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Pulmonary Artery Pressure MonitoringWhen, How, and What Else to Use

AACN Advanced Critical Care

Volume 17, Number 3, pp.286–305

© 2006, AACN

Elizabeth J. Bridges, PhD, RN, CCNS

Adebate continues over the utility of pul-monary artery (PA) catheters in the man-

agement of critically ill patients. In 1996, a ret-rospective study1 evaluating the use of PAcatheters in 5735 critically ill patients sug-gested that PA catheter use may increase mor-bidity and mortality. As a result of this re-search and the lack of studies demonstrating abeneficial effect associated with PA catheteruse, several consensus conferences have beenheld.2–4 Based on these consensus conferences,the patient populations for which PA pressuremonitoring may be beneficial or additionaloutcome studies that are needed include: sepsis/septic shock, acute respiratory distress syn-drome (ARDS), severe refractory heart failure,high-risk surgical patients, and low/moderate-risk surgical patients undergoing high-risk sur-gical procedures.

Since the consensus conferences, a meta-analysis and 4 major outcomes trials have

The integration of data from a pulmonary

artery catheter when used as part of a goal-

directed plan of care may benefit certain

groups of critically ill patients. Integral to

the successful use of the pulmonary artery

catheter is to accurately obtain and interpret

invasive pressure monitoring data. This

article addresses commonly asked clinical

questions and considerations for decision

making under complex care conditions,

such as obtaining hemodynamic measure-

ments when the patient is prone or has

marked respiratory pressure variations or

increased intraabdominal pressure. Recom-

mendations to optimize the invasive pres-

sure monitoring system are presented.

Finally, functional hemodynamic indices,

which are more sensitive and specific in-

dices than static indices (pulmonary artery

and right artrial pressure) of the ability to re-

spond to a fluid bolus, will be introduced.

Keywords: functional hemodynamics, he-

modynamic monitoring, pulmonary artery

catheter

A B S T R A C T

Elizabeth J. Bridges is an Assistant Professor, Biobehavioral

Nursing and Health Systems, University of Washington

School of Nursing, 1959 NE Pacific St, Seattle, WA 98195

(e-mail: ebridges@u.washington.edu).

been completed to evaluate the effects of theuse of PA catheters as a part of care. The meta-analysis5 of 13 randomized clinical trials foundno difference in mortality or length of stay be-tween groups of patients who were random-ized to PA catheter versus no PA cathetergroups. The Evaluation Study of CongestiveHeart Failure and Pulmonary Artery Catheter-ization Effectiveness (ESCAPE)6 evaluated theefficacy and safety of PA catheter use in pa-tients with acute heart failure. In this study,6

endpoints for resuscitation were specified, butthere were no standardized recommendationsfor the use of diuretics or inotropic agents. Thestudy found that the use of a PA catheter didnot increase or decrease the mortality or

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length of stay for acute heart failure patients;however, the group that received PA catheteradjusted therapy had a greater improvement inquality of life and a trend toward improvedexercise capacity. The Pulmonary ArteryCatheter in the Management of ICU Patients(PAC-Man) study7 evaluated PA catheter ver-sus use of an alternative method for cardiacoutput monitoring (eg, transesophagealDoppler) in critically ill patients with ARDS,heart failure, and multiorgan dysfunction.7 Nospecific treatment guidelines or endpoints wereused. There was no significant difference be-tween groups in ICU or 28-day mortality; al-though, in the PA catheter group, 80% of pa-tients had a change in treatment made within 2 hours of insertion. The Sepsis Occurrence inAcutely Ill Patients (SOAP) study8 was an ob-servational study that evaluated the possibleassociation between PA catheter use and out-come. Although patients with PA cathetershad a higher mortality rate, when confoundingfactors such as acuity, age, organ dysfunction,and comorbidities were controlled for, the useof a PA catheter was not independently associ-ated with a higher risk of 60-day mortality.8

Finally, a study9 of the use of PA catheters in patients with shock, ARDS, or both foundno difference in 14 or 28-day mortality in pa-tients treated with routine (nonstandardized)treatment.9

A critical point when reviewing these stud-ies is that the insertion of a PA catheter andsimply monitoring hemodynamic indices doesnot improve outcomes.10 In addition, it may beinsufficient to specify endpoints as goals to bemet and not specify the most effective treat-ment regimen to reach these endpoints.6 He-modynamic indices (to include perfusion in-dices)11 should be used as a part of anevidence-based treatment plan aimed at opti-mizing tissue perfusion before organ dysfunc-tion occurs,12,13 as exemplified by the improvedoutcomes associated with goal-directed ther-apy for patients with septic shock,14 high-risksurgical patients,15–17 and postcardiac surgerypatients.18–19 The challenge remains to identifywhich hemodynamic indices and types ofmonitoring devices (eg, PA catheter, noninva-sive pressure and cardiac output monitors,perfusion indices) improve outcomes, to iden-tify specifically which patient populations (ie,patient type, etiology of shock, severity of ill-ness, and timing of interventions) will benefitmost from the integration of hemodynamic

data into their care, and to develop populationspecific protocols.13–20

Although there are clinical conditions inwhich the integration of hemodynamic datamay improve diagnostic accuracy21 and inte-gration of hemodynamic data into a plan ofcare will improve outcomes, there are 2 gen-eral areas that limit the utility of PA pressuremonitoring. First, critical care clinicians (nurseand physicians) may incorrectly gather and in-terpret the data.22–26 Several excellent resourcesto improve the knowledge and ability to inter-pret and use PA pressure data are the Pul-monary Artery Catheter Education Program(PACEP),27 which is a series of Web-basedtraining modules that cover clinical and tech-nical aspects of care and waveform interpreta-tion and AACN’s Practice Alert: PulmonaryArtery Pressure Monitoring.28 Second, whilethe pulmonary artery occlusion pressure(PAOP) provides useful information regardinghydrostatic pressure and the risk for pul-monary edema, static hemodynamic indices(RAP, PAOP) are not sensitive or specific indi-cators of preload or fluid responsiveness. Theremaining sections of this article focus on: (1)a review of factors that affect the reliabilityand accuracy of hemodynamic indices (ie, ze-roing, referencing, dynamic response charac-teristics, and filter frequency), (2) how to in-terpret the hemodynamic data within thecontext of complex care situations (eg, pron-ing, marked respiratory variation, cardiogenicversus noncardiogenic pulmonary edema), and(3) functional hemodynamic measures, whichare an alternative to static hemodynamicmeasurements.

Factors That Affect the Reliabilityand Accuracy of PulmonaryArtery/Right Atrial PressuresZeroingZeroing of the pressure monitoring system isperformed by opening the system to air to es-tablish atmosphere as zero. The currenttransducers have minimal zero drift and donot require routine rezeroing.29 Of note, reze-roing is not the same as rereferencing, whichis required with any change in the patient’sposition relative to the transducer. A recom-mendation based on older transducer tech-nology was that the pressure system shouldbe rezeroed with changes in barometric pres-sure, such as those that occur with a changein the weather or ascent to altitude during

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aeromedical transport. The current pressuretransducers are vented to air and do not re-quire routine rezeroing with a change inbarometric pressure.30

ReferencingReferencing, which is performed to correctfor the changes in hydrostatic pressure aboveand below the heart, is accomplished by plac-ing the air-fluid interface (stopcock) of thecatheter system at the level of the heart tonegate the weight effect of the catheter tubing.31 Numerous texts identify the midax-illary line as the reference point; however, inthe supine position use of the midaxillary lineas the reference rather than one-half the ante-rior/posterior diameter of the chest, may re-sult in a measurement error of 6 mm Hg inpatients with varied chest wall configura-tions.32,33 Similarly, the use of angle specificreferences is also required for the lateral posi-tion (see Figure 4).

Dynamic Response and FilteringThe dynamic response characteristics of thesystem affect the ability of the pressure moni-toring system to faithfully reproduce a pres-sure waveform. A method to evaluate and op-timize a pressure monitoring system has beenpreviously described.34 One key point in opti-mizing a pressure system is that air bubbles af-fect the dynamic response characteristics ofany pressure monitoring system. Thus, meas-ures must be taken during the set-up andmaintenance of the pressure system to removeair bubbles. The “rocket flush,” which is a 10 mL manual rapid flush of the system, start-ing at the proximal stopcock, is an additionalstep during line preparation to remove airfrom the system.35 The performance of a rocket

flush during line preparation significantly im-proves the dynamic response characteristics ofpressure monitoring systems (Figure 1).30 The“rocket flush” should never be performedwhen the system is attached to a patient be-cause of the risk of retrograde air emboliza-tion. A validated algorithm30 that decreases airbubble formation and optimizes the dynamicresponse characteristics of the pressure systemis provided (Table 1).

Adjusting the filter frequency limits on themonitor is often incorrectly attempted whenthe pressure system is underdamped or whenthere is catheter whip. To understand the func-tion of the filter, it is important to understandhow a waveform is created by the pressuremonitoring system. The oscillations caused bythe pressure wave striking the fluid in thecatheter causes distortion of the diaphragm inthe transducer and the creation of an electricalsignal. The electrical signal from the transduceris sent to the monitor where it is amplified, fil-tered, and converted to the waveform and digi-tal output observed on the monitor. The wave-form that is observed on the monitor is asummation of a series of sine waves or har-monics (Figure 2).36 For a patient with a heartrate of 60 beats per minute, the fundamentalfrequency (first harmonic) is equal to the pulserate and occurs at one cycle/second (1 Hz). Thesecond harmonic occurs at 2 Hz, the third har-monic at 3 Hz, etc. For a patient with a heartrate of 120 beats per minute, the first harmonicoccurs at 2 Hz, the second harmonic at 4 Hz,the third harmonic at 6 Hz, etc. The importantphysiological information is contained in thefirst 6 to 10 harmonics (12 to 20 Hz). Thus, thebandwidth of the filter on the monitor shouldbe set to allow for up to 12 to 20 Hz for a pa-tient with a heart rate of 120 beats per minute.

Figure 1: Effect of a “rocket flush” on the dynamic response characteristics of a pressure monitoring

system. A, Control: pressure system with a VAMP (PXVMP160; Edwards LifeSciences, Irvine, Calif.)

after standard set-up. Fn, 9 Hz; amplitude ratio, 0.3; dynamic response, underdamped. B, Same system

after a 10 mL “rocket flush.” Fn, 13 Hz; amplitude ratio, 0.4; dynamic response, adequate.

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Decreasing the filter frequency below 12 Hzmay cause the waveform to appear cleaner, butimportant physiological waveform informationis being filtered; thus, a true waveform is notbeing observed. Rather than adjusting the filterto clean up the waveform, attention should bepaid to optimizing the dynamic response char-acteristics of the system.

Pulmonary Factors There are numerous pulmonary factors thatadd challenges to accurately and reliably ob-taining PA pressure measurements: (1) the useof digital versus analog data, (2) how to deter-mine if the PA catheter tip is in the correct lungzone, (3) how to interpret the pressures whenthere is marked respiratory variation, and (4)interpretation of invasive pressures when thereis increased pleural pressure.

Analog Versus Digital DataAn assumption of invasive pressure monitor-ing is that the measured pressure (eg, pul-monary artery end diastolic pressure [PAEDP]/

Table 1: Invasive Pressure Monitoring Line Preparation

1. Wash hands.

2. Gather supplies (isotonic sodium chloride

solution IV bag, pressure monitoring kit, 10 mL

syringe, pressure bag).

3. Prime pressure monitoring system to remove all air.

a. Remove pressure monitoring kit from package,

open blood salvage reservoir (if present),

tighten connections, close roller clamp, turn

stopcock OFF to patient (off toward distal end of

the catheter), and remove vented stopcock caps.

b. Vent all air from the IV bag.

c. Invert bag (orient upside down) and using

sterile technique insert spike into IV bag.

d. Leave the spiked bag upside down, open roller

clamp, and simultaneously activate the fast-

flush device continuously while gently

applying pressure to IV bag to slowly clear air

from the IV bag and drip chamber. Completely

fill the drip chamber with IV fluid.

e. Turn the IV bag upright once the fluid is

sufficiently past the drip chamber.

f. Apply gentle pressure (50 mm Hg or hang the

IV bag approximately 30 inches above distal

end of tubing) and activate fast-flush device,

advance fluid, priming the tubing.

g. Orient the blood collection device (if using a

closed-system line) so that all air is removed

by the advancing fluid (tilt distal end up 45�).

h. Complete flushing the line and all stopcocks.

i. Inspect line for any air bubbles.

j. Rocket Flush (never perform when thesystem is attached to a patient)

1. Turn the stopcock off to the distal end of

the catheter

2. Attach 10 mL syringe to the stopcock near

the transducer using sterile technique and

slowly withdraw 10 mL of IV fluid into the

syringe.

3. Turn the stopcock off to the transducer.

4. Flush the pressure line quickly with 10 mL

isotonic sodium chloride solution from

the syringe to remove any remaining air

bubbles; avoid instilling any air into the

line.

5. Turn the stopcock off and remove the

syringe.

6. Cap the stopcock with a solid cap using

sterile technique.

4. Inspect the line, remove any remaining air by

flushing the line with the fast-flush. and repeat

the Rocket Flush.

5. Place IV bag into pressure bag and inflate to

250 to 300 mm Hg and recheck for air in the

line.

6. Perform dynamic response test.

Figure 2: A pressure waveform reflects the

summation of a series of sine waves or harmonics.

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PAOP) is an indicator of atrial and ventriculardistending pressure (transmural pressure). Tomeet this assumption, cardiac pressures aremeasured at end-expiration when juxtacardiacpressure is close to 0 mm Hg. The most accu-rate method for correctly identifying end-expi-ratory pressure is data interpretation from theanalog (hard copy) strip with a correspondingelectrocardiogram (ECG), followed by thestop-cursor method, with digital data from themonitor being the least reliable and accuratemethod.37 For example, with digital data, thePAEDP may be incorrectly identified as thelowest pressure on the PA waveform ratherthan the pressure immediately before the sys-tolic upstroke and without controlling for ven-tilatory-induced changes in pressure. (Note:To accurately identify the PAEDP, the pressureshould be measured 0.08 seconds after the on-set of the QRS complex from a simultaneouslyrecorded ECG strip.)38 The decrease in accu-racy for digital values compared to analogdata is important when deciding whether toautomate the downloading of hemodynamicdata into a clinical information system.

Lung ZonesOne of the first questions to ask when deter-mining if the PAOP accurately reflects leftatrial/ventricular pressures is if the PA cathetertip is in a Zone III vascular field (pulmonary ar-terial pressure [Pa] � pulmonary venous pres-sure [Pv] � pulmonary alveolar pressure (PA).In a Zone III vascular bed during diastole, there

is a continuous column of blood between thePA catheter and the left heart; thus end-dias-tolic pressures measured by the PA catheter re-flect end-diastolic left atrial and ventricularpressures (ie, preload). Clinical clues to detectif the catheter is not in a Zone III vascular bedare summarized in Table 2. Monitoring fornon-Zone III catheter tip placement should beundertaken whenever there is an increase inalveolar pressure (PEEP) and/or a decrease inintravascular volume. One technique to in-crease the likelihood of a Zone III vascularmeasurement is to laterally rotate the patientsuch that the catheter tip is below the leftatrium. For example, in a patient with the PAcatheter in the right pulmonary artery, posi-tioning the patient in the right lateral positionwill place the catheter tip below the left atrium.PA pressure measurements obtained in the 30�and 90� lateral positions are comparable tosupine values as long as an angle-specific refer-ence is used.39,40

Respiratory VariationActive exhalation may increase end-expira-tory pressure. An increase in end-expiratorypressure and the overestimation of the PAOPby as much as 10 mm Hg should be suspectedif there is a greater than 10 to 15 mm Hg res-piratory-induced fluctuation in the PAOP.With marked respiratory variation, the PAOPmeasured at the mid-point between end-expi-ration and the end-inspiratory (nadir) pres-sure is independent of the degree of respira-tory variation and is a better estimate of leftventricular pressure than the end-expiratoryvalue (Figure 3).41

Different mechanical ventilator strategiesmay also affect PA pressure measurements.For example, inverse ratio ventilation, whichdecreases end-expiratory time and increasesend-expiratory lung volumes, may cause anoverestimation of the PAOP. In this case, useof the airway pressure waveform may help toidentify the end-expiratory phase and consid-eration should be given to the need to correctfor PEEP and auto-PEEP. With airway pres-sure release ventilation (APRV), the PAOPshould be measured at the end of the positivepressure plateau,42 which can be observed onthe ventilator and is the point immediately be-fore release of airway pressure and the initia-tion of inspiration. The addition of an airwaypressure signal to the analog tracing may alsoimprove the accuracy of pressure interpretation,

Table 2: Indicators of non-Zone IIIPulmonary Artery Catheter Placement*

• Tip of the PA catheter above the left atrium on a

lateral chest radiograph

• Smoothed PAOP waveform (cannot clearly

visualize the a/v waves)

• PAEDP � PAOP

• Respiratory variation in PAOP � respiratory

variation in PAEDP107

• PAOP increases �50% of an increase in PEEP (eg,

increase PEEP from 5 to 10 cm H2O

(approximately 3.7 mm Hg) and PAOP increases

� 1.9 mm Hg)

*Zone I: PA > Pa > Pv; Zone II: Pa > PA > Pv; Zone III: Pa > Pv > PA.PA, pulmonary alveolar pressure; Pa, pulmonary arterial pressure;PV, pulmonary venous pressure; PA, pulmonary artery; PAOP,pulmonary artery occulusion pressure; PAEDP, pulmonary artery enddiastolic pressure ; PEEP, positive end-expiratory pressure.

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particularly in patients with marked respira-tory-induced pressure variation.43

Increased Pleural PressurePleural pressure may be increased by extrinsicpositive end expiratory pressure (PEEP) or in-trinsic pressure (auto-PEEP), which may leadto an overestimation of the PAOP. In general,PEEP �10 cm H2O does not significantly af-fect the PAOP. However, when PEEP �10 cmH2O is applied, the PAOP should be correctedto account for the pressure that is transmittedto the pleural space. Under conditions of nor-mal lung and chest wall compliance, the pleu-ral pressure will increase by one-half the ap-plied PEEP.44 However, in patients with ARDSwith decreased lung and chest wall compli-ance, a variable amount (1/4 or less) of the ap-plied PEEP may be transmitted to the pleuralspace. Thus, for a patient on 15 cm H2O PEEP(11 mm Hg), a rough correction estimate isthat the PEEP would cause an artifactual in-crease in the PAOP of approximately 3 mmHg. The effect of auto-PEEP should also beconsidered. In contrast to extrinsic PEEP,auto-PEEP, which is often associated with in-creased lung compliance, may transmit agreater percentage of the pressure to the pleu-ral space, with further overestimation of theactual PAOP.

Intraabdominal hypertension (IAH) (in-traabdominal pressure [IAP] �15 mm Hg),which increases pleural pressure, is present inapproximately 20% of critically ill patients onadmission.15–17 Intraabdominal hypertensiondecreases venous return, cardiac output, andventricular compliance and increases intratho-racic and pleural pressures, causing an artifac-tual increase in RAP and PAOP, despite a de-crease in transmural filling pressures andpreload.46,47 Possible solutions for interpretinghemodynamic pressure data in the presence ofintraabdominal hypertension (if resolution ofIAH is not possible) include correction for theeffect of the IAP on pleural pressure (approxi-mately 60% to 70% of the IAP is transmittedto the pleural space),48 the use of volumetricmeasurements or the use of functional hemo-dynamic indices.49 The correction for increasedIAP may not be necessary if the IAP is �15mm Hg; although, further studies are neededin this area.

Finally, position induced changes in in-trathoracic pressure (eg, Trendelenburg) havelead to the misinterpretation that head downposition is beneficial for patients with de-creased blood pressure.50 In a study51 of pa-tients placed in a 30� Trendelenburg position,the RAP increased from 9 to 12 mm Hg andthe PAOP from 8 to 11 mm Hg, despite a rela-tively small increase (20 to 40 mL/m2) in in-trathoracic blood volume. The increase in theRAP and PAOP was due primarily to a position-induced increase in intrathoracic pressure andnot an increase in cardiac volume. Failure torecognize this artifactual increase in RAP orPAOP may lead to inadequate resuscitation.

Position The practice of positioning the patientflat/supine for PA pressure measurements con-tinues despite numerous well-designed studiesdemonstrating clinically insignificant changesin PA pressures in a variety of patient popula-tions in the supine and backrest elevated posi-tion between 30� to 60�.52 One argument fre-quently cited as a rationale for using thesupine position is that for cardiac patients, theinitial pressure measurements were obtainedin the cardiac catheterization lab where the pa-tient was supine; and for comparison, all pres-sures should be standardized to this position.The following questions should be addressedin informing clinical practice related to patientpositioning for hemodynamic measures: (1)

Figure 3: Top: Pulmonary artery occlusion pressure

tracings showing the end expiratory, end inspiratory

(nadir), and the midpoint values in a patient with

marked respiratory variation. Bottom: PAOP in same

patient postmuscle relaxation with paralytic.

Reprinted with permission from Hoyt JD,

Leatherman JW. Interpretation of the pulmonary

artery occlusion pressure in mechanically ventilated

patients with large respiratory excursions in

intrathoracic pressure. Intensive Care Med.

1997;23(11):1126.

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Are there studies in a given patient population(heart failure, ARDS, sepsis, cardiac surgery)that describe the differences in hemodynamicindices (eg, PA pressures, cardiac output) in thesupine versus backrest elevated position orsupine versus lateral position? (2) Are therephysiologically important changes that occurwith repositioning from head of bed elevatedto the supine position? For example, what arethe clinical consequences of the increased or-thopnea observed in patients with heart failurein the supine position? (3) Are the observedpressure differences in the supine compared tohead of bed elevated or lateral position greaterthan the normal variability of the pressuresgiven the patient’s underlying ventricular func-tion? (Normal ventricular function: PAS/PAEDP � 5 mm Hg; PAOP � 4 mm Hg;39 leftventricular dysfunction: PAS � 7 mm Hg or < 8%, PAEDP � 6 mm Hg or � 11%; PAOP� 5 mm Hg or �12%.53) A decision-makingalgorithm54 outlines a process to systematicallyevaluate a patient’s hemodynamic response tovarious positions (Figure 4.)

Prone positioning is used to treat patientswith acute respiratory distress syndrome(ARDS). Hemodynamic measurements aremost often obtained with the patient in thesupine position, which may be the most physi-ologically unstable position for these patients.The patients are subsequently rotated to theprone position for prolonged periods of time,and therapeutic decisions may be made basedon the supine measurements. In several studies,55–57 there were no significant differ-ences in PAOP, RAP, or CO measured 30 to 60minutes after rotation from supine to prone onstandard hospital or air-suspension beds. Aconcern with proning is the potential negativeeffect of abdominal compression and increasedintraabdominal pressure. In non-ARDS med-ical and surgical patients, proning caused a de-crease in venous return and thus cardiac out-put, despite an artifactual increase in measuredPA and RAP pressures.58–60 However, thesefindings have not been found in ARDS pa-tients, as demonstrated in a study61 of the he-modynamic response to manual proning on anair flotation mattress without relief of abdomi-nal pressure. In this study,61 pressure measure-ments were obtained 60 minutes after the position change (supine [S]/prone [P]). The in-traabdominal pressure increased from S: 10 �3 mm Hg to P: 13 � 4 mm Hg (NS), the MAPincreased from S: 75 � 10 mm Hg to

P: 81 � 11 mm Hg (P � .05) and CI increasedfrom S: 3.8 � 0.9 L/min/m2 to P: 4.2 � 0.6L/min/m2(P �.05). There was no significantchange in heart rate (S: 78 � 16 bpm; P: 82 �16 bpm), RAP (S: 16 � 5 mm Hg; P: 15 �5 mm Hg), or intrathoracic blood volume (S: 1008 � 187 mL/m2; P: 1036 � 180 mL/m2).This study,61 and a second study with similarresults,62 are important as they demonstrate aminimal increase in intraabdominal pressureand no significant change in intrathoracic vol-ume in the prone position; both of which arefactors that affect PA pressures. Areas that re-quire further exploration are the time for sta-bilization of hemodynamic pressures afterproning, the effects of proning patients withpreexisting intraabdominal hypertension onPA pressures, the effect on PA pressures ofproning beds that encase the patient withpadding and may increase thoracic/abdominalpressure (eg, RotoProne Bed, KCI, San Anto-nio, TX), and methods to obtain hemody-namic measurements in patients undergoingcombined proning and kinetic therapy.

Clinical Presentation and Cardiac Index/PAOPMany critical care nurses are taught a generalassessment of the patient’s perfusion status(cold/warm) and pulmonary congestion (wet/dry), but may not be aware of the exact rela-tionship between this clinical characterizationand the patient’s cardiac index and PAOP. In1977, the clinical subsets (ie, Forrester subsets)for patients with acute myocardial ischemia/infarction were described.63 According to thesubsets (Figure 5), a cardiac index (CI) �2.2L/min/m2 is consistent with clinical hypoperfu-sion (hypotension, tachycardia, confusion,oliguria, and cyanosis) and a PAOP �18 mmHg is consistent with pulmonary congestion(crackles, abnormal chest radiograph).63 A keypoint regarding the CI and PAOP cutoff pointsis that they were derived in patients with anacute myocardial infarction, who most likelyhad an intact alveolar capillary membrane andnormal colloid osmotic pressure. The impor-tance of these factors with regard to hypoper-fusion and pulmonary congestion is explainedby the Starling equation for fluid flux:

Q � k [Pcap � Pint] – �[πcap – πint]

Hydrostatic Oncotic pressure pressure

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Figure 4: A decision-making algorithm: patient position for pulmonary arterial pressure monitoring.

Adapted with permission from Gawlinski, A. Facts and fallacies of patient positioning and hemodynamic

measurement. J Cardiovasc Nurs. 1997;12(1):1–15.

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where Q is the outward flow of fluid acrossthe capillary membrane, k is the filtration co-efficient (reflecting membrane permeability),Pcap and Pint are the intravascular and intersti-tial hydrostatic pressure, � is the reflection co-efficient for proteins and πcap and πint are theintravascular and interstitial colloid osmoticpressures. In critically ill patients, such asthose with acute respiratory distress syndromeor septic shock, the alveolar capillary mem-brane may be damaged, which affects the fil-tration coefficient, and the colloid osmoticpressure may be decreased. In addition, inARDS or any condition that increases pul-monary venous resistance, the PAOP may un-derestimate the pulmonary capillary pressure(Pcap) by 6 to 8 mm Hg.64,65 A rough approxi-mation is that the Pcap is greater than the PAOPby approximately 40% of the difference be-tween the mean PA pressure and the PAOP(Pcap � PAOP 0.4[PAM – PAOP]) or 2/3 ofthe difference between the PAEDP and PAOP(Pcap � PAOP 0.66[PAEDP-PAOP]).66,67 Thus,under conditions, such as ARDS or septicshock, hydrostatic pulmonary edema may occur at a lower intravascular pressure (ie,PAOP �18 mm Hg).66,68 In addition, in septicshock, myocardial contractility may be alsodecreased despite a normal or increased CI.69,70

Thus, in ARDS and septic shock, the PAOPand CI values must be interpreted with an un-derstanding of the contrast in pathophysiologycompared to an acute MI.

Functional HemodynamicMonitoringThe RAP and PAOP are the traditional pre-load indices used to guide decisions regardingfluid volume therapy. Various recommenda-tions have been set regarding optimal fillingpressures. For example, in the initial volumeresuscitation phase of septic shock, a PAOPbetween 12 to 15 mm Hg is recommended.71,72

However, several assumptions must be met ifthe RAP or PAOP are to be used as indicatorsof end-diastolic volume (Table 3). The pri-mary assumption (pressure � volume) isproblematic because the relationship betweenPAOP and left ventricular end-diastolic vol-ume is curvilinear and different for each indi-vidual; thus, neither an absolute PAOP nor achange in PAOP is reflective of an absoluteend-diastolic volume.68,73 Given the requiredassumptions to establish a relationship be-tween pressure and volume, it is not surpris-ing that there is a poor relationship betweenRAP/PAOP and CI/stroke volume (SV). Al-though measurement of the PAOP remains anindicator of the patient’s risk for the develop-ment of hydrostatic pulmonary edema,68

changes in more direct volumetric indices (eg,stroke volume variation, right and left ven-tricular end-diastolic volume, and intratho-racic blood volume) have a better relation-ship to changes in CI or SV, and may bebetter measures of preload.73–76 In addition,the absolute values of the RAP and PAOP failto differentiate between which patients willincrease their cardiac output in response to afluid challenge (responders) in contrast tothose patients that will not (nonresponders)(Table 4).73,77,78 The latter concern is impor-tant as clinicians need to be able to predict ifa patient with clinical indications of hypoperfusion will respond to a fluid volumechallenge or whether fluid administrationwill cause further cardiopulmonary compro-mise.79,80

Functional hemodynamic indices have beensuggested to better predict which patients willrespond to fluid challenges. These dynamicmeasurements provide insight into the effect ofchanges in intrathoracic pressure on cardiacfunction. To understand why dynamic meas-urements may be more accurate indicators ofpreload dependence than static indices(RAP/PAOP), a review of the relationship be-tween ventilatory-induced changes in intratho-racic pressure and right- and left-heart SV isprovided.

During spontaneous inspiration, pleuraland intrathoracic pressures decrease, with aresultant decrease in RAP. With a decrease inRAP, which is the back pressure to venous fill-ing, venous return increases transiently. Thisincrease in venous return results in an inspira-tory increase in right ventricular (RV) preloadand output (assuming the right ventricle is on

Figure 5: Subsets characterizing the relationship

between clinical presentation and hemodynamic

status in patients with an acute myocardial infarction.

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the steep portion of the ventricular functioncurve). However, if the right ventricle cannotfurther dilate (eg, RV failure), the RAP will notdecrease during inspiration, which indicates

that the right atrium/ventricle are on the flatportion of the cardiac function curve, and theadministration of additional volume will notincrease RV output (nonresponder).81,82

Table 3: Assumptions Underlying Use of Pulmonary Artery Occulusion Pressure asIndicator of End-Diastolic Volume

Assumption Examples of Factors That Negate Assumption

1. Pressure � Volume Pressure-volume relationship is curvilinear

Alteration in ventricular compliance

• Myocardial ischemia/infarction

• Position on the ventricular function curve (steep vs flat

portion)

• Intropic drugs

• Cardiac tamponade/effusion

2. PAOP � LAP Pulmonary venous obstruction

• Atrial myxoma

• Pulmonary venous thromboembolism

3. LAP = LVEDP • Mitral stenosis

• Decreased LV compliance

4. Measured pressure = transmural pressure • Increased intrathoracic pressure (PEEP or auto-PEEP)

(intrathoracic pressure � 0 mm Hg)• Increased intraabdominal pressure causes increase in

intrathoracic pressure

PAOP, pulmonary artery occlusion pressure; LAP, left atrial pressure; LVEDP, left ventricular end diastolic pressure; PEEP, positive endexpiratory pressure.

Table 4: PAOP and RAP Values in Responders and Nonresponders

Indicator Responder Nonresponder P

RAP

Critically ill sepsis/cardiac108 5 � 1 5 � 2 NS

Critically ill patients109 9 � 4 8 � 4 NS

Sepsis/septic shock77 9 � 3 9 � 4 NS

PAOP

Critically ill sepsis/cardiac108 8 � 1 7 � 2 NS

Critically ill patients109 10 � 4 10 � 3 NS

Trauma patients110 16 � 6 15 � 5 NS

Septic shock90 10 � 4 12 � 3 NS

Postcardiac surgery111 12 � 2 16 � 3 �.01

Sepsis/septic shock77 10 � 3 11 � 2 NS

PAOP, pulmonary artery occlusion pressure; RAP, right atrial pressure; NS, not significant.

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During positive pressure mechanical venti-lation, the inspiratory increase in intrathoracicpressure decreases venous return to the heartand increases RV afterload (Figure 6). Thesechanges lead to a decrease in RV stroke vol-ume during inspiration. The decreased RVoutput causes a decrease in left ventricular(LV) preload, which after a few heart beats,decreases LV stroke volume, usually during ex-piration. Thus, the LV stroke volume increasesduring inspiration due to compression of thepulmonary bed and decreases during expira-tion, primarily due to decreased RV output.83–85

Observation of the ventilatory-induced changesin SV can be exploited, based on the findingthat RV preload and SV changes are greaterwhen the ventricle is on the steep versus theflat portion of ventricular function curve.86

The increased RV output is transmitted to theleft heart, and if both ventricles are preload de-pendent, the increased LV preload will be ob-served as a cyclic change in LV stroke volume.The assumption underlying the interpretationof the cyclic SV changes is that a greater cyclic

change is indicative of preload dependence (ie,a patient that will respond to volume loadingwith an increase in SV), whereas a smaller SVchange indicates preload independence. Pa-tients who are preload independent will not in-crease their SV in response to volume loadingand may in fact be compromised by the excessfluid. The cyclic changes in LV stroke volumeare particularly important, as the SV is a pri-mary contributor to the systolic blood pres-sure (SBP) and pulse pressure (PP); thus, varia-tions in SBP, PP, or SV may indicate preloaddependence or independence.

Respiratory Variation in Right Atrial PressureAlthough the absolute RAP has not beenfound to be predictive of which patients willrespond to a volume challenge,77,81 the inspira-tory change in RAP (RAP) may be a usefulpredictor. In medical and cardiac surgery patients who demonstrated an adequate spontaneous inspiratory effort (defined as aninspiratory decrease in PAOP �2 mm Hg), a

Figure 6: Hemodynamic effects of mechanical insufflation. The left ventricle (LV) stroke volume is

maximal at the end of inspiratory period and minimum 2 to 3 heartbeats later during the expiratory

period. The cyclic changes in LV stroke volume are mainly related to the expiratory decrease in LV

preload due to the inspiratory decrease in RV filling and output. Reprinted with permission from

Michard F, Teboul JL. Using heart-lung interactions to assess fluid responsiveness during mechanical

ventilation. Critical Care. 2000;4(5):282.

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spontaneous inspiratory decrease in RAP �1 mm Hg is a positive response (responder),whereas a decrease �1 mm Hg is a negative re-sponse (nonresponder) (Figure 7). For example,in response to a 250 to 500 mL saline fluid bo-lus, 16 of 19 patients in the responder groupdemonstrated an increase in cardiac output ofgreater than 250 mL. Conversely, only 1 of 14patients in the nonresponder group demon-strated an increase in cardiac output. Of note,there were no differences in the baseline RAP,PAOP, or cardiac output between the 2 groups(ie, these values did not aid in determiningwhich patients would or would not respond tovolume loading).81 Similar results were ob-served in a second study87 involving postcar-diac surgery patients. The authors of thesestudies87 suggest that the particular value ofthe RAP is in identifying patients with lowcardiac output who will not respond to fluidvolume expansion, thus avoiding potentiallydeleterious volume overload. An advantage ofthe RAP, unlike the other functional indicesdiscussed in the following sections, is that itcan be measured in a spontaneously breathingpatients, rather than requiring that the patientbe mechanically ventilated and heavily sedatedand/or paralyzed.

Respiratory Variation in Arterial Systolic PressureWith positive pressure inspiration, the RVstroke volume decreases during inspiration.After several beats, the decrease in RV strokevolume is transmitted to the left heart, with asubsequent decrease in LV stroke volume.Stroke volume affects SBP; thus, the ventila-tory-induced change in SV may be observed asa change in SBP. In mechanically ventilated pa-

tients, the systolic pressure variation (Ps) isnormally 8 to 10 mm Hg (Figure 8).88 The Psis described as an absolute value (mm Hg) or apercentage (Ps%), which is described by thefollowing equation:

Ps% � 100 � (Psmax – Psmin)/[(PSmax Psmin)/2]

The Ps is equivalent or more sensitive tovolume-induced changes in CI than thePAOP.89,90 For example, in a group of a venti-lated patients (VT 6 to 12 mL/kg) with acutecirculatory failure related to sepsis, the Ps%was significantly higher in responders (15�5%) than nonresponders (6 � 3%).77 In an-other group of patients undergoing abdomi-nal aortic surgery, a Ps �12 mm Hg wasonly observed in patients with overt hypov-olemia. In one patient in this study,91 duringthe postoperative period, the Ps increasedto �10 mm Hg, which led to the suspicion ofintraabdominal hemorrhage and subsequentreturn to the operating room. In contrast, ina study89 of cardiac surgery patients, al-though the Ps was greater in responders(8.2 � 3.9 mm Hg) than nonresponders (5.3� 2.6 mm Hg), only a pulmonary artery occlusion pressure (PAOP) �10 mm Hg waspredictive of volume response. Note in thislatter study89 that although the respondershad a higher Ps, the Ps did not exceed 10 mm Hg; thus, the lack of predictive abilitywould be expected.

The Ps may also be a useful indicator ofblood loss, particularly occult blood loss thatoccurs before changes occur in the heart rateor blood pressure.92–95 In a study93 of mechani-cally ventilated patients (VT � 10 mL/kg) whohad 500 and 1000 mL of blood phle-botomized, the Ps increased from 9.5 � 4.6mm Hg (Ps% � 9.1 � 5.3%) at baseline to14.3 � 6.5 mm Hg (Ps% � 15.2 � 7.5%) at500 mL blood loss, and 19.6 � 7.5 mm Hg(Ps% � 21.2 � 13.1%) at 1000 mL bloodloss. In this study,93 a Ps of 5 mm Hg or lesswas considered indicative of an absence of hy-povolemia. Similar results were observed incardiac surgery patients on mechanical venti-lation (VT � 8 mL/kg) who were phle-botomized 500 mL over 10 minutes. In thisstudy, the Ps increased from 14 �6 mm Hgat baseline to 18 � mm Hg postbleed. That is,an increase in the Ps of approximately 4 mmHg was indicative of a significant blood loss,

Figure 7: An example of a patient with a positive

ventilatory response in right atrial pressure. Reprinted

from J Crit Care 7(2), Magder S, Georgiadis G,

Cheong T, Respiratory variation in right atrial pressure

predict the response to fluid challenge, p. 79, 1992,

with permission from Elsevier. Pra, right atrial

pressure; INSP, inspiration.

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and in all patients whose blood loss exceeded20% of their circulating volume the Ps ex-ceeded 15 mm Hg.92

Questions remain if the Ps solely reflects achange in SV or whether other factors (eg,lung and chest wall compliance, transmuralpressure, and tidal volume) contribute to theobserved change.91,95,96 However, if these fac-tors are kept constant, the Ps may be a usefulindicator of preload dependence and occulthemorrhage.

Respiratory Variation in Arterial Pulse Pressure Arterial pulse pressure is the difference be-tween the arterial systolic and diastolic pres-sure. Three factors affect the pulse pressure:LV stroke volume, arterial resistance, and arte-rial compliance. Of note, the latter 2 factorsdo not change enough during a single breathto change the beat-to-beat pulse pressure82,97;therefore, the beat-to-beat changes in pulsepressure reflect changes in LV stroke volume.Additionally, unlike the SBP, which is affectedby pleural pressure changes, the pulse pressureis affected only by the SV, as the pleural pres-sure affects the systolic and diastolic pressureequally.

Pulse pressure variation (Pp) is the vari-ability in the difference in the pulse pressureduring mechanical ventilation as defined bythe following equation:98

Pp% � [(PPmax – PPmin)/(PPmax PPmin)/2] � 100

In a study77 of patients with septic shock onmechanical ventilation (VT � 8 to 12 mL/kg),a Pp of 13% of the baseline pulse pressure(eg, if the baseline pulse pressure � 40 mmHg, a 13% change is equal to approximately 5 mm Hg) discriminated between respondersand nonresponders (CI increased �15%) to a500 mL colloid bolus with 94% sensitivity and96% specificity, and was a more sensitive indi-cator than a change in Ps, PAOP, or RAP. Animportant finding in this study was that thegreater the Pp before volume expansion, thegreater the CI response to the fluid bolus. Af-ter volume expansion, the Pp decreased, indi-cating less preload dependence. This latterfinding indicates that the change in the Ppfrom before to after a fluid bolus may be use-ful to determine if the patients requires addi-tional volume expansion.

There are limitations to the use of func-tional measurements. The Ps and Pp can bedetermined only in patients who are on con-trolled ventilation and deeply sedated and/orparalyzed. Changes in tidal volume and pul-monary compliance will alter the magnitude ofthe response. Most of the studies have beenconducted with tidal volumes (10 mL/kg). Re-search is ongoing to evaluate the sensitivityand specificity of these indices under condi-tions of lower tidal volumes (6 mL/kg) asdemonstrated in Figure 8. Significant cardiacdysrhythmias may negate the utility of theseindices and a majority of the studies were con-ducted in patients with relatively normal ven-tricular function; thus, recommendations forpatients with decreased right or left ventricularfunction are limited.85

Stroke Volume VariationA change in LV stroke volume is the primaryfactor that affects beat-to-beat changes inpulse pressure. The LV stroke volume also af-fects the aortic flow, which can be observed asbeat-to-beat changes in SV. Stroke volumevariation (SVV), which can be continuouslymeasured using pulse contour analysis (a newtechnique using a specialized transducerplaced in the femoral, brachial, or axillaryartery), is defined as the change in SV over a30-second period:

SVV � SVVmax – SVVmin/SVVmean

The assumption underlying SVV is that the ob-served SV changes are respiratory-inducedvariations. As with other volumetric measure-ments, the SVV is more closely associated withchanges in SV than are changes in the PAOPand RAP.99,100

The SVV is predictive of fluid response in avarious patient populations. In patients under-going brain surgery (VT � 10 mL/kg), a SVV of9.5% discriminated between responders andnonresponders (defined as an increase in SV�5% in response to a 100 mL colloid bolus),with a sensitivity of 79% and a specificity of93%.101 In cardiac surgery patients (VT � 13to 15 mL/kg), SVV decreased from 11.8 �7.5% to 5.4 � 4.2% after a bolus of 500 mLcolloid, and was correlated with the change inCI (SVV r � –0.64, P �.005).102 In anothergroup of off-pump bypass surgery patientswith preserved left ventricular function, theSVV and Pp were the most sensitive and

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Figure 8: (Continues).

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specific indices of fluid volume responsive-ness.103 Additionally, unlike other functional(Ps) or volumetric indices (intrathoracic bloodvolume), in patients with decreased left ven-tricular function (EF �35%), SVV was relatedto changes in SVI, although no predictive cut-off value has been identified.104

Concerns regarding the measurement ofSVV include the method used (direct measure-ment versus pulse contour analysis).105 Becausethe technology to perform SVV analysis is pro-prietary and it has changed over the past fewyears, comparison of results from the variousmethods is difficult. Additionally, cautionmust be taken when interpreting absolute pre-dictive values, as the SVV% varies dependingon the tidal volume. For example, the SVV be-fore volume loading for 3 different tidal vol-umes were significantly different (SVV 5mL/kg � 7 � 0.7%; SVV 10 mL/kg � 15 �2%, SVV 15 mL/kg � 21 � 2.5%); thus, inter-pretation of the sensitivity and specificity ofexact cutoff point can only be performed inthe context of a standardized tidal volume.106

To achieve a stable tidal volume, SVV analysiscan be performed only in patients who are oncontrolled mechanical ventilation and areheavily sedated/paralyzed.

Clinical Example You are caring for a patient with fibrotic lungdamage due to chemotherapy and radiationand pulmonary tumor metastasis complicatingARDS and septic shock. The patient is me-chanically ventilated (VT � 7 mL/kg, PEEP �12 cm H2O) and sedated. SBP: approximately80 mm Hg; PAOP: 16 mm Hg; CI: 2.4 L/min/m2,and SaO2 89%. Overnight, the interpretationof the patient’s hemodynamic status was chal-lenging, given the potential artifactual increasein PAOP and optimizing the patient’s preloadwithout causing hydrostatic pulmonary edema.The challenging clinical interpretation resultedin the patient being treated first with fluids,followed by diuretics in attempt to increase hisblood pressure and cardiac output withoutcompromising his tenuous pulmonary status.Currently, his Ps is 4 mm Hg. Should this pa-tient be given a fluid bolus to improve his SBPand CI? Answer: No. The Ps indicates thatthe patient will not respond to fluids. In thiscase, 2 decisions were made. First, the alteredpulmonary status was primarily related to theunderlying pulmonary disease, which couldnot be resolved. Adjustments to the ventilatoryparameters would be used to optimize the pa-tient’s oxygenation. Second, if the patient

Figure 8: (Continued) Example of changes in functional indices (Ps, Ps%, and Pp%) in an

experimental animal hemorrhage model (assist-control ventilation, VT � 8 mL/kg). Operating room baseline

� post-50% total blood volume hemorrhage followed by resuscitation with 500 mL Hextend. Blood

resuscitation was with two 400 mL units of whole blood. At baseline, the absolute systolic blood pressure

(100 mm Hg) suggests adequacy of resuscitation; however, the functional indices (Strip 1: Ps � 13 mm

Hg; Ps% � 14%; Pp% � 16%) suggest the subject is preload dependent, and if fluid resuscitation is

indicated, the subject will respond with an increase in stroke volume (SV). In response to a unit of whole

blood (400 mL), the SV increased from 30 mL/beat to 42 mL/beat (40% increase). After the first unit of

blood, the functional indices decreased (Strip 2: Ps � 9 mm Hg; Ps% � 8%; and Pp% � 3%) and the

SV response to the second unit was from 42 mL/beat to 66 mL/beat (57% increase). The interpretation of

the second set of values is equivocal due to the variable effect of VT on the absolute cutoff values. After

the second unit of blood, the functional hemodynamic indices (Strip 3: Ps � 4 mm Hg; Ps% � 9%; and

Pp% � 3%) suggest that the subject will be a nonresponder to additional fluids, which was

demonstrated by the small increase in SV (SV increased from 66 mL/beat to 68 mL/beat � 3% change

in SV).

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demonstrated signs of hypoperfusion, vasoac-tive/inotropic agents would be used to treatthe low blood pressure/CI. Diuresis would notbe appropriate, as the corrected PAOP (ap-proximately 14 mm Hg) was not excessivelyhigh and a diuresis-induced decrease in in-travascular volume in conjunction with thehigh levels of PEEP would potentially decreasecardiac output.

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