Goal Directed Perfusion: theory, clinical results, and key ... 1... · Goal Directed Perfusion:...

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Ranuuci, M et al. 2005 M. Ranucci Director of Clinical Research Dept of Cardiothoracic and Vascular Anesthesia and Intensive Care IRCCS Policlinico S.Donato Goal Directed Perfusion: theory, clinical results, and key rules

Transcript of Goal Directed Perfusion: theory, clinical results, and key ... 1... · Goal Directed Perfusion:...

Ranuuci, M et al. 2005

M. RanucciDirector of Clinical Research

Dept of Cardiothoracic and Vascular

Anesthesia and Intensive Care

IRCCS Policlinico S.Donato

Goal Directed Perfusion: theory, clinical results, and key rules

Outline

• Theory: postoperative organ dysfunction

and oxygen dependency

• Clinical results: the hypothesis generated

by retrospective data

• Key rules: the GDP laws

Outline

• Theory: postoperative organ dysfunction

and oxygen dependency

• Clinical results: the hypothesis generated

by retrospective data

• Key rules: the GDP laws

If this debt is ‘paid back’ within 8 hours, the incidence of postoperative complications decreases, and if it is never paid then cell dysfunction and

death occur.

Performing perioperative optimization of the high-risk surgical patients.

BJA 2006;97:4-11

Lactate

Hemodynamic optimization

Cardiac Index > 4,5 L/min/m2O2 delivery > 600 ml/min /m2O2 consumption > 170 ml/min/m2

Control PAC control PAC hemodynamicoptimization

70

60

50

40

30

20

10

0

FROM NON-CARDIAC SURGERY

TO CPB-CARDIAC OPERATIONS

THE ASSOCIATION BETWEEN ORGANFAILURE AND LOW OXYGEN CONTENT/

DELIVERY

Low HCT levels on CPB have been associated with:

• AKI

• Stroke

• Low cardiac output

THE ASSOCIATION BETWEEN ORGANFAILURE AND LOW OXYGEN CONTENT/

DELIVERY

Low HCT levels on CPB have been associated with:

• KIDNEY

• BRAIN

• HEART

Chang MC. New Horizons 1999;7:35-45

Preload

Cardiac Output

THE ASSOCIATION BETWEEN ORGANFAILURE AND LOW OXYGEN CONTENT/

DELIVERY

Low HCT levels on CPB have been associated with:

• KIDNEY

• BRAIN

•HEART

Crude risk of Low Output Failure (LOF) by Nadir Hematocrit during CPB. Surgenor SD, et al. Circulation

2006;114(Suppl):43–8i.

THE ASSOCIATION BETWEEN ORGANFAILURE AND LOW OXYGEN CONTENT/

DELIVERY

Low HCT levels on CPB have been associated with:

•KIDNEY• BRAIN

• HEART

Possible perfusion-related risk factors

• CPB itself

• Perfusion pressure

• Perfusion flow

• Loss of pulsatility

• Severe hemodilution

• Poor oxygen delivery

• Hemolysis

PRESSURE

FLOW

OXYGEN CONTENT

OXYGEN DELIVERY

STRUCTURE OF THE KIDNEY(after A.Despopoulos & S.Silbernagl , Color Atlas of

Physiology, 2003)

Kidney and oxygen supply

• Renal medulla is chronically hypoxemic

• A low oxygen content (hemodilution) further

worsen kidney hypoxia

• Low blood flow is a major determinant

of reduced oxygen supply

12%

16,000 consecutive patients at the IRCCS PSD

Nadir HCT (%) on CPB

Ris

ko

f A

KI sta

ge 2

10 15 20 25 30 35 400.0

0.1

0.2

0.3

8%

HCTDO2

VCO2

DO2/VCO2

AKI (creatinine change withinfirst 48h)

DO2 262ml/min/m2

DO2/VCO2 5.3

Hct 23.5%

Measurements and calculations

• PA-catheter: Systemic haemodynamics

• Renal vein catheter:– Renal blood flow (RBF)

– Renal oxygen extraction (SaO2-SrvO2) / SaO2

– Filtration fraction (FF), the renal extraction of Cr51-EDTA

• Calculations:• Glomerular Filtration Rate (GFR) = FF x RBF x (1-Hct)

• Renal Oxygen Consumption (RVO2) = RBF x (CaO2 - CvO2)

• Renal Oxygen Delivery (RDO2) = RBF x CaO2

• Urinary excretion of NAG (every 30 minutes)

Lukas lannemyr, M D, Dpt of Cardiothoracic anaesthesia and intensive care,

Sahlgrenska University Hospital, Gothenburg, Sweden

Results –Systemic variables

0

0,5

1

1,5

2

2,5

3

Pre CPB 30' CPB 60' Post CPB

L/m

in/m

2

Cardiac Index

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10

20

30

40

50

60

70

80

90

100

Pre CPB 30' CPB 60' Post CPB

mm

Hg

Mean Arterial Pressure

0

20

40

60

80

100

120

140

Pre CPB 30' CPB 60' Post CPB

g/L

Haemoglobin

*** *** **

*** *** ***

*

* p < 0.05, ** p < 0.01, ** p < 0.001

Results –Renal variables

0

100

200

300

400

500

600

700

Pre CPB 30' CPB 60' Post CPB

ml/

min

Renal blood flow

0

20

40

60

80

Pre CPB 30' CPB 60' Post CPB

ml/

min

Glomerular filtration rate

0

5

10

15

Pre CPB 30' CPB 60' Post CPB

ml/

min

Renal oxygen consumption

*** p < 0.001

***

0

0,05

0,1

0,15

0,2

Pre CPB 30' CPB 60' Post CPB

mm

Hg/

ml/

min

Renal vascular resistance

Systemic and renal oxygen delivery

0

20

40

60

80

100

120

140

0

50

100

150

200

250

300

350

400

Pre CPB CPB 30' CPB 60' Post CPB

RD

O2

ml/

min

DO

2I m

l/m

in/m

2

DO2I

RDO2

* ** *

* *

* p < 0.05, ** p < 0.01 vs Pre

Renal oxygen extraction- oxygen supply demand

relationship

0

0,05

0,1

0,15

0,2

Pre CPB 30' CPB 60' Post CPB

* ****

* p < 0.05, *** p < 0.001 vs Pre

NAG – excretion

0

2

4

6

8

10

12

14

Pre CPB CPB 30' CPB 60' CPB 120' Post CPB30' Post CPB60' 24 hPostCPB

mL/

min

NAG/U-creatinine

*

*

*** ***

* p < 0.05, *** p < 0.001 vs Pre

DO2 600 mL/min

DO2 85 mL/min (14%)

O2ER 10%

BEFORE CPB

DO2 680 mL/min

DO2 68 mL/min (10%)

O2ER 15%

ON CPB

DO2 610 mL/min

DO2 76 mL/min (12%)

O2ER 17%

AFTER CPB

Outline

• Theory: postoperative organ dysfunction

and oxygen dependency

• Clinical results: the hypothesis generated

by retrospective data

• Key rules: the GDP laws

SvO2 not sensitive

• Single center retrospective cohort study• 16.790 non congenital adult patients undergone cardiac surgery on pump from 2000 to

december 2013• 793 (4,7%) AKI stage 2/3 in postop (increasing serum creatinine more than 200%)

Nadir Hct value during CPB was confirmed as an indipendentdeterminant of AKI (increase of 7% per 1% point of nadir Hct value

• Some factors (eGFR and EF) have been improving in the last period• Others (diabetes, redo and nonelective operations, non isolated CABG, peoperative

use of IABP and duration CPB) show a significantly higher severity.

• AKI rate significantly increased until 2005, despite no significant change in RRS• Starting 2006 AKI rate decline, despite the increase in the RRS

7.7% 7.5%

CENTRIFUGAL PUMPS

4.8%

3.7%

NO ANGIOGRAPHY ON THE DAY OF SURGERY – P=0.028

5.8% 3.1%

GOAL DIRECTED PERFUSION – P=0.001

Effect of Goal Directed Perfusion

Outline

• Theory: postoperative organ dysfunction

and oxygen dependency

• Clinical results: the hypothesis generated

by retrospective data

• Key rules: the GDP laws

Gas flowtemperature GDP monitor

Same oldperfusionistas in the 90’s

Pump flowmeasured

Low primeoxygenators

THE FIVE GDP LAWS

1. Limit hemodilution on CPB

Nadir HCT on CPB (%)

AK

I ra

te (

% w

ith

95%

CI)

16 18 20 22 24 26 28 30 32 34 36 380.00

0.05

0.10

0.15

0.20

0.25

THE FIVE GDP LAWS

2. Always stay at a DO2 > 270mL/min/m2

THE FIVE GDP LAWS

3. Increase the DO2 by actingon pump flow, PaO2

Perfusion. 2015 Jul 23. pii: 0267659115595281. [Epub ahead of print]

The effects of hyperoxaemia on tissue oxygenation in patients with a nadir

haematocrit lower than 20% during cardiopulmonary bypass.

Sevuk U(1), Altindag R(2), Baysal E(2), Yaylak B(2), Adiyaman MS(2), Akkaya S(2),

Ay N(3), Alp V(3).

Excessive haemodilution and the resulting anaemia during CPB is accompanied by a

decrease in the total arterial oxygen content, which may impair tissue oxygen

delivery. Hyperoxic ventilation has been proven to improve tissue oxygenation in

different pathophysiological states of anaemic tissue hypoxia. The aim of this

study was to examine the influence of arterial hyperoxaemia on tissue oxygenation

during CPB. Records of patients undergoing isolated CABG with CPB were

retrospectively reviewed. Patients with nadir haematocrit levels below 20% during

CPB were included in the study. Tissue hypoxia was defined as hyperlactataemia

(lactate >2.2 mmol/L) coupled with low ScVO2 (ScVO2 <70%) during CPB. One hundred

patients with normoxaemia and 100 patients with hyperoxaemia were included in the

study. Patients with hyperoxaemia had lower tissue hypoxia incidence than

patients with normoxaemia (p<0.001). Compared with patients without tissue

hypoxia, patients with tissue hypoxia had significantly lower PaO2 values

(p<0.001) and nadir haematocrit levels (p<0.001). Nadir haematocrit levels <18%

(OR: 5.3; 95% CI: 2.67-10.6; p<0.001) and hyperoxaemia (OR: 0.28; 95% CI:

0.14-0.56; p<0.001) were independently associated with tissue

hypoxia.CONCLUSIONS: Hyperoxaemia during CPB may be protective against tissue

hypoxia in patients with nadir haematocrit levels <20%.

THE FIVE GDP LAWS

4. Transfuse RBC based on SvO2and O2ER rather than HCT

THE FIVE GDP LAWS

5. Avoid the anaerobic zone bychecking lactates and VCO2

DO2 , VO2 , SvO2 , and Lactates...and VCO2

0 100 200 300 400 500 600 700 800 900 1,000

DO2 (mL/min)

VO2

(mL/min)300

250

200

150

100

50

0

SvO2

(%) 90

80

70

60

50

40

30

25

Lac

(mMol/L)

12

10

8

6

4

2

0

Critical

DO2

OXYGEN DEBT

VCO2

(mL/min)

THE GDP CONCEPT:

0 100 200 300 400 500 600 700 800 900 1,000

DO2 (mL/min)

VO2

(mL/min)300

250

200

150

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0

SvO2

(%) 90

80

70

60

50

40

30

25

Lac

(mMol/L)

12

10

8

6

4

2

0

Critical

DO2

OXYGEN DEBT

VCO2

(mL/min)

WE WANTTHE PATIENT

IN THISZONE

Lowest HCT on CPB

AK

I 2 r

ate

(%

)

0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 400

5

10

15

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801994

2014

KEEP THEPATIENT

HERE

Lowest Oxygen Delivery (ml/min/mq)

380360340320300280260240220200

Pe

ak A

rte

ria

l B

loo

d L

acta

te (

mM

ol/L

)

3,0

2,5

2,0

1,5

1,0

Critical DO2

GDP: KEEP THEPATIENT HERE

KEEP THEPATIENT

HERE

HERE

HERE

Lowest HCT on CPB

AK

I 2 r

ate

(%

)

0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 400

5

10

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801994

2014

20 years of CPBtechnologiesimprovements

• Centrifugal vs roller pumps• Biocompatible circuits• Flow monitoring• Less transfusions

Same HCTHigher Pump FlowGDP in 2014