Fluid Therapy

Dr. Pangkuwidjaja P

Exsanguination

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 < 34C
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
Crystalloid

Colloid

1. Replace acute loss

(hemorrhage, GI
loss, 3rd space, etc)

Maintenance
Electrolytes

Nutrition

1. Replace normal
loss (IWL + urine +
faecal)
2. Nutrition support

Compartmental Distribution of Total Body

Water

66% ICF

Intracellular Fluid
28 L
Total body
water

33% ECF

Interstitial Fluid
11 L
Plasma

3L
70 kg male TBW

Water Homeostasis
Ingested fluids
Solid food
Metabolic water

1300
800
400

ICF

ECF

Skin
Lungs

500
400

Urine
1500
Faeces 100

Solute Composition of Body Fluid

Compartments
Solutes
Na+
K+
Mg++

Solutes

10 HPO4150SO4-4 HCO3Prot

Na+ 140ClK+ 4 SO4--

Water

114
30

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

ICF

H2O

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 (NS)
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
Solution

Na

Cl-

K+ Ca2 Glucose+

Lactate

R/Plasma

Osmolarity
(mOsmol.L1
)

Hypotonic

253

Hypotonic

154

!! Isotonic

273

Isotonic

308

Dextrose 5%
(D5W)

50

NS

77

77

Lactated Ringer

130

109

N Saline

154

154

D5 NS

38.
5

38.5

50

!! Hypotonic

335

D5 NS

77

77

50

!! Hypotonic

432

3% S

513

513

Hypertonic

1026

28

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
Renal sympathetic nerves
Angitensin II
Catecholamines

Vasodilatory factors
Intrinsic renal
autoregulation
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

750 ml

estimate

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

volume)

15

15 - 30

30 - 40

40

Fluid replacement (3 :
1 rule)

crystalloid crystalloid

crystalloid
and blood

crystalloid
and blood

Pulse rate

< 100

> 100

> 120

14

BP

normal

normal

decreased

decreased

Pulse pressure

Normal or decreased
increased

decreased

decreased

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

confused or
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

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

BUN/creatinine

> 10:11

Delay, not reliable

M 0.4 0.55
F 0.36 0.47

133 148 mEq/L

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.
cholecystectomy)

2-4 ml/kg/hr

Severe (e.g. bowel

resection)

4-8 ml/kg/hr

Blood Replacement Therapy

Replacing Blood Losses

Crystalloid
or
Colloids

Maintain normovolemia
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
Neonates

Blood volume
Premature

95 mL/kg

Full term

85 mL/kg

Infants
Adults

80 mL/kg
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%

RBCV lost = RBCV preop RBCV 30%

1934 1658 = 267 ml

Allowable blood loss = RBCV lost X 3

267 X 3 = 801 ml

Evolution of Transfusion Practices

10 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
Jehovahs 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 oxygencarrying 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
kidney and skin

: 55 70%
: 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 37C 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 patients 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)
-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

Patient
Consent

4
12

Low Risk

High Risk

Younger patient
Slower blood loss
Chronic anemia
Temporary intra-op
hypothermia or
hemodilution

Atherosclerotic
vasc. Dse
Perioperative
ischemia
Pulmonary dse
Rapid blood loss
Anticipated post-op
blood loss
8

Acute Blood
loss and
hypovolemia

10

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
With antibody screen
With complete cross-match

99.8% compatible
99.94% compatible
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 6C
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