and another from JL Vincent Consensus of 16 from Crit Care 2011
Passive Leg raising and End-exp occlusion was good in pts with poor resp compliance; PPV was not (Crit Care Med 2012;40(1):151)
A new article seems to indicate that the best predictor for development of pulmonary edema during fluid loading is reaching plateau of CI, indicated by no additional increase with fluids (CCM 2012; 40:793)
Marik Phillips Curves
The Fluid Challenge
Fluid Challenge Revisited (CCM 2006;34:1333)
Check in at 10 minutes, if CVP increase <2, continue
2-5 Stop infusion, and wait 10 minutes. If it drops back to less than 2, continue
>5 Stop fluid challenge
this one is nice (
A PLR-induced increase in EtCO2 >5 % predicted a fluid induced increase in CI >15 % with sensitivity of 71 % (95 % confidence interval: 48–89 %) and specificity of 100 (82–100) %. (Intensive Care Med (2013) 39:93–100)
Passive leg raise to etco2 New balanced retro study Ccm 2014;42:1585
NICOM – Bioreactance
Marik studied 34 patients in the ICU with PLR, NICOM, SVV, and Carotid Flow (The use of NICOM (Bioreactance) and Carotid Doppler to determine volume responsiveness and blood flow redistribution following passive leg raising in hemodynamically unstable patients Chest 2012 Marik et al.)
Big validation study showed good accuracy (Intensive Care Med (2007) 33:1191–1194)
New study in only 11 pts shows poor correlation with PAC (Fagnoul et al. Critical Care 2012, 16:460)
A 2nd study showing poor correlation in the critically ill (Br J Anaesth 2013;111(6):961)
Passive Leg Raise
Passive leg-raising PLR to 30° transiently increases venous return  in patients who are preload responsive. As PLR only transiently increases CO and blood pressure  in responders, it is only a diagnostic test and cannot be considered as a treatment for hypovolemia. The main advantage of the PLR approach is that it is reversible and easy to perform in patients breathing spontaneously and with arrhythmias . It also can be repeated many times to reassess preload responsiveness without any risk of inducing pulmonary edema or cor pulmonale in potential nonresponders. One of the major limitations of this technique is that in severely hypovolemic patients, the blood volume mobilized by leg-raising which is dependent on total blood volume could be small, which, in turn, can show minimal to no increase in CO and blood pressure, even in responders.
The passive leg-raising test Lifting the legs passively from the horizontal position induces a gravitational transfer of blood from the lower limbs toward the intrathoracic compartment (Fig. 2). Several studies conducted in various hemodynamic conditions have demonstrated an increase in the pulmonary artery occlusion pressure , in the left ventricular end-diastolic dimension , or in the left ventricular ejection time  during passive leg raising (PLR), supporting the evidence that the volume of blood transferred to the heart during PLR is sufficient to increase the left cardiac preload and thus to challenge the Frank-Starling curve. Beyond its ease of use, the method has the advantage of inducing reversible effects once the legs are tilted down [18,38]. Therefore, PLR may act as a reversible self-volume challenge.
The concept of fluid response prediction by using PLR has emerged from the study by Boulain and coworkers , in which the increase in thermodilution stroke volume following a fluid infusion correlated with the increase in arterial pulse pressure produced by PLR. Recently, we demonstrated the full ability of PLR to serve as a test for preload responsiveness . In 71 patients with acute circulatory failure, changes in aortic blood flow (measured by esophageal Doppler) during a 45° leg elevation enabled us to predict the changes in aortic blood flow produced by a 500 ml fluid challenge. This was the case even in the subgroup of patients with cardiac arrhythmias or spontaneous ventilator triggering, situations in which respiratory variation of arterial pulse pressure lost any predictive ability. Probably descending aortic blood flow was a better measure of cardiac output than pulse pressure, volume responsiveness was better predicted by PLR-induced changes in aortic blood flow than by PLR-induced changes in arterial pulse pressure. In another series of patients fully adapted to their ventilator, Lafanechere et al.  also found that fluid responsiveness could be reliably predicted by the response of descending aortic blood flow to PLR. Since the maximal hemodynamic effects of PLR occurred within the first minute of leg elevation , it is important to assess these effects with a method able to track changes in cardiac output or stroke volume on a real-time basis. In this regard, the response of descending aortic blood flow (measured by esophageal Doppler) to PLR [17,18] as well as the response of the velocitytime integral (measured by transthoracic echocardiography)  to PLR have been demonstrated to be helpful in predicting the response to volume administration in patients with spontaneous
17 Lafanechere A, Pene F, Goulenok C, et al. Changes in aortic blood flow induced by passive leg raising predict fluid responsiveness in critically ill patients. Crit Care 2006; 10:R132. Mount Sinai Serials This study confirms the reliability of the PLR test for predicting volume responsiveness by means of esophageal Doppler monitoring, as demonstrated by Monnet et al. . [Context Link] 18 Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts fluid responsiveness in the critically ill. Crit Care Med 2006; 34:14021407. Ovid Full Text Mount Sinai Serials In 71 patients with acute circulatory failure, increases in the aortic blood flow measured by esophageal Doppler by more than 10% allows one to predict volume responsiveness with a sensitivity of 97% and a specificity of 94%. Importantly, in a subgroup of patients with spontaneous breathing activity or cardiac arrhythmias, PLR kept its full predictive value while the respiratory variation of pulse pressure was ineffective for predicting volume responsiveness. [Context Link]
38 Boulain T, Achard JM, Teboul JL, et al. Changes in BP induced by passive leg raising predict response to fluid loading in critically ill patients. Chest 2002; 121:12451252. Mount Sinai Serials Bibliographic Links [Context Link]
Passive leg raising-induced changes in mean radial artery pressure can be used to assess preload dependence if it goes up
Critical Care 2007, 11(Suppl 2):P307
(Chest. 2002;121:1245-1252.) Changes in BP Induced by Passive Leg Raising Predict Response to Fluid Loading in Critically Ill Patients*
Most recent analysis states changes in MAP don’t predict CI increase from fluid load in septic shock (Intensive Care Med (2012) 38:422–428)
Thierry Boulain, MD; Jean-Michel Achard, MD; Jean-Louis Teboul, MD; Christian Richard, MD; Dominique Perrotin, MD and Guy Ginies, MD
Monnet, Xavier MD, PhD; Rienzo, Mario MD; Osman, David MD; Anguel, Nadia MD; Richard, Christian MD; Pinsky, Michael R. MD, Dr hc; Teboul, Jean-Louis MD, PhD
Issue:Volume 34(5), May 2006, pp 1402-1407
Passive leg raising predicts fluid responsiveness in the critically ill *
critical care medicine
>9% change in pulse pressure or > 10% in SV, by PLR predicted volume responsiveness in non-intubated spont breathing patients. (CCM 2010,38:819)
To know if your passive leg raise is accurate, you need to see the CVP increase by at least 2 mm Hg. If this occurs pulse pressure changes are accurate (8%)
(Inten Care Med 2010;36:940)
If there is not an increase, then you need a stroke volume marker and can’t use PP
LR +9, LR-0.14
SR and MA (Inten Care Med 2010;36:1475)
changes in CO are good markers, changes in ABP not as good
Not accurate in IAH patients (CCM 2010;38:1824)
Crit Care Med. 2010 Mar;38(3):819-25.
Passive leg raising is predictive of fluid responsiveness in spontaneously breathing patients with severe sepsis or acute pancreatitis.
Service de Réanimation polyvalente, Centre Hospitalier Jean Bernard, Valenciennes, France. email@example.com
OBJECTIVE: Rapid fluid loading is standard treatment for hypovolemia. Because volume expansion does not always improve hemodynamic status, predictive parameters of fluid responsiveness are needed. Passive leg raising is a reversible maneuver that mimics rapid volume expansion. Passive leg raising-induced changes in stroke volume and its surrogates are reliable predictive indices of volume expansion responsiveness for mechanically ventilated patients. We hypothesized that the hemodynamic response to passive leg raising indicates fluid responsiveness in nonintubated patients without mechanical ventilation.
DESIGN: Prospective study.
SETTING: Intensive care unit of a general hospital.
PATIENTS: We investigated consecutive nonintubated patients, without mechanical ventilation, considered for volume expansion.
INTERVENTIONS: We assessed hemodynamic status at baseline, after passive leg raising, and after volume expansion (500 mL 6% hydroxyethyl starch infusion over 30 mins).
MEASUREMENTS AND MAIN RESULTS: We measured stroke volume using transthoracic echocardiography, radial pulse pressure using an arterial catheter, and peak velocity of femoral artery flow using continuous Doppler. We calculated changes in stroke volume, pulse pressure, and velocity of femoral artery flow induced by passive leg raising (respectively, Deltastroke volume, Deltapulse pressure, and Deltavelocity of femoral artery flow). Among 34 patients included in this study, 14 had a stroke volume increase of >or=15% after volume expansion (responders). All patients included in the study had severe sepsis (n = 28; 82%) or acute pancreatitis (n = 6; 18%). The Deltastroke volume >or=10% predicted fluid responsiveness with sensitivity of 86% and specificity of 90%. The Deltapulse pressure >or=9% predicted fluid responsiveness with sensitivity of 79% and specificity of 85%. The Deltavelocity of femoral artery flow >or=8% predicted fluid responsiveness with sensitivity of 86% and specificity of 80%.
CONCLUSIONS: Changes in stroke volume, radial pulse pressure, and peak velocity of femoral artery flow induced by passive leg raising are accurate and interchangeable indices for predicting fluid responsiveness in nonintubated patients with severe sepsis or acute pancreatitis.
Not predictive if the patient has increased ab pressure
Crit Care Med. 2010 Sep;38(9):1824-9.
5 Rules to Follow
Delta Down and Such
predicting fluid responsiveness in the OR (Br J Anaes 2007;98(4):545) delta down component of SPV minimal resp spv=not fluid responsive
Stroke Volume Variation
A Critical Challenge to the accuracy of SVV during mech vent both for absolute and as a trend (Crit Care Med 2012;40:1186 Biais)
Article on Non-Invasive (Br J Anaesth 2006;97:808)
(Can J Anesth 2003;50:10)
American Journal of Critical Care. 2005;14: 364-368
Use of the Trendelenburg Position as the Resuscitation Position: To T or Not to T?
Expiratory Hold to Predict Volume Responsiveness (Crit Care Med 2009;37(3):951)
15 second expiratory hold
maximal change during last five seconds = test
15% change in arterial pulse pressure predicts volume expansion
Dynamic changes can be false if there is RV dysfunction (will yield false positives) as the PPV means the LA needs more fluid but giving it in the face of the RV failure will not get the fluid to the LA. Put the patient on 10 ml/kg and sedate them. (CCM 2009;37(9):2642)
Art Pressure Wave Interpretation
Slow the arterial line trace to 6.25mm/second to synch with the capnograph. Makes it easy to identify systolic pressure variation (twitter anesthesia tips)
Critical Care 2005;9
The mean systemic pressure is the theoretical pressure value that would be observed in the overall circulatory system under zero flow conditions, assumed to be pressure in the right atrium
MAP=(HR x SV x SVR) -mRAP
13% variation discerned between responders and non to add. fluid resus
Pre-ejection period variations predict the fluid responsiveness of septic ventilated patients [Clinical Investigations] Feissel, Marc MD; Badie, Julio MD; Merlani, Paolo G. MD; Faller, Jean-Pierre MD; Bendjelid, Karim MD, MS Conclusions: The present study found [DELTA]PEPKT and [DELTA]PEPPLET to be as accurate as [DELTA]PP in the prediction of fluid responsiveness in mechanically ventilated septic patients.
Crit Care Med 2005;33(11):2534
Study comparing static pressure markers to Pulse Pressure variation and new proprietary Resp Systolic Variation Test (Br J Anaes 2005;95(6):746)
Driving pressure > 20 is probably necessary to get good PPV (Inten Care Med Volume 36, Number 3 / March, 2010:1432)
When stroke volume variation doesn’t work
(Crit Care Med 2011;39:402)
SOSSmall tidal volume, Open Chest, Sustained cardiac arrhythmia
Less than 1/4 of patients in the ICU will meet the prereqs for art wave analysis ( Dan Med J 2015;62(9):A5136 )
Brachial Artery Peak Velocity
use of doppler ultrasound variation of brachial artery in response to ventilation
Illustrative example of Doppler evaluation of brachial artery peak velocity variation in a responder patient and nonresponder patient. In the responder patient (left), volume expansion (VE) induced a decrease of brachial artery peak velocity variation (ΔVpeakbrach) by 15% (from 23% at baseline to 8% after VE) and an increase of stroke volume index and cardiac index by 27% and 12%, respectively. Radial pulse pressure variation (ΔPPrad) and stroke volume variation (ΔSVVigileo) also significantly decreased in the same patient (from 23% to 4%, and from 24% to 11%, respectively). In nonresponder patients (right), VE did not induce any significant change in ΔVpeakbrach (from 9% to 9% after VE), ΔPPrad (from 10% to 8%) or ΔSVVigileo (from 13% to 12%). Neither cardiac index nor stroke volume index increased significantly after VE (6% and 8%, respectively). SVi = stroke volume index.
Monge García et al. Critical Care 2009 13:R142
Three diastolic filling patterns as assessed by Doppler echocardiography. A = late transmitral velocity occurring with atrial contraction; AF = atrial fibrillation; DTE = deceleration time of early transmitral velocity; E = early transmitral velocity; EA = ratio of early to late transmitral velocity.
The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. (Intensive Care Med. 2004 Sep;30(9):1834-7) OBJECTIVE: To investigate whether the respiratory variation in inferior vena cava diameter (DeltaD(IVC)) could be related to fluid responsiveness in mechanically ventilated patients.DESIGN: Prospective clinical study. SETTING: Medical ICU of a non-university hospital.PATIENTS: Mechanically ventilated patients with septic shock (n=39).INTERVENTIONS: Volume loading with 8 mL/kg of 6% hydroxyethylstarch over 20 min.MEASUREMENTS AND RESULTS: Cardiac output and DeltaD(IVC) were assessed by echography before and immediately after the standardized volume load. Volume loading induced an increase in cardiac output from 5.7+/-2.0 to 6.4+/-1.9 L/min (P<0.001) and a decrease in DeltaD(IVC) from 13.8+/-13.6 vs 5.2+/-5.8% (P<0.001). Sixteen patients responded to volume loading by an increase in cardiac output > or =15% (responders). Before volume loading, the DeltaD(IVC) was greater in responders than in non-responders (25+/-15 vs 6+/-4%, P<0.001), closely correlated with the increase in cardiac output (r=0.82, P<0.001), and a 12% DeltaD(IVC) cut-off value allowed identification of responders with positive and negative predictive values of 93% and 92%, respectively.CONCLUSION: Analysis of DeltaD(IVC) is a simple and non-invasive method to detect fluid responsiveness in mechanically ventilated patients with septic shock. Intensive Care Med. 2004 Sep;30(9):1740-6.Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients.OBJECTIVE: To evaluate the extent to which respiratory changes in inferior vena cava (IVC) diameter can be used to predict fluid responsiveness.DESIGN: Prospective clinical study.SETTING: Hospital intensive care unit.PATIENTS: Twenty-three patients with acute circulatory failure related to sepsis and mechanically ventilated because of an acute lung injury.MEASUREMENTS: Inferior vena cava diameter (D) at end-expiration (Dmin) and at end-inspiration (Dmax) was measured by echocardiography using a subcostal approach. The distensibility index of the IVC (dIVC) was calculated as the ratio of Dmax – Dmin / Dmin, and expressed as a percentage. The Doppler technique was applied in the pulmonary artery trunk to determine cardiac index (CI). Measurements were performed at baseline and after a 7 ml/kg volume expansion using a plasma expander. Patients were separated into responders (increase in CI > or =15%) and non-responders (increase in CI <15%). RESULTS: Using a threshold dIVC of 18%, responders and non-responders were discriminated with 90% sensitivity and 90% specificity. A strong relation (r = 0.9) was observed between dIVC at baseline and the CI increase following blood volume expansion. Baseline central venous pressure did not accurately predict fluid responsiveness.CONCLUSION: Our study suggests that respiratory change in IVC diameter is an accurate predictor of fluid responsiveness in septic patients.
Another True correlation with improved SV, used 16% as cut-off (Neurocrit Care (2010)13:39
measure at the renal vein or just caudad to hepatic vein takeoff. don’t measure at junction with right atrium as the diaphragm may confound (ACAD EMERG MED January 2010, Vol. 17, No. 1:96)
New Annals article shows valid in both mech vent and none, small study, used CVP not SV (Ann Emerg Med 2010;55:290) 2-3 cm from right atrial border
In Mech Vent SAH pts, 16% cut-off predicted fluid responsiveness (Neurocrit Care 2010;13:3)
In a study of sonographic serial measurements of non-traumatic hypotensive patients during fluid resuscitation, sonographic visual estimations of IVCv and LVFv correlated with quantitative sonographic measurements. In addition, there was substantial inter-rater agreement of visual estimates of LVF and IVC respiratory variation. (Annals of Emergency Medicine Volume 56, Issue 3, Supplement , Page S77, September 2010)
SICU study on intubated patients (J Trauma. 2007;63:495502)
Non-intubated Trauma Patients (J Trauma. 2007;63:12451248)
Visual seems to be ok and have reasonable kappa values (acad emerg med 2011;18:98)
IVC diameter may be related to diaphragmatic excursion as well as intrathoracic pressure changes (Eur J of Echocardiography 2011;12:120)
PEEP-induced Increase in CVP
In mech vent patients, a PEEP increase of 10 induced a CVP increase of > 1.5 in fluid responsive patients. Judged against PLR increase in CO. Very small initial study (Br J Anaesth 2011;107(2):150)
Pulse Contour Analysis
doesn’t accurately track pressors/inopressors (Anesth Analg. 2011 Oct;113(4):751-7.)
End-Expiratory Occlusion Test
Crit Care Med. 2012;40:152–157, Crit Care Med. 2009;37:951–956
15 sec end-exp occlusion, look for pulse pressure >=5% during the end-expiratory occlusion with a sensitivity and a specificity of 87% and 100%, respectively, and by an increase in cardiac index >=5% during the end-expiratory occlusion with a sensitivity and a specificity of 91% and 100%, respectively
works even with high PEEPS (Crit Care Med 2013;41:1692)
10 Second Fluid Challenge
Critical Care 2014;18:R108
50 ml bolus over 10 seconds through a central line
Change in VTI measured immediately afterwards
100 ml Colloid over 60 sec (Br J Anaesth 2015; p.449)
Jugular vein distensibility predicts fluid responsiveness in septic patients
(Critical Care 2014, 18:647)
18% during mechanical ventilation