1.
Perioperative hemodynamic
goal-directed therapy
Flow-directed hemodynamic
optimization
宋俊松

2.
Goal-directed hemodynamic therapy
Hemodynamic treatment based on titration of
fluid and inotropic agents infused to
physiologic flow-related end points
(tissue oxygenation)

3.
Perioperative goal-directed
hemodynamic management
Rationale for fluid therapy

4.
Perioperative fluid management (1)
• Previous concept of assumed perioperative fluid
management: insensible perspiration + third space
loss + NPO (fasting and operative period) fluid loss
• Assumptions & myths:
– The preoperatively fasted patient is hypovolemic (ongoing
perspiration and urinary output)
– The insensible perspiration increases dramatically when the
operation begins
– An unpredictable fluid shift toward the third space requires
generous substitution
– Hypervolemia is harmless because the kidneys regulate the
overload

5.
Perioperative fluid management (2)
• Consequence of liberal fluid management:
positive fluid balance and weight gain  increased
incidence of complications
• Truth:
– Blood volume after fasting is normal
– Fluid-consuming third space has never been reliably
shown
– Crystalloids physiologically load the interstitial space
– Colloids deteriorates a vital part of the vascular barrier
– Undifferentiated fluid handling increases the shift
toward the interstitial space

6.
Perioperative fluid management (3)
• Perioperative fluid therapy:
– Lack of standardization
– Liberal (18-20 ml/kg/h) vs. restrictive (≤ 10
ml/kg/h) regimen
– Target:
• Outcome
• Type of surgery: high-risk vs. low-risk surgery
• Demographs of patients
• Cardiac preload
• Volume (fluid) responsiveness

7.
Fluid (volume) responsiveness
• Frank-Starling curve
• Volume responsive – respond
to fluid administration by
increasing C.O.
– e.g. C.I. ≥ 15%
• Predictors
– Spontaneous respiration: PLR
(reversible self-volume
challenge)
– Mechanical ventilation:
respiratory variation of
hemodynamic parameters

8.
Limitations of “volume responsiveness” in
measuring blood volume
• There is no proof that volume responsiveness enables
to maximize stroke volume to achieve the optimal
cardiac preload
• PCWP, CVP, LVEDD, early/late diastolic wave ratio,
and duration of LV ejection time all do not
discriminate responders and non-responders to fluid
therapy
• Systolic pressure variation and pulse pressure
variation: low predictive value in low tidal volume
ventilation (e.g. ARDS), cardiac arrhythmic patients,
and spontaneous ventilation

9.
CVP and PCWP are not appropriate
predictor of volume responsiveness
• Volume resuscitation targets on severe sepsis & septic shock
– CVP 8-12 mmHg: Surviving Sepsis Campaign guidelines (Dellinger et
al., Crit Care Med 2004)
– PCWP 12-15 mmHg: the American College of Critical Care Medicine
(Hollenberg et al., Crit Care Med 2004)
• Osman et al. (Crit Care Med 2007)
– 96 severe septic or septic shock patients monitored with PA catheter
and mechanically ventilated in MICU
– 150 volume challenges (500 ml of 6% hydroxyethyl starch infusion for
20 min)
– Fluid responsiveness: increase in C.I. induced by the volume challenge
of ≥ 15% as responder
– In septic patients receiving mechanical ventilation, cardiac filling
pressures (PCWP & CVP) afford a poor prediction of fluid
responsiveness

10.
SVV and pleth variability index: valid
indicator of fluid responsiveness
Zimmermann et al. Eur J Anaesthsiol 2010
• Compare the accuracy of arterial pressure-based stroke
volume variation (SVV) and variations in the pulse oximeter
plethysmographic waveform amplitude as evaluated with the
noninvasive calculated pleth variability index (PVI) with CVP
to predict the response of stroke volume index (SVI) to
volume replacement in patients undergoing major surgery.
• 20 patients (M/F = 13/7) scheduled for elective major
abdominal surgery
• After induction of anesthesia, all haemodynamic variables
were recorded immediately before (T1) and subsequent to
volume replacement (T2) by infusion of 6% hydroxy-ethyl
starch (HES) 130/0.4 (7 ml/kg) at a rate of 1ml/kg/min
• Fluid responder to volume loading: increase in SVI ≥ 15%.
Time
A-line (FloTrac/Vigileo system)
Pulse oximeter (Masimo Radical-7 monitor)
CVP After
induction
of GA
T1
(Baseline
)
T2 (1 min after
fluid loading)
Fluid loading with 6%
HES 130/0.4 (7 ml/kg) at
a rate of 1 ml/kg/min

11.
SVV and pleth variability index: valid
indicator of fluid responsiveness
Zimmermann et al. Eur J Anaesthsiol 2010
• Baseline SVV and PVI correlate significantly with
∆SVI whereas baseline CVP do not correlate with
∆SVI
• The best threshold value to predict fluid
responsiveness:
– SVV > 11%
– PVI > 9.5%

12.
Current suggestion of perioperative
fluid management
• The extracellular deficit after usual fasting is
low
• The basal fluid loss via insensible perspiration
is approximately 0.5-1 ml/kg/h during major
abdominal surgery
• A primarily fluid-consuming third space does
not exist
• Avoid over-hydration and keep an adequate
fluid replacement improve outcome

13.
Perioperative goal-directed
hemodynamic management
Perfusion pressure

14.
Perfusion pressure
• Cerebral perfusion pressure (CPP)
– MAP – ICP (jugular venous pressure or CVP)
• Coronary perfusion pressure (CPP)
– Right CPP = Aortic diastolic pressure – right atrial
diastolic pressure ( DABP – CVP)
– Left CPP = Aortic diastolic pressure – left atrial
diastolic pressure ( DABP – PCWP)
• Abdominal perfusion pressure (APP)
– MAP – IAP (intra-abdominal pressure)

15.
Suggested optimal perfusion pressure
• Maintaining CPP (cerebral) ≥ 60-70
mmHg (in traumatic brain injury patients)
• Maintaining APP ≥ 60 mmHg

16.
Goal-directed
hemodynamic management
Beneficial effect of
hemodynamic optimization

17.
Decrease the postoperative infection
• Systemic review and meta-analysis: 26 randomized, controlled
trials with a total of 4188 surgical patients (Dalfino et al., Crit
Care 2011)
• Significant reduction in surgical site infection, pneumonia,
urinary tract infection, and total infectious episodes
• Flow-directed hemodyanamic therapy to optimize O2 delivery
protects surgical patients against postoperative hospital-
acquired infections
• Strategies to prevent infection in surgical patients:
– Strict asepsis
– Antibiotic prophylaxis
– Avoidance of glucose imbalance
– Normothermia
– Flow-directed hemodynamic therapy to optimize O2 delivery

18.
Decrease the risks of GI complications
and renal dysfunction
• Reduces GI complications (Giglio et al., Br J
Anaesth 2009)
– 16 RCTs (3410 patients)
– Maintain adequate tissue oxygenation 
reduction in GI complications
• Reduction in complicaitons, renal
dysfunction and duration of hospital stay
(Brienza et al., Crit Care Med 2009)
– 20 RCTs on goal-directed therapy (4220
patients)

19.
Reduces hospital stay duration & postoperative
complications Mayer et al., Crit Care 2010

20.
Goal-directed
hemodynamic management
Some protocols

21.
Algorithm of
hemodynamic
management
cerebral
perfusion
Peter Reilly 1997

22.
Royal Adelaide
Hospital,
Australia 2010

23.
Aimed at abdominal
hypertension/compartment syndrome

24.
Summary
• Maintain adequate blood volume 
hemodynamic stability: avoid hypovolemia &
hypoperfusion
• Improve tissue oxygenation: optimize
oxidative killing ability of neutrophils, tissue
repair, and wound healing
• Flow-directed hemodynamic therapy aims at
optimizing perioperative tissue oxygenation

25.
References
• Chappell D, Jacob M, Hofmann-Kiefer K, Conzen P, Rehm M. A Rational
approach to perioperative fluid management. Anesthesiology 2008;
109(4):723-740.
• Monnet X, Teboul JL. Volume responsiveness. Curr Opin Crit Care 2007;
13(5):549-553.
• Zimmermann M, Feibicke T, Keyl C, Prasser C, Moritz S, Graf BM,
Wiesenack C. accuracy of stroke volume variation compared with pleth
variability index to predict fluid responsiveness in mechanically ventilated
patients undergoing major surgery. Eur J Anaesthesiol 2010; 27(6):551-
561.
• Cannesson M. Arterial pressure variation and goal-directed fluid therapy. J
Cardiothorac Vasc Anesth 2010; 24(3):487-97.
• Osman D, Ridel C, Ray P, Monnet X, Anguel N, Richard C, Teboul JL.
Cardiac filling pressures are not appropriate to predict hemodynamic
response to volume challenge. Crit Care Med 2007; 35(1):64-68.