Hemodynamics in critical care - an overview · Hemodynamics in critical care - an overview J.G. van der Hoeven Radboud University Nijmegen Medical Centre 1. Treatment of shock Cardiac

Hemodynamics in critical care - an overview

J.G. van der HoevenRadboud University Nijmegen Medical Centre

1

Treatment of shock

Cardiac outputHemoglobin

SaO2

Serious defects Serious defects

Macrocirculation Microcirculation Mitochondria

Preload - volume therapyContractility - inotropic agents

Afterload - vasodilatorsTransfusion

Oxygenation

No treatmentVasodilators?

No treatment

2

DO2 - VO2 relationship

0 100 200 300 400 500 600 700 800 900 1000

DO2 (ml/min/m2)

VO2

(ml/m

in/m

2 ) Increase in oxygen extraction

Increa

se in

lactat

e170

3

DO2 - VO2 relationship

0 100 200 300 400 500 600 700 800 900 1000

DO2 (ml/min/m2)

VO2

(ml/m

in/m

2 ) Increase in oxygen extraction

Increa

se in

lactat

e170

3

-0,4

-0,3

-0,2

-0,1

0

0,1

Mor

talit

y d

iffer

ence

bet

wee

n p

roto

col a

nd c

ontr

ol g

roup

Increasing oxygen transport

Supranormalafter OF

Mortality risk > 20%

Supranormalbefore OF

Mortality risk > 20%

SupranormalMortality risk < 15%

4

Early intervention

0

15

30

45

60

Hospital mortality 28 D mortality 60 D mortality

44,3

33,330,5

56,9

49,246,5

Mor

talit

y (%

)

Control Goal directed therapy

Rivers E, et al. N Engl J Med 2001;345:1368-1377

30

40

50

60

70

80

90

100

Baseline 6 hours 7 - 72 hours

Cen

tral

ven

ou o

xyge

n sa

tura

tion

(%)

5

ScvO2 and cardiac output in sepsis

Perner A. Acta Anaesthesiol Scand 2010;54:98-1026







7

What happens during shock?

7


7

65What happens during shock?

7

65What happens during shock?

7

65

62

62


7

Venous saturation in septic shock

50

60

70

80

90

100

Central venous Right atrium Right ventricle Pulmonary artery

70,270,971,5

78,6

Veno

us s

atur

atio

n (%

)

N = 37

Kopterides P. Shock 2009;31:561-5678

Lactate ↑

Lactate production ↑ Lactate clearance ↓

Tissue hypoxia

Local production (lung)Glucose metabolism ↑

Activity PDH ↓

Liver function ↓Decreased liver flow

Anaerobic Aerobic

Increased lactate at admission and persistent lactate elevation have a strong relation with mortality

9

Non-clearance is decrease in lactate < 10%

Initial lactate clearance and mortality

0

20

40

60

80

100

In-Hosptal mortality

%

Lactate clearance Lactate non-clearance

N = 166

N = 38N = 128

Lactate Non-

clearance

Lactate clearance

ScvO2 < 70% 3 20 23

ScvO2 ≥ 70% 11 114 125

14 134 148

P = 0.457

No relation between ScvO2 > 70 and lactate clearance

Arnold RC. Shock 2009;32:35-3910

Lactate driven therapy

0

10

20

30

40

50

33,9

43,5

Mor

talit

y (%

)

Control Lactate driven

N = 348P = 0.067

Admission lactate ≥ 3 mmol/lGoal: lactate ↓ ≥ 20% in 2 hrs

• After correction for risk factors mortality lower in lactate group (HR 0.61, p = 0.006)

• Duration MV ↓, duration ICU stay ↓, lower SOFA score

Jansen TC. Am J Respir Crit Care Med 2010, Epup 12 mei11

Lactate or ScvO2?

Variable Lactate clearance ScvO2 > 70% P-value

Hospital mortality (%) 17 23 ns

ICU stay (D) 5,9 5,6 0,75

Hospital stay (D) 11,4 12,1 0,60

Ventilator free days 9,3 9,9 0,67

MODS (%) 25 22 0,68

Treatment withdrawal (%) 9 15 0,15

N = 300

Noninferiority trialJones AE. JAMA 2010;303:739-746

12

Microcirculation in sepsis

0

25

50

75

100

% perfused vessels % perfused capillaries % absent blood flow % intermittent blood flow

Control Acetylcholine

De Backer D. Am J Respir Crit Care Med 2002;166:98-104

Normal Sepsis

13

Nitroglycerin and microcirculation in sepsis

Boerma EC. Crit Care Med 2010;38:93-100

N = 70

Patients with severe sepsis/septic shock treated with EGDT

14

Boerma EC. Crit Care Med 2010;38:93-10015

Fluid therapy and microcirculation

Proportion perfused small vessels

Baseline Fluids

Early septic shock

Late septic shock Ospina-Tascon G. Intensive Care Med 2010;36:949-955

Despite similar changes in CI

16

17

XXX XXX

Sepsis ONOO- ↑↑

Peroxynitrite

17

XXX XXX

Sepsis ONOO- ↑↑

Peroxynitrite

17

XXX XXX

Sepsis ONOO- ↑↑

Peroxynitrite

PARP + Caspase activation

ApoptosisNecrosis

17

Delayed fluorescence lifetime of endogenous PpIX

Mik EG. Nat Methods 2006;3:939-94518

19

Do we have a circulation problem?

19


Physical examinationUrine production

ScvO2 / BE / lactateNIRS / OPS / SDF

19


No actionNo



19


No actionNo

Is this patient volume responsive?

YesPhysical examination

Urine productionScvO2 / BE / lactateNIRS / OPS / SDF

19


No actionNo

Is this patient volume responsive?



Dynamic parameters

19


No actionNo

Diagnosticechocardiography

No Is this patient volume responsive?



Dynamic parameters

19


No actionNo



Yes

Volume therapy

Yes



Dynamic parameters

19


Volume therapy successful?

No actionNo



Yes

Volume therapy

Yes



Dynamic parameters

19



No actionNo



Yes

Volume therapy

Yes

No



Dynamic parameters

19



No actionNo



Yes

Volume therapy

Yes

YesNo



Dynamic parameters

19



No actionNo



Yes

Volume therapy

Yes

YesNo

Severe LV/RV dysfunction?



Dynamic parameters

19



No actionNo



Yes

Volume therapy

Yes

YesNo


Yes

Specific analysisCO monitoring

Specific measuresInodilator therapy



Dynamic parameters

19



No actionNo



Yes

Volume therapy

Yes

YesNo


Yes



No

Persistent hypotension?



Dynamic parameters

19



No actionNo



Yes

Volume therapy

Yes

YesNo


Yes



No


Yes

AnalysisVasopressor



Dynamic parameters

19



No actionNo



Yes

Volume therapy

Yes

YesNo


Yes



No


Yes

AnalysisVasopressor



Dynamic parameters

No

Reevaluate

19

Documents

Hemodynamics in critical care - an overview · Hemodynamics in critical care - an overview J.G. van der Hoeven Radboud University Nijmegen Medical Centre 1. Treatment of shock Cardiac