Osmolality Goldman
A mole of a substance is the mol wt of that substance in grams
E.g. the mol wt of NaCl is 23+35.5= 58.5
Therefore 1mole NaCl = 58.5 g.
1 millimole is 1/1000 of a mole
Therefore 1millimole of NaCl is 58.5 mg.
The weight of a salt in mg can be converted into millimoles by dividing the weight in mg
by the mol.wt
e.g 1g (1000mg) NaCl = 17.1 millimoles
Mol wt of NaCl =58.5 Therefore 1000/58.5= 17.1
Mol wt of glucose C6H12O6 = 12x6 +1x12 +16x6 = 72+12+96=180
Osmolality – a Molal solution contains a gram mol wt of the substance dissolved in 1000g
of the solvent
(A Molar solution contains a gram mol wt of the substance dissolved in 1 Liter of solvent)
It is determined by measuring the depression of the freezing point of a solution,
compared to water,using an osmometer and expressing the value in *C below 0*C
The value can also be expressed in milliosmoles ,using the factor 1000Osm=186*C or
1*C=538mOsm
The normal range of serum osmolality is 275-290mOsm/kg of serum
NORMAL BODY COMP WashMan
Total Body Water- Water makes up
60% of body wt in males (42l in 70kg male)
50% in females
80% in newborns
2/3 is ICF – Intracellular Fluid ( 40%-28L in 70kg male)
1/3 is ECF-Extracellular (20% body wt-14I) of which1/4 is Intravascular (plasma 5% body
wt-3.5L) and 3/4 Interstitial(10.5L)
Total body water is controlled by ADH
SODIUM-85-90% is in ECF
Change in serum Na (i.e. Intravascular Na) indicates disturbed water homeostasis and
ICF volume
Change in sodium content ( total body Na) are manifest as ECF expansion (edema) or
contraction
Osmolality or tonicity is the solute or particle concentration of a fluid.
Solutes that are restricted to the ICF ( K & organic phosphate esters) or
ECF(Na & accompanying anions) determine the effective tonicity or osmolality
Rule of thumb -Extracellular osmolality = 2x serum Na + 10
Normal body fluid vol and osmolality is maintained by kidneys despite wide variations in
salt and water intake
NORMAL ELECTROLYTE COMP
OF IV &IC mmol/L Schwartz
ELECTROLYTE Intravascular ICF
(SERUM)
Sodium (Na) 135-145 10
Potassium (K) 3.5-4.5 150
Chloride (Cl) 85-115 HPO4+SO4
150
Bicarbonate(HCO3) 22-29 10
Calcium (Ca) 2-2.5
Magnesium (Mg) 0.75-1.25 20
GI –NORMAL VALUES Condon /ACS Manual
Secretion VOL Na Cl K HCO3
ml/d mmol/l mmol/l mmol/l mmol/l
Saliva 1000 100 75 5 25-30
Gastric Juice pH 4 2000 100 100 10
Bile 1500 140 100 10 35
Pancreatic Juice 1000 140 75 10 100
Succus Entericus 3500 100 100 20 35
Diarrhoea 1000- 60 45 20 35
4000
Average Electrolyte Composition Replacement Guidelines per Liter Lost Current diagnosis
Na+ K+ Cl– HCO3– 0.9% 0.45% D5W KCl 7.5% NaHCO3 (45 mmol
(mmol/L) (mmol/ (mmol/ (mmolL) Saline (mL) Saline (mL) (mL) (mmol/L HCO3–/amp)
L) L) )
Sweat 30–50 5 50 500 500 5
Gastric 20 10 10 300 700 20
secretions
Pancreatic 130 5 35 115 400 600 5 2 amps
juice
Bile 145 5 100 25 600 400 5 0.5 amp
Duodenal 60 15 100 10 1000 15 0.25 amp
fluid
Ileal fluid 100 10 60 60 600 400 10 1 amp
Colonic 1401 10 85 60 1000 10 1 amp
diarrhea
ELECTROLYTES/DAY Wash Man
• Na- usually 50-150mmols provided. Renal excretion
can fall to 37* body
temp(2ml/kg/*C)
• Sweating- variable 100-2000ml/hr dep on
physical activity and ambient temp
Replacement with 5% dextrose or ¼ NS
RENAL LOSSES Wash Manual
• Na losses significant in diuretic phase of ATN, diuretic
use,GI losses and catabolic states
• Na retention sig in postop state, dehydration, steroid use
• K loss sig in diuretic use, steroid use, GI losses esp
diarrhoea, ( intracellular shift with Beta agonists like
salbutamol)
• K retention sig in high output renal failure, post trauma,
blood transfusion
RAPID INTERNAL FLUID
SHIFTS Wash Man
• Occurs with peritonitis, burns, intestinal
obstruction, sepsis, crush injury
• Need to replace sequestered fluid with
normal saline
RENAL FUNCTION Condon
Assessed by
Urine sp.gr, pH & osmolality of 1st voided urine in the morning-
• sp.gr should be or > 1.016 and pH 5.8 or lower
• and urine osmolality should be 850mOsmol/Kg water and ratio of
urine to serum osmolality should be at least 3
Tubular Activity Na mmol/L K mmol/L
Normal >40 >40
Conserving 10-30 20-30
Max retention 20mmol/L,make a correction
3. Blood is drawn from an arm with a dextrose drip
The decreased serum Na causes a fall in the osmolallity of extracelluar comp
and there is movement of water intracellularly causing swelling of cells. This
can cause brain edema with inc intracranial pressure
This causes edema, inc in weight, confusion, apathy, weakness, nausea and
vomiting.
If not corrected the water excess will progress to muscle twitching, convulsions,
stupor and even death as serum Na falls H2CO3 H +HCO3- +
Where formation of carbonic acid from carbon
dioxide or reversion of carbonic acid to water
and carbon dioxide will depend on the acid-base
status
ACID BASE BALANCE
H +HCO3- H2CO3 CO2+H2O
+
When acid is added to the system bicarbonate conc will
decrease with a corresponding drop in the
HCO3/H2CO3 ratio
45mmHg, pH decreases. The kidney attempts to
compensate by increasing HCO3 absorption and
H+ excretion
Patient needs ventilatory assistance- intubation
and ventilation to blow off the CO2
Metabolic Acidosis
Metabolic Acidosis- Here there is a deficit of HCO3 due to excessive
acid production eg diabetes with excessive ketone formation or
• renal disease ( inadequate excretion of inorganic acids like
phosphate and sulphate) or
• when there excessive loss of bicarbonate as in diarrhoea,
pancreatic or enterocutaneous fistula or
• Lactic acidosis secondary to shock when anaerobic glycolysis
results in accumulation of lactic acid
Acidosis is dangerous as it
1. decreases myocardial contractility causes a reduction in cardiac
output,
2. decreases responsiveness of peripheral vessels to circulating
cathecholamines causing hypotension and
3. increases refractoriness of the fibrillating heart to defibrillation
making cardiac resuscitation difficult
ACID BASE BALANCE-ALKALOSIS
Alkalosis is better tolerated than acidosis and is fact the most common
acid base abnormality seen in the early postop period.
This is due to post traumatic aldosteronism stimulated by volume
reduction causing retention of Na and HCO3 and secretion of K,
hyperventilation secondary to pain and anxiety and nasogastric
suction causing loss of acid.
Respiratory Alkalosis- Secondary to hyperventilation usually abates when
pain and anxiety subsides. When secondary to hypoxemia it may need
ventilatory support. It results in hypokalemia as extracellular K moves
intracellularly. Hypocapnea results in cerebral vasoconstriction
Metabolic Alkalosis – results from nasogastric suction with loss of H+.(
hypocholeremic, hypokalemic alkalosis) As a result of hypovolemia
the kidney reabsorbs Na exchanging it for K and H – thus resulting in
acid urine – paradoxical aciduria