Ideal MAP for resuscitation
A moving target
Prof. Jean-Louis TEBOUL
Medical ICU
Bicetre hospital
University Paris-South
France
Questions
1- Why do we use vasopressors in septic shock?
2- Which first-line agent?
3- When to start?
4- Which therapeutic target?
Questions
1- Why do we use vasopressors in septic shock?
2- Which first-line agent?
3- When to start?
4- Which therapeutic target?
Why do we use vasopressors in septic shock?
Septic shock is characterized by a decreased vascular tone
(inducible NO synthase activation, etc)
Hypotension
Hypoperfusion worsening
Autoregulation of organ blood flow
organ
blood
flow
mean arterial pressure
Why do we use vasopressors in septic shock?
1- Septic shock is characterized by a decreased vascular tone
(inducible NO synthase activation, etc)
2- Profound hypotension worsens organ hypoperfusion
…… and represents an independent risk of death
48 hrs
65 mmHg
Why do we use vasopressors in septic shock?
1- Septic shock is characterized by a decreased vascular tone
(inducible NO synthase activation, etc)
2- Profound hypotension worsens organ hypoperfusion
…… and represents an independent risk of death
3- Correction of hypotension with a vasopressor allows improving
organ perfusion
Probable “arterial pressure” effect
Urine flow (ml/h)
Creatinine clearance
60
*
*
*
(meq/l)
*
*
30
baseline
4 hrs
54
73
72
mmHg
mmHg
mmHg
Blood lactate
8 hrs
0-2 hrs
54
mmHg
4-6 hrs
72
mmHg
while cardiac output did not change
baseline
4 hrs
8 hrs
54
73
72
mmHg
mmHg
mmHg
Autoregulation of renal blood flow
renal
blood
flow
54
72
mean arterial pressure
Why do we use vasopressors in septic shock?
1- Septic shock is characterized by a decreased vascular tone
(inducible NO synthase activation, etc)
2- Profound hypotension worsens organ hypoperfusion
…… and represents an independent risk of death
3- Correction of hypotension with a vasopressor allows improving
organ perfusion and microcirculation
%
StO2
95
90
85
80
StO2: 75 ± 9%
75
p < 0.05
70
65
healthy
volunteers
60
82 ± 4 *
55
before NE
with NE
NIRS technology
Vascular Occlusion Test
StO2 (%)
Inflation of the
pneumatic cuff
Deflation of the
pneumatic cuff
AUC
90
Start point :
80
70
60
End point : 0.85 x baseline StO2
0.98 x baseline StO2
Recovery
slope
Desaturation
slope
Index of recruitment
of microvessels
50
Start point : 1.05 x minimal StO2
40
Occlusion time
Time
(%/s)
3.5
3.0
StO2 recovery slope
Restoration
of a “good” MAP
with early introduction of NE
2.5
2.0
resulted in recruitment
0.05
1.5
of microvessels
and better tissuep <oxygenation
1.0
0.5
0.0
before NE
with NE
Questions
1- Why do we use vasopressors in septic shock?
2- Which first-line agent?
3- When to start?
4- Which therapeutic target?
Questions
1- Why do we use vasopressors in septic shock?
2- Which first-line agent?
3- When to start?
4- Which therapeutic target?
140
140
SAP
120
100
80
100
MAP
DAP
20
80
60
60
40
120
reflects
the vascular tone
vasodilatation
40
20
low DAP
Consider vasopressors
When to start vasopressors?
• when MAP is < 65 mmHg despite “adequate” fluid resuscitation
• or when MAP is < 65 mmHg and DAP is low
even if the patient has not been yet fully fluid resuscitated
Questions
1- Why do we use vasopressors in septic shock?
2- Which first-line agent?
3- When to start?
4- Which therapeutic target?
Autoregulation of organ blood flow
organ
blood
flow
? 65 mmHg?
mean arterial pressure
MAP: 65 mmHg
MAP: 75 mmHg
MAP: 85 mmHg
%
150
100
13
50
urine
output
capillary
flow
red cell
velocity
tonometry
PCO2 gap
Autoregulation of organ blood flow
organ
blood
flow
65
75
85
Mean Arterial Pressure (mmHg)
Crit Care Med 2000; 28:2729-2732
Crit Care Med 2005; 33:780 –786
increasing MAP above 65 mmHg
results in little benefit
48 hrs
65 mmHg
Crit Care Med 2000; 28:2729-2732
Crit Care Med 2005; 33:780 –786
MAP target value: 65 mmHg
Probably higher target value if:
• History of chronic hypertension
10 patients
none with history
of severe hypertension
MAP: 65 mmHg
MAP: 75 mmHg
MAP: 85 mmHg
%
150
100
13
50
urine
output
capillary
flow
red cell
velocity
tonometry
PCO2 gap
Organ
Blood
flow
no prior hypertension
with prior hypertension
65
Mean arterial pressure
mmHg
pts with chronic hypertension
pts with no chronic hypertension
Probably higher target value if:
• History of chronic hypertension
• High CVP
Probably higher target value if:
• History of chronic hypertension
• High CVP
• Increased abdominal pressure
Is it dangerous to target a MAP value
up to “normal values” (around 85 mmHg)
in septic shock?
13 pts
with septic shock
*
Recovery slope
%/min
*
65
75
MAP
85
mmHg
65
6 pts
with septic shock
Perfused Vessel Density
No worsening but improvement of microcirculation
for MAP target up to 85 mmHg with NE
Microvascular Flow Index
20 pts
with septic shock
Highly variable response among patients
20 pts
with septic shock
Perfused capillary density improved in pts with an altered
sublingual perfusion at baseline, and decreased in patients
with preserved basal microvascular perfusion.
Conclusion
1- Why do we use vasopressors in septic shock?
2- Which first-line agent?
3- When to start?
4- Which therapeutic target?

at least 65 mmHg

probably higher value if:
• History of chronic hypertension
• High CVP
• Increased abdominal pressure
65-85 mmHg
seems to be a safe range
Thank you