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Critical care
tutorial for
chest fellow
Contents

Basic hemodynamic monitoring for
chest physician
 Fluid responsiveness
 Resuscitation target/endpoint
Hemodynamic

BP = CO x SVR

BP = SV x HR x SVR

BP = (EDV-ESV) x HR x SVR

BP = preload x cardiac function x afterload
preload monitoring and
      fluid responsiveness

                             d non-re sponsive
             ive        flui
            ns



CO
            po




                                    Frank- Starling Curve
       res
       id
     flu




                   preload
Frank-Starling
       mechanism
                                       n
                            c fu nctio
                  al c ardia
          Norm

CO
                             a c function
             Impa ired cardi




        preload
preload
      measurement
2 types of preload assessment

  1. static preload monitoring

    pressure: CVP, PAOP

    Volumetric: ITBV, GEDV

    Ultrasound: LVdD, IVCd
preload
     measurement

2. dynamic preload monitoring

 parameter variation: SVV, PPV, SPV

 echocardiographic variation: Ao flow
 velocity, IVC distensibility index.
CVP
(central venous pressure)
Central Venous
                     Pressure
                            B
RAP/RVEDP/LVEDP




                                       A




                     RAV/RVEDV/LVEDV
Central Venous
                     Pressure
                            B
RAP/RVEDP/LVEDP




                                       A




                     RAV/RVEDV/LVEDV
CVP as volume
measurement




            Marik. Chest 2008.
CVP to predict fluid
  responsiveness




                 Michard. Chest 2002.
Neither CVP or Ppao reflect
Ventricular Volumes or tract preload-
           responsiveness




             Kumar et al. Crit Care Med 32:691-9, 2004
CVP
Not a good parameter
   to predict fluid
   responsiveness
  in both CVP and
        dCVP
Predicting Fluid
                       Responsiveness
                   in ICU Patients by CVP
                             Responders / Non-responders      % Responders
Calvin (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
PAOP pressure)
(pulmonary artery occlusive




measure LVEDP, not LVEDV or LV preload

limitation similar to CVP measurement
Predictors for fluid
  responsiveness
              15 % change in
                   CO




                 Michard. AJRCCM 2000.
LVED area
measure under echocardiogram

LV dimension during diastole

LVEDA correlate well to ITBV and GEDV

LVEDd < 25 mm or LVDA < 55 cm2 indicate
hypovolemia

not a good predictor for fluid responsiveness
IVC diameter
collapse IVC indicate volume depletion

Dilate IVC indicate hypervolemia

IVC distensibility/collapsibility index give an
appropriate clue for fluid deficit.

IVC distensibility idex = IVCd (ก่อน) - IVCd
(หลัง) / ก่อน รวมกับหลัง x 0.5...

> 13 percent represent preload deficit.
static volumetric


ITBV

GEDV index
ITBV and GEDV

Measured via PiCCO thermodilution (trans
pulmonary)

ITBV = volume in 4 chambers of heart

GEDV = good estimation of intravascular
volume and preload

Limitation to predict fluid responsiveness.
dynamic indices of
  intravascular
      volume
Correlation to F-S
     curve
fluid responsiveness




- PPV give a best correlation to fluid responsiveness
- Static preload monitoring demonstrated the poor
correlation to fluid responsiveness
passive leg rising
       test
consider as “autotransfusion”

recent study demonstrated the strong
correlation of PLR to predict fluid
responsiveness with ROC of 0.95

Continuous measure SV or CO on a real time
basis eg. echocardiogram, CCO-pulse
contour analysis

CO increase > 10% during PLR indicate fluid
responsiveness.
PLR
The endpoint of
shock resuscitation
PAOP   MAP
Which parameter should
be used for the endpoint
 of shock resuscitation?


                PAOP       MAP
Systolic
 Blood                                   SvO2
pressure                Urine
                        output


   consciousness                        Capillary
                                         refilled

           ScvO2        Lactate level



 CVP               CO       PAOP              MAP
Current aims for shock
     management

              Good tissue
              oxygenation




    Good BP                 Good CO
Upstream and
      downstream theory
                     preload
    Upstream
•   CVP, POAP
•      BP
•      CO          contractility
•     SVR


                    afterload

                                       downstream
                Tissue perfusion and
                    oxygenation
Upstream
   and
Downstream
  theory
Tissue perfusion:
      Oxygen delivery


           Oxygen content
heart
      = O2 in Hb + O2 in plasma
                                  tissue



        Oxygen delivery (DaO2) =
  Cardiac output (CO) x oxygen content
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.
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.
General
       management of
• Reverse hypotension
• Adequate oxygen delivery/ organ
  perfusion
Downstream monitoring
  Global downstream       Regional downstream
      monitoring                monitoring
• Serum lactate
• Mixed/ central venous
  saturation and gases
• Base excess
Venous
 blood
 gases
Venous blood gases
• ScvO2
• SvO2
• PvCO2
• pH
Venous oxygen
          saturation


CvO2 = 13.4              CaO2 = 13.4
x Hb x SvO2              x Hb x SaO2
Venous saturation
                    O2
                consumption




  O2 delivery
Oxygen delivery and
   consumption
Venous
  oxygen
saturation
Mixed venous blood
              sampling
 MvO2
(SvO2)
SvO2
 SvO2                 Consequence
 level
 > 75%   •Normal extraction
         •Oxygen supply > oxygen demand
51%-75% •Compensatory extraction
        •Increase oxygen demand
31%-50% •Decrease oxygen supply
        •Exhaustion of extraction
        •Begin lactic acidosis
25%-30% •Oxygen supply < oxygen demand
        •Severe lactic acidosis

 < 25%   •Cellular death

               Targeted SvO2 > 70%
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.
Central venous
oxygen saturation
ScvO2
SvO2 vs ScvO2
SvO2 vs ScvO2
ScvO2 as a target




               Van Beest. Crit Care 2008.
The first ScvO2 and
                      mortality
Mortality rate




                              Pope. Ann Emerg Med 2010.
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.
PvCO2
               PvCO2


     CO2       Cardiac      CO2
  production   output    elimination




         The higher PvCO2,
           the lower CO
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.
PvCO2 and PaCO2
difference and mortality
            •       dPCO2 is
             significantly higher in
               non survival group
            • The cut of value of
               dPCO2 is 6 mmHg



                      Bakker. Chest 1992.
PcvCO2 vs. PvCO2
           Agreement = 0.978




                     Cuschieri. ICM 2005.
PcvCO2 vs. PvCO2
          R2 = 0.892, p <0.0001




                            Cuschieri. ICM 2005.
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.
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
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.
Metabolism of lactate

glucose

 2 Pyruvate           2 Lactate             47 kcal



Kreb’s cycle
               oxidation     gluconeogenesis


673 kcal       652 kcal           glucose
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
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)
Blood Lactate
serial lactate levels may improve the prognostic value and
                       help guide therapy




                                     Nguyen et al. Crit Care Med 2004
Lactate clearance
   as a target
              Jones. JAMA 2010
Lactate clearance
   as a target
                      Jones. JAMA 2010




    Lactate    <10%
   clearance
  >10%
Lactate clearance
         as a target
           p = NS
23%                           10.0



17%                            7.5
                                        •p = NS

12%                            5.0



6%                             2.5



0%                               0
       mortality (%)                         LOS (D)

                       lactate guided
                                                   Jones. JAMA 2010
                       ScvO2 guided
Lactate clearance
   as a target




              Jansen. AJRCCM 2010.
Lactate clearance
   as a target




              Jansen. AJRCCM 2010.
Lactate clearance
         as a target
44%
                       •p = 0.067
33%

22%

11%

 0%
                            hospital mortality (%)     lactate guided
                                                       non-lactate guided

Lactate guided group                  Hazard ratio     P-value
In hospital mortality               0.61 (0.43-0.87)    0.006
ICU mortality                       0.66 (0.45-0.98)    0.037

                                                         Jansen. AJRCCM 2010.
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.
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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Lecture chest fellow_PSU 2012

  • 2. Contents Basic hemodynamic monitoring for chest physician Fluid responsiveness Resuscitation target/endpoint
  • 3. Hemodynamic BP = CO x SVR BP = SV x HR x SVR BP = (EDV-ESV) x HR x SVR BP = preload x cardiac function x afterload
  • 4. preload monitoring and fluid responsiveness d non-re sponsive ive flui ns CO po Frank- Starling Curve res id flu preload
  • 5. Frank-Starling mechanism n c fu nctio al c ardia Norm CO a c function Impa ired cardi preload
  • 6. preload measurement 2 types of preload assessment 1. static preload monitoring pressure: CVP, PAOP Volumetric: ITBV, GEDV Ultrasound: LVdD, IVCd
  • 7. preload measurement 2. dynamic preload monitoring parameter variation: SVV, PPV, SPV echocardiographic variation: Ao flow velocity, IVC distensibility index.
  • 9. Central Venous Pressure B RAP/RVEDP/LVEDP A RAV/RVEDV/LVEDV
  • 10. Central Venous Pressure B RAP/RVEDP/LVEDP A RAV/RVEDV/LVEDV
  • 11. CVP as volume measurement Marik. Chest 2008.
  • 12. CVP to predict fluid responsiveness Michard. Chest 2002.
  • 13. Neither CVP or Ppao reflect Ventricular Volumes or tract preload- responsiveness Kumar et al. Crit Care Med 32:691-9, 2004
  • 14. CVP Not a good parameter to predict fluid responsiveness in both CVP and dCVP
  • 15. Predicting Fluid Responsiveness in ICU Patients by CVP Responders / Non-responders % Responders Calvin (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. PAOP pressure) (pulmonary artery occlusive measure LVEDP, not LVEDV or LV preload limitation similar to CVP measurement
  • 17. Predictors for fluid responsiveness 15 % change in CO Michard. AJRCCM 2000.
  • 18. LVED area measure under echocardiogram LV dimension during diastole LVEDA correlate well to ITBV and GEDV LVEDd < 25 mm or LVDA < 55 cm2 indicate hypovolemia not a good predictor for fluid responsiveness
  • 19. IVC diameter collapse IVC indicate volume depletion Dilate IVC indicate hypervolemia IVC distensibility/collapsibility index give an appropriate clue for fluid deficit. IVC distensibility idex = IVCd (ก่อน) - IVCd (หลัง) / ก่อน รวมกับหลัง x 0.5... > 13 percent represent preload deficit.
  • 21. ITBV and GEDV Measured via PiCCO thermodilution (trans pulmonary) ITBV = volume in 4 chambers of heart GEDV = good estimation of intravascular volume and preload Limitation to predict fluid responsiveness.
  • 22. dynamic indices of intravascular volume
  • 24. fluid responsiveness - PPV give a best correlation to fluid responsiveness - Static preload monitoring demonstrated the poor correlation to fluid responsiveness
  • 25. passive leg rising test consider as “autotransfusion” recent study demonstrated the strong correlation of PLR to predict fluid responsiveness with ROC of 0.95 Continuous measure SV or CO on a real time basis eg. echocardiogram, CCO-pulse contour analysis CO increase > 10% during PLR indicate fluid responsiveness.
  • 26. PLR
  • 27. The endpoint of shock resuscitation
  • 28. PAOP MAP
  • 29. Which parameter should be used for the endpoint of shock resuscitation? PAOP MAP
  • 30. Systolic Blood SvO2 pressure Urine output consciousness Capillary refilled ScvO2 Lactate level CVP CO PAOP MAP
  • 31. Current aims for shock management Good tissue oxygenation Good BP Good CO
  • 32. Upstream and downstream theory preload Upstream • CVP, POAP • BP • CO contractility • SVR afterload downstream Tissue perfusion and oxygenation
  • 33. Upstream and Downstream theory
  • 34. Tissue perfusion: Oxygen delivery Oxygen content heart = O2 in Hb + O2 in plasma tissue Oxygen delivery (DaO2) = Cardiac output (CO) x oxygen content
  • 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. 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. General management of • Reverse hypotension • Adequate oxygen delivery/ organ perfusion
  • 38. Downstream monitoring Global downstream Regional downstream monitoring monitoring • Serum lactate • Mixed/ central venous saturation and gases • Base excess
  • 40. Venous blood gases • ScvO2 • SvO2 • PvCO2 • pH
  • 41. Venous oxygen saturation CvO2 = 13.4 CaO2 = 13.4 x Hb x SvO2 x Hb x SaO2
  • 42. Venous saturation O2 consumption O2 delivery
  • 43. Oxygen delivery and consumption
  • 45. Mixed venous blood sampling MvO2 (SvO2)
  • 46. SvO2 SvO2 Consequence level > 75% •Normal extraction •Oxygen supply > oxygen demand 51%-75% •Compensatory extraction •Increase oxygen demand 31%-50% •Decrease oxygen supply •Exhaustion of extraction •Begin lactic acidosis 25%-30% •Oxygen supply < oxygen demand •Severe lactic acidosis < 25% •Cellular death Targeted SvO2 > 70%
  • 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.
  • 51. ScvO2 as a target Van Beest. Crit Care 2008.
  • 52. The first ScvO2 and mortality Mortality rate Pope. Ann Emerg Med 2010.
  • 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. PvCO2 PvCO2 CO2 Cardiac CO2 production output elimination The higher PvCO2, the lower CO
  • 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. PvCO2 and PaCO2 difference and mortality • dPCO2 is significantly higher in non survival group • The cut of value of dPCO2 is 6 mmHg Bakker. Chest 1992.
  • 57. PcvCO2 vs. PvCO2 Agreement = 0.978 Cuschieri. ICM 2005.
  • 58. PcvCO2 vs. PvCO2 R2 = 0.892, p <0.0001 Cuschieri. ICM 2005.
  • 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. 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. 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. Metabolism of lactate glucose 2 Pyruvate 2 Lactate 47 kcal Kreb’s cycle oxidation gluconeogenesis 673 kcal 652 kcal glucose
  • 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. 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. Blood Lactate serial lactate levels may improve the prognostic value and help guide therapy Nguyen et al. Crit Care Med 2004
  • 66. Lactate clearance as a target Jones. JAMA 2010
  • 67. Lactate clearance as a target Jones. JAMA 2010 Lactate <10% clearance >10%
  • 68. Lactate clearance as a target p = NS 23% 10.0 17% 7.5 •p = NS 12% 5.0 6% 2.5 0% 0 mortality (%) LOS (D) lactate guided Jones. JAMA 2010 ScvO2 guided
  • 69. Lactate clearance as a target Jansen. AJRCCM 2010.
  • 70. Lactate clearance as a target Jansen. AJRCCM 2010.
  • 71. Lactate clearance as a target 44% •p = 0.067 33% 22% 11% 0% hospital mortality (%) lactate guided non-lactate guided Lactate guided group Hazard ratio P-value In hospital mortality 0.61 (0.43-0.87) 0.006 ICU mortality 0.66 (0.45-0.98) 0.037 Jansen. AJRCCM 2010.
  • 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. 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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