Fluid Shift: Physiology and Pathologic,

and the Concept of Third Space and

Volume Kinetic

Arifin
Head of Medical ICU – Moewardi Hospital
Surakarta - INDONESA
Topic of debate in fluid therapy
๏ Colloids v.s Crystalloids
๏ Colloids v.s Colloids
๏ Saline v.s Balance solution
๏ Perioperative fluid management
➡How much fluid to give ???
➡ Liberal v.s Restrictive regimen
 Rationale for Aggressive Initial
Resuscitative Therapy in Circulatory
Shock

Shock is the immediate systemic Sustained tissue hypoperfusion

result of inadequate O2 delivery result in organ system
in tissue (hypoperfusion) dysfunction and death
 Physical Findings
Impressive but Non-specific:
Increased • Tachycardia, tachypnea,
sympathetic tone hyperpnea, diaphoresis

• Decreased urine output

Decreased organ • Lactic acidosis
perfusion • Ileus, altered sensorium,
peripheral cyanosis

Hypotension • If you wait for hypotension

to treat pts in shock, you
occurs late wait too long
 Autoregulation of Organ Blood Flow

P  Resistance
Autoregulatory
Range Maximum
Organ Vasoconstriction
Blood Flow R = Rmax

Maximum
Vasodilation
R = Rmin
Arterial
5 70 175 Pressure
Critical (mmHg)
Closing Pressure
 Autoregulation when Hypotensive

150
Organ Blood Flow (% baseline)

Autoregulatory Local & regional control

threshold

100

Below their autoregulatory

50
thresholds, organ flows are linearly
dependent on perfusion pressure.

0
20 40 60 80 100
Organ Artery Pressure (mmHg)
 VOLUME KINETICS FOR INFUSION FLUIDS

capillary cell
membrane membrane

Mineral, protein,
ECW ICW gycogen, fat
20% 40% 40%

Plasma Interstitial
o CRYSTALLOID LEAVES THE PLASMA SPACE,
Volume 4.3% fluid 15.7%
EQUILIBRATES WITH INTERSTITIAL SPACE AFTER 20-
30 MIN
colloids
crystalloid:
75-80% leaves vasculature after 20 minutes

5% dextrose
Hahn GR, Anesthesiology 2010
THE PATHOPHYSIOLOGY
BACKGROUND
 CRYSTALLOID
THE VOUME KINETIC OF RESUSCITATION
CRYSTALLOID RESUSCITATION
Hahn GR, Anesthesiology 2010 INTACT GLYCOCALIX

ARDS Hydrostatic

20-30 min
after
Osmotic

Peripheral
edema 75-80%

Burst LYMPH

INTERSTITIAL INTRAVASCULAR Urine

INTRACELLULAR

Endothelial Surface layer (Glycocalix)

Endothelial Capillary Junction
George 2016
WHAT ABOUT COLLOID?
 INTRAVASCULAR VOLUME
EFFECT OF COLLOID
• According classical starling’s principle, infused iso-
oncotic colloids do not change the intravascular
colloid osmotic pressure and cannot cross the barrier.
• Therefore, they should remain theoretically by 100%
within the circulatory space
 WHAT THE EVIDENCE SAY!

Normovolemia/
hemodilution

Interstitial
Volume loading
Hypervolemia
Interstitial

Not only crystalloid are shifted out of the vasculature, but also
colloids
 THE INTRAVASCULAR VOLUME COLLOID COLLOID
EFFECT OF COLLOIDS – THE ROLE OF HYPERVOLEMIA GOAL-DIRECTED

GLYCOCALIX
Not only crystalloids are shifted out ACUTE HYPERVOLEMIA
of the vasculature, but also colloids in SHEDDING GLYCOCALIX
setting of acute hypervolemia LEAKAGE

ARDS

85-98%
LEAKAGE

Peripheral
edema 55-60%

Burst LYMPH

INTRACELLULAR INTERSTITIAL INTRAVASCULAR Urine <<

Endothelial Surface layer (Glycocalix) 6% HES 130/0.4 Jacob 2003, 5% Albumin Rehm 2000, 6% HES
200/0.5 Rehm 2000, 5% Alb Rehm 2001, 6% HES 200/0.5 Rehm 2001
Endothelial Capillary Junction

George 2016
AGGRESSIVE FLUID STRATEGIES
ADVERSELY AFFECT EVERY
SYSTEM AND ORGAN

THE KIDNEY PARADOX;

(oliguria worsened by
Tissue Edema fluid challenge)

Diffusion Distance

Celullar damage
(ORGAN DYSFUNCTION)

FLUID ACCUMULATION AND MULTI ORGAN

DYSFUNCTION
Prowle JR et al. Nat Rev Nephrol 2010;6:107
 Traditional concept of perioperative
fluid loading
5100
3800
5800
2000
Median blood volume status of 13 patients with
1. Preoperatively fasted
ovarian cancer before
1700 and after major abdominal
2. Insensible lost
2450
surgery, receiving a standard infusion regimen
3. 3rd space
750
(crystalloids: approximately 12 ml/kg/h) 4. Vasodilatation of
anesthesia
Direct blood volume
measurements (double-label technique)
4621
Where did they
Fluid shift go?..interstitial
Rehm M. et al: Extra protein loss not caused by surgical bleeding in patients with
ovarian cancer. Acta Anaesthesiol Scand 1998
 Traditional concept of
perioperative fluid loading
 Preoperatively fasted patient is hypovolemic due to ongoing
perspiration and urinary output
 Insensible lost increased dramatically during surgery when
skin barrier is broken
 Unpredictable fluid shift toward 3rd space requires generous
substitution
 Induction of general or neuroaxial anesthesia, is widely spread
treated or even anticipated with fluid loading
✦ Lowered sympathetic tone, relative hypovolemia
• Fluids instead of vasopressors --threaten kidney function?!
Preoperative fasting
 Insensible lost

Basal evaporation = 0.5 mL/kg/hr

 1 mL/kg/hr during large abdominal
surgery with bowel exposure.

Lamke LO. et al: Water loss by evaporation from the abdominal cavity
during surgery. Acta Chir Scan 1977; 143:279-84
• The third-space fluid losses have never been
measured directly, and the actual location of
the lost fluid remains unclear
• Most of the data do not support the
existence of a third space.
 Third-space ?

Perioperative fluid shifting towards the interstitial

space is fact, whereas the classical third space is
fiction
Too much, too little or just right?
Procedure
Morbidity
Comorbidities
Preop hydration
Bowel preparation
Anaesthesia/neuroaxial
Restrictive blockade Liberal

Goal-
Bowel ischemia directed Bowel oedema
 risk of:  risk of:
Organ hypoperfusion Oedema
SIRS Ileus
Sepsis PONV
MOF Pulm complication
 cardiac demands

Hypovolemia normovolemia Hypervolemia

Bundgaard-Neilsen M et al. Acta Anaesthesiol Scan

2009;53:843
  Microvascular pressure (fluid load)(?)  Microvascular permeability (attenuation
 Microcirculatory recruitmenr (vasodilator of tissue oedema (?)
and inhibitor of vasoconstriction)(?)  Blood purification (e.g. CVVH, inhibitors
 Rheology(anti-coagulant,antiaggregants)(?) of cytokines and mediators (?)

Preload is the
Microcirculation
Optimization Oxygen uptake
of oxygen consumption (mitochondrial function
first rule
Perioperative haemodynamic optimization

1. Optimization Optimization 2. Haemoglobin

(arterial oxygen content) of oxygen delivery concentration
 Respiratory support  RBC transfusion
 Additional oxygen and physiotherapy  Blood saving tachnologies

3. Cardiovascular performance
(cardiac output)

1.Contractility 3.Afterload
2.Preload
(heart rate and valvular function (coronary blood flow)
 Contractility (inotropes, beta-blockers)  Fluid load (colloids or crystaloid)  Vasopressor/vasodilators
 Heart rate and rhythm (pacing,chronotropes,  Fluid removal (diuretics,  Regional anaesthesia
anti-arrytmics, anesthetics/sedatives ultrafiltration, restrictive fluid  Intra-aortic baloon pump
 Valvular function (repair, replacement) therapy)

Perioperative haemodynamic therapy, Mukhail Y. Kirov et al. Curr Op Crit Care 2010