The Hemodynamic Puzzle

SVV

NIRS

O2ER Lactate

Oxygen Debt: To Pay or Not to Pay? Full Recovery Possible

Energy Metabolism (Oxygen Consumption) (Ml/min/m2)

Delayed Repayment of O2 Debt

Oxygen Deficit

Oxygen Deficit Oxygen Deficit

Time Excessive O2 Deficit Produces Lethal Cell Injury with Non-recovery Recovery Possible

The principle task of acute care is to avoid or correct oxygen debt by optimization of the oxygen supply and consumption.

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

HR and BP as Resuscitation Endpoint SVV

Heart Rate

GEDV

SV

SvO2

NIRS OPSI

Urine Output Mental Status

Correlation Between Arterial Pressure And Oxygen Delivery 180

MAP mmHg

150

120

90

60

n= 1232

30 100

300

500

700

900

DO2 ml*m-2*min-1

1100

Correlation Between Heart Rate And Oxygen Delivery 180

HR b/min

150

120

90

60

n= 1236

30 100

300

500

700

DO2 ml*m-2*min-1

900

1100

CVP as a Resuscitation Endpoint SVV

Heart Rate

GEDV

SV

SvO2

NIRS OPSI

Urine Output Mental Status

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)

Diagnostic Accuracy of Passive Leg Raising for Prediction of Fluid Responsiveness in Adults: Systematic Review and Metaanalysis of Clinical Studies.

AUC= 0.96

• 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

The pooled sensitivity and specificity of PLR-cCO were 89.4% (84.1-93.4%) and 91.4% (85.9-95.2%) respectively Cavallaro, F. et al. Intensive Care Med. 2010 Sep;36(9):1475-83

CVP as a Resuscitation Endpoint Heart Rate

CVP

SVV

GEDV

SV

SvO2

NIRS OPSI

Urine Output Mental Status

• European survey:

90%

More the 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.

Crit Care Med 2013; 41:1774–1781)

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

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

Osman D1, Ridel C, Ray P, Monnet X, Anguel N, Richard C, Teboul JL. Crit Care Med. 2007 Jan;35(1):64-8.

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..

IVC Diameter and Collapsibility as End Point Heart Rate

CVP

SvO2

SVV

OPSI NIRS GEDV

Urine Output Mental Status

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

Collapsibility Index =

𝑰𝑽𝑪𝒎𝒂𝒙 −𝑰𝑽𝑪𝒎𝒊𝒏 𝑰𝑽𝑪𝒎𝒂𝒙

>12% = responders (PPV 93% and NPV92%).

𝑰𝑽𝑪𝒎𝒂𝒙 −𝑰𝑽𝑪𝒎𝒊𝒏 Collapsibility Index = 𝑰𝑽𝑪𝒎𝒂𝒙

10%

Fluid Non-Responders

Fluid Responders

End-Diastolic Volume

29

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

Dynamic Changes in Arterial Waveform Derived Variables and Fluid Responsiveness in Mechanically Ventilated Patients: A Systematic Review of Literature

Sens. 0.89 Spec. 0.88 AUC= 0.94

Marik, PE et al. (2009). Citi Care Med. 37: 2642-2647

Lactic Acid as Endpoint Resuscitation Heart Rate

CVP

OPSI

SVV SV

GEDV

Urine Output Mental Status

Lactate

Oxygen consumption VO2 mls/min

Critical DO2

DO2 independent in normal patients

DO2 dependent in septic patients

Oxygen Debt

Lactate Oxygen delivery

300mls/min

DO2 mls/min

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

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

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

Oxygen Extraction-based Resuscitation Heart Rate

CVP

SVV

SvO2

SV

GEDV

Urine Output Mental Status

ScvO2

O2ER

Oxygen Extraction-based Resuscitation ScVO2

O2ER = 𝟏𝟎𝟎 𝐗 VO2 DO 2 VO2= CO x [CaO2-CvO2]

CaO2= [Hb X 1.34 x SaO2] + 0.003 x PaO2 DO2= CO x [CaO2]

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

Mixed Venous Saturation in Critically Ill Patient Oxygen Supply: DO2

Oxygen Demand: VO2 SvO2/ScvO2

Low

High

↓DO2

↑VO2

↑DO2

↓VO2

Anemia Bleeding Hypovolemia Hypoxia Heart faliure

Pain Agitation Shivering Seizure Fever

Hg Oxygen Fluids Inotropics

Sedation Analgesia Hypothermia Sepsis

10.0

DO2/ VO2

8.2

6.4

4.6 r= 0.906 y= -9.58 + 0.19*x n= 1149

2.8

1.0 25

40

55

70

SvO2 %

85

100

100 Shock

% SsvO2

80

r= 0.73

60

Normal

r= 0.88 40

20

0 Lee J et al. (1972) Anaesthesiology 36: 472

20

40

60

% SvO2

80

100

SvO2 closely correlates with ScvO2 Mixed venous Central venous

80

Normoxia

Bleeding

Volume Therapy (HAES)

Hyperoxia

20

Normoxia

40

Hypoxia

% Sat

60

Bleeding

0 0

30

60

90

120

Time (min) Reinhart K et al, Chest, 1989; 95:1216-1221

150

180

210

240

ScvO2 of < 70%,

Pope, J et al. Ann Emerg Med. 55:40-46

ScvO2 of > 90%,

Oxygen Parameters as Endpoint Heart Rate

CVP

SVV

SvO2

SV

GEDV

Urine Output Mental Status

P(cv-a)CO2

ScvO2

O2ER

P(cv-a)CO2 ∆PCO2= K X

𝑽𝑪𝑶𝟐 𝑪𝒂𝒓𝒅𝒊𝒂𝒄 𝑶𝒖𝒕𝒑𝒖𝒕

Normal is 2-5 mmHg. Is not a marker of tissue hypoxia but it is a marker of the adequacy of cardiac output

Persistently high venous-to-arterial carbon dioxide differences during early resuscitation are associated with poor outcomes in septic shock 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 (PvaCO2) high at Time 0 (T0) and 6 hours later (T6); L-H, PvaCO2 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

Ospina-Tascón GA et al., Crit Care. 2013; 17(6)

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.

The Hemodynamic Puzzle Heart Rate

CVP

SVV

SvO2

SV

ScvO2

GEDV

Urine Output Mental Status

P(cv-a)CO2

OPSI

NIRS

O2ER

Near-infrared spectroscopy (NIRS)

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.

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

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; bottomleft: septic shock; bottom-right: after cardiac arrest under therapeutic hypothermia

The Hemodynamic Puzzle Heart Rate

CVP

SVV

SvO2

SV

ScvO2

GEDV

Urine Output Mental Status

P(cv-a)CO2

OPSI

O2ER

NIRS Lactate