Crit Care Nurse-2009-Rauen-46-59

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doi: 10.4037/ccn2009287 2009;29:46-59Crit Care Nurse Carol A. Rauen, Mary Beth Flynn Makic and Elizabeth BridgesPracticeEvidence-Based Practice Habits: Transforming Research Into Bedside

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Actions speak louderthan words. If thatstatement is true clin-ically, it could be saidthat nursing practice

is more connected to tradition thanit is evidence based. Many commonpractices in critical care nursingcontinue today despite clear andreliable research that contradictsthem. The barriers to researchimplementation that were identified3 decades ago—lack of time, insuffi-cient administrative support, andlimited access to information—arestill daunting clinicians today.1 Theimportance of basing practice onresearch is well understood. Thebarrier is the actual transformation

Evidence-Based PracticeHabits: Transforming ResearchInto Bedside Practice

This article has been designated for CE credit. Aclosed-book, multiple-choice examination followsthis article, which tests your knowledge of the fol-lowing 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 guidelinesestablished by the Surviving Sepsis Campaign

CEContinuing Education

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

of research findings into practice.1

The accreditation bodies startingto mandate and evaluate evidence-based practices may help move theimplementation of research forward.2

We must create a culture of inquiryin which nurses are not only awareof the current evidence but also areapplying it to practice and askingmore questions about traditionsthat should be supported or refutedwith research.2 Such a culture ofinquiry will help to improve patientcare and clinical outcomes.3

This article is a published reportof a 2008 session at the NationalTeaching Institute and is the secondreport from that annual session onevidence-based practice. We focuson 4 areas common to everydaycritical care practice. ElizabethBridges addresses positioning ofpatients for monitoring hemody-namic parameters. Mary Beth FlynnMakic discusses 2 topics: (1)whether low-dose dopamine pre-vents or can be used to prevent ortreat renal dysfunction and (2) pre-vention of deep vein thrombosis.Carol A. Rauen describes the factsand physiology of fluid replace-ment. The clinical questions and

Carol A. Rauen, RN, MS, CCNS, CCRN, PCCNMary Beth Flynn Makic, RN, PhD, CNS, CCNSElizabeth Bridges, RN, PhD, CCNS

Clinical Article

PRIME POINTS

• Positioning of patientsfor monitoring hemody-namic parameters.

• Can low-dose dopamineprevent or be used to pre-vent or treat renal dys-function?

• How to prevent deepvein thrombosis.

• Facts and physiology offluid replacement.

©2009 American Association of Critical-Care Nurses doi: 10.4037/ccn2009287



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

current body of evidence that canassist clinicians in moving researchto bedside practice are reviewed andrecommendations are outlined.

Positioning Patients forHemodynamic Monitoring

One challenge critical care nursesface is how to answer the question,does my patient need to lie flat forhemodynamic monitoring? In orderto address this challenge, a series ofquestions must be answered: (1) Whatis the correct reference level for a givenposition? (2) Are studies in a givenpopulation of patients (eg, patientswith heart failure, acute respiratorydistress syndrome [ARDS], sepsis,cardiac surgery) available that describethe differences in hemodynamicparameters in the supine vs back-rest elevated position or supine vslateral or prone position? (3) Are theobserved differences in pulmonary

artery pressure (PAP) and centralvenous pressure (CVP) with thepatient in the flat and supine positioncompared with an alternative posi-tion greater than the spontaneousvariability in pressure? An excitingaspect of the evidence to answerthese questions is that most researchon positioning of patients for moni-toring hemodynamic parameters hasbeen conducted by nurse researchers.

Position-Specific Reference LevelRegardless of a patient’s body

position, the key to accurate meas-urements of hemodynamic parame-ters is the use of a position-specificreference level to correct for hydro-static pressure (Table 1, Figure 1).By convention, the phlebostatic axisis the reference point for the rightand left atria.4,5,7,10 The phlebostaticaxis is defined as the intersection of2 reference lines: first, an imaginary

line from the fourth intercostal spaceat the point where the space joinsthe sternum, drawn out to the sideof the body; second, a line drawnmidway between the anterior andposterior surfaces of the chest.11 Thephlebostatic level is a horizontal linethrough the phlebostatic axis. Theair-fluid interface of the stopcock ofthe transducer must be level withthis axis for accurate measurements.In patients with a normal chest wallconfiguration, the midaxillary line isa valid reference level for the rightand left atria; however, use of themidaxillary line in patients with adifferent chest configuration mayresult in a pressure difference of upto 6 mm Hg.12 An alternative refer-ence point is 5 cm below the angleof the sternum. This reference pointreflects the middle of the right atriumand remains the same up to 60º back-rest elevation.13 Use of this alternativereference point, which is also recom-mended for evaluation of jugularvenous distention, results in a CVPmeasurement that is 3 mm Hg lowerthan a CVP measured from a systemreferenced to the phlebostatic axis.13,14

In the lateral position, referencepoints have been validated for the30º and 90º lateral positions with a0º backrest elevation5-7,15 (Table 1).In studies6,16-22 done to evaluate theeffects of a prone position on hemo-dynamic parameters, the midaxil-lary line or the midanteroposterior

Carol A. Rauen is an independent critical care clinical nurse specialist on the Outer Banksof North Carolina and is a staff nurse in the surgical intensive care unit at WashingtonHospital Center, Washington DC.

Mary Beth Flynn Makic is a researcher nurse scientist for critical care and an assistantprofessor at the University of Colorado, Denver.

Elizabeth Bridges is the clinical nurse researcher at the University of Washington MedicalCenter in Seattle and an assistant professor at the University of Washington School ofNursing in Seattle. She is also a colonel in the US Air Force Reserve assigned to the 60thMedical Group at Travis Air Force Base, California.

Corresponding author: Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN, 104 Queen Mary Court, Kill Devil Hills, NC 27948 (e-mail: [email protected]).

To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

Authors

Table 1 Reference level appropriate for various positions of patients

Position

Supine

Supine with head of bed elevated

30º lateral4-6

90º lateral7

Reference level

Half of the anteroposterior diameter of the chest at the fourth intercostal space (not midaxillary)

Half of the anteroposterior diameter of the chest at the fourth intercostal space (not midaxillary)

Half of the vertical distance from the left sternal border to the surface of the bed

Left lateral decubitus: fourth intercostal space/left parasternal border

Right lateral decubitus: fourth intercostal space/midsternum



diameter of the chest has been usedas the reference point, although theaccuracy of this reference has notbeen validated. The reference pointshould be marked on the patient’schest, and the air-fluid interface ofthe system should be leveled by usinga laser or carpenter’s level and notthe “eyeball” method.23

Effect of Position on Hemodynamic Parameters

Supine, Head of Bed Elevated.Studies in a variety of patients inmedical-surgical and cardiac inten-sive care units (ICUs) indicate that ingeneral PAP and CVP can be obtainedreliably with a patient supine withthe head of the bed elevated from 0º

to 60º if the patient’s legs are paral-lel to the floor (ie, the patient is notsitting up with the legs in a depend-ent position).8,24-31 Thermodilutioncardiac 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 wasmeasured with the head of the bedelevated up to 45º. A limitation ofthis research is that it has involvedprimarily patients whose hemody-namic condition was stable; thus,each patient’s response to a givenbody position should be evaluated.

Supine, Trendelenburg/ReverseTrendelenburg. Hemodynamic meas-urements should not be obtainedwith patients in the Trendelenburg

position. Although PAP and CVPincrease when patients are in theTrendelenburg position, neitherintrathoracic blood volume (pre-load) nor cardiac function increases.35

No research has been done on theeffect of the common practice ofelevating the head of the bed andthen placing the entire bed in theTrendelenburg position to preventthe patient from sliding down in thebed. Also, no research has been doneto directly evaluate the effect of useof the reverse Trendelenburg positionon PAP and CVP. However, comparedwith the supine position, a 15º pas-sive tilt decreases cardiac output by10%, and a 45º tilt decreases cardiacoutput by approximately 20%.36 This


Figure 1 Reference levels for various body positions. A, Supine/prone. The reference point is the phlebostatic axis, which is theintersection of 2 reference lines: first, an imaginary line from the fourth intercostal space at the point where the space joins thesternum, drawn out to the side of the body; second, a line drawn midway between the anterior and posterior surfaces of thechest. 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. (Basedon data from VanEtta et al.6) D, 90° lateral position. In the 90° right lateral position, the reference point is the intersection of thefourth intercostal space at the midsternum. In the 90° left lateral position, the reference point is the intersection of the fourthintercostal 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.

Fourthintercostal

space

Lateral marginof sternum

Outermost pointof posterior chest

Left sternalborder

30° Left lateral position 30° Right lateral position

A B

C D

Left sternalborder

Right lateral decubitus position

Sternum

L

LASternum

4th ICS4th ICS/midsternum

Left parasternal border

Left lateral decubitus position

LA LA

L

Outermost pointof sternum

45°

20°

0°

R

LA




research36 suggests that patients’ legsshould be parallel to the groundwhile hemodynamic measurementsare being obtained.

Lateral Position. Results of earlystudies37-43 showed significant differ-ences in PAP and CVP when meas-ured with the patient in the lateralposition (20º-90º) rather than flatand supine. However, in these stud-ies, the phlebostatic axis or the mid-sternum was generally used as thereference point. These referencepoints, which are not accurate dur-ing lateral rotation, introducedmeasurement error into the results.44

For example, in the 30º lateral posi-tion, use of the midsternum ratherthan the validated angle-specificreference6 would introduce an errorof approximately 7 mm Hg. In con-trast, in 2 studies,45,46 in which thevalidated reference point was used,investigators found no clinically sig-nificant changes in CVP and PAP inmost trauma patients45 and patientswho had undergone cardiac surgery.46

In the cardiac surgery patients, thesupine and lateral measurements ofpulmonary artery occlusion pressurediffered by less than 2 mm Hg,44 afinding that most likely reflects the80- to 460-mL position-inducedincrease in cardiac output.47 If theeffects of the incorrect referencepoint were corrected, these originalstudies would on average have resultssimilar to the results of studies thatused the angle-specific reference.46

In addition, in cardiac and medical-surgical ICU patients, PAP and CVPmeasured in patients in the 90º posi-tion were similar to measurementsobtained with the patients supine,as long as the correct angle-specificreference was used.15,40 No studies inwhich the correct angle-specific ref-

erence was used have been completedin patients with severe lung diseaseor in a combined lateral positionwith the head of the bed elevated.

Prone Position. Patients may beplaced prone as a part of therapy forARDS or during surgical procedures.In patients with acute lung injury orARDS, if adequate time (30-60 min-utes) is allowed for stabilization afterrepositioning, no clinically signifi-cant differences in PAP, CVP, orcardiac output are apparent16-22

(Table 2). However, in patients withnormal pulmonary function, suchas those undergoing spinal surgery,cardiac index may be slightly lowerwhen the patient is prone.48-50 Ques-tions to ask include whether abdom-inal compression in the proneposition increases intra-abdominalpressure, and if so, does the increasedintra-abdominal pressure affect theaccuracy of the PAP and CVP meas-urements. As demonstrated in Table3, in patients with normal intra-abdominal pressure, prone position-ing does not significantly increaseintra-abdominal pressure or intratho-racic blood volume and does notfalsely increase CVP.17,18 However, theeffect of the prone position on hemo-dynamic parameters in patients withintra-abdominal hypertension (intra-abdominal pressure>12 mm Hg) isnot known, an important situationbecause intra-abdominal hyperten-sion occurs in up to 50% of ICUpatients.51 Additionally, no studieshave been done in patients in auto-mated proning beds (eg, Rotoprone),and studies are needed to describethe effects that combined prone posi-tioning with lateral rotation with thebed flat and the prone/reverse Tren-delenburg position have on hemo-dynamic parameters.

Normal Variability in Hemodynamic Measurements

The final step is to determine ifthe observed change in pressurebetween having a patient supineand having the patient in an alterna-tive position is within the normalvariability of the measurements.The following changes are clinicallysignificant (ie, do not reflect normalspontaneous variability)46,52-56:

• Change in pulmonary arterysystolic pressure greater than4 to 7 mm Hg

• Change in pulmonary arteryend-diastolic pressure greaterthan 4 to 7 mm Hg

• Change in pulmonary arteryocclusion pressure greaterthan 4 mm Hg

• Change in cardiac outputgreater than 10%

Finally, evidence on the effectof position on hemodynamic param-eters must be interpreted cautiously.Although on average, hemodynamicparameters do not differ signifi-cantly with patients in the variouspositions, individual patients mayrespond to a given position in dif-ferent ways. Thus, it is imperativeto systematically assess each patient’shemodynamic response in a givenposition before assuming that themeasurement will not differ frommeasurements obtained with thepatient supine and flat57,58 (Figure 2).The evidence-based recommenda-tions related to monitoring hemo-dynamic parameters for variousbody positions are summarized inTable 4.

Renal Dose Dopamine:Does It Exist or Not?

Use of low-dose dopamine, orrenal dose dopamine, has become a



widely accepted clinical practice forpreventing or treating renal dys-function.59 Does this agent trulyprotect the kidneys from acute dys-function? The evidence does notsupport the use of low-dose dopamine

to prevent or treat renal dysfunction.In fact, multiple studies59-63 haveshown no evidence that dopamineprevents renal dysfunction or pro-vides renal protection, and the agentmay even be harmful for patients.

Dopamine is a drug with diverseeffects at multiple receptor sites inthe body; this endogenous cate-cholamine regulates cardiac, vascu-lar, and endocrine function.Dopamine is a complex agent; the


Table 2 Measurements of hemodynamic parameters: prone vs supine

Type of patients

ARDS (n = 15)16

ALI (n = 16)18

ALI (n = 12)17

ARDS (n = 23)19

ARDS (n = 11)21

ARDS (n = 19)20

ARDS (n = 14)22

Routine cardiac imaging (n = 48)48

Lumbar spine surgery (n = 15)49

Lumbar spine surgery (n = 40)50

Reference level

Mid-AP

MAL

MAL

Mid-AP

No data

No data

MAL

No data

No data

No data

Supine

84 (19)31 (8)14 (5)

5.1 (1.9)

77 (10)16 (5)

987 (191)4.1 (1.1)

78 (16)75 (10)16 (5)

3.8 (0.9)1008 (187)558 (122)

15 153.5

10 (2) 4.9 (1.1)

87 (9)12 (4)34 (8)15 (5)

5.5 (1.5)

117 (36)61 (15)

9 (2)34 (9)

2.2 (0.5)128 (46)

92 (17)3.1 (0.7)

Position, mean (SD)

Stabilization, min

20

60

60

60-90 (20 minutesafter stabilizationof oxygen satura-tion obtained viapulse oximetry)

90

30

45

No data

15

No data

Abbreviations: ALI, acute lung injury; ARDS, acute respiratory distress syndrome; CI, cardiac index; CO, cardiac output; CVP, central venous pressure; DO2, oxygendelivery; DO2I, oxygen delivery index; EDV, end-diastolic volume; HR, heart rate; ITBVI, intrathoracic blood volume index; MAL, midaxillary line; MAP, mean arterialpressure; 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.

Parameters

MAP, mm HgPAM, mm HgPAOP, mm HgCIa

MAP, mm HgCVP, mm HgITBVIcCIa

HR, beats per minMAP, mm HgCVP, mm HgCIaITBVIcDO2Id

CO, L/minPAOP, mm HgCVP, mm HgHR, beats per minDO2, mL/min

CVP, mm HgPAOP, mm HgCIa

CVP, mm HgCIa

MAP, mm HgCVP, mm HgPAM, mm HgPAOP, mm HgCIa

EDV, mLSV, mL

CVP, mm HgSVIeCIaEDV, mL

MAP, mm HgCIa

Prone

84 (16)29 (8)13 (5)

4.9 (1.6)

82 (11)b

16 (6)1033 (189)

4.4 (0.7)

82 (16)81 (11)b

15 (5)4.2 (0.6)b

1036 (180)620 (74)

14153.4

11 (3)4.8 (1.3)

89 (14)13 (5)37 (8)17 (6)

5.7 (1.7)

111 (39)b

56 (13)b

11 (2)32 (11)2.0 (0.6)100 (48)b

87 (16)2.7 (0.6)

No significant difference for any indices




response to it depends on whichreceptors in the body are stimulated(Table 5). Conventional dosing ofdopamine suggests that low dosages(0.5-3.0 μg/kg per minute) stimulatedopaminergic receptors and resultin coronary and renal vasodilata-tion, natriuresis, and diuresis.Midrange dosing (3-8 μg/kg perminute) activates β-adrenergicreceptors, increasing cardiac inotropyand chronotropy. Dosages greaterthan 8 μg/kg per minute predomi-nantly stimulate α-adrenergicreceptors, resulting in splanchnicand peripheral vasoconstriction.64-67

This conventional dosing is inaccu-rate. Research suggests that dopamineinfusions at similar infusion ratesproduce different responses frompatient to patient.66 One explanationof the variation in responses is thatthe activation of the receptor sitesdepends more on the patient thanon the dose; thus the concept ofdose range affecting specific recep-tors is not universal for all patients.66,67

As a result, traditional dopaminedosing should not be used as a stan-dard regimen. The desired effectsof dopamine infusion depend onthe specific patient’s response tothe agent.59,64,66,67

What is theevidence for theeffectiveness ofrenal dosedopamine inpreventing acuterenal failure?Concern aboutthe use of renaldose dopamineto prevent andtreat renal dys-function beganto appear in theliterature in the

early 1990s.68 Denton et al65 wrote aclassic article discussing the sciencerelated to renal dose dopamine.They reviewed the literature anddiscussed the findings from severalresearch studies in which low-dosedopamine augments renal bloodflow, glomerular filtration rate, andurine output in healthy humans.Denton et al,65 however, did not findsimilar outcomes when critically illpatients were studied. Theyreported that most studies inhumans on the effects of renal dosedopamine and critical illness didnot indicate an improvement inrenal function and prevention ofacute renal failure. Denton et aldiscouraged the use of renal dosedopamine in critically ill patients toprevent or treat renal dysfunction.

In a report published in 1999,Marik and Iglesias63 concluded thatgiving low-dose dopamine to patientswith septic shock and oliguria didnot lead to any significant differ-ences in the incidence of acute renalfailure, need for dialysis, or 28-daysurvival. Then Kellum and Decker59

did a meta-analysis of the use ofdopamine in acute renal failure.They concluded that the use of low-

dose dopamine to treat or preventacute renal failure cannot be justi-fied on the basis of available evidenceand should be eliminated from criti-cal care protocols.59

Despite this evidence, the ongo-ing clinical use of low-dose dopaminecontinued. Friedrich et al62 publisheda meta-analysis and evidence-basedreview on low-dose dopamine, con-cluding that after 15 years of researchon the effectiveness of renal dosedopamine, the evidence indicatesthat low-dose dopamine temporar-ily improves renal output but doesnot prevent renal dysfunction ordeath. Thus, the evidence is conclu-sive: use of low-dose dopaminedoes not prevent or improve renaldysfunction long-term in criticallyill patients.59,60,62,64-66 These findingsshould not be confused withresults of studies that examinedthe effectiveness of higher doses ofdopamine in critically ill patientswith 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 increasewhen a dopamine infusion is started?Dopamine has both natriuretic anddiuretic properties that stimulateurine output, and the responseappears to be more pronounced atlower dosages.64,66,67 This response,however, is often temporary, andurine output tapers off within thefirst 24 hours.62 Dopamine at dosesas low as 2 μg/kg per minute improvescardiac output and mean arterialpressure, enhancing renal perfusionand urine output.66-68

Concerns about the use of low-dose dopamine extend beyond theevidence that the drug is not effec-tive in preventing renal dysfunction.

Table 3 Effect of prone position on abdominal pressureand hemodynamic parametersa

a Based on data from Hering et al.17,18

b Cardiac index, calculated as cardiac output in liters per minute divided bybody surface area in square meters.

Parameter

Abdominal pressure, mm Hg

Mean arterial pressure, mm Hg

Cardiac indexb

Heart rate, beats per min

Right atrial pressure, mm Hg

Intrathoracic blood volume, mL/m2

Supine

10 (3)

75 (10)

3.8 (0.9)

78 (16)

16 (5)

1008 (187)

Position, mean (SD)

Prone

13 (4)

81 (11)

4.2 (0.6)

82 (16)

15 (5)

1036 (180)



Current evidence suggests low-dosedopamine 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 ofdopamine should be continuallyevaluated to match the dose to thedesired outcome without causingadverse consequences for the patient.

Does renal dose dopamineexist? No, it does not. Dopamine

does not protect the kidneys fromrenal dysfunction.59,61,63

Prevention of Deep VeinThrombosis: What Is Best?

Venous thromboembolism is thecombined term that describes both


Figure 2 Algorithm for research-based practice for measurement of central venous pressure, pulmonary artery pressures, andcardiac 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, leftventricular; PAEDP, pulmonary artery end-diastolic pressure; PAOP, pulmonary artery occlusion pressure; PAS, pulmonary artery systolic pressure; SvO2, venousoxygen saturation.

Adapted with permission from Gawlinski.57

Position patient supine/flat if toleratedReference 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 systemSupine (HOB 0° to 45°)

Level and reference to phlebostatic axisLateral (30° or 90°)

30°-Lateral reference: 1⁄2 distance from surface of the bed to the left sternal border90°-Right lateral reference: 4th ICS at midsternum

90°-Left lateral reference: 4th ICS left parasternal borderProne

Reference: phlebostatic axis

Allow for stabilizationSupine with HOB elevated or lateral position

Normal LV function: 5 minutes/LV dysfunction 15 minutesProne

20-30 minutes or until HR ± 10% baseline or SvO2 ± 5%

Perform end-expiratory pressure/CO measurementsUse hard-copy strip and corresponding ECG

Compare hemodynamic parameters in supine, flat position with pressures from alternative positionPAS: Normal LV function: ± 5 mm Hg/Decreased LV function ± 7 mm Hg

PAEDP: Normal LV function: ±5 mm Hg/Decreased LV function ±6 mm HgPAOP: Normal LV function: ±4 mm Hg/Decreased LV function ±5 mm Hg

CO <10%

YesPerform pressure/CO measurements with patient

in the alternative position

NoPerform pressure/CO measurements with patient in the supine/flat position

Are the values within normal spontaneous variability?




deep vein thrombosis (DVT) andpulmonary embolism. Recent esti-mates suggest that venous thrombo -embolism is diagnosed in morethan 900 000 patients in the UnitedStates annually, with approximately400 000 cases manifested as DVTand 500 000 cases as pulmonaryembolism. In 60% of the patientswith pulmonary embolism, theembolism is fatal.71,72 Patients inwhom venous thromboembolismdevelops are also at risk for post-thrombotic syndrome, in which tis-sue injury follows DVT and lastsindefinitely, causing damage of

venous valves,pain, paresthesia,hyperpigmenta-tion, pruritus,venous dilata-tion, edema, andulceration.73,74

Research find-ings71,75 indicatethat clinicalinterventions,includingmechanical andpharmacological therapies, areeffective in preventing venous throm-boembolism; however, only approx-

imately one-third of all patients atrisk for venous thromboembolismreceive prophylactic therapy. The

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

Position-specific reference levels

Supine

Supine with head of bed elevated

30° lateral

90° lateral

Prone/flat

Effect of patient’s position on hemodynamic parameters (compared with supine/flat position)

Supine/head of bed elevated

Supine with Trendelenburg; reverse Trendelenburg

30° lateral

90° lateral

Prone (flat)

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 arterysystolic pressure

Change in pulmonary artery end-diastolic pressure

Change in pulmonary artery occlusion pressure

Change in cardiac output

Phlebostatic axis (half of the anteroposterior diameter of the chest at the fourth intercostal space)

Phlebostatic axis/level (half of the anteroposterior diameter of the chest at the fourth intercostal space)

Half the vertical distance from the left sternal border to the surface of the bed

Left lateral decubitus: fourth intercostal space/left parasternal borderRight lateral decubitus: fourth intercostal space/midsternum

Phlebostatic axis or midaxillary line (limited research to validate this reference level)

Pulmonary artery pressure and central venous pressure: head of bed elevated up to 60°; patient’slegs 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

Not recommended: patient’s legs must be parallel to floor

Pulmonary artery pressure and central venous pressure: pressures can be measured reliably as longas the correct angle-specific reference point/level is used

No studies have validated this position with the head of the bed elevated

Pulmonary artery pressure and central venous pressure: can be measured reliably as long as thecorrect angle-specific reference point/level is used

Pulmonary artery pressure, central venous pressure, and cardiac output: can be measured reliably;allow 20-60 minutes for patient to stabilize after position change

>4-7 mm Hg (increased variability with decreased ejection fraction)

>4-7 mm Hg (increased variability with decreased ejection fraction)

>4 mm Hg

>10%

Table 5 Characteristics of dopamineReceptor sites stimulated

Dopaminergicβ-Adrenergicα-Adrenergic

Physiological actionsImproves cardiac output and mean arterial pressureStimulates natriuresis and diuresis (limited response)Has no effect on renal function/glomerular function

Adverse actionsWorsens splanchnic oxygen consumptionImpairs gastric motilityInduces tachyarrhythmias, especially in elderly patientsBlunts ventilatory response to hypercarbia



most common reasons cited forlack of proper prophylaxis of venousthrombo embolism include lack ofknowledge among providers, under-estimation of patients’ risk for venousthromboembolism, and overestima-tion of the potential risk of bleedingassociated with prophylaxis.74-77

Prevention of venous thromboem-bolism is considered a clear oppor-tunity for improving safe care ofpatients.77 Several national organi-zations and accrediting bodies listthe prevention of venous thromboem-bolism as a patient safety indicatorand measure of quality of care or“never events.”71,78 In 2003, TheAmerican Public Health Associa-tion published guidelines to advancepublic awareness of DVT.76 Geertset al75 published evidence-basedguidelines for the prevention ofvenous thromboembolism, andthat seminal article was followed in2008 with practice guidelines forantithrombotic therapy for venousthromboembolism.79 Evidence isavailable to guide practice for provid-ing interventions to prevent venousthromboembolism. The challenge isto use this evidence in the dailypractice of critical care nursing.

Prevention of venous throm-boembolism begins with assessmentof a patient’s risk factors. A venousthromboembolism is an intravascu-lar fibrin clot that usually forms inregions of slow or disturbed bloodflow. Typically the clot forms in alarge vein in the lower extremities,but it may form in any large vein andposes a great risk when it occludes apulmonary vessel, potentially result-ing in a fatal pulmonary embolism.Classic risk factors for ICU patientsare well known by nurses. The vari-ables are referred to as the Virchowtriad: venous stasis or obstruction,blood vessel injury, and increasedcoagulability. Frequent proceduresdisrupt a patient’s vessels, and thefluid shifts, immobility, and coagu-lation disorders associated with crit-ical illness place ICU patients at highrisk for venous thromboembolism.DVT develops in up to 30% of ICUpatients within the first week ofadmission, a characteristic thatfurther emphasizes the importanceof early interventions.80 To decreasethe prevalence of venous thromboem-bolism, critical care nurses mustevaluate each patient’s risk andimplement preventative interventions

when the patient is admitted tothe unit.

Additional risk factors beyondvenous stasis, immobility, and vas-cular injury should be included inthe assessment of each patient’s riskfor venous thromboembolism. Riskfactors can be grouped in many waysto include patient-specific variables,type of procedure a patient is under-going (eg, orthopedic surgery), andreason for admission (eg, traumaticevent; Table 6). Top risk factorsinclude prolonged immobility,including use of neuromuscularblockade and/or heavy sedation; anindwelling central venous catheter;major surgery; cancer; active infec-tion; pregnancy; hormone therapy;obesity; respiratory failure; heartfailure; cerebral vascular accident;trauma (especially fractures of thepelvis, hip, or leg); history of previ-ous venous thromboembolism; andolder age (ie, risk increases in patients40 years or older).75,81 The more riskfactors a patient has, the more aggres-sive the interventions should be.

Preventive actions are categorizedas mechanical or pharmacologicalinterventions and are implementedon the basis of the assessment of


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

Interventions

Low riskEarly ambulationElastic stockings

Moderate to high riskUnfractionated or low-molecular-

weight heparin Mechanical devices

Highest riskLow-molecular-weight heparin,

fondaparinux, or warfarinMechanical devices

Risk assessment

Low riskAge < 40 yearsMinor surgery

Moderate riskAge > 40 yearsMinor surgery with additional risk factorAge 40-60 years with no additional risk factor

High riskSurgery in patients > 60 years old

Highest riskAge > 40 years with multiple risk factorsHip or knee surgery or interventionsMajor trauma, spinal cord injury




the patient’s risk for venous throm-boembolism (Table 6). Mechanicalprevention encompasses earlyambulation, graduated compressionstockings (also known as elasticcompression stockings), and inter-mittent pneumatic compressiondevices. However, compliance ofpatients and health care practition-ers limits the effectiveness of mechan-ical prevention. For mechanicalprevention to be effective, thedevice(s) must be appropriately fit-ted to each patient and consistentlyapplied to the lower extremities.Often, patients are not appropriatelymeasured for correct fit of a mechan-ical device. In addition, ongoingassessment of the fit of the deviceas body fluids shift may not beaddressed, and the device is notconsistently placed on the patient’sextremities, limiting the effective-ness of mechanical therapy.81-85

Efforts to correctly measure patients’extremities are required to ensurethat the correct size of compressiondevice is used. Also, as body fluidsshift, the fit of the device should bereevaluated. Evidence suggests thatthigh-high graduated compressionstockings are most effective in pro-viding mechanical prevention; how-ever, knee-high stockings are alsoeffective and often have fewer com-plications associated with constric-tion, wrinkles, and compliance withcontinuous wearing.81,86 Intermittentpneumatic compression devices alsoprovide good mechanical preventionif they are continuously used. Theevidence suggests that mechanicaldevices are effective in preventingvenous thromboembolism, providedthe devices fit the patient and areused consistently. Often, patients ornurses remove the devices and do

not reapply them. Nurses shouldbe empowered to correctly assess,measure, and consistently applymechanical interventions to pre-vent the development of venousthromboembolism.

Pharmacological preventionconsists of unfractionated heparin,low-molecular-weight heparin, fon-daparinux, and vitamin K antago-nists (eg, warfarin). Many variablesmust 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, moreaggressive pharmacological therapycombined with mechanical inter-ventions is required. Low-molecular-weight heparin is often prescribedbecause the evidence suggests thatthis 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 asneeded.79,87 High-risk patients mayrequire more aggressive treatmentwith 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 guidelinesof the American College of ChestPhysicians79 provide a full review ofthe evidence supporting antithrom-botic therapy.

What are the best proceduresfor preventing DVT? First and fore-most, preventive interventions mustbe implemented consistently for allcritically ill patients to effectivelydecrease the incidence of venousthromboembolism. Second, patients

should be assessed for severity ofrisk on the basis of age, medical andsurgical history, and projected courseof the critical illness. Third, eachpatient’s plan of care should bereviewed and pharmacologicaltherapy that may help reduce therisk for venous thromboembolismshould be discussed. Fourth, mechan-ical devices must be correctly fittedand consistently applied for effec-tive preventative therapy. Finally,when possible, patients shouldambulate (Table 7). Although allvenous thromboembolism may notbe preventable in critically ill patients,the evidence indicates that its occur-rence can be reduced, and nursesowe it to patients to base practice onthe best evidence to minimize therisk for venous thromboembolism.

Fluid Replacement: Facts and Physiology

Fluid replacement has long beena cornerstone of critical care practice.Historically, the question was notwhether a patient needed fluids butwhat type of fluid would be best. Nowthe physiological value of adminis-tering fluids is being questioned.The goal in fluid replacement is clear:maintain adequate intravascularvolume to ensure cellular oxygendelivery and cardiac output. Themeans to achieve that goal, however,is much more complex.

Both crystalloids and colloidshave significant advantages and dis-advantages. Crystalloids, whichinclude normal saline and lactatedRinger solutions, are isotonic, inex-pensive, readily available, good vol-ume expanders that are easy to storeand administer. These fluids do nottransmit diseases or cause allergicreactions, and both can replace some



electrolytes. However, normal salineand lactated Ringer solutions donot have oxygen-carrying capacity,and approximately 75% of the fluidadministered leaks into the intersti-tial space within hours of adminis-tration. Large volumes of these fluidscan lead to pulmonary edema and,because the blood components arediluted, can actually lead to morebleeding.88 The natural and syntheticblood products (colloids) are muchbetter volume expanders than crys-talloids are and, because of theirmolecular size, tend to stay in theintravascular space longer. Colloidsnot only stay in that space, butbecause of their protein components,they actually can set up an osmoticgradient that will “pull” plasma fromthe interstitium into the intravascu-lar space. These fluids are moreexpensive, are more difficult to storeand administer, often require cross-matching, might transmit diseases ormicroorganisms, and might lead toan allergic or inflammatory response.

Albumin may have many of theadvantages of natural colloids with-out the disadvantages of crystalloids.Finfer et al89 found no significantdifferences between patients givensaline and patients given albumin inthe number of days in the ICU orhospital or in the number of daysthat mechanical ventilation or renal-replacement therapy was required.

Dubois et al90

studied a mixedpopulation ofmedical-surgicalICU patientsand found thatalbumin mighteven have anadvantage overnormal saline:

organ function was improved andtube feedings were more readily tol-erated in the patients who receivedalbumin rather than saline.

Human blood products remainthe best fluid for patients who havelost blood or have symptomaticanemia, but large volumes of bloodare not without risk. The potentialcomplications of using blood prod-ucts include coagulation disorders,metabolic derangements, infection,sepsis, anaphylaxis, and diseasetransmission.91-94 Since the late1990s, administration of blood hasalso been implicated in transfusion-related acute lung injury, transfusion-associated circulatory overload, andtransfusion-related immune modu-lation.91-94 The question of what fluidis best has no risk-free answer.95

Human blood products are alsothe fluid of choice for patients withsymptomatic bleeding whose bloodpressure cannot be increased withcrystalloid administration and whosebleeding has not been controlled.91

The gold standard for treating suchpatients has been fluids and lots ofthem. However, administering crys-talloids to such patients can actuallycause more bleeding. The increase inintravascular volume should increaseblood pressure. If the bleeding sourceis arterial, the increase in bloodpressure could actually disruptclotting and lead to more bleeding.

Crystalloids dilute clotting factorsand platelet volumes. The currentrecommendation for suspectedarterial bleeding is to delay fluidreplacement until surgery to controlthe bleeding is under way.95 It iswidely believed that warm fluid isbetter than cold. Being cold lowersthe core temperature and makescoagulopathies worse. The questionremains: what should the end-pointparameters be for fluid replacement?

The issue of how much fluid toadminister or when to stop is a diffi-cult one. Vincent and Weil96 questionthe traditional clinical parametersthat have been used for decades. His-torically, fluids were cut back whenCVP increased. If the goal is intravas-cular fluid replacement, it must beremembered that CVP reflects onlythe pressure in the central veins. Itdoes not represent total vascularvolume. The same could be said forpulmonary edema. Fluid could beleaking into the lung interstitialspaces because of the high hydrostaticpressure in the pulmonary capillarybed or because of the low oncoticpressure and left ventricular failure.Tachycardia is often used as an indica-tor of anemia or dehydration, butVincent and Weil point out that it isnot a particularly sensitive measure.Tachycardia is a warning sign formany problems in critical care.

In a study of early goal-directedtherapy, Rivers et al97 attempted toanswer the question of replacementend points. Emergency departmentpatients in septic shock had betteroutcomes when they had early goal-directed replacement with the fol-lowing end points:

CVP: 8 to 12 cm H2OMean arterial pressure: greater

than 65 mm Hg


Table 7 Tips for preventing venous thromboembolism

Consistently implement preventative interventions for all patients

Assess patient-specific risk factors for venous thromboembolism

Review plan of care and consider pharmacological therapy

Correctly apply and consistently use mechanical devices (compression stockings, pneumatic devices)

Encourage ambulation




Urine output: greater than 0.5 mL/kg per hour

Central venous oxygen satura-tion: 70%

These parameters were part ofthe Surviving Sepsis Campaignguidelines in 2004 and were recom-mended a second time in the 2008guidelines.98,99 The other recommen-dations in the 2008 guidelines includefluid replacement with 300 to 500mL of colloids or 1 L of crystalloidsin 30 minutes and reducing the fluidchallenge rate if filling pressuresincrease without improvement inhemodynamic status.99

How much blood is the rightamount of blood has also beenresearched. The first hemoglobintrigger that was recommendeddates back to Adam and Lundy100

in 1942. The “10/30” rule was usedin clinical practice for more than 4decades. If a patient’s hemoglobinlevel decreased to less than 10 g/dLor the hematocrit decreased to lessthan 0.30, the patient was givenblood. The discovery that humanimmunodeficiency virus was trans-mitted via blood and the expandingknowledge of the risks of bloodadministration have led clinicians toreevaluate the risks and benefits ofadministering blood and to searchfor a better trigger threshold. Thereport of the current landmarkstudy,92 published in 1999, includedrecommendations that hemoglobin

level be maintained between 7 and 9g/dL. The 2004 and 2008 SurvivingSepsis Campaign guidelinesincluded this recommendation.98,99

The standard exceptions to the trig-ger value of 7 to 9 g/dL are patientswith ischemic heart disease andpatients who have had an acutemyocardial infarction. Corwin et al91

reported that, despite the commonlyknown risks of blood administrationand the new recommendations, clin-ical practice in the United States didnot change much between 1999 and2003. In a 2008 analysis of data onblood transfusions included in theSepsis Occurrence in Acutely IllPatients data base, Vincent et al94

found that administration of bloodwas associated with improved mor-tality. More randomized controlledstudies are needed in critically illpatients to answer these age-oldquestions of which solution, howmuch, and when best to deliver flu-ids to critically ill patients.

In the absence of specific evidence-based practice guidelinesfor fluid replacement in critically illpatients, “For the present, thechoice is best made contingent onthe underlying disease, the type offluid that has been lost, the severityof circulatory failure, the serumalbumin concentration of the patientand the risk of bleeding.”96(p1336) Theshort answer to the simple questionof fluid replacement is that no per-fect solution exists. Patients shouldbe given what they lost or what theyneed that will cause the least harm.Nurses must continue to conductresearch to find a better answer.95

SummaryThis article is the second article

published in Critical Care Nurse that

outlines evidence-based practicesthat should be applied at the bed-side. The challenge before us is 3-fold: we must continue to ask thehard clinical questions, conduct theresearch to answer these questions,and implement the discoveries thatare made. This final challenge is prob-ably the most difficult. We fear thatin today’s environment of cost cut-ting and staffing shortages, uncriti-cal adherence to tradition willbecome the norm again. We mustcreate a culture of inquiry and prac-tice changes based on research andimplement new standards that arebased on the latest available evi-dence. CCN

AcknowledgmentsThe authors served as an expert panel on evidence-based practice at the 2008 National TeachingInstitute in Chicago, Illinois. We thank the Amer-ican Association of Critical-Care Nurses, Linda Bell,Nancy Munro, and the entire Advance PracticeWork Group for their insight in pulling the paneltogether to present this information at the 2008National Teaching Institute.

Financial DisclosuresNone reported.

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eLettersNow that you’ve read the article, create or contributeto an online discussion about this topic using eLetters.Just visit www.ccnonline.org and click “Respondto This Article” in either the full-text or PDF viewof the article.

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82. Amaragiri S, Lees T. Elastic compressionstockings for prevention of DVT. CochraneDatabase Syst Rev. 2000;(3):CD001484.

83. Comerota AJ, Katz ML, White JV. Whydoes prophylaxis with external pneumaticcompression for deep vein thrombosis fail?Am J Surg. 1992;164(3):265-271.

84. Hayes JM, Lehman CA, Castonguay P.Graduated compression stockings: updat-ing practice, improving compliance. MedsurgNurs. 2002;11(4):163-165.

85. Marshall L. Evidence-based nursing mono-graphs: deep vein thrombosis. Mosby’sNursing Consult Web site. http://www.nursingconsult.com/das/ebnm/view/116643613-2. Published October 28, 2007.Accessed January 14, 2009.

86. Graduated compression stockings for theprevention of post operative venous throm-boembolism. Aust Nurs J. 2008;16(2):31-33.

87. Handoll HH, Farrar MJ, McBirnie J, Tyther-leigh-Strong G, Milne AA, Gillespie WJ.Heparin, low molecular weight heparin andphysical methods for preventing deep veinthrombosis and pulmonary embolism fol-lowing surgery for hip fractures. CochraneDatabase Syst Rev. 2002;(4):CD000305.

88. American College of Surgeons’ Committeeon Trauma. Advanced Trauma Life Supportfor Doctors. 8th ed. Chicago, IL: AmericanCollege of Surgeons; 2008.

89. Finfer S, Bellomo R, Boyce N, et al. A com-parison of albumin and saline for fluidresuscitation in the intensive care unit. NEngl J Med. 2004;350(22):2247-2256.

90. Dubois MJ, Orellana-Jimenez C, Melot C,et al. Albumin administration improvesorgan function in critically ill hypoalbu-minemic patients: a prospective, random-ized, controlled, pilot study. Crit Care Med.2006;34(10):2536-2540.

91. Corwin H, Gettinger A, Pearl RG, et al. TheCRIT Study: anemia and blood transfusionin the critically ill—current clinical practicein the United States. Crit Care Med. 2004;32(1):32-39.

92. Hébert PC, Wells G, Blajchman MA, et al.A multicenter, randomized, controlled clin-ical trial of transfusion requirements in crit-ical care. N Engl J Med. 1999;340(6):409-417.

93. Shorr AF, Duh MS, Kelly KM, et al. Redblood cell transfusion and ventilator-associ-ated pneumonia: a potential link? Crit CareMed. 2004;32(3):666-674.

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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 ventilatoryresponse to hypercarbia.

Prevention of Deep Vein Thrombosis: What Is Best?• Patients should be assessed for risk of venous thromboem-

bolism on the basis of age, medical and surgical history, andprojected course of the critical illness (see Table).

• Both mechanical and pharmacological interventions toprevent venous thromboembolism must be implementedconsistently.

Fluid Replacement: Facts and Physiology• More research is needed to determine which solution,

how much, and when best to deliver fluids to critically illpatients.

CCN Fast Facts CRITICALCARENURSEThe journal for high acuity, progressive, and critical care

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 atwww.ccnonline.org

FactsAccording to estimates, 30% to 40% of patients do

not receive care consistent with current scientific evidence.Advanced practice and bedside nurses must evaluatetheir own practice and the needs of their patients andask, Are we doing what is best for our patients with thecurrent evidence available to us?

Positioning Patients for HemodynamicMonitoring• Although, on average, hemodynamic values do not change

markedly when patients are in various body positions,different patients may respond to a given position indifferent ways.

• The key is to systematically assess each patient’s hemo-dynamic response in a given position before assumingthat the measurements will not differ from measurementsobtained with the patient supine and flat.

Evidence-Based Practice Habits: Transforming Research Into Bedside Practice

Table 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

Interventions

Low riskEarly ambulationElastic stockings

Moderate to high riskUnfractionated or low-molecular-

weight heparin Mechanical devices

Highest riskLow-molecular-weight heparin,

fondaparinux, or warfarinMechanical devices

Risk assessment

Low riskAge < 40 yearsMinor surgery

Moderate riskAge > 40 yearsMinor surgery with additional risk factorAge 40-60 years with no additional risk factor

High riskSurgery in patients > 60 years old

Highest riskAge > 40 years with multiple risk factorsHip or knee surgery or interventionsMajor trauma, spinal cord injury




CE Test Test ID C092: Evidence-Based Practice Habits: Transforming Research Into Bedside PracticeLearning 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

Program evaluationYes No

Objective 1 was met � �Objective 2 was met � �Objective 3 was met � �Content was relevant to my

nursing practice � �My expectations were met � �This method of CE is effective

for this content � �The level of difficulty of this test was: � easy � medium � difficult

To complete this program, it took me hours/minutes.

Test answers: Mark only one box for your answer to each question. You may photocopy this form.

1. Which of the following reference levels is used for measuring hemody-namic parameters in supine patients with the head of the bed (HOB)elevated?a. Half of the anterior-posterior diameter of the chest at the second

intercostal spaceb. Half of the anterior-posterior diameter of the chest at the third

intercostal spacec. Half of the anterior-posterior diameter of the chest at the fourth

intercostal spaced. Half of the anterior-posterior diameter of the chest at the fifth

intercostal space

2. Which of the following HOB elevations provides reliable measurementsof pulmonary artery pressure and central venous pressure in supinepatients?a. 0° to 30° c. 0° to 60°b. 0° to 45° d. 0° to 90°

3. Which of the following HOB elevations provides reliable measurementsof thermodilution cardiac output?a. 20° c. 45b. 30° d. 60°

4. The reverse Trendelenburg position has which of the following effectson hemodynamic parameters?a. Decreased pulmonary artery pressureb. Decreased mean arterial pressure c. Decreased central venous pressured. Decreased cardiac output

5. Which of the following dosages of dopamine activates beta-adrenergicreceptors, increasing cardiac inotropy and chronotropy?a. 1 to 3 μg/kg per minuteb. 3 to 8 μg/kg per minutec. 8 to 12 μg/kg per minuted. 12 to 16 μg/kg per minute

6. Current evidence suggests that low-dose dopamine can be harmfuldue to which of the following?a. Worsening splanchnic oxygen consumptionb. Excessive natriuresis and diuresisc. Increased gastric emptyingd. Blunting ventilatory response to hypocarbia

7. Which of the following percentage of patients at risk for venous throm-boembolism receives prophylactic therapy?a. 25% c. 50%b. 33% d. 66%

8. Which of the following patients are at the highest risk for venous throm-boembolism?a. Patients younger than 40 years old who have had minor surgeryb. Patients older than 40 years old who have with minor surgery and an

additional risk factorc. Patients older than 60 years old with surgeryd. Age greater than 40 years with multiple risk factors

9. Evidence suggests that the most effective method for providing mechanical prevention of venous thromboembolism is which of the following?a. Thigh-high compression stockingsb. Knee-high compression stockingsc. Intermittent pneumatic compression devicesd. Compression stockings and compression devices

10. Which of the following endpoints is used for fluid replacement in the Surviving Sepsis Campaign guidelines? a. Central venous pressure of 12 to 15 cm H2Ob. Urine output greater than 1 mL/kg per hourc. Central venous oxygen saturation of 60%d. Mean arterial pressure greater than 65 mm Hg

11. Which of the following is recommended as fluid replacement in the Surviving Sepsis Campaign guidelines?a. 250 mL of colloids over 30 minutesb. 500 mL of colloids over 60 minutesc. 1000 mL of crystalloids over 30 minutesd. 2000 mL of crystalloids over 60 minutes

12. Which of the following hemoglobin levels is recommended as a triggervalue for blood replacement in the Surviving Sepsis Campaign guidelines?a. 6 to 7 g/dLb. 7 to 9 g/dLc. 9 to 10 g/dLd. 9 to 10 g/dL

For faster processing, takethis CE test online atwww.ccnonline.org

(“CE Articles in this issue”)or mail this entire page to:

AACN, 101 Columbia Aliso Viejo, CA 92656.

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 ATest writer: John P. Harper, RN-BC, MSN

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