Diapositive 1

1
8th International Consensus Conference Hemodynamic
Monitoring in Shock and Implications for
Management How Does Hemorrhagic, Cardiogenic and
Septic Shock Differ?
Benoit Vallet Anesthesiology and Critical
Care University Hospital of Lille France bvallet_at_c
hru-lille.fr
2
VO2 DO2 . ERO2

• VO2 O2 consumed 95 to synthesize ATP
• DO2 O2 delivered
• ERO2 O2 extracted

3
VO2 DO2 . ERO2
4
VO2 Q . CaO2 . ERO2
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VO2 ? Q . Hb . SaO2 . 1.39 . ERO2

• ? in intravascular volume hypovolemic shock ?
  Q ? DO2
• ? in cardiac output cardiogenic shock ? Q ?
  DO2
• ? in SaO2 hypoxemic shock ? CaO2 ? DO2
• ? in Hb hemorrhagic shock ? CaO2 ? Q ? DO2
• Abnormal tissue perfusion distributive shock ?
  ERO2
• Altered O2 utilization cytopathic shock ? ERO2
• Result in unmet O2 needs (? VO2) to sustain cell
  mitochondrial function, i.e. ATP synthesis (
  dysoxia)

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Regional Ischemic Hypoxia Low Q Vallet et al. J
Appl Physiol 2000891317-21
10
8
6
Limb O2 Uptake (ml.kg-1. min-1)
4
2
0
5
10
15
20
25
Limb O2 Delivery (ml.kg-1. min-1)
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Regional Hypoxic Hypoxia Low CaO2 Vallet et al.
J Appl Physiol 2000891317-21
10
8
6
Limb O2 Uptake (ml.kg-1. min-1)
4
2
0
5
10
15
20
25
Limb O2 Delivery (ml.kg-1. min-1)
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VO2-to-DO2 Relationship and SvO2 in ICU
PatientsRonco et al. JAMA 19932701724-30
VO2
2.4 ml/kg.min
DO2
ERO2
0.60
DO2
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VO2-to-DO2 Relationship and SvO2 in ICU
PatientsRonco et al. JAMA 19932701724-30
VO2
4 ml/kg.min
DO2
ERO2
0.60 SvO2 0.40
DO2
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Identifying Dysoxia at the Bedside

• SvO2

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• 4 situations responsible for a ? in SvO2
• SaO2 ?
• Q ?
• Hb ?
• VO2 ? not compensated by DO2 ?

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VO2-to-DO2 Relationship and SvO2 in ICU Patients

• SvO2 a gross estimation of the VO2-to-DO2
  relationship
• SvO2 ? as ERO2 ?
• ERO2 VO2/DO2 ? (SaO2 - SvO2)/SaO2
• When SaO2 1, ERO2 ? 1- SvO2
• When ERO2 is 60, SvO2 is 40

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ERO2 ? via 2 Fundamental Adaptive Mechanisms

• Redistribution of blood flow among organs via ?
  in sympathetic adrenergic tone and central
  vascular contraction ? Q in low ERO2 organs
  (skin, gut, kidney) and maintained Q in high ERO2
  organs (heart, brain)
• Capillary recruitment within organs responsible
  for peripheral vasodilation (opposite to central
  vasoconstriction)

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O2 Extraction Role of Vasoconstrictor
Tone Connolly et al. J Clin Invest 199799228-38
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Vascular Endothelium and Tissue Perfusion Curtis
SE, Vallet B, Winn MJ, et al. J Appl Physiol
1995791351-60
? NO et PGI2
? Hyperpolarization, microcirculatory
embolization, endothelial edema
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Pathological Supply Dependence of O2 Uptake
during Bacteremia Nelson et al. J Appl Physiol
1987631487-92
CONTROL
BACTEREMIC
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As Q ?

• When ERO2 and SVR ?, shock is associated with
  preserved vascular reactivity
• Hemorrhagic shock
• Cardiogenic shock
• When ERO2 and SVR do not ?, shock is described as
  associated with non preserved vascular
  reactivity
• Anaphylactic shock
• Septic shock

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Gut Mucosa Perfused Capillary Density during
Endotoxemia Drazenovic et al. J Appl Physiol
199272259-65
ERO2 gt 65
ERO2 lt 50
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Gut DO2 and VO2 in Hemorrhaged or Endotoxemic
Dogs Curtis et al. Am J Physiol
1992262H778-86 Vallet et al. J Appl Physiol
199476793-800
VO2 (ml/kg.min)
DO2 (ml/kg.min)
VO2 (ml/kg.min)
DO2 (ml/kg.min)
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? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
21
Yes
? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
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? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
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? Elevated preload?
? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
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? Elevated preload?
? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
25
? Elevated preload?
No ?
Hypovolemia
? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
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? Elevated preload?
Hemorrhagic shock ? Hb
Yes ?
? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
Hemorrhage?
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? Elevated preload?
? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
28
Cardiogenic or obstructive shock
Yes ?
? Elevated preload?
Hypovolemia
No ?
Hemorrhagic shock ? Hb
Yes ?
? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
Hemorrhage?
Hypovolemic shock Fluid losses (gut, kidney,
fever)
No ?
No
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? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
30
? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
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? DO2 with ? VO2 and ? ScvO2 ? ? Low cardiac
output?
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(No Transcript)
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Identifying Dysoxia at the Bedside

• Lactate
• Base excess
• DPCO2

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VO2, Lactate and P(v-a)CO2 to DO2 Relationship
during Hemorrhage Van der Linden et al. Anesth
Analg 199580269-75
35
Pathological Supply Dependence of O2 Uptake
during Bacteremia Nelson et al. J Appl Physiol
1987631487-92
CONTROL
BACTEREMIC
36
Low Q vs low CaO2
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Arterial Lactate during Ischemic or Hypoxic
Hypoxia Nevière R, Chagnon JL, Teboul JL, Vallet
B, Wattel F. Crit Care Med 200230379-84
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VO2-to-O2 Delivery Relationship and
P(v-a)CO2 during Regional Ischemic or Hypoxic
Hypoxia Vallet et al. J Appl Physiol
2000891317-21
Limb O2 uptake (ml/kg.min)
Limb ?PCO2 (mmHg)




DO2 crit HH 6.9 0.6
DO2 crit IH 6.0 0.5
DO2 crit HH
DO2 crit IH
Limb O2 delivery (ml/kg.min)
Limb O2 delivery (ml/kg.min)
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DpH-to-O2 Delivery Relationship during Regional
Ischemic or Hypoxic Hypoxia Vallet et al. J Appl
Physiol 2000891317-21
DO2 crit IH
DO2 crit HH
40
Muscle vs gut
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Gut-to-Arterial CO2 Gap during Ischemic or
Hypoxic Hypoxia Nevière R, Chagnon JL, Teboul JL,
Vallet B, Wattel F. Crit Care Med 200230379-84
GMBF (perfusion units)
P(r-a)CO2 (Torr)
Ischemia
Ischemia
60
30
40
20
10
20
0
0
0
10
20
30
0
10
20
30
DO2 (mL/kg.min)
DO2 (mL/kg.min)
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? DPCO2 helps in identifying low flow
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SvO2 vs DPCO2 and lactateclinical studies
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Cardiac Index, VO2, SvO2, and P(v-a)CO2
Relationships Dobutamine Effects Teboul et al.
Crit Care Med 1998261007-10
VO2 (ml/min.m2)
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Combination of P(v-a)CO2 with Arteriovenous O2
Content Mekontso-Dessap et al. Intensive Care Med
200228272-77
ROC analysis (lactate gt2mmol/L)
DPCO2/C(a-v)O2 higher in Lac ( n73) 2.00.9
vs. 1.10.6, plt0.0001) threshold value 1.4
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In septic shock, despite increased Q and SvO2 ?
DPCO2 and lactate suggest ? microcirculatory flow
and perfusion heterogeneity
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Excessive activation of cells (macrophages,
neutrophils, and endothelial cells) and
over-production of pro-inflammatory mediators
(prostanoids, NO, kinins) and pyrogens lead to
vasodilatation, vascular hyporeactivity (i.e.
decreased responsiveness to catecholamines) and
capillary leak with third space losses
48
Endotoxin-Induced Impaired Villus
Microcirculation in Pigs Tugtekin et al.
Intensive Care Med 200127757-66
Baseline DP(r-a)CO2 15 (8-17) mmHg
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Endotoxin-Induced Impaired Villus
Microcirculation in Pigs Tugtekin et al.
Intensive Care Med 200127757-66
12 hours of LPS infusion DP(r-a)CO2 18 (15-26)
mmHg
50
Relationship between Gastric Mucosal Blood
Flow and P(r-a)CO2 in Sepsis Nevière et al. Am J
Respir Crit Care Med 19961541684-8
45
40
35
30
25
Gastric intramucosal- arterial PCO2 (mmHg)
20
15
10
5
0
0
100
200
300
400
500
Gastric mucosal blood flow (mvolts)
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Sublingual PCO2 Gap and Perfused
Capillaries Creteur et al. Intensive Care Med
200632516-23
OPS (orthogonal polarisation spectral imaging)
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Sublingual PCO2 Gap and Perfused
Capillaries Creteur et al. Intensive Care Med
200632516-23
OPS (orthogonal polarisation spectral imaging)
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Microvascular Alterations in Patients with
Cardiogenic Shock De Backer et al. Am Heart J
200414791-9

• OPS (orthogonal polarisation spectral imaging)
  for studying sublingual microvascular perfusion
• 40 patients within 48 hrs of ICU admission for
  severe heart failure or cardiogenic shock
• Lower proportion of small vessel perfused in the
  cardiac failure group compared to controls
• The severity of microvascular alterations was
  related with outcome
• Survivors had better perfusion than non survivors
  

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Acute Myocardial Infarction Complicated by
Systemic Hypoperfusion without Hypotension
Report of the SHOCK Trial RegistryMenon V,
Slater JN, White HD et al. Am J Med
2000108374-80

• In patients with cardiogenic shock and absence of
  hypotension, blood pressure was maintained by
  elevated SVR
• Their in-hospital mortality rate (although high
  at 43) was lower than the rate of those patients
  with classic hypotensive shock (66) despite the
  two groups having the same LV ejection fraction
  (34), cardiac index (1.9 L/min per m2), and PAOP
  (25 mmHg)
• A clinically overt systemic inflammatory response
  syndrome was observed

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• Increased production of NO and NO-derived species
  (e.g. peroxynitrite)
• Result in myocardial dysfunction
• And oxidative phosphorylation limitation

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Identifying Dysoxia at the Bedside

• Is the shock hemorrhagic, cardiogenic or septic?

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Is the Shock Hemorrhagic, Cardiogenic or Septic?
Hemorrhagic shock (hypovolemic) Cardiogenic shock (obstructive) Septic shock (SIRS)
Preload Low High Low
Q Low Low High
SVR High High Low
ERO2 ? ? ?
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Is the Shock Hemorrhagic, Cardiogenic or Septic?

• The response to initial therapy helps in
  identifying the type of shock
• Treatment of shock aims at restoring MAP by
  either increasing Q (fluids, inotropes) or SVR
  (vasoconstrictors)
• In face of increasing SVR, adequacy of Q must be
  assessed ( adequate Hb and SaO2)
• This can be done by the following
• ScvO2 or SvO2
• Blood lactate concentration and base deficit
• Venous-to-arterial or tissue-to-arterial DCO2