Fluids and Electrolytes-Seminar

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Fluids and Electrolytes

Dr Tamimi
Assistant Professor of Surgery
University of Aden
The Body Fluids
The Normal Distribution of
3 Fluids
The Normal Distribution of
4 Fluids
 Total body water (TBW) forms about
60% of the lean body mass and is about
40-42L
 Intracellular fluid volume (ICF) forms
60% of TBW and is about 25L
 Extracellular fluid volume (ECF) forms
40% of TBW (and 20% of body weight)
and is about 15-17L
5 Extracellular Fluid (ECF)
 Extracellular fluid further consists of:
Plasma water (IVF) 3L
Extravascular fluid 12-
14L
– Interstitial fluid (ISF) 8-
9L
– Transcellular water 1L
– Bone and dense connective tissue 4-
5L
6 Transcellular Water
 Special body compartments, separate from
ICS, ECS, and plasma
Cerebrospinal Fluid
Fluid in the GI Tract
Bladder
Intraocular Fluids
Fluid in potential spaces (pathological) such as the
pericardial or pleural sacs.
 This volume of fluid is small and is not normally
considered in measurements, but should be
kept in mind, especially in cases of pathology
The Normal Distribution of
7 Fluids

 Distribution
of fluid across the cell
membrane depends on:
High protein content of cells (oncotic
pressure)
Semi-permeability of the cell membrane
The Na-K pump, which is energy
dependent (keeps sodium out of the cells,
and hence water since water movements
follow sodium movements)
The Normal Distribution of
8 Fluids

 Movements of fluid across the capillary


bed depends on:
Hydrostatic pressures at arterial and
venous ends
Semi-permeability of the capillary bed
Plasma oncotic pressure
Interstitial pressure
Normal Fluid Homeostatic
9 Mechanisms

 Totalbody fluids are broadly balanced


by intake and output
Intake is an expression of drinking as a
result of thirst which is the function of
chemoreceptors which detect increased
circulating and cellular osmolarity
Normal Fluid Homeostatic
10 Mechanisms

 Total body fluids are broadly balanced


by intake and output
Volume receptors are less sensitive to fluid
depletion as regards increasing intake, but
play a role in reducing fluid losses in the
kidneys, and stimulating vasoconstriction
and an increased cardiac output to
compensate for the shrunken circulating
volume
Normal Fluid Homeostatic
11 Mechanisms

System for Volume Control


 In hypovolaemia, Va g u s

Hyp o tha la m us

volume receptors in the P ituita ry

heart and great vessels


stimulate the Th yro c a rotid
Re c e p to rs

hypothalamus -
hypophysis system:
Arteria l
Re c e p to rs

ADH for water retention He a rt


ADH

ACTH and hence


Aldosterone for salt AC TH
Ald o s te ro ne

retention Ad re n a l
Gla n d J GA
Ang io te ns in II

Kid ne y
The Renin-Angiotensin-
12 Aldosterone Mechanism
 The enzyme ‘Renin’ is
released from the kidney in
response to a low volume
 This in turn converts
Angiotensinogen to
Angiotensin I, which is
further hydrolyzed to
Angiotensin II in the lungs
Vasoconstriction
 Aldosterone is then released
from the adrenal cortex
Salt and water retention
The Normal Daily Fluid
13 Turnover
The Normal Daily Fluid
14 Requirements
Ionic Composition of Body
15 Fluids
Summary of Ionic
16 Composition
Protein
Organic Phos.
400 Inorganic Phos.
Bicarbonate
300 Chloride
Magnesium
200 Calcium
Potassium
100 Sodium

0
Plasma Interstitial Cell
H2O H2O H2O
Water Depletion:
17 Aetiology

 Purewater depletion may occur in


cases of reduced intake
Inavailability, such as loss in the desert
Incapability, such as in feeble patients or
patients with swallowing disorders
Iatrogenic, caused by doctors !!
Water Depletion:
18 Aetiology

 Or due to increased losses:


Losses in urine – such as in diabetes insipidus or
mellitus, or due to excessive use of osmotic
diuresis
Losses from the GIT – as in patients with profuse
watery diarrhoea
Losses from the lung – as may occur with
hyperventilation using unhumidified air
Losses from the skin - such as increased
insensible losses associated with fever, burns, or
excessive sweating in the tropics
Water Depletion:
19 Features

 Similar
to features of sodium excess,
but associated with a hypovolaemia
Intense thirst
Cellular dehydration with loss of tissue
turgor
Features of hypovolaemia (rapid pulse,
and low BP)
Lethargy or even coma
Water Depletion:
20 Management

 Slow Rehydration with hypotonic solutions


Rapid rehydration may induce the development of
cellular and brain oedema
Conscious stable patients are rehydrated orally
Rough estimation of required fluid volume
calculated by dividing actual serum sodium
concentration by desired concentration, hence if
actual [Na] = 150 mEq/L, then fluid requirement
= 150/140 = 1.07L
21
Water Excess or Intoxication:
Aetiology
 Basically due to excess administration of
fluids
Inappropriate replacement of fluid losses with low
sodium content
Excessive administration of 5% dextrose in water
intravenously
Inappropriate fluid balance in renal failure
Total bowel irrigation with water
Transurethral resection syndrome
Inappropriate ADH syndrome
22
Water Excess or Intoxication:
Features
 Featuresare those of a hyponatraemia,
but associated with a normal or
expanded circulating volume
Low sodium levels of 118 mmol/L or less
Neuromuscular features
– Mental confusion, disorientation, coma and
convulsions
– Muscle weakness and lethargy
Oliguria
23
Water Excess or Intoxication:
Management
 Stop water intake
 Observe and wait for normal diuresis
 200 ml hypertonic saline may induce
diuresis if the patient remains oliguric
after a few days
 Occasionally dialysis or haemo-
filteration may become necessary
Practical
24 Fluid Management
 Surgicallyimportant fluid losses may be
in the form of:
Electrolyte-rich fluids
Protein-rich fluids
Blood
Loss of Electrolyte-Rich
25 Fluids
 Lossof electrolyte-rich fluid, commonly
from the GI tract or the GU tract, such
as:
Vomiting, diarrhoea or losses from fistulae
Intestinal obstruction (sequestration)
Diabetes mellitus or insipidus
Loss of Electrolyte-Rich
26 Fluids
 Pathophysiological changes:
Loss of circulating volume, with features of
hypovolaemia and cellular dehydration
– Interstitial fluids move into the vascular space (net drop
in pressures across the capillary bed), thus temporarily
correcting hypovolaemia
– Intracellular fluids move out into the interstitial space
(drop in interstitial hydrostatic pressure with an
accompanying increase in oncotic pressure), with
resultant cellular dehydration
Loss of electrolytes with clinical features related to
electrolyte deficits
Loss of Electrolyte-Rich
27 Fluids
 Aims of fluid management include:
Correction of circulating volume
Cellular rehydration
Correction of electrolyte imbalances
 Remember that fluid movements follow
sodium movements
 Always Replace What Is Lost
 Don’t Forget to Add Normal Requirements
Loss of Electrolyte-Rich
28 Fluids
 Correction of circulating volume
For best results use a plasma expander, whence
circulating volume is expanded equal to
administered fluid (volume-for-volume)
Alternately use a crystalloid based mainly on
sodium (such as normal saline or Ringer’s
Lactate) - but only ¼ will remain in the circulation
and ¾ will load the interstitial space, causing
peripheral edema
Loss of Electrolyte-Rich
29 Fluids
 Never Use Water or Dextrose for
Volume Replacement, since only 1/12
will remain in the circulation, and 8/12
will enter the cells causing cellular
oedema and damage
You may actually drown the patient
Loss of Electrolyte-Rich
30 Fluids
 Cellular rehydration
As seen from the previous slides, plasma
expanders and saline-containing
crystalloids are not useful in cellular
rehydration
5% dextrose in water, however, is ideal
(remember 8/12 of the given volume will
enter the cells), as well as providing
necessary energy
Loss of Electrolyte-Rich
31 Fluids
 Correction of electrolyte imbalances
Determine imbalance (mostly deficit unless
iatrogenic excess after over-therapy) by
biochemical analysis
Calculate amount of electrolyte(s) required,
add daily requirements, and supplement
slowly with volume replacement
Re-evaluate and manage accordingly
Constituents of Some Common
32 Replacement Fluids
33 Loss of Protein-Rich Fluids
 Protein-rich
fluids are usually lost in
association with:
Burns
Infection and inflammation, such as
peritonitis
Protein-losing enteropathy
Nephritic and nephrotic syndromes
Neoplastic disease involving cavities
34 Loss of Protein-Rich Fluids
 Pathophysiological problems include:
Loss of circulating volume (reduced oncotic
pressure causes reduced fluid return to the
circulation from the interstitial space)
Accumulation of fluids in the interstitial space
(peripheral oedema or even anasarca)
Loss of immune bodies and an increased
susceptibility to infections
Increased catabolism and reduced wound-healing
capabilities
35 Loss of Protein-Rich Fluids
 Aims of fluid management include:
Correction of circulating volume
Reduction of interstitial fluid
Improvement of immunity and correction of
catabolism
 Always Replace What Is Lost
36 Loss of Protein-Rich Fluids
 Correction of circulating volume
Use a plasma expander. Preferably use a
protein-containing expander (replace what
is lost !!)
Do not use a sodium-containing
crystalloid solution (except in the case of
burns in the early phases of fluid management)
since ¾ of the given volume will enter the
interstitial space, which is already flooding
37 Loss of Protein-Rich Fluids
 Reduction of interstitial fluid
Increase the oncotic pressure of the
intravascular space by infusing a protein-
rich fluid
Increase renal losses of water and sodium
using diuretics, but not before correcting
and maintaining circulating volume
38 Loss of Protein-Rich Fluids
 Improvement of immunity and correction
of catabolism
Infuse a protein-rich fluid containing viable
immunoglobulins (and albumin) – such as
fresh plasma
Priority follows correction of circulating
volume and reduction of interstitial fluids
39
Loss of Blood
 Loss of blood may be associated with:
Acute loss from injury or vascular rupture such as
bleeding from an external wound, an internal
bleeding such as splenic rupture, or from
conditions such as oesophageal varices or peptic
ulcer, or intra-operatively
Chronic blood losses from the GIT or the GU
tracts
Damage to RBCs as may occur in burns) in
addition to plasma volume losses)
40
Loss of Blood
 Pathophysiological problems include:
Loss of circulating volume, particularly in acute
bleeding
Loss of oxygen-carrying capacity with higher
incidence of hypoxia and hypoxic injury
An increased circulating volume and heart failure
in cases with chronic bleeding
Problems associated with massive blood
transfusions
41
Loss of Blood

 Aims of fluid management include:


Correction of circulating volume
Correction of oxygen-carrying capacity
Minimizing transfusion complications
 Remember to Always Replace What Is
Lost (Plus The Daily Requirements)
42
Loss of Blood
 Correction of circulating volume
In acute blood loss with hypovolaemia, volume
replacement may start with a saline-rich
crystalloid, but preferrably use a plasma expander.
Once blood is available, it should be given
In chronic blood loss associated with heart failure,
correction of circulating volume (hypervolaemia)
includes potent diuretics, to be followed by
transfusion of packed RBCs
43
Loss of Blood

 Correction of oxygen-carrying capacity


This requires blood transfusion until Hb
concentration is at least in the range of 10
gm/dl
Each 500-ml transfusion unit of blood
will raise the Hb by approximately 1 g/dl
Oxygen mask
44 Oxygen-Carrying Capacity
 Normal oxygen consumption at rest
250 ml per minuite
 Each gm of Hb can deliver
1.14 ml oxygen per minuite (MAX 80% of 1.36 ml)
 Hence total required arterial-side Hb
= 250/1.14 = 220 gm of Hb
 Normal arterial-side blood volume (adult)
= 0.45 x 5L = 2.25L
 Hence required Hb concentration for adequate
oxygen-carrying capacity
= 220gm/(2.25x10)dl = 9.8 gm/dl
Minimizing Transfusion
45 Complications
 Transfuse only if and when
necessary
 Proper grouping and cross-matching
 Meticulous testing for hepatitis and HIV
and other blood-borne diseases
 Use of aseptic techniques in storing,
handling and infusing blood, including
use of proper giving-sets and filters
Minimizing Transfusion
46 Complications
 Use of fresh blood or blood not older
than 14 days
 Addition of calcium gluconate with
massive transfusions
 Careful watch for transfusion reactions,
and early intervention if necessary
 Careful fluid monitoring to avoid
overload
47 Normal Fluid Requirements
 Thenormal requirements of water, Na+
and K+ can effectively be given in a
70Kg man by giving:
2L dextrsoe 5% in water
1L normal saline (0.9%)
Adding 20-30 mmol of K+ in every liter of
fluid running at 1 liter every 8 hours
48 Normal Fluid Requirements
 This regimen will supply:
Water 3L
Sodium 154 mmol
Chloride 154 mmol
Potassium 60-90 mmol
49 Normal Fluid Requirements
 Remember that:
Fever increases daily fluid requirements by up to
10% of the daily insensible water loss (800-1000
ml)
Catabolic patients require more fluid intake to
achieve adequate urinary clearance of waste
products
Maintenance needs are less in the immediate
postoperative period, whence there is water and
sodium retention
Monitoring Fluid
50 Replacement Therapy
 The vital signs
Pulse rhythm, rate and volume
Blood pressure
 The urine output
Should be in the range of 40-60 ml/hour
An accurate fluid input-output chart should
be maintained - including daily weight
measurements
Monitoring Fluid
51 Replacement Therapy
 Clinical evaluation of:
Skin turgor and tongue moisture as
indicators of cellular hydration
Lungs for evidence of pulmonary oedema
(overload)
Lower limbs for evidence of peripheral
oedema (overload)
Monitoring Fluid
52 Replacement Therapy
 Central venous pressure
Essential in critically ill patients
Should be maintained at 4-8 mmHg
 Pulmonary Artery Wedge Pressure
(PAWP)
Useful in patients with right heart failure
Left atrial and pulmonary arterial wedge
pressure should be about 25 mmHg
Monitoring Fluid
53 Replacement Therapy
 Investigations should include:
Hb and Hct - dropping levels in absence of
bleeding indicate haemodilution
Elevated BUN in presence of a normal
creatinine level is a feature of dehydration
Serum electrolytes should be evaluated as
baseline and daily to guide type of fluid
required for correction
The Electrolytes
Gram Molecular Weight
55 (GMW)
 The number of grams of a substance it
takes to provide a mole (mol) of that
substance (i.e., 6.02x1023 molecules)
 The gram molecular weight of a
molecule can be calculated by summing
the atomic weight of its individual atoms
Physiological Molecular
56 Weights
Expressing Fluid
57 Composition
 Percentage
 Molality
 Molarity
 Equivalence
Percent Concentrations:
58 (Solute / Solvent) X 100
 Body solvent is H2O
1 ml weighs 1 g
 (weight/volume) percentages (w/v)
 (weight/weight) percentages (w/w)
 Clinical chemistries: mg % or mg / dl
59
Molality

 Concentration expressed as:


moles per kilogram of solvent.
 Rarely used
60
Molarity (M)
 Concentration expressed as:
moles per liter of solution
 Symbol “M” means moles/liter not moles
 Physiological concentrations are low
millimolar (mM) = 10-3 M
micromolar (M)= 10-6 M
nanomolar (nM) = 10-9 M
picomolar (pM) = 10-12 M
Electrochemical Equivalence
61 (Eq)
 Equivalent weight of an ionic substance
in grams that replaces or combines with
one gram (mole) of monovalent H+ ions
 Physiological Concentration:
Milliequivalent (mEq)
Electrochemical Equivalence
62 (Eq)
 Monovalent Ions (Na+, K+, Cl-):
One equivalent is equal to one GMW.
1 milliequivalent = 1 millimole
 Divalent Ions (Ca++, Mg++, HPO42-)
One equivalent is equal to one-half a
GMW
1 milliequivalent = 0.5 millimole
63
Complications in Determining
Plasma Concentrations
 Incomplete dissociation
e.g. NaCl
 Protein binding
e.g. Ca++
 Plasma volume is only 93% water.
The other 7% is protein and lipid
– Hyperlipidemia
– Hyperproteinemia
64
Osmotic Pressure ()

 The
force/area tending to cause water
movement

p

S S S
S
S S S
S S S
S S S
65 Glucose Example

Initial Gl Gl Gl Gl
10 L 10 L

Final Gl Gl Gl Gl
15 L 5L
66 Osmotic Concentration
 Proportional to the number of osmotic
particles formed
 Assuming complete dissociation:
1.0 mole of NaCl forms a 2.0 osmolar
solution in 1L
1.0 mole of CaCl2 forms a 3.0 osmolar
solution in 1L
67 Osmotic Concentration
 Physiological concentrations:
milliOsmolar units most appropriate
1 mOSM = 10-3 osmoles/L
Plasma Osmolarity
68 Measures ECF Osmolarity
 Plasma is clinically accessible
 Dominated by [Na+] and the associated
anions
 Under normal conditions, ECF
osmolarity can be roughly estimated as:
POSM = 2[Na+]p = 270-290 mOSM
Clinical Laboratory
69 Measurement
 Includes contributions from glucose and
urea
 Contribution from glucose and urea
normally small
Glucose normally 60-100 mg/dl
BUN normally 10-20 mg/dl
Clinical Laboratory
70 Measurement
71 Effective Osmolarity
 Urea (BUN) crosses cell membranes
just as easily as water
[BUN]E = [BUN]i
No effect on water movement
72 Effective Osmolarity
73
Osmolar Gap

 Posm (measured) - Posm (calculated)


 Suggests
the presence of an
unmeasured substance in blood
e.g. following ingestion of a foreign
substance (methanol, ethylene glycol, etc.)
74
Serum Sodium

 Sodium is the main extracellular cation


and is involved in fluid volume control
and fluid movements, as well as in the
resting membrane potential
75
Serum Sodium
 Normal serum Na+
135-148 mEq/L
 Normal total sodium content
Adults 1.09 g/kg lean body weight
Neonates 1.78 g/kg lean body weight
 Normal daily requirements:
1.5-2.0 mmol/kg body weight
76
Serum Sodium

 In a 70 kg man
Total body sodium 4000 mmol
ECF sodium 2100 mmol
ICF sodium 400 mmol
Bony skeleton 1500 mmol
– 700 mmol exchangeable
77
Serum Sodium
 Determining total deficit or excess

Na = (140 - SNa) TBW in mEq

where
Na = Sodium deficit or excess,
SNa = Serum sodium, and
TBW = Total Body water = 60% Bwt (kg)
78
Serum Sodium
 Determining serum deficit or excess

Na = (140 - SNa) ECF in mEq

where
Na = Sodium deficit or excess,
SNa = Serum sodium, and
ECF = ECF volume = 20% Bwt (kg)
79
Serum Sodium
 Example
A 65 kg patient with serum sodium level of
120 mEq/L
The ECF Na deficit is
(140-120) x 20% x 65 = 260 mEq
Each 500 ml bottle of Normal (0.9%)
Saline contains 75 mEq of sodium
Therefore number of bottles required to
correct the deficit = 260/75 = 3.5 bottles
Sodium Disturbances:
80 Aetiology
Sodium Disturbances:
81 Features
Sodium Disturbances:
82 Management
83
Serum Potassium
 Normal serum potassium level
3.8-5.0 mEq/L
 Normal total potassium content
Adults 2.65 g/kg lean body weight
Neonates 1.90 g/kg lean body weight
 Daily excretion of potassium:
50-60 mEq/L
 Normal daily requirements:
1.0 mmol/kg body weight
84
Serum Potassium

 In a 70 kg man
Total body potassium 3800 mmol
ECF potassium 60 mmol
ICF potassium 3740 mmol
85
Serum Potassium
 In the absence of acid-base disturbances,
serum K+ levels closely represent total K+
(although it forms only 2% of the latter)
 Acidosis may result in an outward shift of
potassium from the cells into the ECF space,
with resultant hyperkalaemia, whereas
alkalosis has the opposite effect with
resultant hypokalaemia .
86
Serum Potassium
 Thus, these changes in serum potassium
secondary to changes in pH do not reflect the
true situation regarding the body content of
potassium.
 However, a loss of 10% of total body
potassium gives a true drop of serum K+
levels from 4 to 3 mEq/L at a normal pH.
Potassium Disturbances:
87 Aetiology
Potassium Disturbances:
88 Features
Potassium Disturbances:
89 ECG Changes
Potassium Disturbances:
90 Management
91
Serum Calcium
 Normal serum levels
4.3-5.3 mEq/L (8.5-10.5 mg/100 ml)
 Daily requirements
10 mg/kg body weight
 Total body calcium
Adults 20.1 g/kg lean body
weight
Neonates 9.20 g/kg lean body
weight
92
Serum Calcium

 In a 70 kg man
Total body calcium 30160 mmol
ECF calcium 35 mmol (2.5
mmol/L)
ICF calcium 125 mmol (5 mmol/L)
Bony skeleton 30000 mmol
Calcium Disturbances:
93 Aetiology
Calcium Disturbances:
94 Features
Calcium Disturbances:
95 Management
Investigations in
96 Hypercalcaemia
 Hypercalcaemia
 Hypercalciuria
 Hypophosphataemia
 Hyperphosphatiuria
 Elevated serum alkaline phosphatase
 Elevated serum parathyroid hormone
concentration > 0.5 µgs/L
Investigations in
97 Hypercalcaemia
 X-rays showing subperiosteal bone resorption
in the hands, with generalized cystic bone
disease and renal calculi and/or
nephrocalcinosis.
 Cortisone suppression test-to exclude
hypercalcaemia of:
sarcoidosis
vitamin D intoxication
metastatic bone disease
98 Cortisone Suppression Test
 150 mgs are given daily for 10 days (serum
ionized calcium is measured on the 5th, 8th,
and 10th days before injection).
If the serum ionized calcium level is reduced-then
the likely cause is either sarcoidosis, vitamin D
intoxication, or metastatic bone disease.
If the serum ionized calcium level remains high,
then cause is hyperparathyroidism
Parathyroid Localization
99 Tests
 Isotopescan-using technetium and
thallium subtraction imaging is
extremely sensitive in acurately locating
adenomas
Parathyroid Localization
100 Tests
 Other tests (rarely used now) include:
Cine oesophagography (barium swallow indentation)
Ultrasound scan
Arteriography and digital subtraction angiography
Retrograde venography and venous sampling of
parathormone levels performed by radiologists via the
femoral vein
CT scan
Nuclear medical radiography
Thermography
Lymphangiography
101
Surgical Exploration

 Surgical exploration of the neck is


required for persistent hypercalcaemia
even if all the tests are negative. The
failure rate due to incomplete initial
exploration is 5%, and most undetected
adenomas are in the neck or the upper
thymus
Hypercalcaemia:
102 Differential Diagnosis
 Primary hyperparathyroidism
 Sarcoidosis
 Myelomatosis
 Hyperthyroidism
 Milk-alkali syndrome
 Vitamin D intoxication Immobilization
with Paget's disease
Hypercalcaemia:
103 Differential Diagnosis
 Malignant disease with endocrine function
cancer of the bronchus
renal cancer
 Skeletal metastasis (secondaries) from other
organs or tissues
cancer thyroid
cancer kidney
cancer prostate
cancer breast
Pathways in Calcium
104 Metabolism
105
Serum Magnesium

 Normal serum levels


1.6-2.1 mEq/L
 Total body magnesium
Adults 0.30 g/kg lean body
weight
Neonates 0.27 g/kg lean body
weight
106
Magnesium Disturbances:
Definition
 Hypomagnesaemia  Hypermagnesaemia
Serum Mg < 1 mEq/L Serum Mg > 3 mEq/L
(1.2 mg/dl) (3.6 mg/dl)
Frequently associated
with hypocalcaemia, and
must be sought in all
patients with
hypocalcaemia
Magnesium Disturbances:
107 Aetiology
Magnesium Disturbances:
108 Features
Magnesium Disturbances:
109 Management
110 Chloride Balance
 Normal serum levels (in venous serum or
plasma)
Men 100-106 mEq/L
Women 102-108 mEq/L
 Cell water contains up to 25 mEq/L chloride
 Total body chloride
Adults 1.56 g/kg lean body weight
Neonates 2.00 g/kg lean body weight
111 Chloride Balance
 In a 70 kg man
Total body chloride 2200 mmol
ECF chloride 1500 mmol (100 mmol/L)
ICF chloride 700 mmol (28
mmol/L)
112 Chloride Balance
 Chlorideand potassium follow each
other, hence a deficiency of one is
followed by a deficiency of the other
113 Chloride-Bicarbonate Shift
 When blood is oxygenated, chloride
leaves the RBCs and bicarbonate
enters; water follows the chloride and
hence RBCs become dehydrated when
oxygenated (hence alkaline venous
blood has a lower chloride content than
well oxygenated blood)
114 Bicarbonate Balance
 Normal serum levels
Men 24-28 mmol/l
Women 22-26 mmol/l
 The ratio of dissolved CO2 to
undissociated carbonic acid is 700-
1000:1
 1 mEq of HCO - will release 1 mmol of
3
CO2
Treatment of Acidosis Due
115 to Lowered Bicarbonate
 mEq of HCO3- required
= base deficit x body weight x 0.3
 Bicarbonate may be given i.v. either as
sodium bicarbonate injection (1 ml of 8.4%
sodium bicarbonate solution is equivalent to 1
mEq HCO3-) or as sodium lactate injection (4
ml/kg of M/6 sodium lactate are equivalent to 1
mEq HCO3-)
Treatment of Alkalosis Due
116 to Increased Bicarbonate
 Incase of alkalosis with base excess
more than 5 mEq/L use ammonium
chloride (NH4Cl)
2 ml/kg of M/6 NH4Cl lowers the HCO3- by 1
mEq/L
 mEq of chloride required
= base excess x body weight x 0.3
117 Phosphorous Balance
 Normal serum levels
Adults 3-4 mg/100 ml (1.7-2.4
mEq/L)
Children 4-6 mg/100 ml (2.3-3.5
mEq/L)
 Total body phosphorous
Adults 11.6 g/kg body weight
Neonates 5.40 g/kg body weight
118 Phosphorous Balance
 About 30 mEq of PO43- are excreted in
the urine daily (equivalent to 0.93 grams
of phosphorous).
 Phosphorous is the largest anion
component of cells (80 mEq/L of cell
water)
Disturbances of
119 Phosphorous Balance
 Increased  Reduced
phosphorous levels phosphorous levels
Hypoparathyroidism Hyperparathyroidism
In children during During transfer of
active growth due to blood sugar to cells
increased growth (sugar enters in the
hormone form of Glucose-6-
phosphoric acid,
possibly as a salt of
potassium)

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