2. Objectives
By the end of this presentation the student will
be able to:
-Identify differences among adults, children, and
infants related to fluid requirements, fluid therapy,
and electrolytes..
- Fluid Pressures & movements.
- Explain the causes and clinical manifestations of
the four major types of acid-base imbalances.
3. Introduction
Stable internal environment is maintain by the
balance of body water and electrolyte .
Balance disturbance is very common problem
usually found in association with several disease
conditions ,correction of imbalance and
maintenance of fluid and electrolyte are prime
important for disease management .
8. Body fluids
⢠Water is the largest component of human body.
⢠Water is essential for life.
⢠Present in every cell
⢠Surrounds every cell
9.
10. Variation in body fluid content
Neonates contain more water than adults: 75â
80% water with proportionately more ECF than
adults. At birth, the amount of ISF is
proportionally three times larger than in an adult.
By the age of 12 months this has decreased to
60%, which is the adult value. Total body water
as a percentage of total body weight decreases
progressively with increasing age.
11. Body fluids
Cellular fluid compartments
The two body fluid compartments are
intracellular and extracellular.
The fluid inside the cell is called intracellular
fluid(ICF).
The fluid outside the cell is called extracellular
fluid (ECF).
13. Twoâthirds of body fluid is found inside the
cell and oneâthird of the fluid outside the cell.
The interstitial compartment contains 80% of the
ECF, and 20% is in the intravascular
compartment as plasma
14. Body fluids
Intracellular fluid
â˘â˘ The ICF is primarily a solution of potassium
and organic anions, proteins, and so on.
â˘â˘ The cell membranes and cellular metabolism
control the constituents of this ICF.
â˘â˘ ICF is not consistent in the body. It represents
a collection of fluids from all the different cells.
16. Distribution Of Total Body Water
Fluid Compartments Infants Older children
⢠Intracellular Fluid (ICF) 40% 35 - 40%
⢠Extracellular Fluid (ECF) 35 -40% 20 - 25%
- Interstitial ---- 15%
- Trans vascular (plasma) ---- 5%
- Transcellular ---- 1 -3%
Total body water 75 -80% 60%
17. Body fluids
Regulation of body water is control by it´s intake
and excretion .
Intake is stimulate by thirst ,thirst regulate by
hypothalamus and also by the volume of body
water .
Kidney regulate the water balance and osmolality of
body fluid under the influence of ADH (antidiuretic
hormone ) and natriureteric peptides .
18. Body fluids
Natriureteric peptide are body´s defense against
volume expansion .
Osmolality is the number of osmotically active
particles per 1000g of water in solution - milli
osmole (mOsm/kg) .
Antidiuretic hormone secretion is regulate by
intracellular , plasma osmolality and the volume of
ECF.
19. Body fluids
Antidiuretic hormone secretion is inhibited when
excessive water is administered resulting dilution
of the body fluids and hypotonicity .
The ADH act primarily by increasing the
permeability of the renal collecting ducts to
water .
20. Fluid Pressures & movements
⢠ECF and ICF fluid shifts occur related to
changes in pressure within the compartments
⢠Fluid flows only when there is a difference in
pressure
⢠Always fluid moves from area of low
concentrations to area of high concentrations
21. Fluid Shifting
⢠1st space shifting- normal distribution of
fluid in both the ECF compartment and ICF
compartment.
⢠2nd space shifting- excess accumulation of
interstitial fluid (edema)
⢠3rd space shifting- fluid accumulation in
areas that are normally have no or little
amounts of fluids (ascites)
22. Fluid and Electrolyte Transport
Passive Transport Systems
⢠Diffusion
⢠Filtration
⢠Osmosis
Active Transport System
⢠Pumping
⢠Requires energy expenditure
23. Diffusion
Molecules move across a biological membrane
from an area of higher to an area of lower
concentration
Membrane types :-
ďPermeable
ďSemi-permeable
ďImpermeable
24. Filtration
⢠Movement of solute and solvent across a
membrane caused by hydrostatic (water
pushing) pressure .
⢠Occurs at the capillary level .
⢠If normal pressure gradient changes edema
results from âthird spacingâ.
26. Osmosis
⢠Movement of solvent
from an area of lower
solute concentration to
one of higher concentration.
⢠Occurs through
a semipermeable
membrane using osmotic
(water pulling) pressure.
28. Electrolyte Composition Of Body Fluids
Electrolyte have capability of conducting an
electric current in solution and it may be charge
positively (cations) or charge negatively (anions).
sodium chloride is the principal osmotic agent in
ECF regulation of body water depend on
regulation of sodium .
29. kidney is main organ in regulation of water and
sodium balance âADH . aldosterone and thirst
mechanism .
Both renal and extrarenal mechanisms play role in
regulation of potassium balance which include
aldosterone production and promotion of
potassium movement into the cells by alkalosis
and insulin
31. Crystalloid
⢠Water and electrolyte solution
⢠Does not remain within the intravascular
space but rather distributes to the entire
extracellular space
⢠Only impacts on the intracellular space if it
causes a change in extracellular osmolarity
33. Isotonic Fluids
⢠Osmolality is similar to that of serum.
⢠These fluids remain intravascular momentarily,
thus expanding the volume.
⢠Helpful with patients who are hypotensive or
hypovolemic.
⢠EXAMPLES:
⢠0.9% sodium chloride solution (154 mEq Na/L
308 mOsm/L)
35. Hypotonic Fluids
ďLess osmolarity than serum (meaning: in general
less sodium ion concentration than serum)
ďThese fluids DILUTE serum thus decreasing
osmolarity.
ďWater moves from the vascular compartment into
the interstitial fluid compartment interstitial
fluid becomes diluted Osmolarity decreases
water is drawn into adjacent cells.
36. Hypotonic Fluids
- The purpose of hypotonic fluids is to replace
cellular fluids, because its lower osmotic
pressure(hypotonic) as compared with plasma.
⢠Less salt or more water than isotonic ,It may used
to treat hypernatremia (hypotonic Na solutions).
⢠If infused into blood, RBCs draw water into cells
( can swell & burst )
⢠Solutions move into cells causing them to enlarge.
⢠0.45% Sodium Chloride
⢠0.33% Sodium Chloride
37. Hypotonic Fluids
Complications of excessive use of hypotonic
solutions include:
⢠Intravascular fluid depletion.
⢠Decreased blood pressure.
⢠Cellular edema.
⢠Cell damage
38. Hypertonic solution
⢠Solution of higher osmotic pressure greater
than of ECF.
⢠If infused into blood, water moves out of cells
& into solution (cells wrinkle or shrivel)
⢠Solutions pull fluid from cells
⢠3% NaCl
⢠5% NaCl
⢠TPN
⢠D10%
⢠DNS
40. Crystalloids Advantages
⢠Inexpensive.
⢠Greater urine output.
⢠Replace interstitial fluid.
Disadvantages:
⢠Short duration of hemodynamic improvement.
⢠Peripheral edema.
⢠Pulmonary edema.
⢠Intravascular half-life is about 20-30 min.
41. Colloid
⢠Colloid is a term used to describe fluids which
contain large molecules (Differing molecular
weight & chemical structure).
⢠It remain in the circulation (vascular space)
longer until they are broken down , may be
preferred for increasing intravascular space.
⢠Natural & synthetic plasma protein
⢠It has Higher incidence of severe adverse
reactions.
44. Acid-Base Balance
Acid-base balance is an essential part of fluid
and electrolyte management .
An acid is a chemical substance that dissociates
in solution, resulting hydrogen ions (pH below
7.0 ) .
A base is a substance that combines with acid to
form salts
45. Acid-Base Balance
A buffer is a substance that reduces the change in
free hydrogen ion concentration of a solution
when an acid or base is added .
The concentration of hydrogen ions determines
the acidity of fluids and it is dependent on the
ratio of pCOâand bicarbonate .
46. The term pH is used to indicate acidity
,alkalinity and neutrality.
ď pH = alkalinity
ď pH = acidity
ď A neutral solution has a pH of 7.0
Body pH Regulation Mechanisms :-
- Chemical buffer system of the body .
- Respiratory regulatory mechanism .
- Renal mechanisms
47. Body pH Regulation Mechanisms
Chemical buffer system of the body :-
A buffer is a substance that can absorb or donate Hâş
ion .The four important chemical buffer systems is:-
- Bicarbonate-carbonic acid buffer is most
important system that convert strong acid to a
weak carbonic acid . .
- Phosphate buffer .
- Hemoglobin buffer.
- Protein buffer .
48. Respiratory regulatory mechanism :-
Provide support to the bicarbonate-carbonic acid
buffer system by eliminating excess COâ
Through rapid breathing .
Renal mechanisms:-
It helps in the elimination of excess acid and
base by reabsorption of bicarbonate in the
proximal tubules and excretion of Hâş ion as
phosphate buffer salts and ammonium ions .
49. Fluid imbalance
The imbalance may occur when the normal
physiological requirements of body fluids is not
maintained to replace obligatory urinary and
insensible losses and the water required for
metabolic activity
50. Fluid imbalance
The requirement of fluid depend on :-
ď body weight .
ď body surface area .
ďMetabolic rate .
ďIndividual age .
51. Dehydration
Dehydration is the most common fluid imbalance
due to excessive loss of body water .it is clinical
state that results from fluid deprivation .
It is more common in infant and children .
Important causes is diarrhea and vomiting .it may
also occur in diabetes insipidus ,hyperglycemia
and renal losses .
52. Dehydration types based on type of fluid loss :-
Isotonic dehydration : most common with
proportionate loss of water and solutes from ECF.
ICF remains intact as there is no redistribution of
fluid .
Hypotonic dehydration : the depletion of the
solutes in ECF is much more than the water losses .
Hypotonicity of ECF leads to shift of water from
ECF to ICF causing further contraction of ECF and
shock .
53. Hypertonic dehydration :
excess loss of water proportionate to the solutes
causing movement of water from the cell in the
ECF leading to intracellular dehydration .
54.
55. Dehydration types based on severity :-
Mild :-
When the total fluid loss reaches 5% or less .
Sign and symptoms ( S&S) :-
⢠No dehydration .
⢠Thirsty .
⢠Less than 5% of body weight is lost
56. Moderate :-
When the total fluid loss reaches 5 -10%
S&S :-
⢠Dry skin and mucous membranes .
⢠Thirst .
⢠Decreased urine output .
⢠Muscle weakness .
⢠Drowsiness .
⢠Light headache .
⢠Sunken fontanels .
⢠BP , PR (tachycardia) ,shallow rapid RR .
⢠Crying with tears
57. Severe :-
When the total fluid loss reaches more than 10%
considered in emergency case .
S&S:-
⢠extreme thirst .
⢠Very dry mouth ,skin and mucous membranes .
⢠Sunken eyes and fontanels .
⢠No tears .
⢠Dry skin that lacks elasticity and slowly ââbounces back ââwhen
pinched into fold .
⢠Rapid heartbeat ,rapid and shallow breath .
⢠Delay capillary refill for more than tow seconds .
59. Assessment of dehydration
The successful management of dehydration in
infant and children can be possible by accurate
assessment of degree of dehydration and
initiation of rehydration therapy according to the
child condition .
Clinical history and physical examination are the
major aspect of assessment of hydration status .
62. Laboratory Investigations
Essential for further assessment of fluid and
electrolyte deficits
- Serum electrolyte ,blood urea and creatinine
,acid base status ,plasma osmolality , hematocrit
values and urine specific gravity
64. Management Of Dehydration
Dehydration to be manage after accurate
assessment of dehydration status .
In severe dehydration required to maintain vital
function by rapid intravenous infusion (100 to
120ml /kg ) of isotonic , iso-osmotic solution
(ringer lactate) or normal saline or plasma to
achieve normal urine output , correction of
potassium deficit and acidosis .
65. Management Of Dehydration
Total correction of fluid and electrolyte deficit
can be achieve safely and rapidly through oral
rehydration therapy ORT in most of cases .
Intravenous rehydration is recommended if there
is severe cases or there is persistent vomiting ,
paralytic ileus or unconscious child or too sick to
drink ORS .
66. Management Of Dehydration
Hydration should be assessed at regular interval
to determine whether rehydration therapy is
essential furthermore or not .
Mother should be involved during rehydration
therapy .
Intake and output is vital responsibility of the
nurse .
67. Fluid Maintenance
⢠100 mL/kg for first 10 kg
⢠50 mL/kg for next 10 kg
⢠20 mL/kg for remaining kg
⢠Add together for total mL needed per 24-hour
period.
⢠Divide by 24 for mL/hour fluid requirement.
71. Rehydration Solution
Dosage:
⢠Children 0-2. Ÿ to ½ cup after each loose
stool. Max 2 cups/day.
⢠Children 2-9. ½ to 1 cup after each loose
stool. Max 4 ½ cups/ day.
⢠10+ yrs. Approximately 2 L/day.
74. Hyponatremia
Is the termed when serum sodium level is less
than 130 mEq/L it occurs due to water retention
,sodium loss or both .
Is commonly found in hospitalized children with
acute diarrhea, pneumonia, meningitis, sepsis,
heart failure ,hepatic failure and renal disease .
75. Etiology Of Hyponatremia
ďPrimary sodium deficit with sodium depletion
resulting in :
1- renal sodium losses in prematurity, chronic
diuretic therapy, osmotic diuresis in diabetes
mellitus, adrenal insufficiency .
76. 2- extrarenal sodium losses due to vomiting,
diarrhea, nasogastric drainage, burn and
excessive sweating .
3- nutritional deficit in water intoxication, poor
sodium concentration in IV fluid, paracentesis,
CSF drainage and burns .
77. ďPrimary water excess with water gain due to :
Excess IV fluid, tap ware enema,
hypothyroidism and syndrome of inappropriate
ADH secretion .
ďAbnormal retention of sodium and water in :
nephrotic syndrome, liver cirrhosis CCF and
renal failure .
78. Clinical Manifestation
⢠The features depend on the severity of the
condition usually if the sodium level between 120
to130mEq/L the patient may be a symptomatic .
⢠Restlessness .
⢠Confusion .
⢠Convulsion .
⢠Hypotension .
⢠Unconsciousness .
79. Management
Symptomatic hyponatremia is managed by
administering 10ml/kg sodium chloride (saline)
at rate 1ml/minute in 24 to 48 hours.
Restrict fluid in some cases (renal failure) to
avoid pulmonary oedema and CCF .
Furosemide with 3 percent saline if CNS
symptoms are associated with condition .
80. Hypernatremia
Is the termed when serum sodium level is more
than 150 mEq/L . It is result from deficit of water
with respect to sodium stores due to water loss in
diarrhea, vomiting, diuresis, and burn or
excessive sodium intake .
81. Etiology of Hypernatremia
Excessive sodium gain in faulty preparation of
ORS formula, excessive sodium bicarbonate
during resuscitation, IV administration of
hypertonic saline, high Naâş content in breast
milk and salt poisoning .
Excessive water loss or deficit in diabetes
mellitus ,poor water in take ,increased insensible
loss in fever and hyperventilation .
82. Clinical Manifestation
⢠Irritability .
⢠Confusion .
⢠Twitching .
⢠Seizer .
⢠Tough and doughy skin and subcutaneous
tissue .
⢠Metabolic acidosis with deep rapid breathing .
83. Management
⢠Rapid IV Ringer Lactate or saline to correct
hypovolemia .
⢠Specific treatment of underline cause.
⢠Withholding diuretics, hypokalemia and
hypercalcemia treatment ad correction of
faulty ORS therapy .
84. Hypokalemia
Is the termed when serum potassium level is
more than 3.5 mEq/L the most common causes
are acute gastroenteritis AGE, septicemia,
diuretic therapy and hepatic failure
85.
86. Etiology Of Hypokalemia
⢠Reduced potassium intake in PEM .
⢠High renal losses of potassium in diuretic
therapy, renal tubular defect, acid-base
imbalance(alkalosis, diabetic ketoacidosis)
endocrinopathies .
⢠High extrarenal losses of potassium in diarrhea,
vomiting, frequent enemas,
87. Clinical Manifestation
Hypokalemia affect the bioelectric processes
(muscle contraction, nerve conduction and
myocardial pacing.
The features is :-
Weakness of the skeletal muscle, hypotonia,
diminished reflexes, abdominal distention,
paralytic ileus, respiratory distress, arrhythmias,
ECG changes, hypokalemic nephropathy and
polyuria .
88.
89.
90. Management
⢠Administration of potassium over 24 to 48 hours.
⢠Treat underline cause.
⢠Oral administration is safer than IV route.
⢠In life-threating hypokalemia and ECG changes
rapid correction is recommended
⢠Potassium infusion at rate of 0.3 to
0.35mEq/kg/hour till ECG become normal
91. Management
⢠Infusion rate should not exceed 0.6 mEq/kg /hour.
⢠Infusion fluid should not contain more than 40
mEq/L of potassium.
⢠High rate and concentration cause cardiac
depression .
⢠Potassium should be administered only when
urinary flow is stablished
92.
93. Hyperkalemia
⢠Hyperkalemia is defined as a potassium
concentration > 5.5 mmol/L.
⢠Hyperkalemia is a true medical emergency.
⢠The most serious effect of hyperkalemia is
cardiac toxicity, which does not correlate well
with the plasma [K].
94. Hyperkalemia
Earliest ECG changes include:
- increased T wave amplitude with
- tall T waves (especially in leads V2-V3).
More severe hyperkalemia results in a
prolonged PR interval and QRS duration,
atrioventricular conduction delay, and loss of P
waves.
95. The terminal event is usually ventricular
fibrillation or asystole which are resistant to the
treatment until hyperkalemia is corrected.
Hyperkalemia causes also a partial
depolarization of cell membranes, which is
manifested as weakness that may progress to
flaccid paralysis and hypoventilation.
96. Causes of hyperkalemia:
Increased [Kâş] intake (e.g. iatrogenic, rapid
transfusion of relatively old blood).
Transcellular shift (most common cause).
Tumor lysis syndrome.
Rhabdomyolysis,
intravascular hemolysis.
97. Causes of hyperkalemia:
Metabolic acidosis, especially in renal failure or
in renal tubular acidosis.
- Less evident with lactic acidosis.
Succinylcholine, especially in patients with
anterior motor neuron disease, myopathies burns
or prolonged immobilization.
- Familial periodic paralysis.
98. Causes of hyperkalemia:
Impaired renal [Kâş] excretion:
Renal failure with GFR < 10 mL/min, and
oliguria < 500 mL/day.
Diabetic nephropathy.
Adrenal insufficiency, hyporeninemic
hypoaldosteronism.
Drug related ([Kâş]-sparing diuretics, (angiotensin-
converting enzyme) ACE inhibitors, non-selective
beta-blockers, cyclosporine, NSAIDs).
99. Treatment Of Hyperkalemia
Calcium: A physiologic membrane antagonist
of [Kâş].
- Calcium gluconate (10 ml 10% solution)
should be immediately given over 2-3 min to
prevent potassium-induced cardiotoxicity.
- Ca chloride is preferable in patients with
circulatory instability.
100. Treatment Of Hyperkalemia
The duration of the therapeutic effect is limited
(20-30 min).
The dose can be repeated if no change in the
ECG is seen after 5-10 min.
Ca should be used cautiously in patients with
digitalis toxicity.
101. Treatment Of Hyperkalemia
Induction of intracellular shift of potassium:
Glucose-insulin:
Pediatric: IV 0.5 g/kg glucose with 0.1 units/kg
regular insulin over 30 min (use 25% glucose).
Neonate: 2 mL/kg 10% dextrose with 0.05
units/kg regular insulin.
102. Treatment Of Hyperkalemia
Na bicarbonate should be reserved for severe
hyperkalemia associated with metabolic acidosis.
The onset of action is nearly immediate, with a
duration of 1-2 h
103. Treatment Of Hyperkalemia
Beta2-adrenergic agonists (salbutamol) are
readily available by the IV or by the inhalation
route and directly induce cellular uptake of [Kâş].
The onset of action is in 30 min.
These drugs may lower [Kâş] by 0.5-1.0 mmol/L
and this effect may last for 2-4 h.
104. Treatment Of Hyperkalemia
Increase of potassium excretion:
Loop and thiazide diuretics (if renal function is
adequate).
Cation exchange resins (kayexalate).
Usual dose is 25-50 g PO, mixed with 100 ml
20% sorbitol (lasts for 4-6 h) or 50 g in tap water
administered as a retention enema (should be
avoided in postoperative patients).
108. Acid-base imbalances
are common in children and fall into four
categories: respiratory acidosis, respiratory
alkalosis, metabolic acidosis, and metabolic
alkalosis.
The body will compensate for these
disturbances by using a renal or a respiratory
buffering mechanism. These responses are
monitored by ABG analysis.
109. Respiratory acidosis
can be caused by any condition that decreases a
childâs respiratory effort. Slowed or shallow
respirations will result in a buildup of carbon
dioxide, which
combined with water forms carbonic acid and
leads to acidosis ( pH , pCO2).
110. Clinical Conditions Associated With Respiratory
Acidosis :
Head trauma . Asthma.
General anesthesia . Croup or epiglottitis.
Drug overdose . Cystic fibrosis.
Brain tumor . Atelectasis.
Sleep apnea . Muscular dystrophy.
Mechanical underventilation . Pneumothorax.
111. Acidosis causes central nervous system
depression. As a result, the child will be
lethargic, confused, and disoriented, may
complain of a headache, and, if not treated,
may become comatose. Efforts to improve
ventilation help correct the underlying cause
of respiratory acidosis. Without correction,
the body, via the kidneys, will retain
bicarbonate to help neutralize the increased
acid.
112. The kidneys attempt to compensate is slow and
does not correct the underlying respiratory
problem.
Compensation is a body process to restore blood
pH to normal by changing the partial pressure of
carbon dioxide (pCO2) or the bicarbonic ion
concentration.
114. Respiratory alkalosis
occurs when the carbon dioxide level is too low.
This most commonly occurs from conditions that
cause the child to hyperventilate (e.g., anxiety,
pain, meningitis, gram-negative septicemia,
early response to salicylate poisoning,
mechanical overventilation).
child will often feel numbness or tingling in toes
and fingers, lightheadedness, and confusion, and
may faint
115. Renal compensation for respiratory alkalosis is
rarely seen clinically because the underlying
condition is often corrected before the kidneys
have time to respond.
the kidneys would retain free hydrogen ions and
excrete bicarbonate. The childâs urine pH would
increase as a result of the increased bicarbonate
excretion.
116. Clinical Manifestations
⢠Tachypnea
⢠Numbness, tingling of
toes and fingers
⢠Lightheaded, dizzy
⢠Syncope
⢠Diaphoresis
Management Approaches
⢠Monitor blood gases
⢠Encourage slow
ventilation
⢠Use rebreathing
oxygen masks or bag
⢠Administer sedative, if
ordered
⢠Monitor vital signs
117. Metabolic acidosis
is most commonly caused by a loss of bicarbonate
in the stool or an increase in ketone bodies (e.g.,
acetoacetic acid, acetone, beta-hydroxybutyric
acid) in the blood. These conditions most
frequently result from diarrhea and diabetic
ketoacidosis. Children are often confused,
lethargic, and tachycardic..
118. The body compensates by increasing the depth and
rate of respirations in order to blow off carbon
dioxide, thus decreasing pCO2 and carbonic acid
119. Clinical Manifestations
⢠Confusion
⢠Lethargy
⢠Deep, rapid
respirations
⢠Acetone odor to breath
⢠Tachycardia
⢠Cold, clammy skin
(mild acidosis)
⢠Warm, dry skin (severe
acidosis)
Management Approaches
⢠Correct underlying
problem
⢠Administer sodium
bicarbonate
⢠Administer oxygen
⢠Correct DKA with
insulin or glucose
⢠Monitor vital signs
120. Metabolic alkalosis
occurs as a result of bicarbonate retention or
hydrogen ion loss. It is most commonly seen in
children with prolonged vomiting as emesis is
acidic stomach contents. It can also occur with
ingestion of large quantities of bicarbonate
antacids, massive blood transfusions, loss of
nasogastric fluids due to gastric suction, and
hypokalemia.
121. A child experiencing metabolic alkalosis is often
weak and dizzy and may complain of muscle
cramps. The respiratory response would be to
increase pCO2 by decreasing the rate and depth
of respirations (hypoventilation).
122. Clinical Manifestations
⢠Slow, shallow
respirations
⢠Tremors, muscle
twitching
⢠Disorientation
⢠Seizures
Management Approaches
⢠Correct underlying
problem
⢠Administer sodium
NaCl and KCl
⢠Replace loss of fluids
⢠Take seizure precautions
⢠Monitor intake and
output
⢠Monitor electrolyte
status
123. Normal Arterial Blood Gas Values
pH 7.35 - 7.45
PaCO2 35 - 45 mm Hg
PaO2 70 - 100 mm Hg **
SaO2 93 - 98%
HCO3
ÂŻ 22 - 26 mEq/L
%MetHb < 2.0%
%COHb < 3.0%
Base excess -2.0 to 2.0 mEq/L
CaO2 16 - 22 ml O2/dl