Lecture chest fellow_PSU 2012

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สอน fellow chest เรื่อง hemodynamic

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Lecture chest fellow_PSU 2012

  1. 1. Critical caretutorial forchest fellow
  2. 2. ContentsBasic hemodynamic monitoring forchest physician Fluid responsiveness Resuscitation target/endpoint
  3. 3. HemodynamicBP = CO x SVRBP = SV x HR x SVRBP = (EDV-ESV) x HR x SVRBP = preload x cardiac function x afterload
  4. 4. preload monitoring and fluid responsiveness d non-re sponsive ive flui nsCO po Frank- Starling Curve res id flu preload
  5. 5. Frank-Starling mechanism n c fu nctio al c ardia NormCO a c function Impa ired cardi preload
  6. 6. preload measurement2 types of preload assessment 1. static preload monitoring pressure: CVP, PAOP Volumetric: ITBV, GEDV Ultrasound: LVdD, IVCd
  7. 7. preload measurement2. dynamic preload monitoring parameter variation: SVV, PPV, SPV echocardiographic variation: Ao flow velocity, IVC distensibility index.
  8. 8. CVP(central venous pressure)
  9. 9. Central Venous Pressure BRAP/RVEDP/LVEDP A RAV/RVEDV/LVEDV
  10. 10. Central Venous Pressure BRAP/RVEDP/LVEDP A RAV/RVEDV/LVEDV
  11. 11. CVP as volumemeasurement Marik. Chest 2008.
  12. 12. CVP to predict fluid responsiveness Michard. Chest 2002.
  13. 13. Neither CVP or Ppao reflectVentricular Volumes or tract preload- responsiveness Kumar et al. Crit Care Med 32:691-9, 2004
  14. 14. CVPNot a good parameter to predict fluid responsiveness in both CVP and dCVP
  15. 15. Predicting Fluid Responsiveness in ICU Patients by CVP Responders / Non-responders % RespondersCalvin (Surgery 81) 20 / 8 71%Schneider (Am Heart J 88) 13 / 5 72%Reuse (Chest 90) 26 / 15 63%Magder (J Crit Care 92) 17 / 16 52%Diebel (Arch Surgery 92) 13 / 9 59%Diebel (J Trauma 94) 26 / 39 40%Wagner (Chest 98) 20 / 16 56%Tavernier (Anesthesio 98) 21 / 14 60%Magder (J Crit Care 99) 13 / 16 45%Tousignant (A Analg 00) 16 / 24 40%Michard (AJRCCM 00) 16 / 24 40%Feissel (Chest 01) 10 / 9 53%Mean 211 / 195 52% Michard & Teboul. Chest 121:2000-8, 2002
  16. 16. PAOP pressure)(pulmonary artery occlusivemeasure LVEDP, not LVEDV or LV preloadlimitation similar to CVP measurement
  17. 17. Predictors for fluid responsiveness 15 % change in CO Michard. AJRCCM 2000.
  18. 18. LVED areameasure under echocardiogramLV dimension during diastoleLVEDA correlate well to ITBV and GEDVLVEDd < 25 mm or LVDA < 55 cm2 indicatehypovolemianot a good predictor for fluid responsiveness
  19. 19. IVC diametercollapse IVC indicate volume depletionDilate IVC indicate hypervolemiaIVC distensibility/collapsibility index give anappropriate clue for fluid deficit.IVC distensibility idex = IVCd (ก่อน) - IVCd(หลัง) / ก่อน รวมกับหลัง x 0.5...> 13 percent represent preload deficit.
  20. 20. static volumetricITBVGEDV index
  21. 21. ITBV and GEDVMeasured via PiCCO thermodilution (transpulmonary)ITBV = volume in 4 chambers of heartGEDV = good estimation of intravascularvolume and preloadLimitation to predict fluid responsiveness.
  22. 22. dynamic indices of intravascular volume
  23. 23. Correlation to F-S curve
  24. 24. fluid responsiveness- PPV give a best correlation to fluid responsiveness- Static preload monitoring demonstrated the poorcorrelation to fluid responsiveness
  25. 25. passive leg rising testconsider as “autotransfusion”recent study demonstrated the strongcorrelation of PLR to predict fluidresponsiveness with ROC of 0.95Continuous measure SV or CO on a real timebasis eg. echocardiogram, CCO-pulsecontour analysisCO increase > 10% during PLR indicate fluidresponsiveness.
  26. 26. PLR
  27. 27. The endpoint ofshock resuscitation
  28. 28. PAOP MAP
  29. 29. Which parameter shouldbe used for the endpoint of shock resuscitation? PAOP MAP
  30. 30. Systolic Blood SvO2pressure Urine output consciousness Capillary refilled ScvO2 Lactate level CVP CO PAOP MAP
  31. 31. Current aims for shock management Good tissue oxygenation Good BP Good CO
  32. 32. Upstream and downstream theory preload Upstream• CVP, POAP• BP• CO contractility• SVR afterload downstream Tissue perfusion and oxygenation
  33. 33. Upstream andDownstream theory
  34. 34. Tissue perfusion: Oxygen delivery Oxygen contentheart = O2 in Hb + O2 in plasma tissue Oxygen delivery (DaO2) = Cardiac output (CO) x oxygen content
  35. 35. Blood pressure• Represent organ perfusion pressure• MAP –More reliable indication of tissue perfusion than SBP and DBP –Reflect autoregulation limit of organ blood flow – CPP = MAP –ICP (normal 60-90 mmHg) –APP = MAP – IAP (normal 50-70 mmHg) –RPP normal 70-90 mmHg Goodrich. AACN 2006.
  36. 36. Blood pressure• Optimal MAP is unknown• MAP > 65 mmHg is now recommended as EGDT study• Targeted BP does not necessarily equate to tissue perfusion, but have to achieve for the first step.• Elderly may require higher MAP due to vasculopathy• Previous hypertensive group may require MAP higher than normotensive one.
  37. 37. General management of• Reverse hypotension• Adequate oxygen delivery/ organ perfusion
  38. 38. Downstream monitoring Global downstream Regional downstream monitoring monitoring• Serum lactate• Mixed/ central venous saturation and gases• Base excess
  39. 39. Venous blood gases
  40. 40. Venous blood gases• ScvO2• SvO2• PvCO2• pH
  41. 41. Venous oxygen saturationCvO2 = 13.4 CaO2 = 13.4x Hb x SvO2 x Hb x SaO2
  42. 42. Venous saturation O2 consumption O2 delivery
  43. 43. Oxygen delivery and consumption
  44. 44. Venous oxygensaturation
  45. 45. Mixed venous blood sampling MvO2(SvO2)
  46. 46. SvO2 SvO2 Consequence level > 75% •Normal extraction •Oxygen supply > oxygen demand51%-75% •Compensatory extraction •Increase oxygen demand31%-50% •Decrease oxygen supply •Exhaustion of extraction •Begin lactic acidosis25%-30% •Oxygen supply < oxygen demand •Severe lactic acidosis < 25% •Cellular death Targeted SvO2 > 70%
  47. 47. SvO2 as a treatment endpoint• Goal directed therapy to keep SvO2 > 70% over 5 days did not lower the mortality in septic shock. Gattinoni. NEJM 1995.• MAP > 65 mmHg and SvO2 > 70% in the first 48 hours after resuscitation shown less septic mortality. (retrospective study) Varpula.ICM 2005.
  48. 48. Central venousoxygen saturationScvO2
  49. 49. SvO2 vs ScvO2
  50. 50. SvO2 vs ScvO2
  51. 51. ScvO2 as a target Van Beest. Crit Care 2008.
  52. 52. The first ScvO2 and mortalityMortality rate Pope. Ann Emerg Med 2010.
  53. 53. Targeted ScvO2• ScvO2 > 70 % reflected adequate tissue perfusion (normoxia)• Do not keep ScvO2 too high.• Immediate ScvO2 level will be used for the endpoint if it is on lower side.• May require addition parameter to assess perfusion state.
  54. 54. PvCO2 PvCO2 CO2 Cardiac CO2 production output elimination The higher PvCO2, the lower CO
  55. 55. PvCO2 and PaCO2 difference• Inverse non linear significant relation between oxygen delivery, P(v-a)CO2 and pH(v-a) Brandi. Minerva Anestesio 1995.• Increase P(v-a)CO2 mainly related to decrease in cardiac output and increased in ischemic hypoxia not in hypoxic hypoxia Vallet. J Appl Physiol 2000.
  56. 56. PvCO2 and PaCO2difference and mortality • dPCO2 is significantly higher in non survival group • The cut of value of dPCO2 is 6 mmHg Bakker. Chest 1992.
  57. 57. PcvCO2 vs. PvCO2 Agreement = 0.978 Cuschieri. ICM 2005.
  58. 58. PcvCO2 vs. PvCO2 R2 = 0.892, p <0.0001 Cuschieri. ICM 2005.
  59. 59. PcvCO2 as a target for resuscitation P(cv-a)CO2 may serve as a global tissue perfusion index when ScvO2 goal reached Vallee. ICM 2008.
  60. 60. PcvCO2 as a target for resuscitation Vallee. ICM 2008. • High dPCO2 associated with lower CI and higher lactate level R=0.58, p<0.0001
  61. 61. PvCO2 or PcvCO2• Interchangeable• Level of PvCO2 and PcvCO2 invert correlation to cardiac index• dPCO2 or P(cv-a)CO2 may be a better parameter to indicate global tissue perfusion than ScvO2• Clinical study should be done to confirm the hypothesis.
  62. 62. Metabolism of lactateglucose 2 Pyruvate 2 Lactate 47 kcalKreb’s cycle oxidation gluconeogenesis673 kcal 652 kcal glucose
  63. 63. Lactate• generated through anaerobic metabolism• advocated as index of tissue hypoperfusion• Endotoxin induced lactate production without hypoperfusion• level represents a balance between generation and elimination• Hyperlactatemia: lactate level > 2 mmol/L• Lactic acidosis: lactate level > 4 mmol/L
  64. 64. Lactate• high lactate levels (> 4mmol/L) in critically ill patients associated with increased mortality (Bakker et al. Chest 1991)• lactate clearance better predictor of mortality – lac-time: time in which blood lactate > 2 mmol/l – survivors had decreased lac-time – lac-time also directed correlated with number of organ failures (Bakker et al. (Am J Surg 1996)
  65. 65. Blood Lactateserial lactate levels may improve the prognostic value and help guide therapy Nguyen et al. Crit Care Med 2004
  66. 66. Lactate clearance as a target Jones. JAMA 2010
  67. 67. Lactate clearance as a target Jones. JAMA 2010 Lactate <10% clearance >10%
  68. 68. Lactate clearance as a target p = NS23% 10.017% 7.5 •p = NS12% 5.06% 2.50% 0 mortality (%) LOS (D) lactate guided Jones. JAMA 2010 ScvO2 guided
  69. 69. Lactate clearance as a target Jansen. AJRCCM 2010.
  70. 70. Lactate clearance as a target Jansen. AJRCCM 2010.
  71. 71. Lactate clearance as a target44% •p = 0.06733%22%11% 0% hospital mortality (%) lactate guided non-lactate guidedLactate guided group Hazard ratio P-valueIn hospital mortality 0.61 (0.43-0.87) 0.006ICU mortality 0.66 (0.45-0.98) 0.037 Jansen. AJRCCM 2010.
  72. 72. Lactate as a target• Hyperlactatemia associated with mortality• Rapid lactate clearance improved ICU outcome• Lactate guided resuscitation is feasible.• Aggressive fluid resuscitation, inotropes and vasodilator will reduce blood lactate.
  73. 73. Goal of shock resuscitationReverse of hypotension (macro)Clinically well perfusedAdequate tissue perfusion and oxygenation (micro) There has been no the best parameter to date.  combine parameter is suggested Use common parameters such as ScvO2 or lactate is reasonable The supporting data of sophisticated device is now scanty.

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