stroke volume optimization: the new hemodynamic · pdf file criticalcarenurse vol 35, ... 2...

Nurses commonly experience scenarios where hemodynamic monitoring is focused

on hypovolemia (see case study) in clinical practice. In this article, we provide

an overview of the use of stroke volume (the amount of blood ejected from the left

ventricle with each beat) for hemodynamic management of critically ill patients.

We also discuss the limitations of conventional assessment parameters, methods

of measuring stroke volume, hemodynamic variables that influence stroke volume, the stroke volume

optimization (SVO) replacement algorithm, supporting literature, and nursing considerations.

Much of the supporting literature (mostly studies in perioperative patients) on stroke volume as a

primary hemodynamic monitoring parameter focuses on the treatment of hypovolemia, as in the case

Stroke Volume Optimization: The NewHemodynamic AlgorithmALEXANDER JOHNSON, RN, MSN, ACNP-BC, CCNS, CCRN

THOMAS AHRENS, RN, PhD

This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article,which tests your knowledge of the following objectives:

1. Discuss the use of stroke volume optimization in a hypovolemic patient2. Define corrected flow time, peak velocity, stroke distance, and stroke index3. State various methods used to obtain blood flow measurement

©2015 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2015427

CNE Continuing Nursing Education

Cover

www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 11

Critical care practices have evolved to rely more on physical assessments for monitoring cardiac output

and evaluating fluid volume status because these assessments are less invasive and more convenient to

use than is a pulmonary artery catheter. Despite this trend, level of consciousness, central venous pressure,

urine output, heart rate, and blood pressure remain assessments that are slow to be changed, potentially

misleading, and often manifested as late indications of decreased cardiac output. The hemodynamic

optimization strategy called stroke volume optimization might provide a proactive guide for clinicians to

optimize a patient’s status before late indications of a worsening condition occur. The evidence supporting

use of the stroke volume optimization algorithm to treat hypovolemia is increasing. Many of the cardiac

output monitor technologies today measure stroke volume, as well as the parameters that comprise stroke

volume: preload, afterload, and contractility. (Critical Care Nurse. 2015;35[1]:11-28)

study. In the following section, we review the clinical

importance of hypovolemia that may go undetected

(occult hypovolemia) when conventional assessment

techniques are used.

Importance of Occult HypovolemiaTo illustrate the nature of subclinical or occult

hypovolemia and to test the sensitivity of gastrointestinal

tonometry for detecting such hypovolemia, Hamilton-

Davies et al1 conducted a study on 6 healthy volunteers

in the critical care unit at University College of London

Hospitals, London, England. Each of the volunteers had

a mean of 25% (21%-31%) of their overall blood volume

removed during a 1-hour period, and the volunteers’

response was measured. Variables such as heart rate,

blood pressure, serum levels of lactate, and stroke volume

were measured every 30 minutes throughout the study.

After 90 minutes, decreases in gut intramucosal pH were

observed, as well as marked decreases in stroke volume,

by a mean of 16.5 mL (P < .01). Despite this compromised

flow, no clinically significant or consistent postinterven-

tional changes were noted in serum levels of lactate,

arterial blood pressure, heart rate, or arterial blood gases

according to serial measurements obtained throughout

the study period. Retransfusion was started after 90 min-

utes. The results of this study1 may provide insight into

the reliability of routinely used measurements such as

heart rate and systolic blood pressure as volume deple-

tion progressed in these volunteers.

Hypovolemia (defined as inadequate left ventricular

filling volumes)2 affects the cardiovascular system in a

characteristic sequence of events as the hypovolemia

worsens3-6 (Table 1). First, stroke volume decreases

Alexander Johnson is a clinical nurse specialist, Central DuPage Hospital, Cadence Health System–Northwestern Medicine, Winfield, Illinois.

Thomas Ahrens is a research scientist, Barnes-Jewish Hospital, St Louis, Missouri.

Corresponding author: Alexander Johnson, 4007 Schillinger Dr, Naperville, IL 60564 (e-mail: [email protected]).

To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 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

12 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org

Acritical care nurse cares for a patient who had

a 3-vessel coronary artery bypass graft approx-

imately 30 minutes earlier. No indications of

bleeding are present, and both cardiac output and urine

output are within the reference limits. However, the

patient’s systolic arterial blood pressure has decreased

to 77 mm Hg 3 times in the past 20 minutes. Because

the decrease seems to respond to fluid administration,

the nurse begins administering a fourth bottle of 5%

albumin via the rapid infuser in accordance with the sur-

geon’s standing orders. Even though the patient’s central

venous pressure has remained at 3-4 mm Hg since the

patient arrived from surgery, the nurse notes that the

stroke volume has remained between 75 and 80 mL

since the second bottle of albumin. On the basis of the

patient’s hemodynamic profile and this recent

sequence of events, the nurse calls the surgeon to inquire

about an order to administer a vasoactive agent. In

this case, decreased stroke volume response to fluid

suggests adequate volume expansion even though low

central venous pressure values suggest hypovolemia.

CASE STUDY

Blood loss, %

Heart rate, beats per minute

Blood pressure, mm Hg

Pulse pressure

Respiratory rate, breaths per minute

Mental status

Class 4

> 40%

> 140

Decreased

Decreased

> 35

Confused, lethargic

Class 3

30%-40%

> 120

Decreased

Decreased

30-40

Anxious, confused

Class 2

15%-30%

> 100

Normal

Decreased

20-30

Mildly anxious

Class 1

< 15%

< 100

Normal

Normal or increased

14-20

Slightly anxious

Table 1 Classes of shock by Advanced Trauma Life Support (ATLS) designationa

a Reprinted from American College of Surgeons,5 with permission.

because of decreased overall circulating volume (class 1).

Next, heart rate increases and vasoconstriction occurs to

maintain blood pressure and cardiac output (the volume

of blood pumped by the heart per minute)7 (class 2). A

surge of endogenous catecholamines helps shunt blood

from the periphery and splanchnic circulation to the brain

and great vessels to preserve vital organs. Once compen-

satory mechanisms are exhausted, cellular respiration

begins to change from aerobic metabolism to anaerobic

metabolism, and tissue oxygenation is threatened. Oxy-

gen extraction rates increase, and mixed venous oxygen

saturation (Sv̄O2) and central venous oxygen saturation

(ScvO2) decrease because of decreased cardiac output,

compromised blood flow, and decreased oxygen deliv-

ery to tissues (class 3).2,7 Finally, urine output, level of

consciousness, and blood pressure decrease (class 4).3-5

Each event may take minutes to hours. Despite this known

sequence, aggressive intervention often is not implemented

until hypotension occurs.8,9 Traditionally, clinicians are

trained to monitor for early indications of decompensa-

tion, and the first hemodynamic monitoring parameter

to decrease in hypovolemia is stroke volume.1-5

Hypovolemia frequently occurs in patients during

surgery and in the critical care unit because of bleeding,

hypoalbuminemia, capillary leak and interstitial edema,

diarrhea, vomiting, and insensible water loss. If the hypo-

volemia is left untreated (or undertreated), circulatory

hypoxia may develop because of the decreased blood flow

and hypoperfusion. Compensatory diversion of blood

flow centrally, away from the peripheral and splanchnic

circulation, often masks hypoperfusion.2

If not recognized and treated promptly, decreased

circulating volume (particularly at the microvascular level)

leads to diminished oxygen delivery, depletion of intra-

cellular energy reserves, acidosis, anaerobic glycolysis,

and lactate accumulation. Hypovolemia can also lead to

ischemic gastrointestinal complications, including nau-

sea, vomiting, and intolerance of oral intake. Therefore,

diligent monitoring, via accurate assessment of cardiac

output and stroke volume, for hypovolemia is important

for monitoring blood flow.

Limitations of Conventional AssessmentsCurrent conventional assessments such as heart rate,

blood pressure, urine output, central venous pressure

(CVP), and level of consciousness often lack precision as

indicators of changes in a patient’s status. Although the

values obtained in these assessments somewhat correlate

with hemodynamic variables, the values are slow to

change and the changes are often late indications of a

patient’s worsening condition.3-5 Several studies10-17 suggest

that using physical assessment to evaluate cardiac output

may yield inaccurate findings. More recent data18-20 sug-

gest that the predictive power of blood lactate levels for

mortality and morbidity are independent of blood pres-

sure and common physiological triage variables (eg,

heart rate, blood pressure, mental status, capillary refill).

Despite these limitations, assessments such as blood

pressure are still considered a standard of care, and cur-

rent practice mandates use of the assessments. However,

blood pressure itself is a composite of so many factors2-5

(Figure 1) that it is of limited value as an early sign of

hemodynamic derangements such as hypovolemia.

Compensatory mechanisms such as vasoconstriction

and tachycardia influence the cardiovascular system to

keep blood pressure normal,2 making the correlation

between blood pressure and blood flow slow to change

as circulating volume decreases.1-5 The terms compensated

shock and cryptic shock are now being used to define

patient scenarios that meet clinical criteria for shock in


Figure 1 A, Complexity of blood pressure (BP): interrela-tionship of variables comprising BP. BP is the cardiacoutput (CO) multiplied by systemic vascular resistance(SVR). CO is the product of heart rate (HR) and strokevolume (SV). SV is influenced by preload, afterload, contractility, and rhythm. SVR is calculated by dividingthe difference between mean arterial pressure (MAP) and central venous pressure (CVP) by the CO and thenmultiplying by 80. (Derivation of content as described inAlspach.2) B, CO and SVR coexist in a balanced “seesaw”-type relationship. In general, when one decreases, the otherincreases (and vice versa) to maintain normal blood pressure.

BP = CO x SVR

A

B

HR x SV

MAP – CVP x 80

• Preload• Afterload• Contractility• Rhythm

CO

CO SVR

the presence of normal blood pressures.18 Blood pressure

measurements are more useful for conditions that involve

treatment of hypertension rather than treatment of

hypovolemia or shock.21,22 International guidelines such

as the Seventh Report of the Joint National Committee on

Prevention, Detection, Evaluation, and Treatment of High

Blood Pressure22 help guide care providers in the man-

agement of hypertension according to a systematic and

stepwise approach. However, currently no such guidelines

exist for the management of hypotension.

Reconsidering Fluid Replacement End Points

In an article published in 1996, Connors et al23 sug-

gested that use of a pulmonary artery catheter (PAC) was

associated with an increased likelihood of patient death.

Since then, use of PACs has generally decreased. Although

values obtained via a PAC were once considered the gold

standard for bedside hemodynamic monitoring,24,25 the

precision of a PAC for assessing preload status via filling

pressures is limited. As early as 1971, Forrester et al26

pointed out the inaccuracies of CVP monitoring. In a more

recent systematic review of CVP as a predictor of cardiac

output and fluid responsiveness, Marik et al27 concluded

that CVP should

not be used as a

basis for clinical

decisions on fluid

management. In

fact, Marik et al27

noted that the

only published study28 suggesting CVP could be an accurate

indication of preload was done in horses. Even though

guidelines such as those of the Surviving Sepsis Campaign29

recommend using CVP to monitor preload, no study of

CVP or pulmonary artery occlusive pressure (PAOP) has

shown that these pressures consistently correlate with

blood flow or volume status.30 Early and aggressive use

of fluid replacement to preestablished end points such

as ScvO2 is more likely than the measurement of CVP

itself to provide patients benefit.31,32 The limitations of

CVP are further pointed out in the landmark study on

septic shock by Rivers et al33 published in 2001. These

investigators randomized 263 patients with septic shock

to receive either treatment according to a protocol on

fluid replacement known as early goal-directed therapy

or conventional care (control group). The patients treated

according to the protocol had a 17% reduction in mortality,

even though CVP was used as part of the basis for treat-

ment in both the interventional and the control group.33

PAOP is also an inaccurate predictor of fluid respon-

siveness in critically ill patients, further indicating that

blood pressures do not correlate with blood flow param-

eters such as cardiac output and stroke volume.34,35 This

lack of correlation occurs because many factors can

alter the pressure-volume relationship within the heart.

For example, conditions that increase PAOP but not

preload include, but are not limited to, positive-pressure

mechanical ventilation, positive end-expiratory pressure,

and decreased ventricular compliance. Conditions that

alter cardiac compliance include aging, obesity, diabetes,

myocardial ischemia, and sepsis.36 The challenge encoun-

tered with interpreting PAOP is further illustrated in

Figure 2; the 3 hearts in the drawing have different cardio -

myopathies and various left ventricular end-diastolic vol-

umes (LVEDVs), but each heart has the same PAOP. As a

result, the baseline Frank-Starling pressure-volume

curves for the 3 hearts differ vastly (Figure 3). When

LVEDV increases in normal hearts, pressure increases in

a characteristic curvilinear relationship. However, in con-

ditions such as left ventricular hypertrophy, decreased

wall compliance increases intracardiac pressure without

a concomitant increase in volume. Measurements based

on blood flow, such as stroke volume, help clinicians

avoid incorrect assumptions based on pressure-volume

curves.36 Ultimately, blood flow is more reliable and pre-

cise than are blood pressures, and blood flow can decrease

before blood pressures decrease.1,3,5,18

CVP and PAOP were never intended to be used alone;

both are filling pressures meant to guide the optimiza-

tion of stroke volume.27,32 The fundamental reason to

administer a fluid bolus to a patient is to increase stroke

volume.27,35,37 Although stroke volume monitoring is not

considered a standard of care, as is conventional moni-

toring of vital signs, plotting or documenting stroke

volume in response to a fluid challenge may be the clos-

est clinicians can come to using the Frank-Starling curve

in routine bedside practice. Stroke volume is more likely

to indicate hypovolemia before other monitoring param-

eters do because the former is not influenced by most

compensatory mechanisms.1-5 Treatments that include

giving fluids and medications such as drugs that improve

contractility (inotropes) are often administered with the

goal of improving stroke volume. Specifically targeting


Ultimately, blood flow is more reliableand precise than blood pressures, andblood flow can decrease before bloodpressures decrease.

stroke volume for hemodynamic management is termed

SVO. Indications for use of SVO include age, heart failure,

low urine output, bleeding, monitoring of fluid boluses

and vasoactive infusions, cardiac conditions, and risk for

hypoperfusion or organ dysfunction. Awareness of con-

traindications is just as important: for example, esophageal

Doppler monitoring is contraindicated in patients with

esophageal strictures or varices.

Stroke Volume As the Newest CardiacVital SignAssessing for Adequate Perfusion

Using mean arterial pressure to evaluate a patient for

adequate perfusion to the vital organs is a controversial

but important idea for bedside clinicians to consider.38,39

As oxygen supply decreases or oxygen demand increases,

tissue hypoxia can develop. However, exactly when the

hypoxia occurs in an individual patient is unclear. ScvO2

can be a helpful global indicator; however, monitoring

microcirculatory perfusion at the end-organ level is not

readily available yet.40 When compromised perfusion

progresses to the point of eventual acidosis, organ dam-

age most likely is occurring, even when blood pressures

are normal.1

The complexity of these changes defies overreliance

on parameters such as blood pressure. Ongoing fluid

replacement decisions should be based on stroke volume,

variations in pulse pressure, cardiac output derived by

using a minimally invasive method, and passive leg-raising

maneuvers supported by integrated assessment to more


Figure 2 Challenges associated with interpreting pulmonary artery occlusion pressure (PAOP). Left ventricular end-diastolicvolume (LVEDV) can be independent of PAOP. A, PAOP is 22 mm Hg. Normal left ventricle has very high LVEDV. B, PAOP is22 mm Hg. Dilated right ventricle creates increased juxtacardiac pressure; LVEDV is normal. C, PAOP is 22 mm Hg. Left ventric-ular hypertrophy with noncompliant myocardium creates decreased space within the left ventricle; LVEDV is low. Use of PAOPalone to reflect LVEDV may not be accurate.Based on data from Marik et al27 and Turner.36

Illustration courtesy of Lisa Merry, RN, Merry Studio, Bloomington, Illinois.

B CA

Figure 3 Fluid replacement to optimize stroke volume(SV) vs cardiac filling pressures as primary end point.Information in blue is displayed when filling pressuresform the basis for routine bedside preload monitoring.Patient-specific differences in myocardial compliance and filling capacity markedly limit ability to estimate end-diastolic volume and thus, SV, on the basis of cardiac fill-ing pressures. Note also the widening of the Doppleraortic pulse waveform (systolic flow time, or FTc) as pre-load increases. SV measurements (in red) are the primarytarget for fluid in SV optimization. Blood-flow-based tech-nology allows clinicians to estimate SV more directlyalong this pressure-volume curve. This approach helpseliminate “guesstimation” of blood flow based on cardiacfilling pressures.

Stro

ke v

olum

e, m

L

25

Fluid bolus administered

Pulmonary arteryocclusive pressure

50

SV 100 mL

SV 75 mL

SV 40 mL

500 mL 1000 mL 1500 mL4 mm Hg➔➔

12 mm Hg 18 mm Hg

75

100

120

precisely determine the response to the replacement

efforts.32,35,41,42 Methods of actually measuring blood flow

by more direct methods are becoming increasingly

available. These methods can provide true blood-flow

measurements, such as stroke volume, stroke distance,

variation in stroke volume, and systolic flow time.

Methods of Measuring Stroke VolumeTraditionally, echocardiography has been the most

commonly used method to measure stroke volume at the

bedside. However, this method is expensive and technically

difficult and continuous or serial measurements are often

not practical in critical care. Several new technologies

enable ongoing measurement of stroke volume at the

bedside, including noninvasive Doppler imaging

(USCOM), esophageal Doppler imaging (Deltex Medical;

Figure 4), bioimpedance (SonoSite), endotracheally applied

bioimpedance (ConMed Corporation), bioreactance

(Cheetah Medical), pulse contour methods (Edwards

Lifesciences, LidCo Ltd, Pulsion Medical Systems), an

exhaled carbon dioxide method (Philips, Respironics),

and the PAC. All use various methods to calculate stroke

volume, and the results have various degrees of accuracy.

Some devices measure stroke volume directly (eg,

esophageal Doppler imaging) and may be considered

the preferred method because of the high degree of

accuracy of the results.43 Other technologies simply

divide the cardiac output by the heart rate to obtain

stroke volume (eg, PAC). Table 2 provides a more

detailed comparison.44-59

Clinical application of technology is based on

knowledge and experience in obtaining and applying

the information received. If a care provider targets the

wrong hemodynamic end points or interprets a poor

waveform as an

accurate tracing,

benefits may be

limited. These

concerns were

cited in the tech-

nology assessment report published by the Agency for

Healthcare Research and Quality60 in 2008 as some of the

most likely reasons studies have collectively suggested

no benefit for monitoring with PACs.

Disagreement may exist about which technology is best

for monitoring stroke volume because none of the tech-

nologies is appropriate for all patients in all situations.

Each technology has a unique profile of advantages and

limitations, and a patient’s situation may dictate which

technology is best at a given time. Regardless of the

technology used, the device will provide measurements

of preload, afterload, and contractility for optimizing

stroke volume.

Hemodynamic Variables That InfluenceStroke Volume

Three variables affect stroke volume: preload,

contractility, and afterload.

Measurement of Preload: Corrected Flow TimeCorrected flow time (FTc) is a measure obtained in

esophageal and noninvasive Doppler imaging via ultra-

sound technology. The FTc is an estimate of circulating

blood volume based on the amount of red blood cells


Each technology has a unique profileof advantages and limitations, and apatient’s situation may dictate whichtechnology is best at a give time.

Figure 4 Examples of minimally invasive hemodynamicmonitoring. A, Esophageal Doppler monitor: displayallows real-time measurement of preload (flow time, cor-rected, FTc), contractility (peak velocity, PV), stroke vol-ume (SV), and stroke distance (SD). B, Sagittal view ofesophageal Doppler probe in place to monitor cardiac out-put variables. Ultrasound transducer measures blood flowin the descending thoracic aorta.Images courtesy of Deltex Medical, Inc, West Sussex, England.

A

B


Description

Stroke volume estimate obtained viaultrasound probe placed at the sternalnotch or parasternally; ultrasound beamdirected at the aortic or pulmonic valve

Stroke volume estimate directly obtainedvia Doppler signal of descending aorta;typically, patient must be sedated;inserted similarly to a nasogastric tube

Bioimpedance technology via endotra-cheal tube; stroke volume obtainedfrom impedance signal from ascendingaorta; patient must be intubated

Transcutaneous electrodes placed onneck and chest; electrical impedancebetween electrodes during cardiaccycle entered into nomogram to com-pute stroke volume; for best readings,patient must have normal anatomy

Stroke volume estimated from arterialpressure waveform via methods suchas lithium infusion, pulse pressurevariation, or thermodilution; continu-ous cardiac output and beat-to-beatvariability proportional to stroke volume; changes in systemic vascularresistance and arterial pressure neces-sitate recalibration; dampening, dys-rhythmias, and ventilator triggeringalso limit accuracy

Exhaled carbon dioxide method, withFick equation; needs controlledmechanical ventilation to work; addi-tional personnel, such as respiratorytherapist, may be required; patientmust be intubated

Measures cardiac output via thermodi-lution, temperature sensed by thecatheter thermistor; stroke volumecalculated by dividing cardiac outputby heart rate; central venous accessrequired via catheterization of rightside of heart

Like bioimpedance, uses transcutaneouselectrodes; however, signal acquisitioneliminates impedance errors presentwith the first-generation technology

Randomized controlled trials regarding patient outcome

None

9 trials44-52 (2 trials hadconflicts of interest todisclose) showing reducedlength of stay, complica-tions, use of vasopres-sors, renal insufficiency, and mortality and lowerlactate levels

None

None

3 trials (each with conflictsof interest to disclose)suggesting decreasedcomplications and length of stay (LidCO),53

(FloTrac),54 and (PiCCO)55

3 trials suggesting unclearbenefit (PiCCO)56 (conflictof interest disclosed) orno benefit (FloTrac)57

and (PiCCO)58

None

Several trials,59,60 with both pro and con findings

None

Where used

Anywhere

Operating room,intensive careunit, emergencydepartment

Operating room,intensive care unit

Anywhere





Manufacturer

USCOM, Sydney, Australia

Deltex Medical, WestSussex, England

ConMed Corporation,Utica, New York

SonoSite, Bothell,Washington

FloTrac, Edwards Lifesciences, IrvineCalifornia

LidCo Ltd, Cambridge,United Kingdom

PiCCO, Pulsion Medical Systems,Munich, Germany

Philips Respironics,Andover, Massachusetts

Cheetah Medical, Portland, Oregon

Technology

External Dopplerimaging

Esophageal Doppler imaging

Endotrachealbioimpedance

Transcutaneousbioimpedance

Pulse contour

Exhaled carbondioxide method

Pulmonary arterycatheter

Bioreactance

Table 2 Technology for measuring stroke volume

that cross the ultrasound transducer beam through the

aorta during the systolic phase (Figures 4A and 4B). FTc

corresponds to the width of the pulse waveform base

and can be used to estimate preload. For example, a longer

FTc suggests that the left ventricle is pumping forward

an increased amount of blood (ie, increased preload).

The width of the pulse wave is measured in milliseconds

and represents the amount of time spent in systole com-

pared with total cardiac cycle time, and FTc is also cor-

rected for heart rate.61 The correction is based on a heart

rate of 60/min,

although the

current heart

rate is taken into

account. If a

patient’s heart

rate is 60/min, then each cardiac cycle will last 1 second,

or 1000 ms. Normal FTc is 330 to 360 ms.61,62 In other

words, for a cardiac cycle lasting 1 second, the systolic flow

period should last approximately 330 to 360 ms, provided

that adequate preload exists. An easy way to remember

the reference range is to remember that the heart is in

diastole two-thirds of the time and that normal FTc

multiplied by 3 equals 1 second, or 1000 ms62 (Figure 5).

But normal reference ranges are really just reference points,

not necessarily static physiological targets to be used for

all patients. The most important value of FTc is the degree

to which it changes in response to intravenous adminis-

tration of fluids.62 Increases in FTc in response to volume

challenge help confirm hypovolemia, which is manifested

as a narrow waveform base and a low FTc (Figure 3).

The accuracy of FTc has been questioned.63-65 However,

a complete understanding of the variable is critical before

FTc and be used effectively in clinical practice.66-68 Simply

put, FTc is suggestive of the amount of circulating volume

that passes the tip of the ultrasound probe during systole.36

Therefore, conditions such as bleeding (hypovolemia),

heart failure (low contractility), and high afterload (eg,

vasoconstriction) may contribute to low blood-flow

states and thus low FTc. These influences must be con-

sidered before FTc is accepted as a surrogate for preload

in individual patients. Several investigators66,69-72 have

suggested that FTc is as good as or better than PAOP for

indicating changes in preload. Most important, however,

improvement in stroke volume after fluid administration

is what was intended to form the basis on which preload


The most important value of correctedflow time is the degree to which itchanges in response to intraveousadministration of fluids.

Figure 5 Waveform components for stroke volume optimization (SVO): aortic pulse waveform from an esophageal Dopplerexamination. Corrected flow time (ie, the time spent in systole) corresponds to the width of the pulse waveform and is an indexof preload. Peak velocity corresponds to the height of the wave and is a measure of contractility. Stroke distance represents thearea under the curve and is used to compute stroke volume.

Peak velocity (cm/s)

Velo

city

, cm

/s

Flow time, ms

Stroke distance (cm)= area under curve

1/3 Systole 2/3 Diastole

1 Cardiac cycle

responsiveness is ultimately determined (in each of the

outcome trials studying SVO).44-52,73,74 In other words,

FTc (as well as CVP and PAOP) is best used as a decision-

making aid for optimizing stroke volume.

Measurement of Contractility: Peak VelocityPeak velocity, a measure of contractility, is indicated

by the amplitude of a Doppler waveform (Figure 5). It

indicates the acceleration of blood flow in the systolic

phase, or the speed at which a pressure wave goes from

baseline to the peak height of contraction. An overall

reference range is 50 to 120 cm/s. Peak velocity can be

age dependent; the expected range for a 20- to 30-year-

old is 90 to 120 cm/s, with gradually decreasing expected

peak velocity as a person ages. Patients more than 65

years old are expected to have a peak velocity greater

than 50 cm/s. Values less than 50 cm/s are suggestive

of poor left ventricular contractility, as in heart failure.

However, peak velocity should be evaluated with respect

to a patient’s baseline values and how those values

respond to treatments. For example, an increase in peak

velocity is expected with administration of an inotrope.

A low stroke volume can occur for 1 of 2 main rea-

sons: hypovolemia or decreased ventricular contractility.

The immediate measured availability of peak velocity

with Doppler techniques provides better information

than do the derived contractility parameters of the PAC

regarding why stroke volume may be low. For example,

if stroke volume is low but peak velocity is normal, the

problem most likely is hypovolemia.21 However, if both

stroke volume and peak velocity are low, the problem

most likely is left ventricular dysfunction.62 A patient’s

response to medications such as preload reducers, after-

load reducers, or inotropes can help differentiate the

cause of the left ventricular dysfunction (eg, fluid over-

load, high afterload, or low contractility, respectively).

Peak velocity may also help detect acute decompen-

sating systolic heart failure earlier than do other tech-

niques for monitoring cardiac output. In critical illness,

poor left ventricular contractility (low ejection fraction)

may initially lead to a compensatory increase in end-

diastolic volume, a change that implies a normal stroke

volume. The ability to monitor peak velocity allows cli-

nicians to recognize this decrease in contractility in real

time and intervene before a decrease in stroke volume

occurs. Further research is needed to better establish

SVO treatment guidelines for patients with heart failure.

Measurement of Afterload: Systemic Vascular Resistance

Systemic vascular resistance (SVR) is the resistance

that must be overcome by the ventricles to develop force

and contract, propelling blood into the arterial circulation.2

Most of the newer hemodynamic monitoring technolo-

gies (eg, esophageal Doppler imaging, bioimpedance,

pulse contour methods) have the capability to calculate

SVR. However, SVR was not a major parameter in the

algorithms used in any of the SVO trials that showed

improved outcomes in surgical patients.44-52,73,74

Evidence of lack of inclusion suggests that SVR is a

more of a secondary monitoring parameter. Elevated SVR

usually occurs in response to systemic hypertension or

as a compensatory mechanism due to decreased cardiac

output, as in shock states (Figures 1A and 1B). Therefore,

nurses must know why the SVR is elevated. If the value is

elevated in response to low cardiac output, once cardiac

output is improved with treatment (eg, fluid, inotropes),

SVR should decrease because of a decreased need for

compensatory vasoconstriction. If SVR is elevated

because of systemic hypertension, treatment may include

administration of an afterload reducer.2

When SVR decreases, the left ventricular ejection of

blood encounters lower resistance. Low afterload states

may be less problematic when blood pressure and car-

diac output are normal (Figure 1A). However, attempts

to increase low SVR generally include administration of

vasopressors.2 ScvO2 and stroke volume should also be

followed as end points to ensure that blood flow and tis-

sue oxygenation improve in response to the vasopressor21

(Figure 6). Titrating the dose of a vasopressor used to

alter ScvO2 and stroke volume allows clinicians to focus

on optimizing blood flow to both the microcirculation

and the macrocirculation. Several studies of fluid replace-

ment protocols that include use of vasopressors suggest

that optimizing ScvO231,33,75 and stroke volume47,76 improve

patients’ outcomes. However, further research is needed

to better establish how vasopressors and ScvO2 are best

used in SVO protocols.

Stroke Volume, Stroke Index, and Stroke Distance

Stroke volume is one of the primary end points for

detecting fluid responsiveness and guiding goal-directed

therapy.27,32,62 Stroke index is a standardized parameter in

which a patient’s body surface area is taken into account.


However, monitoring both stroke volume and stroke index

is generally not necessary, because they use different units

of measure to quantify the same value. Table 3 gives ref-

erence ranges for these parameters.21,77-79 However, the

ideal stroke volume value is the one that contributes to

adequate blood flow for tissue oxygenation without

increasing heart rate.

Despite the unique advantages of measuring stroke

volume, available technologies to measure this parameter

at the bedside have some limitations. Even esophageal

Doppler imaging, which provides a highly flow-directed

estimation of stroke volume, uses a calculated estimation

of aortic diameter based on the patient’s height and

weight.80 Stroke distance may be a more accurate reflec-

tion of the Doppler estimation of stroke volume. Stroke

distance is the distance a column of blood moves through

the descending thoracic aorta during each systolic phase.61

Because stroke distance is used to calculate stroke vol-

ume, the recommendation is that stroke distance be

evaluated to determine if the measurement of stroke

volume is accurate.

The SVO Algorithm: Putting It All Together

The Frank-Starling principle states that the strength

of cardiac contraction is directly related to the length of

muscle fibers at end diastole, or preload.81 Administration

of fluid on the basis of stroke volume allows clinicians to

directly apply this principle. Figure 7 displays a standard

example of an SVO fluid replacement algorithm, cited by

Schober et al,62 that is based on a synthesis of experimen-

tal SVO protocols and literature.44-52,73,74 In this type of

algorithm, determination of fluid responsiveness is used:

fluid boluses are administered as long as stroke volume

continues to improve by 10% or more. When administra-

tion of fluid boluses ceases to improve stroke volume by


Figure 6 Response of stroke volume to norepinephrine. Increasing vasopressor doses to previously established, prescribedthresholds for mean arterial pressure (MAP) and systemic vascular resistance may in turn decrease stroke volume and overallblood flow. The case example graph suggests that stroke volume is optimized at 8 μg/min of norepinephrine, even though aMAP of only 55 mm Hg is achieved at that dose. Note: patients’ responses to norepinephrine dosing may vary.

Stro

ke v

olum

e, m

L

MAP response to increasing doses of norepinephrine, mm Hg

Increasing norepinephrine dose, μg/min 2 5

75

50

25

10 15 20

65605550

Parameter

Cardiac output, L/min

Stroke volume, mL

Stroke indexb

Flow time corrected, ms

Peak velocity, cm/s

Stroke distance, cm

Cardiac indexc

Systemic vascular resistance, dyne sec cm-5

Saturation of central venous oxyhemoglobin, %

Central venous pressure, mm Hg

Stroke volume variation, %

Referencerange

4-8

50-100

25-45

330-360

30-120

10-20

2.8-4.2

900-1600

65-80

2-8

< 10-15

Table 3 Reference ranges for hemodynamic parametersa

a Based on data from Ahrens,21 Lynn-McHale Wiegand,77 Lynn-McHale Wiegand and Carlson,78 and Edwards Lifesciences.79

b Calculated as stroke volume in milliliters per heartbeat divided by bodysurface area in square meters.

c Calculated as cardiac output in liters per minute divided by body surfacearea in square meters.

10% or more, no more fluid is needed. Using this method

of fluid administration can mitigate the risk of pulmonary

edema, and bedside clinicians can be better assured that

the patient is receiving enough fluid to optimize the

macrocirculation but not more fluid than is needed.

SVR and blood pressure are usually not included in

SVO algorithms and are considered secondary monitor-

ing parameters in SVO.44-52 According to the SVO algo-

rithm, SVR and blood pressure are evaluated only after

peak velocity (contractility) and stroke volume are opti-

mized, because SVR and blood pressure are more indi-

rect reflections of cardiac output and are influenced by

other factors (see Figures 1A and 1B). Furthermore,

when blood flow and tissue oxygenation are measured

rather than assumed, doses of vasopressors can be adjusted

to optimize the end points of stroke volume (macrocir-

culation) and ScvO2 (microcirculation) rather than SVR

and blood pressure (Figure 6). Stroke volume may improve

initially with initiation and escalating doses of vasopres-

sors, but changes in afterload due to further increases in

the medication may impede stroke volume and cardiac

output.82 Surveillance of ongoing stroke volume and

cardiac output may help clinicians avoid this decrease

in stroke volume and cardiac output.

Challenges to SVO implementation may include incor-

porating new hemodynamic monitoring technology into

daily practice (eg, esophageal Doppler imaging, pulse

contour method), education of staff members, support

from physicians and leaders, and the paucity of literature

to support use in nonsurgical patients. However, potential

benefits include use of minimally invasive techniques,

allowing earlier detection of unstable hemodynamic status,

and reductions in morbidity, mortality, and length of stay.

More research is needed to determine how values

such as peak velocity and ScvO2 can be incorporated into

the SVO algorithm. The following case studies illustrate

these points and indicate how SVO can be applied in cases

involving alterations in preload, afterload, and contractility.

Case Study 1: Decreased PreloadA 59-year-old man was admitted to the surgical

intensive care unit after having a partial liver lobectomy


Figure 7 Example of an algorithm for stroke volume optimization.

Other therapies as appropriate, for example:

• High afterload state: dilators (± more fluid) if low correctedflow time, low peak velocity, and blood pressure acceptable

• Low contractility state: inotropic agents if low peak velocityand blood pressure

• Low afterload state: vasopressors if high corrected flowtime, high stroke volume, and low blood pressure

If stroke volume or correctedflow time is low

Give 200 mL of colloid or500 mL of crystalloid

Stop giving fluids;monitor stroke

volume as indicated

If stroke volume decreased > 10%

Yes (stroke volumeincreased < 10%)

No (stroke volumeincreased > 10%)

Is the heart pumping

enough blood?

after a motor vehicle accident (Table 4). On postopera-

tive day 5, he was evaluated for discharge to a general

care unit. His urine output had decreased during the

preceding 12 hours, suggestive of hypovolemia. The

hypovolemia was evidenced by low stroke volume, low

FTc, and low ScvO2 in the presence of a normal peak

velocity. After injection of a 1000-mL bolus of physiolog-

ical saline, stroke volume improved from 34 mL to 48

mL, more than a 10% (3.4 mL) improvement. So,

another bolus was given. Satisfactory response to the

bolus was manifested by normal FTc and ScvO2. Stroke

volume improved to 49 mL only with the second bolus

(<10% improvement), indicating the beginning of the

plateau along the Frank-Starling curve where increased

stretching of the ventricular myocytes does not improve

stroke volume. Thus, no further administration of fluid

was indicated.

Case Study 2: Decreased Preload Leads toDecreased Afterload

A 55-year-old woman was admitted because of sepsis

(Table 5). The patient had a dangerously reduced stroke

volume, decreased FTc, decreased ScvO2, and a normal

peak velocity, indicating hypovolemia. She was deemed

fluid responsive as indicated by an improvement in

stroke volume from 26 mL to 50 mL, a greater than 10%

(2.6 mL) improvement, after administration of a bolus of

1000 mL of physiological saline. So, another saline bolus

was indicated. However, the patient did not respond to

the second bolus, as evidenced by an improvement in

stroke volume from 50 mL to only 51 mL (<10%), suggest-

ing that the macrocirculation had been optimized. Nor-

epinephrine was started because of the reduced ScvO2

and persistent hypotension despite volume correction.

The patient responded appropriately as evidenced by the


Heart rate, beats

per minute

102

100

99

Central venousoxygen

saturation, %

49

69

70

Central venouspressure,mm Hg

3

5

6

Blood pres-sure, mean

(SD), mm Hg

100/48 (64)

94/55 (68)

100/60 (73)

Peak velocity,

cm/s

96

95

95

Flow time, corrected, ms

300

335

337

Stroke volume,

mL

34

48

49

Intervention

Administer 1000-mLbolus of physio-logical saline


Response

Table 4 Interventions used and response of 59-year-old man admitted after a motor vehicle accident

Heart rate, beats

per minute

107

105

105

106

Central venousoxygen

saturation, %

26

48

50

68

Central venouspressure,mm Hg

4

9

9

8

Blood pres-sure, mean

(SD), mm Hg

68/36 (47)

76/42 (53)

80/44 (59)

92/62 (72)

Peak velocity,

cm/s

78

76

76

72

Flow time, corrected, ms

254

341

341

344

Stroke volume,

mL

26

50

51

55

Intervention

Administer 1000-mLbolus of 0.9% normal saline


Administer norepinephrine 10 μg/min

Response

Table 5 Interventions used and response of 55-year-old woman admitted for sepsis

increase in ScvO2 to 68%, suggesting normalization of

the microcirculation.

Literature Supporting Clinical Usefulness of SVO

Before they adopt a new practice, astute clinicians

want to know that the practice is strongly supported in

the literature. Randomized controlled trials are the

highest-level research design, and the number of well-

designed randomized controlled trials is directly correlated

with the level of evidence assigned to a given practice.83-85

The findings of 11 randomized controlled trials,44-52,73,74

including 9 prospective trials,44-52 suggest that SVO results

in improved patient outcomes. Despite a thorough liter-

ature review, we were unable to find a fluid replacement

strategy supported by more research. The results of the

9 prospective trials,44-52 which included a total of about

1000 patients, consistently suggested that compared with

conventional fluid replacement, SVO fluid replacement

protocols contribute to decreases in overall hospital length

of stay (by 2 days or more), complication rates, renal

insufficiency, infection, use of vasopressors, blood lactate

levels, and time-to-tolerance of oral intake. Appropriately

implemented SVO programs that replicate these outcomes

may also be associated with decreased costs.86

Notably, the sample in all 11 trials44-52,73,74 included

perioperative patients. Although 2 of these trials44,47 also

focused on postoperative care in the critical care unit,

more research is needed to indicate the efficacy of SVO

in nonsurgical patients. However, in perioperative

patients, the strength of the supporting evidence in

favor of SVO has been substantiated by large-scale sys-

tematic literature reviews conducted by the Agency for

Healthcare Research and Quality,87 the National Health

Service,86 and third-party payers such as the Centers for

Medicare and Medicaid Services88 and Aetna.89

In 3 of these studies,86-88 the agencies recommended

SVO protocols be used for monitoring cardiac output of

patients receiving mechanical ventilation in the critical

care unit and for surgical patients who require intra -

operative fluid optimization. Esophageal Doppler imag-

ing,88 bioimpedance,90 and PACs91 are all reimbursed by

the Centers for Medicare and Medicaid Services88 on the

basis of systematic literature reviews. However,

esophageal Doppler imaging is the only technology also

supported by the Agency for Healthcare Research and

Quality.87

Similarly, the Cochrane Collaborative59 and the

Agency for Healthcare Research and Quality60 have pub-

lished technology assessments based on meta-analyses

of outcomes related to use of PACs. The analyses indi-

cated that the patients studied showed no evidence of

benefit or harm from PACs. Among the reasons cited

for the perceived lack of benefit was clinician-to-clinician

variability in management of hemodynamic data obtained

via PACs. In addition, the authors59,60 questioned the

accuracy of the interpretation of the hemodynamic

information in the studies analyzed and whether or not

patient management strategies based on hemodynamic

data were appropriate. Furthermore, none of the studies

included use of a specific protocol for PAC use. This lack

of a protocol is a key difference between PAC studies and

SVO studies. Each of the 9 randomized control trials44-52

on SVO

included a

protocol for

use of SVO.

Use of a pro-

tocol is con-

sistent with

other studies of replacement protocols that include

fluid therapy, which can be lifesaving when initiated

early in the course of treatment. Findings from a meta-

analysis of hemodynamic optimization by Poeze et al92

also suggest that replacement strategies such as SVO

improve outcomes, including patient mortality, in

high-risk surgical patients.

Nursing ConsiderationsNursing considerations associated with incorporat-

ing SVO into bedside practice include acquiring and

evaluating hemodynamic data, maintenance of skin

integrity, sedation and analgesia, and nursing research.

Acquisition and Evaluation of Hemodynamic Information

Clinical proficiency with applying or inserting the

hemodynamic monitoring device and adequate signal

acquisition are key.93 Each device has its own unique signal

acquisition technique and competency requirements.

Inappropriate application of the device may produce inac-

curate hemodynamic readings, leading to improper treat-

ment decisions.77,78 Once accurate readings are obtained,

understanding the appropriate application of “normal”


Stroke volume may improve initially with initiation and escalating doses ofvasopressors, but changes in afterloaddue to further pressor dose increases mayimpede stroke volume and cardiac output.

hemodynamic reference ranges to all patients is crucial.

Tracking trends in hemodynamic values over time is

generally more useful than is monitoring and treating

on the basis of single data points, because transient

changes in values may not be clinically importantly.

When readings are considered accurate and hypo -

volemia is identified, rapid infusion of a fluid bolus may

optimize a patient’s response. Fluid infused via a pres-

sure bag often produces a more dramatic increase in

stroke volume than does fluid administered via an intra-

venous infusion pump. A maximum rate of commonly

used intravenous pumps is 999 mL/h. Because hypo -

volemia and hypoperfusion are time-sensitive conditions,

the provider’s judgment and the patient’s condition may

determine that a more rapid infusion rate is needed.

The latest revision of the Surviving Sepsis Campaign

guidelines also suggests an increased emphasis on earlier

and more aggressive fluid replacement. For example, the

2008 guidelines94 recommended a 20 mL/kg crystalloid

fluid challenge in a 6-hour replacement bundle. In the

2012 revised guideline,29 the recommended amount of

fluid was increased (to 30 mL/kg) in a shorter time (3-hour

bundle). Clinicians must strongly consider strategies to

infuse such a volume rapidly enough, in accordance with

institutional policy as appropriate.

Maintenance of Skin IntegrityCare must be taken to avoid skin breakdown under

and around skin electrodes. With bioimpedance and

bioreactance, signals are acquired transcutaneously, and

skin care should be in accordance with the manufacturer’s

recommendations and institutional policy. Mouth ulcer-

ations are also possible with monitoring devices such as

those used for esophageal Doppler imaging93 and endo-

tracheally applied bioimpedance. Diligent oral care should

be performed as

needed while

those devices are

in place. Site care

is also important

when caring for

patients moni-

tored with intravenous pulse contour devices or PACs.

Catheter infections can be minimized by using sterile

conditions during insertion and aseptic technique during

dressing changes.77,78

Sedation and AnalgesiaSedation is sometimes required with techniques such

as the exhaled carbon dioxide method, which requires

controlled mechanical ventilation, and esophageal Doppler

imaging. These techniques may have limited accuracy

when increased respiratory rates or restlessness, respec-

tively, occur. Therefore, sedative agents or analgesics

may be administered as needed.77,78 Although not a major

focus with respect to SVO, pain cannot be overlooked;

it is not only an overall priority but can also influence

hemodynamic readings.

Nurse ResearchThe implications of patient advocacy extend beyond

routine patient care and include nurses’ participation in

designing and implementing future research on the clini-

cal usefulness of SVO in critical care. Critical care nurses

monitor and treat hypovolemia daily and have a unique

opportunity to contribute to the existing scientific body

of knowledge through participation in SVO studies in

medical critical care patients.

SummaryThe growing body of evidence supporting SVO

suggests that implementation of SVO into daily practice

should be considered.61,62,88 A new era is emerging in

which blood-flow monitoring is taking precedence over

the monitoring of blood pressures. Cardiac pressures

help provide estimates of blood volume; however, normal

cardiac pressures can be observed in a patient in shock

and provide little information about blood flow.30,95-97

Interpretation and treatment of blood pressures incor-

porate assumptions, whereas stroke volume may be

considered a more precise measure of fluid responsive-

ness and an earlier warning sign of volume depletion

than are urine output, altered mental status, CVP, heart

rate, and blood pressure.1-5 Earlier signals allow clini-

cians to anticipate rather than react to changes, improv-

ing the likelihood for maintaining a stable metabolic

state at the organ and cellular level. In addition to the

evidence supporting SVO, minimally invasive applica-

tions and improvements in accuracy also add to safety

advantages when inherent limitations of the various

methods are considered.

For years, strategies for use of SVO were not feasible

because no practical measurement method for SVO


Earlier signals such as stroke volumeallow clinicians to anticipate rather thanreact to changes, improving the likeli-hood of maintaining a stable metabolicstate at the organ and cellular level.

existed for bedside clinicians. Fortunately, technology

has improved the hemodynamic monitoring landscape.

Compared with old devices, newer technology is less inva-

sive, safe, evidence based, flow directed, cost-effective,

easier to use, and accurate. Although further research

on SVO and dynamic indices are needed to establish the

clinical efficacy of SVO in critical care units, the current

body of literature indicates that SVO is associated with

fewer complications and reduced hospital lengths of stay,

particularly in patients receiving mechanical ventilation

and in surgical patients. Until more randomized trials

on the impact of SVO protocols on the outcomes of

critical care patients are published, SVO is supported

by more evidence than is use of filling pressures for fluid

replacement in critical care units.27,32,44-52,73,74,86-88 On the

basis of our review of the current available literature, we

suggest that the SVO algorithm for fluid replacement be

considered in place of use of cardiac filling pressures for

patients in critical care, as appropriate, with attention to

outcomes. In the meantime, more research is needed to

evaluate the impact of SVO on patients other than peri-

operative patients and on nonintubated patients. CCN

AcknowledgmentsThe authors thank Terry Sears and Julie Stielstra for their contributions. Wealso thank the critical care staff, physicians, and leaders at Central DuPageHospital–Northwestern Medicine. Without their help and support, this man-uscript would have been much more difficult to complete.

Financial DisclosuresTom Ahrens has lectured for hemodynamic monitoring companies (includingDeltex Medical Inc) and is a hemodynamic monitoring consultant.

References1. Hamilton-Davies C, Mythen M, Salmon J, Jacobson D, Shukla A, Webb A.

Comparison of commonly used clinical indicators of hypovolaemia withgastrointestinal tonometry. Intensive Care Med. 1997;23(3):276-281.

2. Alspach J, ed. Core Curriculum for Critical Care Nursing. 6th ed. St Louis,MO: Saunders Elsevier; 2006:83, 195, 361, 365, 368.

3. Gutierrez G, Reines HD, Wulf-Gutierrez M. Clinical review: hemorrhagicshock. Crit Care. 2004;8(5):373-381.

4. McLean B, Zimmerman J, Baldisseri M,et al. Fundamental Critical CareSupport. 4th ed. Mount Prospect, IL: Society of Critical Care Medicine;2007:9-6.

5. American College of Surgeons. Advanced Trauma Life Support for Doctors:ATLS. 8th ed. Chicago, IL: American College of Surgeons; 2008.

6. McCance KL, Huether SE, Brashers VL, Rote NS. Pathophysiology: TheBiologic Basis for Disease in Adults and Children. 6th ed. St Louis, MO:Mosby, Elsevier: 2010.

7. Ahrens T, Rutherford K. Essentials of Oxygenation: Implication for ClinicalPractice. Boston, MA: Jones & Bartlett Publishers Inc; 1993:51.

8. Hillman KM, Bristow PJ, Chey T, et al. Antecedents to hospital deaths.Intern Med J. 2001;31(6):343-348.

9. Kause J, Smith G, Prytherch D, et al; Intensive Care Society (UK); Aus-tralian and New Zealand Intensive Care Society Clinical Trials Group.A comparison of antecedents to cardiac arrests, deaths and emergencyintensive care admissions in Australia and New Zealand, and the UnitedKingdom—the ACADEMIA study. Resuscitation. 2004;62(3):275-282.

10. Connors AF Jr, Dawson NV, Shaw PK, Montenegro HD, Nara AR, Martin L. Hemodynamic status in critically ill patients with and withoutacute heart disease. Chest. 1990;98(5):1200-1206.

11. Dawson NV, Connors AF Jr, Speroff T, Kemka A, Shaw P, Arkes HR.Hemodynamic assessment in managing the critically ill: is physicianconfidence warranted? Med Decis Making. 1993;13(3):258-266.

12. Eisenberg PR, Jaffe AS, Schuster DP. Clinical evaluation compared topulmonary artery catheterization in the hemodynamic assessment ofcritically ill patients. Crit Care Med. 1984;12(7):549-553.

13. Hoeft A, Schorn B, Weyland A, et al. Bedside assessment of intravascularvolume status in patients undergoing coronary bypass surgery. Anesthe-siology. 1994;81(1):76-86.

14 Iregui MG, Prentice D, Sherman G, Schallom L, Sona C, Kollef MH.Physicians’ estimates of cardiac index and intravascular volume basedon clinical assessment versus transesophageal Doppler measurementsobtained by critical care nurses. Am J Crit Care. 2003;12(4):336-342.

15. Neath SX, Lazio L, Guss DA. Utility of impedance cardiography toimprove physician estimation of hemodynamic parameters in the emer-gency department. Congest Heart Fail. 2005;11(1):17-20.

16. Staudinger T, Locker GJ, Laczika K, et al. Diagnostic validity of pulmonaryartery catheterization for residents at an intensive care unit. J Trauma.1998;44(5):902-906.

17. Celoria G, Steingrub J, Vickers-Lahti M, et al. Clinical assessment ofhemodynamic values in two surgical intensive care units: effects of ther-apy. Arch Surg. 1990;125(8):1036-1039.

18. Bakker J, Jansen T. Don’t take vitals, take a lactate. Intensive Care Med.2007;33:1863-1865.

19. Howell MD, Donnino M, Clardy P, Talmor D, Shapiro NI. Occult hypop-erfusion and mortality in patients with suspected infection. Intensive CareMed. 2007;33(11):1892-1899.

20. Mikkelsen M, Miltiades A, Gaieski D, et al. Serum lactate is associatedwith mortality in severe sepsis independent of organ failure and shock.Crit Care Med. 2009;37(5):1670-1677.

21. Ahrens T. Hemodynamics in sepsis. AACN Adv Crit Care. 2006;17(4):435-445.

22. Department of Health and Human Services, National Institutes ofHealth, National Heart, Lung, and Blood Institute. The Seventh Report ofthe Joint National Committee on Prevention, Detection, Evaluation, andTreatment of High Blood Pressure. Bethesda MD: National Heart, Lung,and Blood Institute; August 2004. NIH Publication No. 04-5230.

23. Connors A, Speroff T, Dawson N, et al. The effectiveness of right heartcatheterization in the initial care of critically ill patients. SUPPORTInvestigators. JAMA. 1996;276(11):889-897.

24. Smartt S. The pulmonary artery catheter: gold standard or redundantrelic. J Perianesth Nurs. 2005;20(6):373-379.

25. Pugsley J, Lerner A. Cardiac output monitoring: is there a gold standardand how do the newer technologies compare? Semin Cardiothorac VascAnesth. 2010;14(4):274-282.

26. Forrester JS, Diamond G, McHugh TJ, Swan HJ. Filling pressures in theright and left sides of the heart in acute myocardial infarction: a reappraisalof central-venous-pressure monitoring. N Engl J Med. 1971;285(4):190-193.

27. Marik P, Baram M, Vahid B. Does central venous pressure predict fluidresponsiveness? A systematic review of the literature and the tale ofseven mares. Chest. 2008;134(1):172-178.

28. Magdesian KG, Fielding CL, Rhodes DM, Ruby RE. Changes in centralvenous pressure and blood lactate concentration in response to acuteblood loss in horses. J Am Vet Med Assoc. 2006;229(9):1458-1462.

29. Dellinger RP, Levy MM, Rhodes A, et al; Surviving Sepsis CampaignGuidelines Committee including the Pediatric Subgroup. SurvivingSepsis Campaign: International guidelines for management of severesepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580-637.

30. Ahrens T. Stroke volume optimization vs central venous pressure influid management. Crit Care Nurse. 2010;30(2):71-73.

31. Pope JV, Jones AE, Gaieski DF, Arnold RC, Trzeciak S, Shapiro NI; Emer-gency Medicine Shock Research Network (EMShockNet) Investigators.


Now that you’ve read the article, create or contribute to an online discussionabout this topic using eLetters. Just visit www.ccnonline.org and select the articleyou want to comment on. In the full-text or PDF view of the article, click“Responses” in the middle column and then “Submit a response.”

To learn more about stroke volume optimization, read “StrokeVolume Optimization Versus Central Venous Pressure in FluidManagement” by Ahrens in Critical Care Nurse, April 2010;30:71-72. Available at www.ccnonline.org.

Multicenter study of central venous oxygen saturation (ScvO2) as a pre-dictor of mortality in patients with sepsis. Ann Emerg Med. 2010;55(1):40-46.e1.

32. Marik P. Surviving sepsis: going beyond the guidelines. Ann IntensiveCare. 2011;1(17):1-6.

33. Rivers E, Nguyen B, Havstad S, et al; Early Goal-Directed Therapy Col-laborative Group. Early goal-directed therapy in the treatment of severesepsis and septic shock. N Engl J Med. 2001;345(19):1368-1377.

34. Benington S, Ferris P, Nirmalan M. Emerging trends in minimally inva-sive haemodynamic monitoring and optimization of fluid therapy. Eur JAnaesthesiol. 2009;26(11):893-905.

35. Marik P, Monnet X, Teboul JL. Hemodynamic parameters to guide fluidtherapy. Ann Intensive Care. 2011;1(1):1-9.

36. Turner MA. Doppler-based hemodynamic monitoring: a minimallyinvasive alternative. AACN Clin Issues. 2003;14(2):220-231.

37. Michard F, Teboul J. Predicting fluid responsiveness in ICU patients: acritical analysis of the evidence. Chest. 2002;121:2000-2008.

38. Dünser M, Takala J, Brunauer A, Bakker J. Re-thinking resuscitation:leaving blood pressure cosmetics behind and moving forward to permis-sive hypotension and a tissue perfusion-based approach. Crit Care. 2013;17:326. doi:10.1186/cc12727.

39. Marik P, Bellomo R. Re-thinking resuscitation goals: an alternativepoint of view! Crit Care. 2013;17:458. doi:10.1186/cc12775.

40. Knotzer H, Hasibeder W. Microcirculation function monitoring at thebedside—a view from the intensive care. Physiol Meas. 2007;28(9):R65-R86.

41. Marik P, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterialwaveform derived variables and fluid responsiveness in mechanicallyventilated patients: a systematic review of the literature. Crit Care Med.2009;37(9):2642-2647.

42. Marik P. Techniques for assessment of intravascular volume in criticallyill patients. Intensive Care Med. 2009;24(5):329-337.

43. Dark P, Singer M. The validity of trans-esophageal Doppler ultrasonog-raphy as a measure of cardiac output in critically ill adults. Intensive CareMed. 2004;30:2060-2066.

44. Chytra I, Pradl R, Bosman R, Pelnar P, Kasal E, Zidkova A. EsophagealDoppler-guided fluid management decreases blood lactate levels inmultiple-trauma patients: a randomized controlled trial. Crit Care.2007;11(1):R24.

45. Conway DH, Mayall R, Abdul-Latif MS, Gilligan S, Tackaberry C. Ran-domized controlled trial investigating the influence of intravenous fluidtitration using esophageal Doppler monitoring during bowel surgery.Anaesthesia. 2002;57(9):845-849.

46. Gan TJ, Soppitt A, Maroof M, et al. Goal-directed intraoperative fluidadministration reduces length of hospital stay after major surgery. Anes-thesiology. 2002;97(4):820-826.

47. McKendry M, McGloin H, Saberi D, Caudwell L, Brady AR, Singer M.Randomised controlled trial assessing the impact of a nurse delivered,flow monitored protocol for optimisation of circulatory status after car-diac surgery. BMJ. 2004;329(7460):258-261.

48. Mythen MG, Webb AR. Perioperative plasma volume expansionreduces the incidence of gut mucosal hypoperfusion during cardiac sur-gery. Arch Surg. 1995;130(4):423-429.

49. Sinclair S, James S, Singer M. Intraoperative intravascular volume opti-misation and length of hospital stay after repair of proximal femoralfracture: randomised controlled trial. BMJ. 1997;315(7113):909-912.

50. Venn R, Steele A, Richardson P, Poloniecki J, Grounds M, Newman P.Randomized controlled trial to investigate influence of the fluid chal-lenge on duration of hospital stay and perioperative morbidity inpatients with hip fractures. Br J Anaesth. 2002;88(1):65-71.

51. Wakeling HG, McFall MR, Jenkins CS, et al. Intraoperative oesophagealDoppler guided fluid management shortens postoperative hospital stayafter major bowel surgery. Br J Anaesth. 2005;95(5):634-642.

52. Noblett S, Snowden C, Shenton B, Horgan A. Randomized clinical trialassessing the effect of Doppler-optimized fluid management on out-come after elective colorectal resection. Br J Surg. 2006;93(9):1069-1076.

53. Pearse R, Dawson D, Fawcett J, Rhodes A, Grounds RM, Bennett ED.Early goal-directed therapy after major surgery reduces complicationsand duration of hospital stay: a randomized, controlled trial[ISRCTN38797445]. Crit Care. 2005;9(6):R687-R693.

54. Mayer J, Boldt J, Mengistu AM, Röhm KD, Suttner S. Goal-directedintraoperative therapy based on autocalibrated arterial pressure wave-form analysis reduces hospital stay in high-risk surgical patients: a ran-domized, controlled trial. Crit Care. 2010;14(1):R18. doi:10.1186/cc8875.

55. Goepfert M, Richter H, Eulenburg C, et al. Individually optimizedhemodynamic therapy reduces complications and length of stay in theintensive care unit: a prospective, randomized controlled trial. Anesthe-siology. 2013;119(4):824-836.

56. Salzwedel C, Puig J, Carstens A, et al. Perioperative goal-directed hemo-dynamic therapy based on radial arterial pulse pressure variation andcontinuous cardiac index trending reduces postoperative complicationsafter major abdominal surgery: a multi-center, prospective, randomizedstudy. Crit Care. 2013;17(5):R191. doi:10.1186/cc12885.

57. Van der Linden PJ, Dierick A, Wilmin S, Bellens B, De Hert SG. A ran-domized controlled trial comparing an intraoperative goal-directedstrategy with routine clinical practice in patients undergoing peripheralarterial surgery. Eur J Anaesthesiol. 2010;27(9):788-793.

58. Szakmany T, Toth I, Kovacs Z, et al. Effects of volumetric vs pressure-guided fluid therapy on postoperative inflammatory response: a prospec-tive, randomized clinical trial. Intensive Care Med. 2005;31(5):656-663.

59. Rajaram SS, Desai NK, Kalra A, et al. Pulmonary artery catheters foradult patients in intensive care. Cochrane Database Syst Rev. 2013;2:CD003408. doi:10.1002/14651858.CD003408.pub3.

60. Balk E, Raman G, Chung M, et al. Evaluation of the Evidence on Benefitsand Harms of Pulmonary Artery Catheter Use in Critical Care Settings.Rockville, MD: Agency for Healthcare Research and Quality; March 28,2008. http://www.cms.gov/determinationprocess/downloads/id55TA.pdf. Accessed October 29, 2014.

61. Roche A, Miller T, Gan T. Goal-directed fluid management with trans-oesophageal Doppler. Best Pract Res Clin Anaesthesiol. 2009;23(3):327-334.

62. Schober P, Loer S, Schwarte L. Perioperative hemodynamic monitoringwith transesophageal Doppler technology. Anesth Analg. 2009;109:340-353.

63. Chew HC, Devanand A, Phua GC, Loo CM. Oesophageal Doppler ultra-sound in the assessment of haemodynamic status of patients admittedto the medical intensive care unit with septic shock. Ann Acad Med Sin-gapore. 2009;38(8):699-703.

64. Bendjelid K. Assessing fluid responsiveness with esophageal Dopplerdynamic indices: concepts and methods [comment]. Intensive Care Med.2006;32(7):1088.

65. Monnet X, Pinsky M, Teboul J. FTc is not an accurate predictor of fluidresponsiveness. Intensive Care Med. 2006;32:1090-1091.

66. Johnson A, Schweitzer D. Putting the wedge under pressure [comment].Ann Acad Med Singapore. 2010;39(10):815.

67. Singer M. The FTc is not an accurate marker of left ventricular preload:reply to the comment by Chemla and Nitenberg. Intensive Care Med.2006;32(9):1456-1457.

68. Singer M. The FTc is not an accurate marker of left ventricular preload.Intensive Care Med. 2006;32(7):1089.

69. Madan AK, UyBarreta VV, Aliabadi-Wahle S, et al. Esophageal Dopplerultrasound monitor versus pulmonary artery catheter in the hemody-namic management of critically ill surgical patients. J Trauma. 1999;46(4):607-611.

70. Seoudi H, Perkal M, Hanrahan A, Angood P. The esophageal Dopplermonitor in mechanically ventilated surgical patients: does it work[abstract]? J Trauma. 1999;47(6):1171.

71. DiCorte CJ, Latham P, Greilich PE, Cooley MV, Grayburn PA, Jessen ME.Esophageal Doppler monitor determinations of cardiac output and pre-load during cardiac operations. Ann Thoracic Surg. 2000;69(6):1782-1786.

72. Kincaid H, Fly M, Chang M. Noninvasive measurements of preloadusing esophageal Doppler are superior to pressure-based estimates incritically injured patients [abstract]. Crit Care Med. 1999;27(1):A111.

73. Mark JB, Steinbrook RA, Gugino LD, et al. Continuous noninvasivemonitoring of cardiac output with esophageal Doppler ultrasound dur-ing cardiac surgery. Anesth Analg. 1986;65(10):1013-1020.

74. Valtier B, Cholley BP, Belot JP, Coussay JE, Mateo J, Payen DM. Nonin-vasive monitoring of cardiac output in critically ill patients using trans-esophageal Doppler. Am J Respir Crit Care Med. 1998;158:77-83.

75. Micek ST, Roubinian N, Heuring T, et al. Before-after study of a stan-dardized hospital order set for the management of septic shock. CritCare Med. 2006;34(11):2707-2713.

76. Saberi D, Caudwell L, McGloin H, Singer M. Proactive circulatory man-agement in the first 4 hours postcardiac surgery: interim analysis of anurse-led, oesophageal Doppler-guided protocol [abstract]. IntensiveCare Med. 2000;26(3 suppl):S220.

77. Lynn-McHale Wiegand D, ed. AACN Procedure Manual for Critical Care.6th ed. St Louis, MO: Elsevier Saunders: 2011.

78. Lynn-McHale Wiegand D, Carlson K, eds. AACN Procedure Manual forCritical Care. 5th ed. St Louis, MO: Elsevier; 2005.

79. Edwards Lifesciences. Advanced hemodynamic monitoring. The FloTracsensor: stroke volume variation. http://www.edwards.com/products/mininvasive/Pages/strokevolumevariationwp.aspx. Accessed October30, 2014.

80. Singer M. Continuous Haemodynamic Monitoring by Oesophageal Doppler[doctoral dissertation]. London, England: University of London; April 1989.

81. Starling EH. The Linacre Lecture on the Law of the Heart. London, England:Longmans, Green & Co; 1918.


82. Ahrens T, Taylor L. Hemodynamic Waveform Analysis. St Louis, MO: WBSaunders; 1992:432, 444-447.

83. Atkins D, Best D, Briss PA, et al; GRADE Working Group. Grading quality ofevidence and strength of recommendations. BMJ. 2004;328(7454):1490-1498.

84. Guyatt G, Gutterman D, Baumann MH, et al. Grading strength of recom-mendations and quality of evidence in clinical guidelines: report from anAmerican College of Chest Physicians task force. Chest. 2006;129(1):174-181.

85. Schünemann HJ, Jaeschke R, Cook DJ, et al; ATS Documents Developmentand Implementation Committee. An official ATS statement: grading thequality of evidence and strength of recommendations in ATS guidelinesand recommendations. Am J Respir Crit Care Med. 2006;174(5):605-614.

86. Mowatt G, Houston G, Hernández R, et al. Systematic review of the clini-cal effectiveness and cost-effectiveness of oesophageal Doppler monitor-ing in critically ill and high-risk surgical patients. Health Technol Assess.2009;13(7):iii-iv, ix-xii, 1-95. doi:10.3310/hta13070.

87. Agency for Healthcare Research and Quality. Esophageal Doppler ultra-sound-based cardiac output monitoring for real-time therapeutic manage-ment of hospitalized patients: a review. http://www.cms.hhs.gov/determinationprocess/downloads/id45TA.pdf. Published January 16,2007. Accessed October 30, 2014.

88. Centers for Medicare and Medicaid Services. CMS manual system: pub100-03 Medicare national coverage determinations. http://www.cms.hhs.gov/Transmittals/Downloads/R72NCD.pdf. Published August 28,2007. Accessed October 31, 2014.

89. Aetna Health Insurance. Clinical policy bulletin: esophageal Dopplermonitoring. Publication No. 0793. http://www.aetna.com/cpb/medical/data/700_799/0793.html. Accessed October 31, 2014.

90. Centers for Medicare and Medicaid Services. CMS manual system: pub100-03 Medicare national coverage determinations. https://www.cms.gov/transmittals/downloads/R63NCD.pdf. Published December 15, 2006.Accessed October 31, 2014.

91. CMS.gov. Billing and coding guidelines. Cardiac catheterization andcoronary angiography. http://downloads.cms.gov/medicare-coverage-database/lcd_attachments/30719_6/L30719_CV006_CBG_010111.pdf. Accessed November 24, 2014.

92. Poeze M, Greve J, Ramsay G. Meta-analysis of hemodynamic optimization:relationship to methodological quality. Critical Care. 2005;9(6):R771-R779.

93. Prentice D, Sona C. Esophageal Doppler monitoring for hemodynamicassessment. Crit Care Nurs Clin North Am. 2006;18:189-193.

94. Dellinger P, Levy M, Carlet J, et al; International Surviving Sepsis Cam-paign Guidelines Committee; American Association of Critical-CareNurses; American College of Chest Physicians; American College ofEmergency Physicians; Canadian Critical Care Society; European Societyof Clinical Microbiology and Infectious Diseases; European Society ofIntensive Care Medicine; European Respiratory Society; InternationalSepsis Forum; Japanese Association for Acute Medicine; Japanese Soci-ety of Intensive Care Medicine; Society of Critical Care Medicine; Societyof Hospital Medicine; Surgical Infection Society; World Federation ofSocieties of Intensive and Critical Care Medicine. Surviving Sepsis Cam-paign: international guidelines for management of severe sepsis and sep-tic shock: 2008 [published correction appears in Crit Care Med.2008;36(4):1394-1396]. Crit Care Med. 2008;36(1):296-327.

95. Wo CC, Shoemaker WC, Appel PL, Bishop MH, Kram HB, Hardin E.Unreliability of blood pressure and heart rate to evaluate cardiac outputin emergency resuscitation and critical illness. Crit Care Med. 1993;21(2):218-223.

96. Shippy C, Appel P, Shoemaker W. Reliability of clinical monitoring to assessblood volume in critically ill patients. Crit Care Med. 1984;12:107-112.

97. Ferrer R, Artigas A, Suarez D, et al; Edusepsis Study Group. Effectivenessof treatments for severe sepsis: a prospective, multicenter, observationalstudy. Am J Respir Crit Care Med. 2009;180(9):861-866.
