How to evaluate the different moralities available in the assessment of fluid status for the critically ill patient!

1. The Hemodynamic Puzzle
O2ER
NIRS
SVV
Lactate

2. EnergyMetabolism
(OxygenConsumption)
(Ml/min/m2)
Delayed Repayment of
O2 Debt
Full Recovery
Possible
Excessive O2 Deficit
Produces Lethal Cell Injury
with Non-recovery
Recovery Possible
Time
Oxygen Deficit
Oxygen
Deficit
Oxygen Deficit
Oxygen Debt: To Pay or Not to Pay?
The principle task of acute care is
to avoid or correct oxygen debt
by optimization of the oxygen
supply and consumption.

3. Providing the right amount of fluid is vital in a
critically ill patient, as both too little and too much
can result in poor outcomes
Under Resuscitation Over Resuscitation
It is just as important to recognize that DO2 and tissue perfusion has
normalized, therefore any further measures to increase DO2 may do harm
by unnecessary over resuscitation

4. HR and BP as Resuscitation Endpoint
NIRS
SVV SvO2
Heart Rate
Urine Output
Mental Status
OPSI
GEDV
SV

6. DO2 ml*m-2*min-1
100 300 500 700 900 1100
n= 1232
30
60
90
120
150
180
MAPmmHg
Correlation Between Arterial Pressure
And Oxygen Delivery

7. DO2 ml*m-2*min-1
100 300 500 700 900 1100
n= 1236
30
60
90
120
150
180
HRb/min
Correlation Between Heart Rate
And Oxygen Delivery

8. CVP as a Resuscitation Endpoint
NIRS
SVV SvO2
Heart Rate
Urine Output
Mental Status
OPSI
GEDV
SV

9. Passive leg raising (PLR)
Volume of blood transferred (usually 200-300 mL) to the heart during PLR is sufficient to increase the left cardiac preload
and thus challenge the Frank-Starling curve.
Maximal effect occurs at 30-90 seconds and assess for a 10% increase in stroke volume (cardiac output monitor) or using
a surrogate such as pulse pressure (using an arterial line)

10. Diagnostic Accuracy of Passive Leg Raising for Prediction of Fluid
Responsiveness in Adults: Systematic Review and Meta-analysis
of Clinical Studies.
• Meta-analysis 9 studies
• PLR changes in CO predicts fluid
responsiveness
• Regardless of ventilation mode
and cardiac rhythm
• Difference in CO of 18%
distinguished responder from NR
Cavallaro, F. et al. Intensive Care Med. 2010 Sep;36(9):1475-83
The pooled sensitivity and specificity of PLR-cCO were
89.4% (84.1-93.4%) and 91.4% (85.9-95.2%) respectively
AUC= 0.96

11. CVP as a Resuscitation Endpoint
NIRS
SVV SvO2
Heart Rate
Urine Output
Mental Status
OPSI
GEDV
SV
CVP

12. • European survey:
More the 90%of intensivist
or anesthesiologists used
the CVP to guide fluid
management.
• Canadian survey:
90% of intensivists used the
CVP to monitor fluid
resuscitation in patients with
septic shock.

13. Crit Care Med 2013; 41:1774–1781)

14. Paul E. Marik, MD, FCCP; Michael Baram, MD, FCCP; BobbakVahid, MD Chest. 2008;134(1):172-178.

15. Osman D1, Ridel C, Ray P, Monnet X, Anguel N, Richard C,Teboul JL. Crit Care Med. 2007 Jan;35(1):64-8.
The study demonstrates that cardiac filling pressures are poor
predictors of fluid responsiveness in septic patients. Therefore,
their use as targets for volume resuscitation must be
discouraged, at least after the early phase of sepsis has
concluded

16. There are no data to support the widespread
practice of using central venous pressure to
guide fluid therapy.This approach to fluid
resuscitation should be abandoned.
Marik PE, Cavallazzi R . Crit Care Med. 2013 Jul;41(7):1774-81..

17. IVC Diameter and Collapsibility as End Point
NIRS
SVV SvO2
Heart Rate
Urine Output
Mental Status
OPSI
GEDV
CVP

18. Simultaneous measurements of the central venous pressure (CVP) and
IVC diameter at the end of expiration in 108 mechanically ventilated
patients

19. Collapsibility Index =
𝑰𝑽𝑪 𝒎𝒂𝒙
−𝑰𝑽𝑪𝒎𝒊𝒏
𝑰𝑽𝑪 𝒎𝒂𝒙
>12% = responders
(PPV 93% and NPV92%).

20. Collapsibility Index =
𝑰𝑽𝑪 𝒎𝒂𝒙
−𝑰𝑽𝑪𝒎𝒊𝒏
𝑰𝑽𝑪 𝒎𝒂𝒙
<12% = non-responders
(PPV 93% and NPV92%).

21. Zhongheng Zhang, Xiao Xu, ShengYe, Lei Xu. Ultrasound in Medicine and Biology.Volume 40, Issue 5, Pages 845–853, May 2014
Total of 8 studies/235 Pts
ΔIVC measured is of great value in predicting fluid
responsiveness, particularly in patients on
controlled mechanical ventilation

22. CO/SV as a Resuscitation Endpoint
NIRS
SVV SvO2
Heart Rate
Urine Output
Mental Status
OPSI
SV/CO
CVP
GEDV

23. Effects of Cardiac Output and Stroke Volume Guided
Hemorrhage and Fluid Resuscitation
CI-group SVI-group
Tbsl T0 tend Tbsl T0 Tend
SVI (ml/m2) 33.6 ± 6.2 14.6 ± 10.1 23.4 ± 7.9 26.8 ± 4.7 13.4 ± 2.3 26.6 ± 4.1
CI (l/min/m2) 2.88 ± 0.42 1.79 ± 0.53 2.73 ± 0.35 2.6 ± 0.4 1.8 ± 0.3 2.9 ± 0.5
MAP (mmHg) 127 ± 13.07 75 ± 25 85 ± 22 112 ± 23 74 ± 18 91 ± 19
Heart rate (beats/min) 87 ± 16 140 ± 40 124 ± 37 95 ± 12 131 ± 27 107 ± 16
Central venous oxygen
saturation (%)
81 ± 8 58 ± 18 64 ± 15 78 ± 7 61 ± 5 73 ± 9
Venous to arterial carbon
dioxide gap (mm Hg)
3.3 ± 3.1 8.9 ± 3.3 7.8 ± 4.8 5.3 ± 2 9.6 ± 2.3 5.1 ± 2.6
GEDV (ml/m2) 317 ± 36 198 ± 57 249 ± 46 309 ± 57 231 ± 61 287 ± 49
Stroke volume variation (%) 10.8 ± 5.5 17.3 ± 5.1 16.4 ± 8.2 13.6 ± 4.3 22.6 ± 5.6 12.2 ± 4.3
Nemeth, M. et al. Acta Anaesthesiol Scand (2014). doi:10.1111/aas.12312
21 animal subjects were bled until CI (n=9) or SVI (n=12) decreased by 50% then resuscitated during 60 minutes with LR till
target is achieved

24. SVV & PPV as End Point
SvO2
Heart Rate
Urine Output
Mental Status
OPSI
SV
GEDV
SVVCVP

25. Hemodynamics During Positive Pressure
Ventilation: SVV and PPV

26. Preload
Stroke
Volume
0
0
Higher PVI = More likely to respond to fluid administration
24 %
10 %
Lower PVI = Less likely to respond
to fluid administration
PVI to Help Clinicians
Optimize Preload / Cardiac Output
Frank-Starling Relationship

27. Determine success of fluid by the response in stroke
volume/index and SvO2
30
Stroke Volume
End-Diastolic Volume
D < 10%
D > 10%
D 0%
Fluid Responders
Fluid Non-Responders

28. Dynamic parameters should be used preferentially to static parameters to
predict fluid responsiveness in ICU patients

29. Dynamic Changes in Arterial Waveform DerivedVariables and Fluid
Responsiveness in MechanicallyVentilated Patients: A Systematic
Review of Literature
Marik, PE et al. (2009). Citi Care Med. 37: 2642-2647
Sens. 0.89
Spec. 0.88
AUC= 0.94

30. Lactic Acid as Endpoint Resuscitation
Heart Rate
Urine Output
Mental Status
OPSI
SV
Lactate
CVP
GEDV
SVV

31. Oxygen consumption
VO2 mls/min
Oxygen delivery
DO2 mls/min
300mls/min
Lactate
Critical
DO2
Oxygen
Debt
DO2 independent in
normal patients
DO2 dependent in
septic patients

32. Prolonged lactate clearance is associated with increased
mortality in the surgical intensive care unit
J. McNelis et al. The American Journal of Surgery 182 (2001) 481–485

33. Early lactate-guided therapy in intensive care unit
patients: a multicenter, open-label, randomized
controlled trial.
Jansen TC,van Bommel J, Schoonderbeek FJ,Sleeswijk Visser SJ, vander Klooster JM, Lima AP, et al. Am J Respir Crit Care Med (2010) 182:752–
61.doi:10.1164/rccm.200912-1918OC

34. Effects of Cardiac Output and Stroke Volume
Guided Hemorrhage and Fluid Resuscitation
CI-group SVI-group
Tbsl T0 tend Tbsl T0 Tend
Oxygen delivery
(ml/min/m2)
335 ± 63 158 ± 62 284 ± 52 419 ± 62 272 ± 56 341 ± 62
VO2 (ml/min/m2) 44 ± 25 62 ± 38 76 ± 34 77 ± 26 96 ± 19 82 ± 27
Oxygen extraction
(VO2/DO2)
0.13 ± 0.08 0.38 ± 0.19 0.32 ± 0.14 0.20 ± 0.07 0.36 ± 0.05 0.24 ± 0.09
Central venous oxygen
saturation (%)
81 ± 8 58 ± 18 64 ± 15 78 ± 7 61 ± 5 73 ± 9
Venous to arterial carbon
dioxide gap (mm Hg)
3.3 ± 3.1 8.9 ± 3.3 7.8 ± 4.8 5.3 ± 2 9.6 ± 2.3 5.1 ± 2.6
Lactate (mmol/L) 3.6 ± 1.1 5.0 ± 1.6 4.6 ± 2.0 1.62 ± 0.43 3.86 ± 1.49 3.54 ± 1.9
Hemoglobin (g/L) 9.0 ± 0.7 8.0 ± 2.7 6.9 ± 1.3 12.05 ± 1.37 11.22 ± 1.39 8.45 ± 1.1
Nemeth, M. et al. Acta Anaesthesiol Scand (2014). doi:10.1111/aas.12312

35. Oxygen Extraction-based Resuscitation
SVVHeart Rate
Urine Output
Mental Status
SV
GEDV
SVV
O2ER
SvO2
ScvO2
CVP

36. DO2= CO x [CaO2]
CaO2= [Hb X 1.34 x SaO2] + 0.003 x PaO2
VO2= CO x [CaO2-CvO2]
O2ER = 𝟏𝟎𝟎 𝐗 VO2
DO2
Oxygen Extraction-based Resuscitation
ScVO2

37. Effects of Cardiac Output and Stroke Volume
Guided Hemorrhage and Fluid Resuscitation
CI-group SVI-group
Tbsl T0 tend Tbsl T0 Tend
Oxygen delivery
(ml/min/m2)
335 ± 63 158 ± 62 284 ± 52 419 ± 62 272 ± 56 341 ± 62
VO2 (ml/min/m2) 44 ± 25 62 ± 38 76 ± 34 77 ± 26 96 ± 19 82 ± 27
Oxygen extraction
(VO2/DO2)
0.13 ± 0.08 0.38 ± 0.19 0.32 ± 0.14 0.20 ± 0.07 0.36 ± 0.05 0.24 ± 0.09
Central venous oxygen
saturation (%)
81 ± 8 58 ± 18 64 ± 15 78 ± 7 61 ± 5 73 ± 9
Venous to arterial carbon
dioxide gap (mm Hg)
3.3 ± 3.1 8.9 ± 3.3 7.8 ± 4.8 5.3 ± 2 9.6 ± 2.3 5.1 ± 2.6
Lactate (mmol/L) 3.6 ± 1.1 5.0 ± 1.6 4.6 ± 2.0 1.62 ± 0.43 3.86 ± 1.49 3.54 ± 1.9
Hemoglobin (g/L) 9.0 ± 0.7 8.0 ± 2.7 6.9 ± 1.3 12.05 ± 1.37 11.22 ± 1.39 8.45 ± 1.1
Nemeth, M. et al. Acta Anaesthesiol Scand (2014). doi:10.1111/aas.12312

38. Mixed Venous Saturation in Critically Ill Patient
Oxygen Supply: DO2 Oxygen Demand: VO2
SvO2/ScvO2
Low
↓DO2 ↑VO2
Anemia
Bleeding
Hypovolemia
Hypoxia
Heart faliure
Pain
Agitation
Shivering
Seizure
Fever
High
↑DO2 ↓VO2
Hg
Oxygen
Fluids
Inotropics
Sedation
Analgesia
Hypothermia
Sepsis

39. SvO2 %
DO2/VO2
25 705540 85 100
1.0
2.8
4.6
6.4
8.2
10.0
r= 0.906
y= -9.58 + 0.19*x
n= 1149

40. Lee J et al. (1972) Anaesthesiology 36: 472
%SsvO2
% SvO2
100
80
60
40
20
0 20 40 60 80 100
r= 0.73
r= 0.88
Shock
Normal

41. Reinhart K et al, Chest, 1989; 95:1216-1221
SvO2 closely correlates with ScvO2
Time (min)
%Sat
80
60
40
20
0
300 60 90 120 150 180 210 240
Normoxia Bleeding VolumeTherapy (HAES) Bleeding
Hypoxia
Normoxia
Hyperoxia
Mixed venous
Central venous

42. Pope, J et al. Ann Emerg Med. 55:40-46
ScvO2 of > 90%,ScvO2 of < 70%,

43. Oxygen Parameters as Endpoint
SVVHeart Rate
Urine Output
Mental Status
SV
GEDV
SVV
O2ER
SvO2
ScvO2
P(cv-a)CO2
CVP

44. P(cv-a)CO2
Normal is 2-5 mmHg.
Is not a marker of tissue hypoxia
but it is a marker of the adequacy
of cardiac output
∆PCO2= K X
𝑽𝑪𝑶 𝟐
𝑪𝒂𝒓𝒅𝒊𝒂𝒄 𝑶𝒖𝒕𝒑𝒖𝒕

45. Persistently high venous-to-arterial carbon dioxide differences
during early resuscitation are associated with poor outcomes in
septic shock
Ospina-Tascón GA et al., Crit Care. 2013; 17(6)
The persistence of high Pv-aCO2
during the early resuscitation of
septic shock was associated with
more severe multi-organ
dysfunction and worse outcomes at
day-28
H-H, mixed venous-to-arterial carbon dioxide difference (Pv-
aCO2) high at Time 0 (T0) and 6 hours later (T6); L-H, Pv-
aCO2 normal at T0 and high at T6; H-L, Pv-aCO2 high at T0 and
normal at T6; and L-L, Pv-aCO2 normal at T0 and T6

46. Central Venous-to-Arterial Gap Is a Useful Parameter in
Monitoring Hypovolemia-Caused Altered Oxygen Balance:
Animal Study
ScvO2 < 73% and CO2
gap >6 mmHg can be
complementary tools
in detecting
hypovolemia-caused
imbalance of oxygen
extraction.
Kocsi S et al, Crit Care Res Pract. 2013; 583-598.

47. The Hemodynamic Puzzle
SVVHeart Rate
Urine Output
Mental Status
SV
GEDV
SVV
O2ER
SvO2
ScvO2
P(cv-a)CO2 NIRSOPSI
CVP

48. Near-infrared spectroscopy (NIRS)

49. NIRS
StO2 (at 20 mm, skeletal muscle) is an index of profusion that tracks
DO2 during active resuscitation
Crit Care. 2009; 13(Suppl 5): S10.

50. Orthogonal Polarization Spectral Imaging
(OPS): Sublingual capillaroscopy.
Orthogonal polarization
spectral (OPS) imaging is an
optical imaging technique
that uses a handheld
microscope and green
polarized light to visualize
the red blood cells in the
microcirculation of organ
surfaces

51. Orthogonal Polarization Spectral Imaging
(OPS): Sublingual capillaroscopy.
Red blood cells are visualised as black-grey points flowing along the vessels. Up-right and up-left: normal findings; bottom-
left: septic shock; bottom-right: after cardiac arrest under therapeutic hypothermia

53. The Hemodynamic Puzzle
O2ER
NIRS
SVV SvO2
ScvO2
Heart Rate
Urine Output
Mental Status
OPSI
GEDV
P(cv-a)CO2
Lactate
SV
CVP