Fluid Therapy

Dr. Pangkuwidjaja P
Exsanguination
Undetermined
Other
CNS +
Exsanguination 4% 2%
6%

Organ failure
7%

CNS
42%

Exsanguination
39%
 Predictors of death
• Estimated blood loss > 5,000 mls
• Red cell transfusion > 4,000 mls
• Total blood transfusion > 5,000 mls
OR fluid transfusion > 12,000 mls
• Transfusion rates > 12 mls/min
– pH < 7.2
– Temp < 34ºC
– HCO3 < 15 mmol/l
Trauma and surgery
 Alters volumes and composition of IC and EC
spaces

Therapeutic infusion
 further alters compartmental volumes
and composition
 Emergency Resuscitation
• How much?

• What Fluid?

• Which Endpoints?
 Goals of Fluid Administration
• Maintain good tissue perfusion
• Maintain adequate oxygen delivery
• Normal electrolyte concentration
• Normoglycemia & pH
 Goal of Fluid Resuscitation
↑ Cardiac Output
↓Hb

 DaO2
CO x CaO2
(Hb x SaO2 x 1,34) + (PaO2 x 0,003)

BP = CO x SVR
 FLUID THERAPY

Resuscitation Maintenance

Crystalloid Colloid Electrolytes Nutrition

1. Replace normal
1. Replace acute loss
loss (IWL + urine +
(hemorrhage, GI
faecal)
loss, 3rd space, etc)
2. Nutrition support
 Compartmental Distribution of Total Body
Water

Intracellular Fluid
66% ICF 28 L
Total body water

Interstitial Fluid
33% ECF 11 L

Plasma 3L
70 kg male TBW 42 L
 Water Homeostasis
Ingested fluids 1300
Solid food 800
Metabolic water 400

ICF ECF

Skin 500
Lungs 400

Urine 1500
Faeces 100
 Solute Composition of Body Fluid
Compartments
Solutes Solutes

Na+ 10 HPO4- Na+ 140 Cl- 114

K+ 150 SO4-- K+ 4 SO4-- 30
Mg++ 4 HCO3-
Prot

Water Water
280 – 310 mOsm/l

ICF ECF
 Practical Fluid Balance
Rule 1

Water without Na expands the TBW (enter both ICF & ECF in
proportion to their initial volume)

H2O H2O H2O

ICF ECF
 Practical Fluid Balance
Rule 2

All infused Na+ can not gain access to the ICF because of the Sodium
Pump

Na+
Na+
Na+
Na+
Na+

Na+

ICF ECF
Isotonic = NO Water Exchange
 Practical Fluid Balance
Rule 3

Change in tonicity of Na solutions (relative to Plasma) causes water

exchange

a. Hypotonic saline (¼NS)

Hypotonic = Water Exchange

H2O
 Practical Fluid Balance
b. Hypertonic solution

Hypertonic = Water Exchange

Increase Plasma Volume (x times) the originally infused

amount
from IFV & ICF

H2O
 Dynamics of IV Fluids
• Water solution  Intracellularly
All hypotonic solutions e.g. 5% dextrose called as maintenance type
of fluids

• Electrolyte solutions
Interstitial compartment
Isotonic
Called replacement of fluids
 Electrolyte Contents
Electrolyte contents (mEq/l)
+ g/L Osmolarity
Solution R/Plasma (mOsmol.L-
Na Cl- K+ Ca2 Glucose+ Lactate 1)
+ +

Dextrose 5% 50 Hypotonic 253

(D5W)
½ NS 77 77 Hypotonic 154
Lactated Ringer 130 109 4 3 28 !! Isotonic 273
N Saline 154 154 Isotonic 308
D5 ¼ NS 38. 38.5 50 !! Hypotonic 335
5
D5 ½ NS 77 77 50 !! Hypotonic 432
3% S 513 513 Hypertonic 1026
 Regulation of Extracellular Fluid Volume

Renal adaptation to hypovolemia

• Renal autoregulation
↓/↑ renal afferent arteriolar resistance
• Reduction in RBF
↑ renal afferent arteriolar resistance
 redistributed from the kidney
• Reduction in GFR
• Increased tubular reabsorption
Regulation of Extracellular Fluid Volume

Renal perfusion during hypovolemia

Vasoconstrictive factors Vasodilatory factors

• Renal sympathetic nerves • Intrinsic renal
• Angitensin II autoregulation
• Catecholamines • Renal vasodilatory effect
of prostaglandins
 Regulation of Extracellular Fluid Volume

PV preservation:

↑ reabsorption of filtered water and Na

ADH
Aldosterone
hypoperfusion  renin secretion
↓ ANP
vasodilatory effect
↑ renal excretion of Na and water
 Clinical Implications of Choices
Between Crystalloid and Colloid

If membrane permeability intact

Colloids preferentially expand PV rather than IF

PV expansion unaccompanied by IF expansion
lower fluid requirements
less peripheral and pulmonary edema accumulation
reduce concern about later fluid mobilization
 Crystalloids and colloids
Crystalloid Colloid
Intravascular persistance Poor Good
Haemodynamic stabilisation Transient Prolonged
Required infusion volume Large Moderate
Risk of tissue oedema Obvious Insignificant
Enhancement of capillary perfusion Poor Good
Risk of anaphylaxis Nil Low to
moderate
Plasma colloid osmotic pressure Reduced Maintained
Cost Inexpensive Expensive
 Persistence of Fluids in
Circulation
• IMG_2009
Crystalloids (Hypertonic Saline)
• Hypertonic Saline 3% and 7.5%

• Increase Plasma Volume from IFV & ICF

• Small Volume Resuscitation

250 ml

H2O

estimate
750 ml
 Clinical Implication of Hypertonic
Fluid Administration
Hypertonic solutions may improve
Hemodynamics
Cerebral hemodynamic
impermeability of BBB to sodium in uninjured brain
 cause brain to shrink in response to acute increase of Na
Microvascular perfusion
through PV expansion

To prolong the therapeutic effect

continued infusion
subsequent infusion of blood or conventional fluids or addition of
colloid
Evaluation of Intravascular Volume
• Physical Examination
• Laboratory
 Class I Class II Class III Class IV
Blood loss (ml) ≤ 750 750 - 1500 1500 – 2000 ≥ 2000
Blood loss (% of blood ≤ 15 15 - 30 30 - 40 ≥ 40
volume)
Fluid replacement (3 : crystalloid crystalloid crystalloid crystalloid
1 rule) and blood and blood
Pulse rate < 100 > 100 > 120 ≤ 14
BP normal normal decreased decreased
Pulse pressure Normal or decreased decreased decreased
increased
Capillary refill test normal positive positive positive
Respiratory rate (bpm) 14 – 20 20 – 30 30 – 40 > 35
Urine output (ml/h) ≥ 30 20 - 30 5 - 15 negligible
Mental status sl. anxiety Mild anxiety anxious or confused or
confused lethargic
 Hemodynamic Parameters
Parameter findings Comment

HR Increase

BP Decrease

CVP Decrease < 5 mmHg

Fluid Challenge (250 ml) Increase > 1 – 2 mmHg

> 5 mmHg
> 12 mmHg (rule out RV
dysfunction)
PAOP Decrease < 8 mmHg
> 12 mmHg (rule out LV
dysfunction)
Laboratory Signs of Dehydration
Test Findings
HCT Increase M 0.4 – 0.55
F 0.36 – 0.47
pH < 7.36
Urine Specific Gravity > 1010
UO < 0.5 ml/kg/h
Urinary Sodium < 10 mEq/L
Urinary Osmolality > 450 mOsm/kg
Blood Na+ > 145 mEq/L 133 – 148 mEq/L
BUN/creatinine > 10:11

Delay, not reliable

 Surgical Fluid Requirements
Surgical patients require:
replacement of PV and ECF
must compensate for the acute reduction of
functional IF
3rd space loss

Degree of Tissue Trauma Fluid Requirement

Minimal (e.g. hemiorraphy) 0-2 ml/kg/hr
Moderate (e.g. 2-4 ml/kg/hr
cholecystectomy)
Severe (e.g. bowel 4-8 ml/kg/hr
resection)
Blood Replacement Therapy
 Replacing Blood Losses

Crystalloid
or Maintain normovolemia
Colloids
till the danger of anemia outweighs
the risk of transfusion
ie. 7-8 Gm/dl (HCT of 21-24%)
 Replacing Blood Loses (Vol)

Patients with normal HCT should only be transfused after 10-20% loss of blood volume

One unit of blood pack cells

Increases Hb by 1 gm/dl
Or HCT by 2-3%

10 ml pack cells/kg
Increases Hb by 3 gm/dl
Or HCT by 10%
 Estimated Blood Volumes
Age Blood volume

Neonates Premature 95 mL/kg

Full term 85 mL/kg

Infants 80 mL/kg

Adults Men 75 mL/kg

Women 65 mL/kg
 Replacing Blood Loses (HCT)
An 85 kg woman has a preoperative HCT 35%.
How much blood loss to decrease her HCT to 30%?

Estimate blood volume 65 ml X kg 85 = 5525 ml

Estimate RBCV at preoperative HCT RBCV preop 5525 X 35% = 1934 ml

Estimate RBCV at HCT 30% RBCV 30% 5525 X 30% = 1658 ml

Calculate RCV lost when HCT 30% 1934 – 1658 = 267 ml

RBCV lost = RBCV preop – RBCV 30%

Allowable blood loss = RBCV lost X 3 267 X 3 = 801 ml

 Evolution of Transfusion Practices
• 10 ε 30 rule
• AIDS

 A patient specific approach to the decision

to transfuse blood components
 RBC transfusion threshold
The rationale
??? What Hgb/Hct level poses greater risk to the patient than
the threat of contacting a transfusion-transmitted disease

• greater degrees of anemia could be well tolerated

chronically anemic renal failure
• Jehovah’s witness

 morbidity and mortality rates did not increase

until Hgb level fell below 7 g/dl
 RBC transfusion threshold
The rationale

Adverse physiologic effects of anemia

No evidence that mild to moderate anemia impairs:
• Wound healing
Hct < 15
• Increases bleeding
• Increases the length of hospital stay
• Increases the frequency or severity of postoperative infection
 RBC transfusion threshold
The rationale

• The cause of anemia is thought to be more important in influencing

the perioperative course than the severity of anemia
• Maintaining of blood volume was more critical than correcting
anemia
 RBC transfusion threshold
The rationale
• Goal:
to anticipate, on a patient-by-patient basis, the minimum Hgb
level that will avoid organ damage due to O2 deprivation
Do2
Vo2
physiologic capacity for compensatory mechanism

• Decision:
should be based upon the clinical judgment that oxygen-
carrying capacity of the blood must be increased to prevent Vo2 from
outstripping Do2
Calculation of oxygen delivery (Do2)

Cao2 = Sao2 x Hg x 1.34 + Pao2 x 0.0031

Do2 = Cao2 x CO x 10
Calculation of oxygen consumption
(Vo2)

Vo2 = CO x (Cao2 – Cvo2)

normal arteriovenous oxygen content difference is 5 vol%

~ Svo2 = 75%

↑Vo2 :
sepsis
hyperthermia
↑ metabolic activity
hyperthyroidism
 Oxygen extraction ratio
Fraction of total oxygen delivered is
consumed or extracted by the tissues

ER = Vo2 / Do2
= [CO x (Cao2 – Cvo2)] / Cao2 x CO
= (Cao2 – Cvo2) / Cao2
 Oxygen extraction ratio
Global ≠ Regional
normal global oxygen delivery may occur in spite of critical
levels of regional ischemia

Svo2:
vo2 of many vascular beds (global)

heart, under basal condition : 55 – 70%

kidney and skin : 7 – 10%

organ with the greatest ER will have the least O2 reserve

 Compensatory mechanisms during anemia

• Increased cardiac output

• Redistribution of cardiac output
• Increased oxygen extraction
• Changes in Oxygen-Hemoglobin affinity
 Compensatory mechanisms during anemia

Increased cardiac output

With isovolemic hemodilution
↑ SV
↓ SVR
vascular tone
viscosity
age
acute or develops slowly

 self correcting
↓ oxygen carrying capacity
↑ oxygen transport
 Compensatory mechanisms during anemia

Redistribution of cardiac output

 to organ with greater O2 requirement (brain and heart)

The heart
has a high extraction ratio
 must rely upon redistribution blood flow to ↑ O2 supply
greatest risk !!!
 Compensatory mechanisms during anemia

Increased oxygen extraction

Play an important adaptive role

when the normovolemic Hct drops below 25%

 ↓ mixed venous oxygen saturation

Organs with high ER under basal condition

 limited capacity to increase Do2 by this mechanism
 Compensatory mechanisms during anemia

Changes in Oxygen-Hemoglobin affinity

The sigmoid-shaped oxygen-Hemoglobin dissociation curve:

P50 for normal adult Hgb at 37ºC and a pH of 7.4 : 27 mmHg

Left-shifting
hypothermia, alkalosis
Hgb molecule is more ‘stingy’ and requires lower Po2
to release O2 to tissues
Hgb molecules does not release 50% of its O2
until ambient Po2 less than 27 mmHg
 Compensatory mechanisms during anemia

Changes in Oxygen-Hemoglobin affinity

When anemia develops slowly

the affinity of Hgb for O2 may be decreased (right-shifted)
 accumulation of 2,3 - DPG
 Hypovolemic anemia vs Acute blood loss

Acute blood loss

stimulation of adrenergic nervous system
 vasoconstriction and tachycardia
! Increased CO does not contribute

Chronic anemia
CO may not change until Hgb decreases to 7 – 8 g/dl
synthesis of supranormal level of 2,3 – DPG begin at Hgb 9
g/dl
 right shifted
 Establishing the RBC transfusion threshold

Transfusion ‘trigger’
the Hgb or Hct threshold that justifies RBC transfusion for
individual patient
it is presumed that the benefits of RBC transfusion
outweigh the risks

• No single criterion could replace clinical judgment as the basis of

decision-making
• No evidence that mild-moderate anemia contribute to perioperative
morbidity

NIH – Consensus conference on Perioperative Red Cell Transfusion 1988

 Establishing the RBC transfusion threshold

Guide therapy
clinical assessment
Hgb value
Laboratory data (when indicated)
arterial oxygenation
mixed venous oxygen tension
cardiac output
oxygen extraction ratio
blood volume

 estimation of the patient’s myocardial/coronary reserve !!!

Condition that may decrease tolerance for anemia
and influence the RBC transfusion threshold
Increased oxygen demand
Hyperthermia
Hyperthyroidism
Pregnancy
Limited ability to increase CO
Coronary artery disease
Myocardial dysfunction (infarction, cardiomyopathy)
β-adrenergic blockade
Inability to redistribute CO
Low SVR state (sepsis, post-CPB)
Occlusive vascular disease (cerebral, coronary)
Left shift of O2-Hgb curve
Alkalosis
Hypothermia
Abnormal Hemoglobins
Presence of stored Hgb (decreased 2,3-DPG)
Hgb S
Acute anemia (limited 2,3-DPG compensation)
Impaired oxygenation
Pulmonary disease
High altitude
 Low Risk High Risk
Patient • Younger patient • Atherosclerotic
Acute Blood loss
• Slower blood loss vasc. Dse
Consent • Chronic anemia • Perioperative
and hypovolemia
• Temporary intra-op ischemia
hypothermia or • Pulmonary dse
hemodilution • Rapid blood loss
• Anticipated post-
op blood loss
4 6 8 10 12

Target Hemoglobin concentration (g/dl)

 What donor blood group type may be compatible
for transfusion to a particular recipient ?

Focus on which antibodies will be present in the recipient serum !!!

reaction of these antibodies with donor RBC antigens
can activate complement
 hemolysis of RBC

Type O-negative blood  universal donors

Type AB-positive blood  universal recipients
 Compatibility testing
The cross-match

Donor RBCs mixed with recipient serum

stimulating the actual anticipated transfusion

3 phases
1. Immediate phase
2. Incubation phase
3. Antiglobulin phase
 Is cross-match necessary?
ABO-Rh status alone 99.8% compatible
With antibody screen 99.94% compatible
With complete cross-match 99.95% compatible

Those who have not previously exposed or pregnant

incompatibility : 1 in 1000
Those who have previously exposed or pregnant
incompatibility : 1 in 100
 Type and Screen orders
• When blood is ordered preoperatively for surgical cases in which
transfusion is unlikely
• If the need arises the blood can be cross-matched prior to
transfusion

Advantages:
• If the blood is not needed
the additional expenses for cross-match is eliminated
• If cross-match is performed and compatible unit identified
those unit are held in reserve
 temporarily out of blood supply
 if the blood is not used
 wastage by outdating
 Risk of blood product administration

1. Problems related to blood storage

2. Problems related to immune-mediated
transfusion reaction
3. Infectious risks
 Risk of blood product administration
Problems related to blood storage

• Citrate intoxication
Citrate prevent coagulation of stored blood
by chelating ionized Calcium
large volume (>1 blood volume)
administered rapidly (> 1 ml/kg/minor 1 unit/5 mins)
impaired liver function
 temporary reduction of ionized Ca levels

Signs:
hypotension
narrow pulse pressure
↑ VEDP
↑ CVP
ECG
prolonged QT interval
widened QRS complexes
flattened T waves
 Risk of blood product administration
Problems related to blood storage

• Acid-base Changes
CPD  ↓ pH to 7.0 – 7.1
during storage
 ongoing metabolism of glucose to lactate
 production of CO2
Citrate metabolized to bicarbonate

• Decreases in 2,3-DPG
left shift of O2-Hgb dissociation curve
 less efficient O2
 Risk of blood product administration
Problems related to blood storage

• Hyperkalemia
to maintain electrochemical neutrality
H+ generated during storage
RBCs lysis

with normal infusion rate K+ is distributed

rates > 90 – 120 ml/min  hyperkalemia
aggravated by
hypovolemia
hypothermia
acidosis
 Risk of blood product administration
Problems related to blood storage

• Hypothermia
from rapid transfusion of large volumes of cold blood
stored at temp 1 – 6ºC

↓ CO
tissue perfusion impaired
vasoconstriction
left-shifting of O2-Hgb dissociation curve
metabolic acidosis
shivering
↑ O2 consumption by 300-400%
hemostatic dysfunction
citrate toxicity
ventricular irritability
 Risk of blood product administration
Problems related to blood storage

• Dilutional coagulopathy
platelets
clotting factors
V and VIII
Immediate Hemolytic Transfusion Reactions
 hemolysis
 release hemoglobin to the blood
 renal damage
↓ renal blood flow
mechanical obstruction in the renal tubule
free Hgb, RBC stroma
deposition of antigen-antibody complexes (G)
deposition of fibrin (DIC)

Signs and symptoms

fever, chill, nausea and vomiting
hypotension and tachycardia
flushed and dyspneic
chest and back pain
restless
hemoglobinuria
diffuse bleeding
renal failure
 Massive Blood Transfusion
≥ one blood volume
< 24 h

• Coagulopathy
• Hypothermia
• Citrate toxicity
• Hyperkalemia
• ↓ 2,3 DPG
Emergency Transfusion

Choices:
• Type-specific partially cross-matched blood
• Type-specific uncross-matched blood
• O-negative (universal donor) PRBCs

O-negative (universal donor) whole blood

contains high titers of antibodies