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New concepts in thepathophysiology of shock
D. Georgopoulos, Professor of Medicine,
Director of ICU, University Hospital of Heraklion,University of Crete, Heraklion
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VO2
(2)
CaO2 = 1.36 x Hb x SaO2 + (0.003xPaO2)
Amount of O2 = Truck volume x CaO2
CaO2
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VO2
2
CaO2 = 1.36 x Hb x SaO2 + (0.003xPaO2)
Amount of arterial O2 = Truck volume x CaO2
CaO2CvO2
CvO2 = 1.36 x Hb x SvO2 + (0.003xPvO2)
Amount of venous O2 = Truck volume x CvO2
VO2 = Truck volume x (CaO2 - CvO2)
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VO2
2
CaO2CvO2
DO2 = SV x HR x CaO2
Fick equation
VO2/min = SV x HR x (CaO2 - CvO2)
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DO2 = SVxHRx(CaO2-CvO2)
VO2
Critical value
Sepsis
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Shock - Definition
Shock = Tissue hypoxia
Arterial blood pressure should not be
used for shock definition
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Shock
Hypovolemic Cardiogenic ObstructiveDistributive
(Vasodilatory)
Cardiac output Cardiac output
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Vasodilatory shock is the final
common pathway for long-
lasting and severe shock ofany cause
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Shock
Hypovolemic Cardiogenic ObstructiveDistributive
(Vasodilatory)
Cardiac output Cardiac output
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Why?
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Landry and Oliver New Engl J Med 2001;345:588
Tissue
hypoxia
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Activation of ATP-sensitive
Potassium Channels
(Open ATP-K+)
Increased synthesis
of NO
Deficiency of
vasopressin
Energy depth
(tissue hypoxia)
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A section of the neurohypophysis from a normal dog
Before After 1 hr of severe hemorrhagichypotension (mean AP
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Tissue hypoxia
(Shock)
Nitric Oxidesynthase
ATP, H+
, lactatein vascular smooth muscle
Vasopressinsecretion
Open KATP
Nitric Oxide
cGMP
Cytoplasmic Ca++
Phosphorylated
myosin
Vasodilation
Vasopressinstores
PlasmaVasopressin
Landry and Oliver New Engl J Med 2001;345:588
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Vasodilatory shock is the final
common pathway for long-
lasting and severe shock ofany cause
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Microcirculation
The microcirculation, with its hugeendothelial surface, is in fact the
largest organ in the human body
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Shock: Complete stasis in
the capillaries
Healthy volunteer
Shock: Some capillariesshowing stasis and others
showing high flow
Orthogonal polarisation
spectral imaging
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Normal Sepsis
De Backer et al. Am J Respir Crit Care Med 2002
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De Backer et al. Am J Respir Crit Care Med 2002;166:98
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De Backer et al. Am J Respir Crit Care Med 2002;166:98
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De Backer Am Heart J 2004;147:91
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De Backer Am Heart J 2004;147:91
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De Backer Am Heart J 2004;147:91
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De Backer et al. Am J Respir Crit Care Med 2002;166:98
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Sakr et al. Crit Care Med 2004;32:1825
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Sakr et al. Crit Care Med 2004;32:1825
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Sakr et al. Crit Care Med 2004;32:1825
Evolution of small vessel perfusion
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Sakr et al. Crit Care Med 2004;32:1825
ROC curve for the change in small vessel perfusion
within 24 hrs of the onset of shock
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It is rational to open the
microcirculation during tissuehypoxia
Evidence?
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8 patients with septic shock were fluidresuscitated such as mean AP was > 60 mmHgand CVP > 12 mmHg
After the pressure goal had been reachednitroglycerin infusion was started with an I.Vbolus dose of 0.5 mg and followed bycontinuous infusion of2 mg/hr
The dose was increased and fluids were infuseduntil peripheral circulation seemed to berestored
Lancet 2002; 360:1395
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Patients characteristics
Age 59 (range 27-79)
APACHE-II27 (range 11-37)
The amount of fluids ranged between 2.2and 8.3 L
CVP ranged between 11 and 25 mmHg
Mean AP ranged between 60 to 80 mmHg
Spronk et al. Lancet 2002;360:1395
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Spronk et al. Lancet 2002;360:1395
Sludged erythrocytes
Before After nitroglycerin
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Spronk et al. Lancet 2002;360:1395
7 out of 8 patients were discharged from the hospital
1 required renal replacement therapy
1 patient died 6 days after treatment from cerebral haemorrhage
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Take home messages
Vasodilatory shock is the final commonpathway for long-lasting and severe shockof any cause
Microcirculation plays an important(probably the most important) role in thepathophysiology of shock
Therapies targeting the microcirculationmight influence the outcome of patientswith shock