’ knowledge of arterial pressure monitoring. Am J Crit Care. 2001;10:43-51.
2. Bridges EJ. Evaluation of Critical Care
Nurses’ Knowledge and Ability to Utilize
Information Related to Pulmonary
Artery Pressure Measurement [master’s
thesis]. Seattle, Wash: University of
Washington; 1991.
3. Kondrat P. Critical Care Nurses’
Knowledge of Pressure Waveforms
Obtained From the Pulmonary Artery
Catheter [master’s thesis]. Seattle, Wash:
University of Washington; 1994.
4. Iberti TJ, Daily EK, Leibowitz AB,
Schecter CB, Fischer EP, Silverstein JH.
Assessment of critical care nurses’ knowl-
78 CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
edge of the pulmonary artery catheter.
The Pulmonary Artery Catheter Study
Group. Crit Care Med. 1994;22:1674-1678.
Burns D, Burns D, Shively M. Critical
care nurses’ knowledge of pulmonary
artery catheters. Am J Crit Care. 1996;
5:49-54.
Rhoades RA, Tanner GA. Medical
Physiology. Boston, Mass: Little Brown &
Co; 1995.
Scher A, Feigl EO. Introduction and
physical principles. In: Patton D, Fuchs
AF, Hille B, Scher AM, Steiner R, eds.
Textbook of Physiology. Vol 2. 21st ed.
Philadelphia, Pa: WB Saunders Co;
1989:771-781.
Gorny DA. Arterial blood pressure measurement technique. AACN Clin Issues.
1993;4:66-80.
Halpenny C. The systemic circulation.
In: Woods SL, Sivarajan-Froelicher ES,
Halpenny C, Motzer S, eds. Cardiac
Nursing. 3rd ed. Philadelphia, Pa: JB
Lippincott; 1995:58-71.
Darovic GO. Hemodynamic Monitoring:
Invasive and Noninvasive Clinical
Application. 2nd ed. Philadelphia, Pa:
WB Saunders Co; 1995.
Bridges EJ. The systemic circulation. In:
Woods SL, Motzer S, SivarajanFroelicher ES, eds. Cardiac Nursing. 4th
ed. Philadelphia, Pa: JB Lippincott;
1999:51-71.
Nutter D. Measurement of the systolic
blood pressure. In: Hurst J, ed. The
Heart, Arteries, and Veins. 5th ed. New
York, NY: McGraw-Hill; 1982:182-187.
O’Rourke MF. The measurement of systemic blood pressure: normal and
abnormal pulsations of the arteries and
veins. In: Hurst J, Schlant R, eds. The
Heart, Arteries, and Veins. 7th ed. New
York, NY: McGraw-Hill; 1990:149-162.
Bridges EJ. Control of blood pressure
and cardiac output. In: Woods SL,
Motzer S, Sivarajan-Froelicher ES, eds.
Cardiac Nursing. 4th ed. Philadelphia,
Pa: JB Lippincott; 1999:82-106.
Hedges JR. Preload and afterload revisited. Emerg Nurs. 1983;9:262-267.
O’Rourke MF. What is blood pressure?
Am J Hypertens. 1990;3:803-810.
Folkow B, Svanborg A. Physiology of cardiovascular aging. Physiol Rev.
1993;73:725-764.
Franklin S, Gustin W, Wong N, et al.
Hemodynamic patterns of age-related
changes in blood pressure. The
Framingham Heart Study. Circulation.
1997;96:308-315.
Lakatta E. Cardiovascular system. In:
Masora E, ed. Handbook of Physiology:
Aging. Bethesda, Md: American
Physiological Society; 1995:413-474.
Feigl EO. Coronary circulation. In:
Patton HD, Fuchs AF, Hille B, Scher AM,
Steiner R, eds. Textbook of Physiology.
Vol 2. 21st ed. Philadelphia, Pa: WB
Saunders Co; 1989:933-950.
Marino PL. The ICU Book. Philadelphia,
Pa: Lea & Febiger; 1998.
Henneman E, Henneman P. Intricacies
of blood pressure measurement. Heart
Lung. 1989;19:263-273.
Grossman W. Pressure measurement. In:
Grossman W, Baim D, eds. Cardiac
Catheterization, Angiography and
Intervention. 5th ed. Baltimore, Md:
Williams & Wilkins; 1996:125-142.
Venus B, Mathru M, Smith RA, Pham
CG. Direct versus indirect blood pressure measurements in critically ill
patients. Heart Lung. 1985;14:228-231.
25. Loubser PG. Comparison of intra-arterial and automated oscillometric blood
pressure measurement methods in postoperative hypertensive patients. Med
Instrum. 1986;20:255-259.
26. Gardner RM. Direct blood pressure measurement: dynamic response requirements. Anesthesiology. 1981;54:227-236.
27. Gibbs N, Gardner RM. Dynamics of
invasive pressure monitoring systems:
clinical and laboratory evaluation. Heart
Lung. 1988;17:43-51.
28. Gardner RM, Hollingsworth K.
Optimizing the electrocardiogram and
pressure monitoring. Crit Care Med.
1986;14:651-658.
29. Kee L, Simonson J, Stotts N, Skov P,
Schiller N. Echocardiographic determination of valid zero reference levels in
supine and lateral positions. Am J Crit
Care. 1993;2:72-78.
30. Winsor T, Burch GE. Phlebostatic axis
and phlebostatic level: reference levels
for venous pressure measurement in
man. Proc Soc Exp Biol Med.
1945;58:165-169.
31. Bartz B, Maroun C, Underhill S. Differences in mid-anterioposterior level
and midaxillary level in patients with a
range of chest configurations. Heart
Lung. 1988;17:308.
32. Bridges EJ, Bond EF, Ahrens T, Daly E,
Woods SL. Direct arterial vs oscillometric
monitoring of blood pressure: stop comparing and pick one. Crit Care Nurse.
December 1997;17:96-97, 101-102.
33. Ahrens T, Penick J, Tucker M. Frequency
requirements for zeroing transducers in
hemodynamic monitoring. Am J Crit
Care. 1995;4:466-471.
34. Gardner RM, Hujcs M. Fundamentals of
physiologic monitoring. AACN Clin
Issues. 1993;4:11-24.
35. Hoover L. Comparison of blood pressure
readings between cuff pressures and
radial arterial catheters with changes in
transducer level and patient position
[abstract]. Am J Crit Care. 2000;9:220-221.
36. Bridges EJ, Middleton R. Direct arterial
vs oscillometric monitoring of blood
pressure: stop comparing and pick one
(a decision-making algorithm). Crit Care
Nurse. June 1997;17:58-66, 68-72.
37. Campbell B. Arterial waveforms: monitoring changes in configuration. Heart
Lung. 1997;26:204-214.
38. Gardner PE, Bridges EJ. Hemodynamic
monitoring. In: Woods SL, SivarajanFroelicher ES, Halpenny C, Motzer S,
eds. Cardiac Nursing. 3rd ed.
Philadelphia, Pa: JB Lippincott;
1995:424-458.
39. O’Rourke MF, Yaginuma M. Wave reflections and the arterial pulse. Arch Intern
Med. 1984;144:366-371.
40. O’Rourke MF. Arterial mechanics and
wave reflection with antihypertensive
therapy. J Hypertens. 1992;10:43-49.
41. Imperial-Perez F, McRae M. Arterial
Pressure Monitoring. Aliso Viejo, Calif:
American Association of Critical-Care
Nurses; 1998.
42. Evaluation of the effects of heparinized
and nonheparinized flush solutions on
the patency of arterial pressure monitoring lines: the AACN Thunder Project. Am
J Crit Care. 1993;2:3-15.
43. Maloy L, Gardner RM. Monitoring systemic arterial blood pressure: strip chart
recording versus digital display. Heart
Lung. 1986;15:627-635.
44. Lundstedt JL. Comparison of methods of
measuring pulmonary artery pressure.
Am J Crit Care. 1997;6:324-332.
45. Ellis D. Interpretation of beat-to-beat
blood pressure values in the presence of
ventilatory changes. J Clin Monit.
1985;1:65-70.
46. Christensen B. Hemodynamic monitoring: what it tells you and what it doesn’t,
I. J Post Anesth Nurs. 1992;7:330-337.
47. Topol E, ed. Textbook of Cardiovascular
Medicine. Philadelphia, Pa: LippincottRaven Publishers; 1998.
48. Daily E, Speer-Schroeder J. Techniques
in Bedside Hemodynamic Monitoring. St
Louis, Mo: Mosby-Year Book Inc; 1994.
49. Nora A, Burns M, Downs W. Blood
Pressure. Richmond, Wash: Space Labs
Medical Inc; 1993.
CRITICAL CARE NURSE Vol 22, No. 2, APRIL 2002 79
Downloaded from ccn.aacnjournals.org by guest on July 3, 2011