Evidence-Based Practice Habits: Transforming Research Into Bedside

Practice
Carol A. Rauen, Mary Beth Flynn Makic and Elizabeth Bridges
Crit Care Nurse 2009;29:46-59 doi: 10.4037/ccn2009287
© 2009 American Association of Critical-Care Nurses
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 Clinical Article
Evidence-Based Practice
Habits: Transforming Research
Into Bedside Practice
Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN
Mary Beth Flynn Makic, RN, PhD, CNS, CCNS
Elizabeth Bridges, RN, PhD, CCNS
A
ctions speak louder
than words. If that
statement is true clin-
ically, it could be said
that nursing practice
is more connected to tradition than
it is evidence based. Many common
practices in critical care nursing
continue today despite clear and
reliable research that contradicts
them. The barriers to research
implementation that were identified
3 decades ago—lack of time, insuffi-
cient administrative support, and
limited access to information—are
still daunting clinicians today.1 The
PRIME POINTS importance of basing practice on
research is well understood. The
barrier is the actual transformation
• Positioning of patients
for monitoring hemody-
namic parameters.
CEContinuing Education
• Can low-dose dopamine This article has been designated for CE credit. A
prevent or be used to pre- closed-book, multiple-choice examination follows
this article, which tests your knowledge of the fol-
vent or treat renal dys- lowing objectives:
function? 1. Identify the reference lines for the
phlebostatic axis
2. Describe the best procedures for prevention
• How to prevent deep of venous thromboembolism
vein thrombosis. 3. Discuss the fluid replacement guidelines
established by the Surviving Sepsis Campaign
• Facts and physiology of ©2009 American Association of Critical-
fluid replacement. Care Nurses doi: 10.4037/ccn2009287
46 CRITICALCARENURSE Vol 29, No. 2, APRIL 2009
Downloaded from ccn.aacnjournals.org by guest on March 7, 2011
of research findings into practice.1
The accreditation bodies starting
to mandate and evaluate evidence-
based practices may help move the
implementation of research forward.2
We must create a culture of inquiry
in which nurses are not only aware
of the current evidence but also are
applying it to practice and asking
more questions about traditions
that should be supported or refuted
with research.2 Such a culture of
inquiry will help to improve patient
care and clinical outcomes.3
This article is a published report
of a 2008 session at the National
Teaching Institute and is the second
report from that annual session on
evidence-based practice. We focus
on 4 areas common to everyday
critical care practice. Elizabeth
Bridges addresses positioning of
patients for monitoring hemody-
namic parameters. Mary Beth Flynn
Makic discusses 2 topics: (1)
whether low-dose dopamine pre-
vents or can be used to prevent or
treat renal dysfunction and (2) pre-
vention of deep vein thrombosis.
Carol A. Rauen describes the facts
and physiology of fluid replace-
ment. The clinical questions and
www.ccnonline.org
 Table 1 Reference level appropriate for various positions of patients
Position Reference level
Supine Half of the anteroposterior diameter of the chest at the fourth intercostal space (not midaxillary)
Supine with head of bed elevated Half of the anteroposterior diameter of the chest at the fourth intercostal space (not midaxillary)
30º lateral4-6 Half of the vertical distance from the left sternal border to the surface of the bed
90º lateral 7
Left lateral decubitus: fourth intercostal space/left parasternal border
Right lateral decubitus: fourth intercostal space/midsternum

current body of evidence that can artery pressure (PAP) and central line from the fourth intercostal space
assist clinicians in moving research venous pressure (CVP) with the at the point where the space joins
to bedside practice are reviewed and patient in the flat and supine position the sternum, drawn out to the side
recommendations are outlined. compared with an alternative posi- of the body; second, a line drawn
tion greater than the spontaneous midway between the anterior and
Positioning Patients for variability in pressure? An exciting posterior surfaces of the chest.11 The
Hemodynamic Monitoring aspect of the evidence to answer phlebostatic level is a horizontal line
One challenge critical care nurses these questions is that most research through the phlebostatic axis. The
face is how to answer the question, on positioning of patients for moni- air-fluid interface of the stopcock of
does my patient need to lie flat for toring hemodynamic parameters has the transducer must be level with
hemodynamic monitoring? In order been conducted by nurse researchers. this axis for accurate measurements.
to address this challenge, a series of In patients with a normal chest wall
questions must be answered: (1) What Position-Specific Reference Level configuration, the midaxillary line is
is the correct reference level for a given Regardless of a patient’s body a valid reference level for the right
position? (2) Are studies in a given position, the key to accurate meas- and left atria; however, use of the
population of patients (eg, patients urements of hemodynamic parame- midaxillary line in patients with a
with heart failure, acute respiratory ters is the use of a position-specific different chest configuration may
distress syndrome [ARDS], sepsis, reference level to correct for hydro- result in a pressure difference of up
cardiac surgery) available that describe static pressure (Table 1, Figure 1). to 6 mm Hg.12 An alternative refer-
the differences in hemodynamic By convention, the phlebostatic axis ence point is 5 cm below the angle
parameters in the supine vs back- is the reference point for the right of the sternum. This reference point
rest elevated position or supine vs and left atria.4,5,7,10 The phlebostatic reflects the middle of the right atrium
lateral or prone position? (3) Are the axis is defined as the intersection of and remains the same up to 60º back-
observed differences in pulmonary 2 reference lines: first, an imaginary rest elevation.13 Use of this alternative
reference point, which is also recom-
mended for evaluation of jugular
Authors
venous distention, results in a CVP
Carol A. Rauen is an independent critical care clinical nurse specialist on the Outer Banks measurement that is 3 mm Hg lower
of North Carolina and is a staff nurse in the surgical intensive care unit at Washington than a CVP measured from a system
Hospital Center, Washington DC.
referenced to the phlebostatic axis.13,14
Mary Beth Flynn Makic is a researcher nurse scientist for critical care and an assistant
professor at the University of Colorado, Denver. In the lateral position, reference
Elizabeth Bridges is the clinical nurse researcher at the University of Washington Medical points have been validated for the
Center in Seattle and an assistant professor at the University of Washington School of 30º and 90º lateral positions with a
Nursing in Seattle. She is also a colonel in the US Air Force Reserve assigned to the 60th 0º backrest elevation5-7,15 (Table 1).
Medical Group at Travis Air Force Base, California.
In studies6,16-22 done to evaluate the
Corresponding author: Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN, 104 Queen Mary Court, Kill Devil Hills,
NC 27948 (e-mail: carol.rauen@charter.net).
effects of a prone position on hemo-
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.
dynamic parameters, the midaxil-
Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org. lary line or the midanteroposterior

www.ccnonline.org CRITICALCARENURSE Vol 29, No. 2, APRIL 2009 47

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 A B
Fourth
intercostal
space
45°

20°
Lateral margin
of sternum Outermost point
of sternum 0°
Outermost point
of posterior chest

C D
30° Left lateral position 30° Right lateral position Right lateral decubitus position Left lateral decubitus position

Left sternal Left sternal

border LA Sternum
border Sternum
4th ICS/midsternum LA
LA LA 4th ICS
L R Left parasternal border
L

Figure 1 Reference levels for various body positions. A, Supine/prone. The reference point is the phlebostatic axis, which is the
intersection of 2 reference lines: first, an imaginary line from the fourth intercostal space at the point where the space joins the
sternum, drawn out to the side of the body; second, a line drawn midway between the anterior and posterior surfaces of the
chest. B, Supine with the head of the bed elevated. The phlebostatic level is a horizontal line through the phlebostatic axis.
Measurements of pulmonary artery pressure and central venous pressure can be obtained at backrest elevations of up to 60°.
C, 30° lateral position. The reference point is one-half the distance from the left sternal border to the surface of the bed. (Based
on data from VanEtta et al.6) D, 90° lateral position. In the 90° right lateral position, the reference point is the intersection of the
fourth intercostal space at the midsternum. In the 90° left lateral position, the reference point is the intersection of the fourth
intercostal space at the left parasternal border.
Abbreviations: ICS, intercostal space; L, left; LA, left atrium; R, right.
A and B, Reprinted from Woods and Mansfield,8 with permission. ©Elsevier (1976).
C and D, Reprinted from Bridges and Woods,9 with permission.

diameter of the chest has been used
as the reference point, although the
accuracy of this reference has not
been validated. The reference point
should be marked on the patient’s
chest, and the air-fluid interface of
the system should be leveled by using
a laser or carpenter’s level and not
the “eyeball” method.23
Effect of Position on
Hemodynamic Parameters
Supine, Head of Bed Elevated.
Studies in a variety of patients in
medical-surgical and cardiac inten-
sive care units (ICUs) indicate that in
general PAP and CVP can be obtained
reliably with a patient supine with
the head of the bed elevated from 0º
to 60º if the patient’s legs are paral-
lel to the floor (ie, the patient is not
sitting up with the legs in a depend-
ent position).8,24-31 Thermodilution
cardiac output can be reliably meas-
ured with the head of the bed ele-
vated up to 20º.32,33 In one study,34
continuous cardiac output was
measured with the head of the bed
elevated up to 45º. A limitation of
this research is that it has involved
primarily patients whose hemody-
namic condition was stable; thus,
each patient’s response to a given
body position should be evaluated.
Supine, Trendelenburg/Reverse
Trendelenburg. Hemodynamic meas-
urements should not be obtained
with patients in the Trendelenburg
position. Although PAP and CVP
increase when patients are in the
Trendelenburg position, neither
intrathoracic blood volume (pre-
load) nor cardiac function increases.35
No research has been done on the
effect of the common practice of
elevating the head of the bed and
then placing the entire bed in the
Trendelenburg position to prevent
the patient from sliding down in the
bed. Also, no research has been done
to directly evaluate the effect of use
of the reverse Trendelenburg position
on PAP and CVP. However, compared
with the supine position, a 15º pas-
sive tilt decreases cardiac output by
10%, and a 45º tilt decreases cardiac
output by approximately 20%.36 This

48 CRITICALCARENURSE Vol 29, No. 2, APRIL 2009 www.ccnonline.org

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research36 suggests that patients’ legs
should be parallel to the ground
while hemodynamic measurements
are being obtained.
Lateral Position. Results of early
studies37-43 showed significant differ-
ences in PAP and CVP when meas-
ured with the patient in the lateral
position (20º-90º) rather than flat
and supine. However, in these stud-
ies, the phlebostatic axis or the mid-
sternum was generally used as the
reference point. These reference
points, which are not accurate dur-
ing lateral rotation, introduced
measurement error into the results.44
For example, in the 30º lateral posi-
tion, use of the midsternum rather
than the validated angle-specific
reference6 would introduce an error
of approximately 7 mm Hg. In con-
trast, in 2 studies,45,46 in which the
validated reference point was used,
investigators found no clinically sig-
nificant changes in CVP and PAP in
most trauma patients45 and patients
who had undergone cardiac surgery.46
In the cardiac surgery patients, the
supine and lateral measurements of
pulmonary artery occlusion pressure
differed by less than 2 mm Hg,44 a
finding that most likely reflects the
80- to 460-mL position-induced
increase in cardiac output.47 If the
effects of the incorrect reference
point were corrected, these original
studies would on average have results
similar to the results of studies that
used the angle-specific reference.46
In addition, in cardiac and medical-
surgical ICU patients, PAP and CVP
measured in patients in the 90º posi-
tion were similar to measurements
obtained with the patients supine,
as long as the correct angle-specific
reference was used.15,40 No studies in
which the correct angle-specific ref-
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erence was used have been completed
in patients with severe lung disease
or in a combined lateral position
with the head of the bed elevated.
Prone Position. Patients may be
placed prone as a part of therapy for
ARDS or during surgical procedures.
In patients with acute lung injury or
ARDS, if adequate time (30-60 min-
utes) is allowed for stabilization after
repositioning, no clinically signifi-
cant differences in PAP, CVP, or
cardiac output are apparent16-22
(Table 2). However, in patients with
normal pulmonary function, such
as those undergoing spinal surgery,
cardiac index may be slightly lower
when the patient is prone.48-50 Ques-
tions to ask include whether abdom-
inal compression in the prone
position increases intra-abdominal
pressure, and if so, does the increased
intra-abdominal pressure affect the
accuracy of the PAP and CVP meas-
urements. As demonstrated in Table
3, in patients with normal intra-
abdominal pressure, prone position-
ing does not significantly increase
intra-abdominal pressure or intratho-
racic blood volume and does not
falsely increase CVP.17,18 However, the
effect of the prone position on hemo-
dynamic parameters in patients with
intra-abdominal hypertension (intra-
abdominal pressure>12 mm Hg) is
not known, an important situation
because intra-abdominal hyperten-
sion occurs in up to 50% of ICU
patients.51 Additionally, no studies
have been done in patients in auto-
mated proning beds (eg, Rotoprone),
and studies are needed to describe
the effects that combined prone posi-
tioning with lateral rotation with the
bed flat and the prone/reverse Tren-
delenburg position have on hemo-
dynamic parameters.
CRITICALCARENURSE Vol 29, No. 2, APRIL 2009 49
Normal Variability in
Hemodynamic Measurements
The final step is to determine if
the observed change in pressure
between having a patient supine
and having the patient in an alterna-
tive position is within the normal
variability of the measurements.
The following changes are clinically
significant (ie, do not reflect normal
spontaneous variability)46,52-56:
• Change in pulmonary artery
systolic pressure greater than
4 to 7 mm Hg
• Change in pulmonary artery
end-diastolic pressure greater
than 4 to 7 mm Hg
• Change in pulmonary artery
occlusion pressure greater
than 4 mm Hg
• Change in cardiac output
greater than 10%
Finally, evidence on the effect
of position on hemodynamic param-
eters must be interpreted cautiously.
Although on average, hemodynamic
parameters do not differ signifi-
cantly with patients in the various
positions, individual patients may
respond to a given position in dif-
ferent ways. Thus, it is imperative
to systematically assess each patient’s
hemodynamic response in a given
position before assuming that the
measurement will not differ from
measurements obtained with the
patient supine and flat57,58 (Figure 2).
The evidence-based recommenda-
tions related to monitoring hemo-
dynamic parameters for various
body positions are summarized in
Table 4.
Renal Dose Dopamine:
Does It Exist or Not?
Use of low-dose dopamine, or
renal dose dopamine, has become a
 Table 2 Measurements of hemodynamic parameters: prone vs supine
Position, mean (SD)
Type of patients Reference level Parameters Supine Prone Stabilization, min
ARDS (n = 15)16 Mid-AP MAP, mm Hg 84 (19) 84 (16) 20
PAM, mm Hg 31 (8) 29 (8)
PAOP, mm Hg 14 (5) 13 (5)
CIa 5.1 (1.9) 4.9 (1.6)
ALI (n = 16)18 MAL MAP, mm Hg 77 (10) 82 (11)b 60
CVP, mm Hg 16 (5) 16 (6)
ITBVIc 987 (191) 1033 (189)
CIa 4.1 (1.1) 4.4 (0.7)
ALI (n = 12)17 MAL HR, beats per min 78 (16) 82 (16) 60
MAP, mm Hg 75 (10) 81 (11)b
CVP, mm Hg 16 (5) 15 (5)
CIa 3.8 (0.9) 4.2 (0.6)b
ITBVIc 1008 (187) 1036 (180)
DO2Id 558 (122) 620 (74)
ARDS (n = 23)19 Mid-AP CO, L/min No significant difference for any indices 60-90 (20 minutes
PAOP, mm Hg after stabilization
CVP, mm Hg of oxygen satura-
HR, beats per min tion obtained via
DO2, mL/min pulse oximetry)
ARDS (n = 11)21 No data CVP, mm Hg 15 14 90
PAOP, mm Hg 15 15
CIa 3.5 3.4
ARDS (n = 19)20 No data CVP, mm Hg 10 (2) 11 (3) 30
CIa 4.9 (1.1) 4.8 (1.3)
ARDS (n = 14)22 MAL MAP, mm Hg 87 (9) 89 (14) 45
CVP, mm Hg 12 (4) 13 (5)
PAM, mm Hg 34 (8) 37 (8)
PAOP, mm Hg 15 (5) 17 (6)
CIa 5.5 (1.5) 5.7 (1.7)
Routine cardiac imaging (n = 48)48 No data EDV, mL 117 (36) 111 (39)b No data
SV, mL 61 (15) 56 (13)b
Lumbar spine surgery (n = 15)49 No data CVP, mm Hg 9 (2) 11 (2) 15
SVIe 34 (9) 32 (11)
CIa 2.2 (0.5) 2.0 (0.6)
EDV, mL 128 (46) 100 (48)b
Lumbar spine surgery (n = 40)50 No data MAP, mm Hg 92 (17) 87 (16) No data
CIa 3.1 (0.7) 2.7 (0.6)

Abbreviations: ALI, acute lung injury; ARDS, acute respiratory distress syndrome; CI, cardiac index; CO, cardiac output; CVP, central venous pressure; DO2, oxygen
delivery; DO2I, oxygen delivery index; EDV, end-diastolic volume; HR, heart rate; ITBVI, intrathoracic blood volume index; MAL, midaxillary line; MAP, mean arterial
pressure; Mid-AP, midanteroposterior chest diameter; PAM, mean pulmonary artery pressure; PAOP, pulmonary artery occlusion pressure; SV, stroke volume; SVI,
stroke volume index.
a P < .05 (prone vs supine measurement).
b Cardiac index, calculated as cardiac output in liters per minute divided by body surface area in square meters.
c Intrathoracic blood volume index, calculated as intrathoracic blood volume in milliliters divided by body surface area in square meters.
d Oxygen delivery index, calculated as oxygen delivery in milliliters per minute divided by body surface area in square meters.
e Stroke volume index, calculated as stroke volume in milliliters divided by body surface area in square meters.

widely accepted clinical practice for
preventing or treating renal dys-
function.59 Does this agent truly
protect the kidneys from acute dys-
function? The evidence does not
support the use of low-dose dopamine
to prevent or treat renal dysfunction.
In fact, multiple studies59-63 have
shown no evidence that dopamine
prevents renal dysfunction or pro-
vides renal protection, and the agent
may even be harmful for patients.
Dopamine is a drug with diverse
effects at multiple receptor sites in
the body; this endogenous cate-
cholamine regulates cardiac, vascu-
lar, and endocrine function.
Dopamine is a complex agent; the

50 CRITICALCARENURSE Vol 29, No. 2, APRIL 2009 www.ccnonline.org

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Table 3 Effect of prone position on abdominal pressure
and hemodynamic parametersa
Parameter
Abdominal pressure, mm Hg
Mean arterial pressure, mm Hg
Cardiac index b 3.8 (0.9)
Heart rate, beats per min
Right atrial pressure, mm Hg
Intrathoracic blood volume, mL/m2 1008 (187)
a Based on data from Hering et al.
17,18
b Cardiac index, calculated as cardiac output in liters per minute divided by
body surface area in square meters.
response to it depends on which
receptors in the body are stimulated
(Table 5). Conventional dosing of
dopamine suggests that low dosages
(0.5-3.0 μg/kg per minute) stimulate
dopaminergic receptors and result
in coronary and renal vasodilata-
tion, natriuresis, and diuresis.
Midrange dosing (3-8 μg/kg per
minute) activates β-adrenergic
receptors, increasing cardiac inotropy
and chronotropy. Dosages greater
than 8 μg/kg per minute predomi-
nantly stimulate α-adrenergic
receptors, resulting in splanchnic
64-67
and peripheral vasoconstriction.
This conventional dosing is inaccu-
rate. Research suggests that dopamine
infusions at similar infusion rates
produce different responses from
patient to patient.66 One explanation
of the variation in responses is that
the activation of the receptor sites
depends more on the patient than
on the dose; thus the concept of
dose range affecting specific recep-
tors is not universal for all patients.66,67
As a result, traditional dopamine
dosing should not be used as a stan-
dard regimen. The desired effects
of dopamine infusion depend on
the specific patient’s response to
the agent.59,64,66,67
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What is the
evidence for the
Position, mean (SD) effectiveness of
Supine Prone renal dose
10 (3) 13 (4) dopamine in
75 (10) 81 (11) preventing acute
4.2 (0.6) renal failure?
78 (16) 82 (16) Concern about
16 (5) 15 (5)
the use of renal
dose dopamine
1036 (180)
to prevent and
treat renal dys-
function began
to appear in the
literature in the
early 1990s. Denton et al65 wrote a
68
classic article discussing the science
related to renal dose dopamine.
They reviewed the literature and
discussed the findings from several
research studies in which low-dose
dopamine augments renal blood
flow, glomerular filtration rate, and
urine output in healthy humans.
Denton et al,65 however, did not find
similar outcomes when critically ill
patients were studied. They
reported that most studies in
humans on the effects of renal dose
dopamine and critical illness did
not indicate an improvement in
renal function and prevention of
acute renal failure. Denton et al
discouraged the use of renal dose
dopamine in critically ill patients to
prevent or treat renal dysfunction.
In a report published in 1999,
Marik and Iglesias63 concluded that
giving low-dose dopamine to patients
with septic shock and oliguria did
not lead to any significant differ-
ences in the incidence of acute renal
failure, need for dialysis, or 28-day
survival. Then Kellum and Decker59
did a meta-analysis of the use of
dopamine in acute renal failure.
They concluded that the use of low-
CRITICALCARENURSE Vol 29, No. 2, APRIL 2009 51
dose dopamine to treat or prevent
acute renal failure cannot be justi-
fied on the basis of available evidence
and should be eliminated from criti-
cal care protocols.59
Despite this evidence, the ongo-
ing clinical use of low-dose dopamine
continued. Friedrich et al62 published
a meta-analysis and evidence-based
review on low-dose dopamine, con-
cluding that after 15 years of research
on the effectiveness of renal dose
dopamine, the evidence indicates
that low-dose dopamine temporar-
ily improves renal output but does
not prevent renal dysfunction or
death. Thus, the evidence is conclu-
sive: use of low-dose dopamine
does not prevent or improve renal
dysfunction long-term in critically
ill patients.59,60,62,64-66 These findings
should not be confused with
results of studies that examined
the effectiveness of higher doses of
dopamine in critically ill patients
with heart failure and septic shock.
In such patients, dopamine is bene-
ficial for its inotropic and vasoac-
tive properties.60,65
So why does urine output increase
when a dopamine infusion is started?
Dopamine has both natriuretic and
diuretic properties that stimulate
urine output, and the response
appears to be more pronounced at
lower dosages.64,66,67 This response,
however, is often temporary, and
urine output tapers off within the
first 24 hours.62 Dopamine at doses
as low as 2 μg/kg per minute improves
cardiac output and mean arterial
pressure, enhancing renal perfusion
and urine output.66-68
Concerns about the use of low-
dose dopamine extend beyond the
evidence that the drug is not effec-
tive in preventing renal dysfunction.
 Position patient supine/flat if tolerated
Reference system: 1⁄2 AP diameter at 4th ICS
Allow 5 minutes after position change (ensure stability: <10% BP compared to baseline)
Measure end-expiratory hemodynamic parameters (use hard copy with corresponding ECG)

Reposition and re-reference the system

Supine (HOB 0° to 45°)
Level and reference to phlebostatic axis
Lateral (30° or 90°)
30°-Lateral reference: 1⁄2 distance from surface of the bed to the left sternal border
90°-Right lateral reference: 4th ICS at midsternum
90°-Left lateral reference: 4th ICS left parasternal border
Prone
Reference: phlebostatic axis

Allow for stabilization

Supine with HOB elevated or lateral position
Normal LV function: 5 minutes/LV dysfunction 15 minutes
Prone
20-30 minutes or until HR ± 10% baseline or SvO2 ± 5%

Perform end-expiratory pressure/CO measurements

Use hard-copy strip and corresponding ECG

Compare hemodynamic parameters in supine, flat position with pressures from alternative position
PAS: Normal LV function: ± 5 mm Hg/Decreased LV function ± 7 mm Hg
PAEDP: Normal LV function: ±5 mm Hg/Decreased LV function ±6 mm Hg
PAOP: Normal LV function: ±4 mm Hg/Decreased LV function ±5 mm Hg
CO <10%

Are the values within normal spontaneous variability?

Yes No
Perform pressure/CO measurements with patient Perform pressure/CO measurements
in the alternative position with patient in the supine/flat position

Figure 2 Algorithm for research-based practice for measurement of central venous pressure, pulmonary artery pressures, and
cardiac output with the head of the bed elevated and the patient in lateral or prone position.
Abbreviations: AP, anteroposterior; BP, blood pressure; CO, cardiac output; ECG, electrocardiogram; HOB, head of bed; HR, heart rate; ICS, intercostal space; LV, left
ventricular; PAEDP, pulmonary artery end-diastolic pressure; PAOP, pulmonary artery occlusion pressure; PAS, pulmonary artery systolic pressure; SvO2, venous
oxygen saturation.
Adapted with permission from Gawlinski.57

Current evidence suggests low-dose
dopamine may cause harm by wors-
ening splanchnic oxygen consump-
tion, impairing gastric motility,
inducing tachyarrhythmias (espe-
cially in elderly patients), and blunt-
ing ventilatory response to
hypercarbia.61,69,70 Administration of does not protect the kidneys from
dopamine should be continually renal dysfunction.59,61,63
evaluated to match the dose to the
desired outcome without causing Prevention of Deep Vein
adverse consequences for the patient. Thrombosis: What Is Best?
Does renal dose dopamine Venous thromboembolism is the
exist? No, it does not. Dopamine combined term that describes both

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 Table 4 Summary of recommendations for hemodynamic pressure measurements with patients in different body positions

Position-specific reference levels

Supine Phlebostatic axis (half of the anteroposterior diameter of the chest at the fourth intercostal space)
Supine with head of bed elevated Phlebostatic axis/level (half of the anteroposterior diameter of the chest at the fourth intercostal space)
30° lateral Half the vertical distance from the left sternal border to the surface of the bed
90° lateral Left lateral decubitus: fourth intercostal space/left parasternal border
Right lateral decubitus: fourth intercostal space/midsternum
Prone/flat Phlebostatic axis or midaxillary line (limited research to validate this reference level)
Effect of patient’s position on hemodynamic parameters (compared with supine/flat position)
Supine/head of bed elevated Pulmonary artery pressure and central venous pressure: head of bed elevated up to 60°; patient’s
legs must be parallel to the floor8,24-31
Thermodilution cardiac output: head of bed up to 20°32,33
Continuous cardiac output: head of bed elevated up to 45°34
Supine with Trendelenburg; Not recommended: patient’s legs must be parallel to floor
reverse Trendelenburg
30° lateral Pulmonary artery pressure and central venous pressure: pressures can be measured reliably as long
as the correct angle-specific reference point/level is used
No studies have validated this position with the head of the bed elevated
90° lateral Pulmonary artery pressure and central venous pressure: can be measured reliably as long as the
correct angle-specific reference point/level is used
Prone (flat) Pulmonary artery pressure, central venous pressure, and cardiac output: can be measured reliably;
allow 20-60 minutes for patient to stabilize after position change
Normal variability in hemodynamic parameters (use this information to evaluate if change in value is greater than expected
variability for that parameter)
Change in pulmonary artery >4-7 mm Hg (increased variability with decreased ejection fraction)
systolic pressure
Change in pulmonary artery >4-7 mm Hg (increased variability with decreased ejection fraction)
end-diastolic pressure
Change in pulmonary artery >4 mm Hg
occlusion pressure
Change in cardiac output >10%

deep vein thrombosis (DVT) and venous valves,

Table 5 Characteristics of dopamine
pulmonary embolism. Recent esti- pain, paresthesia,
Receptor sites stimulated
mates suggest that venous thrombo- hyperpigmenta- Dopaminergic
embolism is diagnosed in more tion, pruritus, β-Adrenergic
α-Adrenergic
than 900 000 patients in the United venous dilata-
Physiological actions
States annually, with approximately tion, edema, and Improves cardiac output and mean arterial pressure
73,74
400 000 cases manifested as DVT ulceration. Stimulates natriuresis and diuresis (limited response)
and 500 000 cases as pulmonary Research find- Has no effect on renal function/glomerular function
embolism. In 60% of the patients 71,75
ings indicate Adverse actions
Worsens splanchnic oxygen consumption
with pulmonary embolism, the that clinical Impairs gastric motility
embolism is fatal.71,72 Patients in interventions, Induces tachyarrhythmias, especially in elderly patients
whom venous thromboembolism including Blunts ventilatory response to hypercarbia

develops are also at risk for post- mechanical and

thrombotic syndrome, in which tis- pharmacological therapies, are imately one-third of all patients at
sue injury follows DVT and lasts effective in preventing venous throm- risk for venous thromboembolism
indefinitely, causing damage of boembolism; however, only approx- receive prophylactic therapy. The

www.ccnonline.org CRITICALCARENURSE Vol 29, No. 2, APRIL 2009 53

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 Table 6 Risk assessment and interventions for venous thromboembolism
General risk factors for all patients
Immobility
Surgery
Cancer
Pregnancy
Hormone therapy
Obesity
Trauma
Acute infection
History of venous thromboembolism
Age >40 years
most common reasons cited for
lack of proper prophylaxis of venous
thromboembolism include lack of
knowledge among providers, under-
estimation of patients’ risk for venous
thromboembolism, and overestima-
tion of the potential risk of bleeding
associated with prophylaxis.74-77
Prevention of venous thromboem-
bolism is considered a clear oppor-
tunity for improving safe care of
patients.77 Several national organi-
zations and accrediting bodies list
the prevention of venous thromboem-
bolism as a patient safety indicator
and measure of quality of care or
“never events.”71,78 In 2003, The
American Public Health Associa-
tion published guidelines to advance
public awareness of DVT.76 Geerts
et al75 published evidence-based
guidelines for the prevention of
venous thromboembolism, and
that seminal article was followed in
2008 with practice guidelines for
antithrombotic therapy for venous
thromboembolism.79 Evidence is
available to guide practice for provid-
ing interventions to prevent venous
thromboembolism. The challenge is
to use this evidence in the daily
practice of critical care nursing.
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Risk assessment
Low risk
Age < 40 years
Minor surgery
Moderate risk
Age > 40 years
Minor surgery with additional risk factor
Age 40-60 years with no additional risk factor
High risk
Surgery in patients > 60 years old
Highest risk
Age > 40 years with multiple risk factors
Hip or knee surgery or interventions
Major trauma, spinal cord injury
Prevention of venous throm-
boembolism begins with assessment
of a patient’s risk factors. A venous
thromboembolism is an intravascu-
lar fibrin clot that usually forms in
regions of slow or disturbed blood
flow. Typically the clot forms in a
large vein in the lower extremities,
but it may form in any large vein and
poses a great risk when it occludes a
pulmonary vessel, potentially result-
ing in a fatal pulmonary embolism.
Classic risk factors for ICU patients
are well known by nurses. The vari-
ables are referred to as the Virchow
triad: venous stasis or obstruction,
blood vessel injury, and increased
coagulability. Frequent procedures
disrupt a patient’s vessels, and the
fluid shifts, immobility, and coagu-
lation disorders associated with crit-
ical illness place ICU patients at high
risk for venous thromboembolism.
DVT develops in up to 30% of ICU
patients within the first week of
admission, a characteristic that
further emphasizes the importance
of early interventions.80 To decrease
the prevalence of venous thromboem-
bolism, critical care nurses must
evaluate each patient’s risk and
implement preventative interventions
Interventions
Low risk
Early ambulation
Elastic stockings
Moderate to high risk
Unfractionated or low-molecular-
weight heparin
Mechanical devices
Highest risk
Low-molecular-weight heparin,
fondaparinux, or warfarin
Mechanical devices
when the patient is admitted to
the unit.
Additional risk factors beyond
venous stasis, immobility, and vas-
cular injury should be included in
the assessment of each patient’s risk
for venous thromboembolism. Risk
factors can be grouped in many ways
to include patient-specific variables,
type of procedure a patient is under-
going (eg, orthopedic surgery), and
reason for admission (eg, traumatic
event; Table 6). Top risk factors
include prolonged immobility,
including use of neuromuscular
blockade and/or heavy sedation; an
indwelling central venous catheter;
major surgery; cancer; active infec-
tion; pregnancy; hormone therapy;
obesity; respiratory failure; heart
failure; cerebral vascular accident;
trauma (especially fractures of the
pelvis, hip, or leg); history of previ-
ous venous thromboembolism; and
older age (ie, risk increases in patients
40 years or older).75,81 The more risk
factors a patient has, the more aggres-
sive the interventions should be.
Preventive actions are categorized
as mechanical or pharmacological
interventions and are implemented
on the basis of the assessment of
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the patient’s risk for venous throm-
boembolism (Table 6). Mechanical
prevention encompasses early
ambulation, graduated compression
stockings (also known as elastic
compression stockings), and inter-
mittent pneumatic compression
devices. However, compliance of
patients and health care practition-
ers limits the effectiveness of mechan-
ical prevention. For mechanical
prevention to be effective, the
device(s) must be appropriately fit-
ted to each patient and consistently
applied to the lower extremities.
Often, patients are not appropriately
measured for correct fit of a mechan-
ical device. In addition, ongoing
assessment of the fit of the device
as body fluids shift may not be
addressed, and the device is not
consistently placed on the patient’s
extremities, limiting the effective-
ness of mechanical therapy.81-85
Efforts to correctly measure patients’
extremities are required to ensure
that the correct size of compression
device is used. Also, as body fluids
shift, the fit of the device should be
reevaluated. Evidence suggests that
thigh-high graduated compression
stockings are most effective in pro-
viding mechanical prevention; how-
ever, knee-high stockings are also
effective and often have fewer com-
plications associated with constric-
tion, wrinkles, and compliance with
continuous wearing.81,86 Intermittent
pneumatic compression devices also
provide good mechanical prevention
if they are continuously used. The
evidence suggests that mechanical
devices are effective in preventing
venous thromboembolism, provided
the devices fit the patient and are
used consistently. Often, patients or
nurses remove the devices and do
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not reapply them. Nurses should
be empowered to correctly assess,
measure, and consistently apply
mechanical interventions to pre-
vent the development of venous
thromboembolism.
Pharmacological prevention
consists of unfractionated heparin,
low-molecular-weight heparin, fon-
daparinux, and vitamin K antago-
nists (eg, warfarin). Many variables
must be assessed before pharmaco-
logical interventions are started,
including the risk for venous throm-
boembolism, presence of bleeding,
and desired duration of therapy.
As a patient’s risk increases, more
aggressive pharmacological therapy
combined with mechanical inter-
ventions is required. Low-molecular-
weight heparin is often prescribed
because the evidence suggests that
this agent is as effective as unfrac-
tionated heparin in preventing DVT,
has fewer adverse effects (eg, bleed-
ing, heparin-induced thrombocy-
topenia) and better bioavailability,
and is safe in the outpatient setting,
allowing for long-term therapy as
needed.79,87 High-risk patients may
require more aggressive treatment
with low-molecular-weight heparin,
fondaparinux, or warfarin. The evi-
dence on aspirin is well established:
aspirin alone is not effective in pre-
venting DVT.75 The 2008 guidelines
of the American College of Chest
Physicians79 provide a full review of
the evidence supporting antithrom-
botic therapy.
What are the best procedures
for preventing DVT? First and fore-
most, preventive interventions must
be implemented consistently for all
critically ill patients to effectively
decrease the incidence of venous
thromboembolism. Second, patients
CRITICALCARENURSE Vol 29, No. 2, APRIL 2009 55
should be assessed for severity of
risk on the basis of age, medical and
surgical history, and projected course
of the critical illness. Third, each
patient’s plan of care should be
reviewed and pharmacological
therapy that may help reduce the
risk for venous thromboembolism
should be discussed. Fourth, mechan-
ical devices must be correctly fitted
and consistently applied for effec-
tive preventative therapy. Finally,
when possible, patients should
ambulate (Table 7). Although all
venous thromboembolism may not
be preventable in critically ill patients,
the evidence indicates that its occur-
rence can be reduced, and nurses
owe it to patients to base practice on
the best evidence to minimize the
risk for venous thromboembolism.
Fluid Replacement:
Facts and Physiology
Fluid replacement has long been
a cornerstone of critical care practice.
Historically, the question was not
whether a patient needed fluids but
what type of fluid would be best. Now
the physiological value of adminis-
tering fluids is being questioned.
The goal in fluid replacement is clear:
maintain adequate intravascular
volume to ensure cellular oxygen
delivery and cardiac output. The
means to achieve that goal, however,
is much more complex.
Both crystalloids and colloids
have significant advantages and dis-
advantages. Crystalloids, which
include normal saline and lactated
Ringer solutions, are isotonic, inex-
pensive, readily available, good vol-
ume expanders that are easy to store
and administer. These fluids do not
transmit diseases or cause allergic
reactions, and both can replace some
 Dubois et al90
Table 7 Tips for preventing venous thromboembolism
studied a mixed
Consistently implement preventative interventions for all patients population of
Assess patient-specific risk factors for venous thromboembolism medical-surgical
Review plan of care and consider pharmacological therapy ICU patients
Correctly apply and consistently use mechanical devices
and found that
(compression stockings, pneumatic devices) albumin might
Encourage ambulation even have an
advantage over
normal saline:
electrolytes. However, normal saline organ function was improved and
and lactated Ringer solutions do tube feedings were more readily tol-
not have oxygen-carrying capacity, erated in the patients who received
and approximately 75% of the fluid albumin rather than saline.
administered leaks into the intersti- Human blood products remain
tial space within hours of adminis- the best fluid for patients who have
tration. Large volumes of these fluids lost blood or have symptomatic
can lead to pulmonary edema and, anemia, but large volumes of blood
because the blood components are are not without risk. The potential
diluted, can actually lead to more complications of using blood prod-
bleeding.88 The natural and synthetic ucts include coagulation disorders,
blood products (colloids) are much metabolic derangements, infection,
better volume expanders than crys- sepsis, anaphylaxis, and disease
talloids are and, because of their transmission.91-94 Since the late
molecular size, tend to stay in the 1990s, administration of blood has
intravascular space longer. Colloids also been implicated in transfusion-
not only stay in that space, but related acute lung injury, transfusion-
because of their protein components, associated circulatory overload, and
they actually can set up an osmotic transfusion-related immune modu-
gradient that will “pull” plasma from lation.91-94 The question of what fluid
the interstitium into the intravascu- is best has no risk-free answer.95
lar space. These fluids are more Human blood products are also
expensive, are more difficult to store the fluid of choice for patients with
and administer, often require cross- symptomatic bleeding whose blood
matching, might transmit diseases or pressure cannot be increased with
microorganisms, and might lead to crystalloid administration and whose
an allergic or inflammatory response. bleeding has not been controlled.91
Albumin may have many of the The gold standard for treating such
advantages of natural colloids with- patients has been fluids and lots of
out the disadvantages of crystalloids. them. However, administering crys-
Finfer et al89 found no significant talloids to such patients can actually
differences between patients given cause more bleeding. The increase in
saline and patients given albumin in intravascular volume should increase
the number of days in the ICU or blood pressure. If the bleeding source
hospital or in the number of days is arterial, the increase in blood
that mechanical ventilation or renal- pressure could actually disrupt
replacement therapy was required. clotting and lead to more bleeding.
56 CRITICALCARENURSE Vol 29, No. 2, APRIL 2009
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Crystalloids dilute clotting factors
and platelet volumes. The current
recommendation for suspected
arterial bleeding is to delay fluid
replacement until surgery to control
the bleeding is under way.95 It is
widely believed that warm fluid is
better than cold. Being cold lowers
the core temperature and makes
coagulopathies worse. The question
remains: what should the end-point
parameters be for fluid replacement?
The issue of how much fluid to
administer or when to stop is a diffi-
cult one. Vincent and Weil96 question
the traditional clinical parameters
that have been used for decades. His-
torically, fluids were cut back when
CVP increased. If the goal is intravas-
cular fluid replacement, it must be
remembered that CVP reflects only
the pressure in the central veins. It
does not represent total vascular
volume. The same could be said for
pulmonary edema. Fluid could be
leaking into the lung interstitial
spaces because of the high hydrostatic
pressure in the pulmonary capillary
bed or because of the low oncotic
pressure and left ventricular failure.
Tachycardia is often used as an indica-
tor of anemia or dehydration, but
Vincent and Weil point out that it is
not a particularly sensitive measure.
Tachycardia is a warning sign for
many problems in critical care.
In a study of early goal-directed
therapy, Rivers et al97 attempted to
answer the question of replacement
end points. Emergency department
patients in septic shock had better
outcomes when they had early goal-
directed replacement with the fol-
lowing end points:
CVP: 8 to 12 cm H2O
Mean arterial pressure: greater
than 65 mm Hg
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 Urine output: greater than
0.5 mL/kg per hour
Central venous oxygen satura-
tion: 70%
These parameters were part of
the Surviving Sepsis Campaign
guidelines in 2004 and were recom-
mended a second time in the 2008
guidelines.98,99 The other recommen-
dations in the 2008 guidelines include
fluid replacement with 300 to 500
mL of colloids or 1 L of crystalloids
in 30 minutes and reducing the fluid
challenge rate if filling pressures
increase without improvement in
hemodynamic status.99
How much blood is the right
amount of blood has also been
researched. The first hemoglobin
trigger that was recommended
dates back to Adam and Lundy100
in 1942. The “10/30” rule was used
in clinical practice for more than 4
decades. If a patient’s hemoglobin
level decreased to less than 10 g/dL
or the hematocrit decreased to less
than 0.30, the patient was given
blood. The discovery that human
immunodeficiency virus was trans-
mitted via blood and the expanding
knowledge of the risks of blood
administration have led clinicians to
reevaluate the risks and benefits of
administering blood and to search
for a better trigger threshold. The
report of the current landmark
study,92 published in 1999, included
recommendations that hemoglobin
•
d tmore
To learn more about fluid replacement, read
“Weaning Readiness and Fluid Balance in
Older Critically Ill Surgical Patients” by
Carol Diane Epstein and Joel R. Peerless in
the American Journal of Critical Care,
2006;15(1):54-64. Available at
www.ajcconline.org.
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Downloaded from ccn.aacnjournals.org by guest on March 7, 2011
level be maintained between 7 and 9
g/dL. The 2004 and 2008 Surviving
Sepsis Campaign guidelines
included this recommendation.98,99
The standard exceptions to the trig-
ger value of 7 to 9 g/dL are patients
with ischemic heart disease and
patients who have had an acute
myocardial infarction. Corwin et al91
reported that, despite the commonly
known risks of blood administration
and the new recommendations, clin-
ical practice in the United States did
not change much between 1999 and
2003. In a 2008 analysis of data on
blood transfusions included in the
Sepsis Occurrence in Acutely Ill
Patients data base, Vincent et al94
found that administration of blood
was associated with improved mor-
tality. More randomized controlled
studies are needed in critically ill
patients to answer these age-old
questions of which solution, how
much, and when best to deliver flu-
ids to critically ill patients.
In the absence of specific
evidence-based practice guidelines
for fluid replacement in critically ill
patients, “For the present, the
choice is best made contingent on
the underlying disease, the type of
fluid that has been lost, the severity
of circulatory failure, the serum
albumin concentration of the patient
and the risk of bleeding.”96(p1336) The
short answer to the simple question
of fluid replacement is that no per-
fect solution exists. Patients should
be given what they lost or what they
need that will cause the least harm.
Nurses must continue to conduct
research to find a better answer.95
Summary
This article is the second article
published in Critical Care Nurse that
CRITICALCARENURSE Vol 29, No. 2, APRIL 2009 57
outlines evidence-based practices
that should be applied at the bed-
side. The challenge before us is 3-
fold: we must continue to ask the
hard clinical questions, conduct the
research to answer these questions,
and implement the discoveries that
are made. This final challenge is prob-
ably the most difficult. We fear that
in today’s environment of cost cut-
ting and staffing shortages, uncriti-
cal adherence to tradition will
become the norm again. We must
create a culture of inquiry and prac-
tice changes based on research and
implement new standards that are
based on the latest available evi-
dence. CCN
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Acknowledgments
The authors served as an expert panel on evidence-
based practice at the 2008 National Teaching
Institute in Chicago, Illinois. We thank the Amer-
ican Association of Critical-Care Nurses, Linda Bell,
Nancy Munro, and the entire Advance Practice
Work Group for their insight in pulling the panel
together to present this information at the 2008
National Teaching Institute.
Financial Disclosures
None reported.
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70. Lauschke A, Teichgraber UK, Frei U,
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CRITICALCARENURSE Vol 29, No. 2, APRIL 2009 59
CCN Fast Facts CRITICALCARENURSE
The journal for high acuity, progressive, and critical care

Evidence-Based Practice Habits:

Transforming Research Into Bedside Practice
Facts
According to estimates, 30% to 40% of patients do
not receive care consistent with current scientific evidence.
Advanced practice and bedside nurses must evaluate
their own practice and the needs of their patients and
ask, Are we doing what is best for our patients with the
current evidence available to us?
Renal Dose Dopamine: Does It Exist or Not?
• Low-dose dopamine does not prevent or improve renal
dysfunction long term in critically ill patients.
• Low-dose dopamine may worsen splanchnic oxygen con-
sumption, impair gastric motility, induce tachyarrhythmias
(especially in elderly patients), and blunt the ventilatory
response to hypercarbia.

Positioning Patients for Hemodynamic Prevention of Deep Vein Thrombosis:

Monitoring
• Although, on average, hemodynamic values do not change
markedly when patients are in various body positions,
different patients may respond to a given position in
different ways.
• The key is to systematically assess each patient’s hemo-
dynamic response in a given position before assuming
that the measurements will not differ from measurements
obtained with the patient supine and flat.
What Is Best?
• Patients should be assessed for risk of venous thromboem-
bolism on the basis of age, medical and surgical history, and
projected course of the critical illness (see Table).
• Both mechanical and pharmacological interventions to
prevent venous thromboembolism must be implemented
consistently.
Fluid Replacement: Facts and Physiology
• More research is needed to determine which solution,
how much, and when best to deliver fluids to critically ill
patients.

Table Risk assessment and interventions for venous thromboembolism

General risk factors for all patients Risk assessment Interventions
Immobility Low risk Low risk
Age < 40 years Early ambulation
Surgery
Minor surgery Elastic stockings
Cancer
Moderate risk Moderate to high risk
Pregnancy Age > 40 years Unfractionated or low-molecular-
Minor surgery with additional risk factor weight heparin
Hormone therapy
Age 40-60 years with no additional risk factor Mechanical devices
Obesity
High risk
Trauma Surgery in patients > 60 years old
Acute infection Highest risk Highest risk
Age > 40 years with multiple risk factors Low-molecular-weight heparin,
History of venous thromboembolism
Hip or knee surgery or interventions fondaparinux, or warfarin
Age >40 years Major trauma, spinal cord injury Mechanical devices

Rauen CA, Makic MB, Bridges E. Evidence-based practice habits:

transforming research into bedside practice. Crit Care Nurse.
2009;29(2):46-61.
This article and an online version of the CE test may be found online at
www.ccnonline.org

60 CRITICALCARENURSE Vol 29, No. 2, APRIL 2009 www.ccnonline.org

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 CE Test Test ID C092: Evidence-Based Practice Habits: Transforming Research Into Bedside Practice
Learning objectives: 1. Identify the reference lines for the phlebostatic axis 2. Describe the best procedures for prevention of venous thromboembolism
3. Discuss the fluid replacement guidelines established by the Surviving Sepsis Campaign

1. Which of the following reference levels is used for measuring hemody- 7. Which of the following percentage of patients at risk for venous throm-
namic parameters in supine patients with the head of the bed (HOB) boembolism receives prophylactic therapy?
elevated? a. 25% c. 50%
a. Half of the anterior-posterior diameter of the chest at the second b. 33% d. 66%
intercostal space
b. Half of the anterior-posterior diameter of the chest at the third 8. Which of the following patients are at the highest risk for venous throm-
intercostal space boembolism?
c. Half of the anterior-posterior diameter of the chest at the fourth a. Patients younger than 40 years old who have had minor surgery
intercostal space b. Patients older than 40 years old who have with minor surgery and an
d. Half of the anterior-posterior diameter of the chest at the fifth additional risk factor
intercostal space c. Patients older than 60 years old with surgery
d. Age greater than 40 years with multiple risk factors
2. Which of the following HOB elevations provides reliable measurements
of pulmonary artery pressure and central venous pressure in supine 9. Evidence suggests that the most effective method for providing mechanical
patients? prevention of venous thromboembolism is which of the following?
a. 0° to 30° c. 0° to 60° a. Thigh-high compression stockings
b. 0° to 45° d. 0° to 90° b. Knee-high compression stockings
c. Intermittent pneumatic compression devices
3. Which of the following HOB elevations provides reliable measurements d. Compression stockings and compression devices
of thermodilution cardiac output?
a. 20° c. 45 10. Which of the following endpoints is used for fluid replacement in the
b. 30° d. 60° Surviving Sepsis Campaign guidelines?
a. Central venous pressure of 12 to 15 cm H2O
4. The reverse Trendelenburg position has which of the following effects b. Urine output greater than 1 mL/kg per hour
on hemodynamic parameters? c. Central venous oxygen saturation of 60%
a. Decreased pulmonary artery pressure d. Mean arterial pressure greater than 65 mm Hg
b. Decreased mean arterial pressure
c. Decreased central venous pressure 11. Which of the following is recommended as fluid replacement in the
d. Decreased cardiac output Surviving Sepsis Campaign guidelines?
a. 250 mL of colloids over 30 minutes
5. Which of the following dosages of dopamine activates beta-adrenergic b. 500 mL of colloids over 60 minutes
receptors, increasing cardiac inotropy and chronotropy? c. 1000 mL of crystalloids over 30 minutes
a. 1 to 3 μg/kg per minute d. 2000 mL of crystalloids over 60 minutes
b. 3 to 8 μg/kg per minute
12. Which of the following hemoglobin levels is recommended as a trigger
c. 8 to 12 μg/kg per minute
value for blood replacement in the Surviving Sepsis Campaign guidelines?
d. 12 to 16 μg/kg per minute
a. 6 to 7 g/dL
b. 7 to 9 g/dL
6. Current evidence suggests that low-dose dopamine can be harmful
c. 9 to 10 g/dL
due to which of the following?
d. 9 to 10 g/dL
a. Worsening splanchnic oxygen consumption
b. Excessive natriuresis and diuresis
c. Increased gastric emptying
d. Blunting ventilatory response to hypocarbia
Test answers: Mark only one box for your answer to each question. You may photocopy this form.
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Kb Kb Kb Kb Kb Kb Kb Kb Kb Kb Kb Kb
Kc Kc Kc Kc Kc Kc Kc Kc Kc Kc Kc Kc
Kd Kd Kd Kd Kd Kd Kd Kd Kd Kd Kd Kd
Test ID: C092 Form expires: April 1, 2011 Contact hours: 1.25 Fee: AACN members, $0; nonmembers, $10.50 Passing score: 9 correct (75%) Category: CERP A Synergy CERP A
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