Total Body Water, Represents approximately, 45-70% of total Body Weight, (60% in an idealized sense)
(TBW) Note: TBW is NOT total body weight…!!

Factors influencing this number include – Age, and obesity.

The older and more obese – The LESS the total body water is a % of Total Body WEIGHT. This makes sense because the more fat cells you possess the more they will contribute to the TOTAL BODY WEIGHT and LESS of it will be attributed to TOTAL BODY WATER.

Extra-cellular Fluids account for approximately 1/3 of Total Body Water.
Plasma Volume = 1/3 of ECF thus 1/12th TBW
Interstitial Fluid = 2/3 of ECF thus 1/6th TBW

Intracellular Fluids account for approximately 2/3 of Total Body Water.

Electrolyte Imbalances
Daily Sodium and Potassium Requirements = 1meq/Kg of body weight per day K+ excretion is due mainly to secretion of K+ after filtration.
Osmolarity is a measure of the number of Solute particles per solvent. Normal Osmolarity is around the 300 Range.

Osmolarity = 2[Na] + {BUN /2.8}+ Glucose /18
TOOL: ( bun has 3 letters so it is 2.8=3.0)
Based on the equation Na accounts for over 75 % of the Osmolarity.
Typical Value for Na is 140 = 2x that is 280 there is your osmolarity right there.

When assessing sodium concentrations in the blood one must understand an important concept.
There are 2 components to Serum, 93% is Water and the other 7% is Dry Weight for lipids and
Proteins. The Na+ is dissolved in the water portion which is 930cc of 1 liter of Serum,
Most Laboratory Machines Measure Na+ levels in serum ( ie NA/1000cc),
The Ramifications of this will be evident later on
Do not Confuse Natremia with osmolarity. THEY ARE DIFFERENT !!

Factitious Hyponatrimia
In cases where there is elevated Dry weight due to disease and the Dry weight is increased to say 14% then, the laboratory will give a reading of Na levels that are low, ie 130/860 cc will be read as 130meq/L but in actuality its the same as 140/930cc which is 151 (Do the math) Thus this is Factitious Hyponatrimia.

Let’s See this mathematically

Ok Normal is 140/930cc which translates to 151meq/L but it is READ as 140/L by lab machines.

Now if we have normal Na concentrations 120.4meq/L in a volume of 860cc this gives 120.4 meq/860 cc But it is READ as 120/L thus this Shows A LOW NA+ [ ] when in Actuality it is NORMAL.

Hypo Natremia with HYPER OSMOLARITY
This is a situation of Na concentrations less than 135 meq/dl and there is elevations of glucose levels as seen in diabetics that cause the osmolarity to skyrocket. For every 100mg/dl INCREASE in GLUCOSE there is a 1.6 meq/dl DEC in Na Concentration. The elevated Glucose also pulls in water so that’s why sodium levels go down.


NA values are fine but Water is excess ( dec in [NA+] This can be rather confusing because the Na+ Content may be fine or high but because there is a disturbance in the volume of Water it may dilute the sodium to low levels, IE in cases of CHF, LIVER DISEASE , NEPHROTIC SYNDROME, all cause this.

Symptoms of HYPO-Natremia with HYPER-Volemia include ascities, Edema.

Factors Causing EDEMA

A decrease in intravascular Oncotic Pressure as seen in cases of Nephrotic Syndrome (due to proteinuria), can lead to edema in the legs, Facial edema may also be evident by a puffy face and droopy eyes. There is a decrease in urinary Surface tension due to the presence of urine and the urine becomes frothy (A Dipstick Test is helpful in making the diagnosis of proteinuria).

HypoNatrimia with HypoVolemia is seen in cases of GI disturbances, Blood Loss, and
the Na loss is greater than the water loss leading to HYPOOSMOLARITY.

HypoNatrimia with ISOVolemia, occurs in cases of Syndrome of Inappropriate ADH secretion (SiADH) , as well as renal failure. There is no Presence of Edema because The volume is normal but that doesn’t mean that there isn’t an increase in Interstitial Fluid, just not enough to be Noticeable ( remember edema is a visual sign).

Treatment – Will depend on the severity of the abnormality.
In most cases, the first component of treatment is Fluid Restriction. If fluid restriction cannot correct the Hyponatrimia, THEN DEMOCYCLINE SHOULD BE INITIATED. BUT FIRST TRY FLUID RESTRICTION.

IF However, the Hyponatrimia is SEVERE IE BELOW 115mg/dl THEN SLOW INFUSION of HYPERTONIC Solution will dictate Treatment.

Severe Hyponatrimia is a serious condition that can lead to instability and EVEN DEATH, CORRECTING IT TO QUICKLY CAN Cause Cerebral Pontine Myolisis…Which can also cause death…


K+ Imbalance

K+ Imbalance can have numerous causative factors, Gastrointestinal disturbances, Renal Impairment, Aldosterone,
K+ is present mainly within the ICF at a concentration of about [ 150] ECF values range from 3.5-6.4 Plasma Values of K+ equal 3.5-4.5 Insulin, Alkalosis, (vomitus ) Aldosterone, 􀃆 DEC Intracellular Uptake of K+.

This is defined as a condition where plasma values are less then 3.5meq/l, in conditions of Alkalosis K+ is exchanged with H+ Ions to shift the balance. In cases of increased insulin, Glucose is transported using a K+, Glucose pump. Thus Insulin acts to influence up regulation of K+.

An important special condition worth noting is RTA ( Renal Tubular Acidosis) a condition where there is an inability to conserve bicarbonate and or an inability to excrete H+ ions leading to acidosis, and in this case there is increased Na absorption at the expense of oK+ loss. ( Resulting in the hypokalemia). This is a severe Acidosis and there is absorption and the ANION GAP REMAINS UNCHANGED. This Hypokalemic situation occurs when the metabolic acidosis lasts for several days aka it is Prolonged and thus the Acidosis must be corrected, once this acid base disturbance is returned to normal then these cells take up the K+ they lost during the crisis and thus the patient becomes Hypokalemic. ( The Kidney pissed out all the K+ the cells put out )>

Diuretics also work on the same mechanism in the Distal Tubule, There is elevated exchange of Na+ for K+.

GI Disturbances can lead to K+ loss in the stool but they also contribute to the Na+, K+ pump within the kidneys.


Ficticious HyperKalemia
A Condition which is seen in Serum specimens due to the coagulation of blood that leads to a release of K+ by the White Blood Cells, There is no elevation in serum levels, This situation occurs when WBC and Platelets are elevated greater the 500,000/ ml.

Factors influencing True HyperKalemia Include
1) Acidosis
2) Diabetes ( No insulin thus no K+ uptake into the Cells )
3) Cellular Necrosis ( Destruction leading to leakage of K+)
4) Renal Failure

Treatment Options Include

1) Insulin
2) Bicarbonate
3) Diuretics ( Not the K+ Sparing kind)
4) Ion Exchange Resins ( Kakalating Enema )
a. This exchanges K+ for Na+ within the Gi so you excrete K+ out into the GI Lumen while taking up Na+
5) Calcium Glucoronate ( Good for K+ Induced Arrythmias) TOOL
This is very important. In patients with hyperkalemia, the heart is a very vulnerable to excess K+ floating around in the blood. So the next step in patients suspected of hyperkalemia is to give CALCIUM GLUCOCORNATE. It protects the heart from life-threatening K+ induced arrhythmias.
6) Dialysis