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Prof. Jean-Louis TEBOUL Medical ICU Bicetre hospital University Paris XI France

What is the best way to assess fluid responsiveness in a spontaneously breathing patient ?. Prof. Jean-Louis TEBOUL Medical ICU Bicetre hospital University Paris XI France. Member of the Medical Advisory Board of Pulsion . Three different scenarios.

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Prof. Jean-Louis TEBOUL Medical ICU Bicetre hospital University Paris XI France

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  1. What is the best way to assess fluid responsiveness in a spontaneously breathing patient ? Prof. Jean-Louis TEBOUL Medical ICU Bicetre hospital University Paris XI France Member of the Medical Advisory Board of Pulsion

  2. Three different scenarios 1- Patients in the ER for acute blood losses or body fluid losses 2- Patients in the ER for high suspicion of septic shock 3- Patients in the ICU, already resuscitated for several hours or days

  3. goodprediction of volume responsiveness althoughlacking of sensitivity 1- Patients in the ER for acute blood losses or body fluid losses Diagnosis of hypovolemia is almost certain Presence ofclinical signs of hemodynamic instability No therapeutic dilemma

  4. 2- Patients in the ER for high suspicion of septic shock Most often,no needsfor searching sophisticatedpredictors of volume responsiveness since volume resuscitation is mandatory in the first hours (see Rivers et al NEJM 2001)

  5. 3- Patients in the ICU, already resuscitated for several hours or days - with hemodynamic instability requiring therapy - without certainty of volume responsiveness • with potential risks of pulmonary edema • and/or excessive cumulative fluid balance

  6. 3- Patients in the ICU, already resuscitated for several hours or days - with hemodynamic instability requiring therapy - without certainty of volume responsiveness • with potential risks of pulmonary edema • and/or excessive cumulative fluid balance How to deal with this therapeutic dilemma? Fluid challenge ? Prediction of volume responsiveness ?

  7. Crit Care Med 2006; 34:1333-1337 Rate of infusion:500-1000 mL crystalloids or 300-500 mL colloids over30 mins Goal:reversal of the marker of perfusion failure that prompted the fluid challenge (ex: hypotension, tachycardia, oliguria, etc) Safety limits: CVP of 15 mmHg measured every 10 mins

  8. Crit Care Med 2006; 34:1333-1337 Rate of infusion: 500-1000 mL crystalloids or 300-500 mL colloids over 30 mins Goal: reversal of the marker of perfusion failure that prompted the fluid challenge (ex: hypotension, tachycardia, oliguria, etc) Safety limits: CVP of 15 mmHg measured every 10 mins Question: benefit/risk ratio ? Fluid challenge successful in only 50% cases

  9. CHEST 2002, 121:2000-8

  10. Crit Care Med 2006; 34:1333-1337 Rate of infusion: 500-1000 mL crystalloids or 300-500 mL colloids over 30 mins Goal: reversal of the marker of perfusion failure that prompted the fluid challenge (ex: hypotension, tachycardia, oliguria, etc) Safety limits: CVP of 15 mmHg measured every 10 mins Question: benefit/risk ratio ? Fluid challenge successful in only 50% cases Fluid challenge potentially risky Is a CVP of 15 mmHg a reasonable safety limit? 1) PAOP often > CVP 2) Pulmonary capillary pressure (Pcap) > PAOP

  11. Pcap-PAOP difference is high in ALI/ARDS Collee et al. Anesthesiology 1987 Radermacher et al. Anesthesiology 1989 Radermacher et al. Anesthesiology 1990 Teboul et al J. Appl Physiol 1992 Benzing et al. Acta Anaesthesiol Scand.1994 Rossetti et al. Am J Respir Crit Care Med 1996 Benzing et al. Br J Anaesth. 1998 Nunes et al. Intensive Care Med. 2003 Her et al. Anesthesiology 2005

  12. Crit Care Med 2006; 34:1333-1337 Rate of infusion: 500-1000 mL crystalloids or 300-500 mL colloids over 30 mins Goal: reversal of the marker of perfusion failure that prompted the fluid challenge (ex: hypotension, tachycardia, oliguria, etc) Safety limits: CVP of 15 mmHg measured every 10 mins Question: benefit/risk ratio ? Fluid challenge successful in only 50% cases Fluid challenge potentially risky Is a CVP of 15 mmHg a reasonable safety limit? 1) PAOP often > CVP 2) Pulmonary capillary pressure (Pcap) > PAOP 3) Degree of pulmonary edema poorly evaluated by Pcap since lung capillary permeability is often altered in ICU pts

  13. Increased lung capillary permeability EVLW normal lung capillary permeability Pcrit mmHg PVC: 15, PAOP:19 Pulmonary capillary hydrostatic pressure

  14. Crit Care Med 2006; 34:1333-1337 Rate of infusion: 500-1000 mL crystalloids or 300-500 mL colloids over 30 mins Goal: reversal of the marker of perfusion failure that prompted the fluid challenge (ex: hypotension, tachycardia, oliguria, etc) Safety limits: CVP of 15 mmHg measured every 10 mins Question:benefit/risk ratio ? Fluid challenge successful in only 50% cases Fluid challenge potentially risky

  15. 3- Patients in the ICU, already resuscitated for several hours or days - with hemodynamic instability requiring therapy - without certainty of volume responsiveness • with potential risks of pulmonary edema • and/or excessive cumulative fluid balance How to deal with this therapeutic dilemma? Fluid challenge ? Prediction of volume responsiveness ?

  16. preload-independence preload-dependence Volume expansion will increase stroke volume only if ventricles are preload-dependent Stroke Volume Ventricular preload

  17. How to predict preload-dependence and hence volume responsiveness? • 1- By estimating cardiac preload - using filling pressures:RAP, PAOP

  18. preload-independence preload-dependence The lower the ventricular preload, the more likely the preload-dependency Stroke Volume Ventricular preload

  19. responders nonresponders RAP before volume expansion in responders (R) and non-responders (NR) mmHg 20 10 * * 0 Calvin Schneider Reuse Wagner 1981 1988 1990 1998 number of pts28 18 41 25 SB pts (%) 54 33 24 6

  20. r = 0.45 Changes in stroke volume (%) Baseline PRA(mmHg) Wagner et al. Chest 1998

  21. responders nonresponders PAOP before volume expansion in responders (R) and non-responders (NR) mmHg 20 10 0 Calvin Schneider Reuse Diebel 1981 1988 1990 1994 number of pts28 18 41 32 SB pts (%) 54 33 24 31

  22. How to predict preload-dependence and hence volume responsiveness? • 1- By estimating cardiac preload - using filling pressures: RAP, PAOP - using dimensions:RVEDVi, LVEDVi

  23. responders nonresponders RVEDVi before volume expansion in responders (R) and non-responders (NR) * * Calvin Schneider Reuse Diebel Diebel Wagner 1981 1988 1990 1992 1994 1998 number of pts28 18 41 22 32 25 SB pts (%) 54 33 24 16 31 6

  24. responders nonresponders LVEDVi before volume expansion in responders (R) and non-responders (NR) mL/m2 120 80 40 0 Calvin Schneider 1981 1988 number of pts 28 18 SB pts (%) 54 33

  25. How to predict preload-dependence and hence volume responsiveness? • 1- By estimating cardiac preload - using filling pressures: RAP, PAOP - using dimensions: RVEDVi, LVEDVi markers of preload: poor markers of volume responsiveness Why ?

  26. Why do ventricular preload indicators not predict fluid responsiveness ? 1- In the available studies, pts were already resuscitated so that values of markers of preload were rarely low. On the other hand, values were rarely high before fluid challenges It cannot be excluded that low values predict volume responsiveness, whereas high values well predict the absence of hemodynamic response to volume 2- Because RAP, PAOP, RVEDVi, LVEDVi are not always accurate indicators of preload 3- Because assessment of preload is not assessment of preload-dependence

  27. normal heart preload-dependence failing heart preload-independence Stroke volume . Ventricular preload

  28. How to detect fluid responsiveness ? • 1- By estimating cardiac preload ? • 2- By using dynamic tests detecting • cardiac preload reserve ? 2.1- using heart-lung interaction - SPV, PPV? . for physiological reasons, these indices must not work . as confirmed in clinical studies

  29. Systolic pressure variation(mmHg) Patients with SB Systolic pressure variation(mmHg) Patients with MV Rooke et al Anesth & Analg 1995

  30. Patients breathing without mechanical support 23 % PPV before volume infusion 12 % 3 % responders nonresponders Soubrier et al. ATS 2005

  31. PPV PPV (threshold: 12 %) sedated patients patients with SB sensitivity 1 - specificity

  32. How to detect fluid responsiveness ? • 1- By estimating cardiac preload ? • 2- By using dynamic tests detecting • cardiac preload reserve ? 2.1- using heart-lung interaction - SPV, PPV? NO - Inspiratory decrease in RAP?

  33. J Crit Care 1992, 7:76-85 negative respiratory response positive respiratory response RAP mmHg RAP decrease by < 1 mmHg at inspiration RAP decrease by ≥1 mmHg at inspiration Inspiration 20 RAP mmHg 0 20 Inspiration 0 no hemodynamic response to volume challenge hemodynamic response to volume challenge

  34. 2.4 1.8 1.2 Changes in CO after volume loading(L/min) 0.6 0.0 - 0.6 negative respiratory response positive respiratory response Magder et al J Crit Care 1992 Limitation : to be sure that the inspiratory effort is sufficient

  35. How to detect fluid responsiveness ? • 1- By estimating cardiac preload ? • 2- By using dynamic tests detecting • cardiac preload reserve ? 2.1- using heart-lung interaction - SPV, PPV? NO - Inspiratory decrease in RAP? 2.2- using passive leg raising

  36. Venous blood shift (Rutlen et al. 1981, Reich et al. 1989) 45 ° Passive Leg Raising Increase in right ventricular preload(Thomas et al 1965) Reversible effects Increase in left ventricular preload(Rocha 1987, Takagi 1989, De Hert 1999, Kyriades 1994 )

  37. Chest 2002; 121: 1245-52 PAOP (mmHg) RAP (mmHg) 30 20 25 15 20 15 10 10 5 5 0 0 PLR PLR post-PLR post-PLR Base Base

  38. Venous blood shift (Rutlen et al. 1981, Reich et al. 1989) 45 ° Passive Leg Raising PLR could be used as a test to detect volume responsiveness rather than as a therapy Increase in right ventricular preload (Thomas et al 1965) Increase in left ventricular preload (Rocha 1987, Takagi 1989, De Hert 1999, Kyriades 1994 ) Transient effect (Gaffney 1982)

  39. Chest 2002; 121: 1245-1252 Hypothesis The increase in pulse pressure during PLR predicts theincrease in stroke volume afler volume loading

  40. Chest 2002; 121: 1245-52 Fluid-induced changes in Stroke Volume (%) n = 39 r = 0.74 PLR-induced changes in Pulse Pressure (mmHg)

  41. Hypothesis : a better surrogate of stroke volume than PP could do better Real-time CO monitoring is mandatory

  42. Hypothesis PLR-induced increase in mean aortic blood flow provides a better prediction of volume responsiveness than PLR-induced increase in pulse pressure Hypothesis : a better surrogate of stroke volume than PP could do better

  43. Base 1 Base 2 PLR Post VE 500 mL saline

  44. responders 40 nonresponders Changes in aortic blood flow (%) 30 20 10 0 -10 Base 1 PLR Base 2 Post VE

  45. PLR-induced changes in pulse pressure PLR-induced changes in aortic blood flow 80 60 40 * * 20 % change from Baseline 10 0 -20 NR R NR R -40

  46. 100 100 PLR-induced changes in ABF 80 80 60 60 PLR-induced changes in PP 40 40 20 20 PPV 0 0 0 0 20 20 40 40 60 60 80 80 100 100 100 - specificity 100 - specificity patients with spontaneous breathing n = 19 sensitivity Monnet et al. Crit Care Med 2006

  47. Hypothesis PLR-induced increase in Pulse Contour CO provides a better prediction of volume responsiveness than PLR-induced increase in pulse pressure Hypothesis : a better surrogate of stroke volume than PP could do better

  48. % increase in Pulse Contour CO during PLR 100 90 80 70 60 50 40 30 * 20 Se = 70 % Sp = 92 % cut-off = 12 % 10 0 -10 nonresponders responders Ridel ATS 2006

  49. Conclusion In spontaneously breathing patients Prediction of volume responsiveness is a difficult issue markers of preload unreliable PPV, SPV, SVV Inspiratory decrease in RAP valuable Response to passive leg raising but need to be confirmed Thank you for your attention

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