Current Status of Dynamic PArameters of Fluid Loading

Current Status of Dynamic

Parameters of Fluid Loading

Amit Asopa, MD, FRCA

Swaminathan Karthik, MBBS

Balachundhar Subramaniam,

MBBS, MD, MPHAnesthesia, Critical Care and Pain MedicineBeth Israel Deaconess Medical CenterBoston, Massachusetts

Perioperative fluid management plays a critical role in the outcomesof surgical patients. There is an ongoing controversy between advocatesof a liberal fluid management regimen and a more restrictive fluidreplacement strategy. Traditional fluid management emphasizes thereplacement of fluid deficits from fasting, insensible, and evaporativelosses as well as estimating maintenance fluid and blood loss.1 Suchcalculations are thought to overestimate fluid requirements and lead tointerstitial fluid accumulation and weight gain.2 Another approach usesthe measurement of central venous pressures and pulmonary arterydiastolic or wedge pressures as measures of cardiac preload. But theseparameters have been shown to be completely unrelated to cardiacpreload both in healthy volunteers as well as the critically ill.3–5 Recentlya more restrictive fluid management regimen has been proposed, whichinvolves replacing only definite fluid losses. This fluid strategy wasshown to improve outcomes in certain critically ill surgical populations.6

Brandstrup et al6 demonstrated in a randomized trial that postoperativecomplications were fewer in the fluid restricted group of patientsundergoing colon surgery. McArdle et al showed that positive fluidbalance is predictive of major adverse events and increased high

INTERNATIONAL ANESTHESIOLOGY CLINICSVolume 48, Number 1, 23–36r 2010, Lippincott Williams & Wilkins

www.anesthesiaclinics.com | 23

REPRINTS: SWAMINATHAN KARTHIK, MBBS, MD, MPH, DEPARTMENT OF ANESTHESIOLOGY, HARVARD MEDICAL

SCHOOL, BETH ISRAEL DEACONESS MEDICAL CENTER, BOSTON, MA 02215, E-MAIL: [email protected]

dependency unit, intensive care unit (ICU), and overall hospital stay.7

Appropriate fluid therapy in critically ill patients may result in earlyextubation, less incidence of pulmonary edema, and renal failure. Thus,it is clear that current fluid management strategies have significantdeficiencies and adversely influence outcomes in a variety of patientpopulations. A new paradigm to guide fluid management is essential.A growing body of evidence support the usage of underused dynamicparameters for assessing fluid responsiveness.8 These parameters arebased on the cardiopulmonary interaction during positive pressureventilation. The resulting transpulmonary pressure changes causevariations in venous return, blood pressure (BP), and stroke volume.The amplitude of this variation is inversely proportional to volumestatus. Thus, hypovolemia is characterized by larger swings in BP andstroke volume.9 Clinicians have subjectively used these for a long timeby observing swings in the arterial or plethysmographic waveform.Pulsus paradoxus seen in pericardial tamponade, is an exaggeratedexample of the same variation. However, the physiologic variation duringspontaneous ventilation was not objectively quantified to be a meaningfulmeasure of intravascular volume status for a long period of time.

’ Physiology of Cardiopulmonary Interaction

Effects on Venous Return

Venous blood flows along a gradient from a high peripheral venoushigher pressure to a lower right atrial pressure (RAP). During mechanicalinspiration, intrathoracic pressure rises and venous return falls,decreasing the ventricular preload. This leads to a decreased rightventricular (RV) stroke volume. The resulting decrease in pulmonary bloodflow eventually causes a decrease in left ventricular (LV) stroke volume.

Two mechanisms may explain this decrease in venous return.9 A risein intrathoracic pressure would increase the transmural RAP. This increasein downstream pressure would decrease venous flow. A second mechan-ism may involve compression of the intrathoracic vena cava by an increasein intrathoracic pressure. Mechanical expiration results in a decrease inintrathoracic pressure and the peripherally pooled venous blood returnsto the right atrium in greater quantity, increasing the ventricular preloadand thus RV stroke volume. Higher pulmonary blood flow eventuallyresults in increased LV stoke volume.

Effect of Pulmonary Transit Time

Changes in the RV stroke volume get reflected in the LV strokevolume only after 2 to 3 seconds due to pulmonary transit time.Therefore, mechanical ventilation seems to have opposite effects on RVand LV stroke volumes, but the effect on the LV stroke volume is

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predominantly the effect of the previous ventilatory cycle. Thus,mechanical inspiration decreases venous return and RV stroke volumewhereas LV stroke volume seems to increase. Although mechanicalexpiration increases venous return and RV stroke volume, LV strokevolume seems to decrease.

Effect on Pulmonary Vascular Bed

Variations in stroke volume may also be caused by the effect of mecha-nical ventilation on the pulmonary vascular bed. Mechanical inspirationincreases pulmonary vascular resistance by the effect of alveolar distentionon pulmonary capillaries. This increased RVafterload adds to the decreasein RV stroke volume during mechanical inspiration. The opposite effect isseen on the LV. Increased alveolar pressure from mechanical inspirationcauses improved emptying of the pulmonary venous system increasing LVpreload and thus increasing LV stroke volume. The opposite effect is seenduring mechanical expiration.

Interdependence of the Ventricles

With an intact pericardium, the ventricles are interdependent. Theyinfluence the compliance of the other across the interventricular septum.An increase in RV preload during expiration causes decreased LVcompliance and hence decreased preload. During inspiration, RV preloaddecreases and this is reflected as improved LV compliance and preload.

Transmural LV Pressure

Mechanical inspiration increases intrathoracic pressure and thisextrapericardial pressure acts on the LV to increase its transmuralpressure with reference to systemic vascular resistance. Increased LVtransmural pressure increases LV ejection velocity and ejection fraction.During mechanical expiration, LV emptying is decreased.

The sum total of all these effects as well as the pulmonary bloodtransit time is that mechanical inspiration causes RV output to drop butthe arterial BP transiently increases due to improved LV output (Fig. 1).The reverse happens during mechanical expiration and the arterialpressure transiently decreases.

’ Cardiopulmonary Interaction Under Special Conditions

Spontaneous Ventilation

Although cardiopulmonary interactions occur during spontaneousventilation, these are more difficult to standardize. Tidal volumes and

Dynamic Parameters of Fluid Loading ’ 25


hence transpulmonary pressure changes vary from breath to breathadding to the variation in venous return and stroke volume.10

Hypovolemia

The cardiorespiratory variation described previously is exaggeratedduring hypovolemic conditions. This occurs due to the transmission ofairway and pleural pressures to the heart directly and through the Westzones of the lung. There is predominance of zones I and II, wherealveolar pressure is greater than pulmonary arterial and venous pressures,and RV afterload increases (Fig. 2). In West zone III, where pulmonaryvenous pressure is greater than alveolar pressure, blood is pushed forwardduring inspiration, thus augmenting the LV preload (Fig. 2).

Hypervolemia

Cardiorespiratory variation is less pronounced during fluid over-load states. This is due to the higher intramural pressures in thechambers of the heart as well as the predominance of West zone III inthe lungs (Fig. 3).

’ Dynamic Parameters of Fluid Responsiveness

During mechanical ventilation, where standard tidal volumes(< = 8 mL/kg body weight) are used, this cardiopulmonary interactioncan be objectively quantified to create useful parameters (Table 1).1

Figure 1. Aortic flow represents arterial blood pressure tracing. Pulmonary artery flow representspulmonary arterial blood pressure tracings. Vena cava flow represents filling pressure. 1, 2, and 3represent the beginning of positive pressure inspiration.

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Figure 2. Zone I-III are West lung zones. LA indicates left atrium; LV, left ventricle; Palv,alveolar pressure; Ppl, pleural pressure; RA, right atrium; RV, right ventricle.

Figure 3. Zones 1, II, and III are West lung zones. LA indicates left atrium; LV, left ventricle;Palv, alveolar pressure; Ppl, pleural pressure; RA, right atrium; RV, right ventricle.



Systolic Pressure Variation

Systolic pressure variation (SPV) is defined as the differencebetween the maximal and minimal values of systolic arterial pressurerecorded over a respiratory cycle. Normal value is <10 mm Hg.

SPV ¼ SBP max�SBP min =ðSBP maxþSBP min =2Þ

SPV can also be determined by: SPV =DUp+DDown, whereDUp = SBP max – Apneic baseline (represents the augmentation of systolicpressure due to the increase in Left Ventricular End Diastolic Volumeand the decrease in LV afterload during inspiration) and DDown =Apneic baseline – SBP min (represents the fall in Left Ventricular EndDiastolic Volume and the increase in LV afterload during earlyexpiration).

Delta Up and Delta Down

Delta Up increases in proportion to the increases in LV preloadand a reduction in LV afterload. Delta Down reflects the degree ofRV preload reduction due to reduced venous return and henceindicates volume responsiveness in a patient. SPV is calculated fromthe minimum and maximum systolic pressure across a respiratory cycle(Figs. 4, 5).

Pulse Pressure Variation

Pulse pressure is difference of the systolic and diastolic BP. Thearterial pulse pressure is directly proportional to stroke volume and

Table 1. Current Dynamic Parameters of Fluid Resuscitation

Monitor Dynamic Parameter Measured

Arterial line Systolic pressure variation

Pulse pressure variation

Delta down

Delta up

Aortic Doppler Ejection time

Stroke volume variation

Echocardiography SVC collapsibility index

IVC collapsibility index

Stroke volume variation

Flotrac Stroke volume variation

LidCO Stroke volume variation

PiCCO Stroke volume variation

Pulse pressure variation

IVC indicates inferior vena cava; LidCO, lithium dilution cardiacoutput monitor; PiCCO, pulsion continuous cardiac output moni-tor; SVC, superior vena cava.

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inversely related to arterial compliance. Therefore, for a given arterialcompliance, the amplitude of pulse pressure is directly related to LVstroke volume. In this regard, the respiratory variation in LV strokevolume has been shown to be the main determinant of the respiratoryvariation in pulse pressure.11

Pulse pressure variation (PPV) is the maximal difference in pulsepressure seen over a respiratory cycle. PPV is expressed as a percentage(Fig. 6).

PPV ¼½ðSBP�DBPÞmax�ðSBP�DBPÞmin�=

½ðSBP�DBPÞmaxþðSBP�DBPÞmin =2�

¼ PP max�PP min =ðPP maxþPPmin=2Þ

Normal value <13%.

Stroke Volume Variation

Stroke volume variation (SVV) is the percentage of change bet-ween the maximal and minimal stroke volumes divided by the average

Figure 4. The arterial pressure is the continuous arterial waveform and the airway pressure isshown as a flat line with 1 positive pressure breath in the middle of the screen. With intermittentpositive pressure ventilation, there is a fluctuation in blood pressure. There is increase in bloodpressure during inspiration and is followed by a decrease in blood pressure during expiration beforethe baseline pressure plateaus in the expiratory pause. SPMax indicates maximum systolic pressure;SPMin, minimum systolic pressure during the respiratory cycle.22



of the minimum and maximum over a floating period of 10 seconds(Figs. 7, 8).

SVV ¼ SV max�SV min =ðSV maxþSV min =2Þ

Normal value <10%.

Esophageal Aortic Doppler

The esophageal Doppler monitor measures blood flow velocity inthe descending thoracic aorta using a flexible ultrasound probe, whichproduces ultrasound wave of 4 MHz. This is then combined withestimated aortic cross-sectional area to give stroke volume and cardiacoutput measurements. Thus, linear variables are converted to volu-metric variables. Stroke distance (SD) is described as the distance acolumn of blood travels down the descending thoracic aorta with eachsystole (cm) and is represented by the area under the velocity timewaveform (Fig. 9).

As volume of a cylinder is given by Length (distance) � cross-sectional area, stroke volume = SD� aortic cross-sectional area.

Deltex Medical’s CardioQ monitor gives a continuous display of thepatient’s hemodynamic parameters such as, (a) CO (cardiac output), (b)SV (stroke volume), (c) corrected flow time, (d) peak velocity, (e) minutedistance, (f ) heart rate.

Figure 5. The changes in arterial blood pressure observed during the respiratory cycle. Systolicpressure variation (SPV) is the sum of delta Up (DUp) and delta Down (DDown) as measured fromthe apneic baseline.

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On the basis of these parameters, it can be determined whetherpatients need fluids, vasopressors, or inotropes.

However, it makes certain assumptions:1. It is assumed that the patient’s actual aortic dimensions are accurately

represented by the stored nomogram.2. The angle of the CardioQ esophageal probe to blood flow in the

descending aorta is 45 degrees. Velocity measurements from theDoppler equation use the cosine of this value. A wider angle willresult in a greater reduction in measured velocity compared with truevelocity.

3. Descending aortic flow represents 70% of the LV output and that thisremains constant throughout the spectrum of hemodynamic changes.

Arterial Pulse Contour Analysis

The origin of the pulse contour method for estimation of beat-to-beat stroke volume is based on the Windkessel model described byOtto Frank in 1899. Windkessel effect is the distension of the aorta whenblood is ejected from the LV. The aorta recoils and smoothes out

Figure 6. Fluctuation of pulse pressure observed with intermittent positive pressure ventilation.Pulse pressure is maximal during inspiration (PPmax) and minimal in early expiration (PPmin).



pressure and blood flow, this helps perfuse coronary arteries by pushingblood back to the opening of the coronary arteries. Wesseling et al12

reintroduced the Windkessel effect for pulse contour analysis. Cardiacoutput (CO) is calculated from pulse wave contour analysis, which is alsoinfluenced by the compliance and impedance of the arterial system. Thecompliance varies individually and pressure/volume relations of arteriesare not linear. Therefore, an independent technique is requiredto provide initial calibration of the pulse contour CO analysis. Thiscalibration is done usually by calibration with thermo or lithium dilutionusing the Stewart-Hamilton formula (PICCO System; PULSIONMedical Systems AG, Munich, Germany, and LIDCO; LiDCO Ltd,London, UK).These monitors still need a central line and/or specialarterial lines, whereas FloTrac monitor (FloTrac/Vigileo, EdwardsLifesciences, Irvine, CA), requires only a standard arterial line formeasurement of continuous CO. FloTrac calculates CO with a newalgorithm, which eliminates the necessity for independent calibrationand insertion of a central venous catheter. It performs continuous self-calibration through its automatic vascular tone adjustment.

Figure 7. Pulse contour analysis of the arterial pressure wave provides beat-to-beat measurementof the stroke volume. The change in stroke volume over the respiratory cycle (taken from maximumand minimum values over 10 s) is the stoke volume variation (www.edwards.com accessed on August30, 2009).

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Photoplethysmographic Waveform Analysis

This technique makes use of photoelectric plethysmography todetect changes in blood volume. It has been shown that systolic BPvariation and DDown correlated with similar indexes measured on thephotoplethysmographic waveform after blood withdrawal.13 Nataliniet al14 compared the ventilation-induced variation in arterial andphotoplethysmographic waveforms in randomly selected patients in theoperating room and ICU undergoing controlled mechanical ventilation.Their study showed that pulse variations observed in the arterialpressure waveform and photoplethysmogram are similar in response

Figure 9. Measurements obtained from the aortic Doppler. The corrected flow time is the importantparameter to which some studies have optimized fluid management. (Reproduced with permissionfrom Anaesthesia UK website accessed on August 30, 2009 at http://frca.co.uk/article.aspx?articleid = 100557).

Figure 8. SV max is the maximum stroke volume, SVmin is the minimum stroke volume. Differentdevices use all or a part of the pressure wave in their algorithms for the calculation of stroke volume(www.edwards.com accessed on August 30, 2009).



to positive pressure ventilation. Furthermore, photoplethysmographicpulse variation >9% identifies patients with ventilation-induced arterialBP variation who are likely to respond to fluid administration.14

Change in RAP

Michard at al15 analyzed the clinical studies investigating predictivefactors of fluid responsiveness in critically ill patients to assess the valueof each parameter tested. They reported that dynamic parameters[inspiratory decrease in RAP (DRAP), expiratory decrease in arterialsystolic pressure (D down), respiratory changes in pulse pressure (DPP),and respiratory changes in aortic blood velocity (DV peak)] should beused preferentially to static parameters to predict fluid responsiveness inICU patients.15

Passive Leg Raising

Passive leg raising induces a translocation of venous blood from thelegs to the intrathoracic compartment resulting in a ‘‘reversible volumechallenge’’ that is proportional to body size, and does not result in volumeoverload in nonpreload-responsive subjects. This causes transient increasein RV and LV preload. The effects of passive leg raising on cardiac outputare variable depending on the existence of cardiac preload reserve.16

Limitations Sakka et al17 analyzed SPV and SVV in comparisonwith static preload parameters during an increase in arterial BP andairway pressure in postoperative mechanically ventilated cardiac surgicalpatients. They concluded that in cardiac surgical patients with preservedcardiac index, SVV, but not SPV, decreased during an acute increase inBP, whereas both parameters, in contrast to cardiac filling pressures,significantly increased with higher tidal volume.

Normal sinus rhythm, presence of mechanical ventilation with atidal volume more 7 mL/kg18 are essential requirements to haveappropriate PPV or SVV measurements reflecting fluid responsiveness.These changes happen largely due to the increase in RVafterload, whichis related to the inspiratory increase in transpulmonary pressure(alveolar pressure minus intrathoracic pressure). Open chest conditionsmay disturb this relationship and may make these parametersunpredictable.19 In a study by de Waal et al, open-chest conditionshad a higher unreliability of these dynamic parameters, and theyconcluded that they fail during these conditions.20 However, theaccompanying editorial pointed out the other half of the patients whohad a good response.19 These observations reinforce the fact thatabsence of fluid responsiveness by PPV or SVV during open chestsurgery does not imply lack of fluid responsiveness. However, presence

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of fluid responsiveness really means that patients will be responsive tofluid boluses under open chest conditions.

The utility of these parameters in increasing abdominal pressureshave been studied.21 In a porcine model, PPV, SVV and global enddiastolic volume all predicted fluid responsiveness (as indicated by a15% increase in stroke volume) with thresholds at 11.5%, 9.5%, and963 mL. However, with increased intra-abdominal pressure of 25 mm ofHg, SVV did not predict fluid responsiveness. PPV and global enddiastolic volume predicted fluid responsiveness with increased intra-abdominal pressure although with a higher thresholds (20.5% for PPV).

Outcomes and Utilization There is growing literature to supportthe use of dynamic hemodynamic parameters in identifying patients thatwill respond to fluid resuscitation. However, what is not clear is whetherthis will lead to improved clinical outcomes. These issues of volumeresponsiveness and outcome are dealt elsewhere in this issue ofInternational Anesthesia Clinics.

’ References

1. Shires T, Williams J, Brown F. Acute change in extracellular fluids associated withmajor surgical procedures. Ann Surg. 1961;154:803–810.

2. Chappell D, Jacob M, Hofmann-Kiefer K, et al. A rational approach to perioperativefluid management. Anesthesiology. 2008;109:723–740.

3. Hamilton-Davies C, Mythen MG, Salmon JB, et al. Comparison of commonly usedclinical indicators of hypovolaemia with gastrointestinal tonometry. Intensive Care Med.1997;23:276–281.

4. Kumar A, Anel R, Bunnell E, et al. Pulmonary artery occlusion pressure and centralvenous pressure fail to predict ventricular filling volume, cardiac performance, or theresponse to volume infusion in normal subjects. Crit Care Med. 2004;32:691–699.

5. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluidresponsiveness? A systematic review of the literature and the tale of seven mares.Chest. 2008;134:172–178.

6. Brandstrup B, Tonnesen H, Beier-Holgersen R, et al. Effects of intravenous fluidrestriction on postoperative complications: comparison of two perioperativefluid regimens: a randomized assessor-blinded multicenter trial. Ann Surg. 2003;238:641–648.

7. McArdle GT, Price G, Lewis A, et al. Positive fluid balance is associated withcomplications after elective open infrarenal abdominal aortic aneurysm repair. EurJ Vasc Endovasc Surg. 2007;34:522–527.

8. Michard F. Underutilized tools for the assessment of intravascular volume status.Chest. 2003;124:414–445; author reply 5–6.

9. Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology.2005;103:419–428; quiz 49–45.

10. Michard F, Teboul JL, Richard C. Influence of tidal volume on stroke volumevariation. Does it really matter? Intensive Care Med. 2003;29:1613.

11. Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes inarterial pulse pressure and fluid responsiveness in septic patients with acutecirculatory failure. Am J Respir Crit Care Med. 2000;162:134–138.



12. Wesseling KH, Purschke R, Smith NT, et al. A computer module for the continuousmonitoring of cardiac output in the operating theatre and the ICU. Acta AnaesthesiolBelg. 1976;27 (suppl):327–341.

13. Shamir M, Eidelman LA, Floman Y, et al. Pulse oximetry plethysmographic waveformduring changes in blood volume. Br J Anaesth. 1999;82:178–181.

14. Natalini G, Rosano A, Franceschetti ME, et al. Variations in arterial blood pressureand photoplethysmography during mechanical ventilation. Anesth Analg. 2006;103:1182–1188.

15. Michard F, Teboul JL. Predicting fluid responsiveness in ICU patients: a criticalanalysis of the evidence. Chest. 2002;121:2000–2008.

16. Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts fluid responsivenessin the critically ill. Crit Care Med. 2006;34:1402–1407.

17. Sakka SG, Becher L, Kozieras J, et al. Effects of changes in blood pressure and airwaypressures on parameters of fluid responsiveness. Eur J Anaesthesiol. 2009;26:322–327.

18. De Backer D, Heenen S, Piagnerelli M, et al. Pulse pressure variations to predict fluidresponsiveness: influence of tidal volume. Intensive Care Med. 2005;31:517–523.

19. Teboul JL. Meaning of pulse pressure variation during cardiac surgery: everythingis open. Crit Care Med. 2009;37:757–758.

20. de Waal EE, Rex S, Kruitwagen CL, et al. Dynamic preload indicators fail to predictfluid responsiveness in open-chest conditions. Crit Care Med. 2009;37:510–515.

21. Renner J, Gruenewald M, Quaden R, et al. Influence of increased intra-abdominalpressure on fluid responsiveness predicted by pulse pressure variation and strokevolume variation in a porcine model. Crit Care Med. 2009;37:650–658.

22. Parry-Jones AJD, Pittman JAL. Arterial pressure and stroke volume variability asmeasurements for cardiovascular optimization. Int J Intens Care. 2003:67–72.

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Current Status of Dynamic PArameters of Fluid Loading

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