This document provides an overview of fluid and electrolyte balance in the human body. It discusses water balance and the roles of ADH and thirst in maintaining appropriate plasma osmolality. Sodium balance is also reviewed, including the causes and management of hyponatremia and hypernatremia. Potassium disorders like hypokalemia and hyperkalemia are examined as well. Treatment approaches aim to correct fluid deficits and shifts while avoiding overly rapid changes in electrolyte concentrations.

1. FLUID AND ELECTROLYTE
Prepared by Mersha M(MD)
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2. CONTENT
Water balance
Osmolality
Sodium abnormality
Potassium bnormality
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3. OBJECTIVES
 All of you should know the fluid balance of our body
 You should know the mechanism by which our body maintain
 Should know causes and management of hypernatremia and h
 Should know causes and management of hypokalemia and hy
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4. WATER BALANCE
 In the average normal subject, the body water
comprises 60% of the body weight in males and about
55 % in females
 Body water is functionally divided into the ECF and ICF,
separated from each other by the cell membrane
 The cell membrane is freely permeable to water and to
some solutes
 Movement of fluids due to:
• hydrostatic pressure
• osmotic pressure
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5. FLUID COMPARTMENTS OF THE BODY
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6. 6

7. ELECTROLYTE AND MINERAL
CONCENTRATIONS IN BODY WATER
COMPARTMENTS
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8. OSMOLALITY AND TONICITY
 Osmolality- is defined as the concentration of all solutes in a given
weight of water
 The total osmolality of plasma is not always equivalent to the
“effective” osmolality
 Effective osmolality (Tonicity)-is a function of the relative solute
permeability the cell membrane to the solute.
 Solutes that cannot freely traverse cell membranes (Na,mannitol) are
effective osmoles
 Solutes that traverse cell membranes (urea,
ethanol) are ineffective osmoles, because they do not create osmotic
pressure gradients
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9. WATER BALANCE- ROLE OF ADH
 ADH
- secreted in response to changes in osmolality and in circulatory
volume.Produced by the posterior pituitary .
- The “osmoreceptor” cells are located in the anterior hypothalamus and
they are sensitive to changes in plasma osmolality of as little as 1%.
- In humans, the osmotic threshold for ADH release is 280 to 290
mOsm/kg.
- This system is so efficient that the plasma osmolality usually does not
vary by more than 1% to 2%despite wide fluctuations in water intake
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10. ADH
 Non-osmotic stimuli for ADH secretion.
- decreased arterial circulating volume (eg, heart failure,
cirrhosis etc )
- Nausea
- postoperative pain
- pregnancy.
- hypoglycemia
 Much higher ADH levels can be achieved with
hypovolemia than with hyperosmolarity, although a large
fall in blood volume is required before this response is
initiated.
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11. ADH
 It affects increases free water absorption
via binding to AVP V2 receptors in the collecting
duct of the kidney
o It causes increased water permeability
through the insertion of the aquaporin-2 (AQP-
2) water channel .
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12. WATER BALANCE- ROLE OF THIRST
 In humans the thirst mechanism plays an important role in water
balance.
 Hypertonicity is the most potent stimulus for thirst: only 2% to 3 %
changes in plasma osmolality produce a strong desire to drink water.
 The absolute level of plasma osmolality at which a person develops a
consciousurge to seek and drink water is called osmotic threshold for
thirst, usually averages about 290 to 295 mOsm/kg H2O.
 The thirst center is located close to the osmoreceptors but is
anatomically distinct.
 In general, overall intake and output come into balance at a plasma
osmolality of 288 mOsm/kg, roughly halfway between the thresholds
for ADH release and thirst
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13. 13

14. Decreased Blood Volume
and Pressure
Volume Receptors
Atria/Carotid/Baroreceptors
CVS Renal
 CO and
Vasoconstriction
Retain salt and
Water
 ECF and ICF
Volume
 Blood pressure
Body Responses
to changes in
Volume
Trigger Homeostatic
reflexes
Renin-angiotensin system
ADH
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15. WATER AND SODIUM IMBALANCES
 Hyponatremia
 Hypernatremia
 Hypovolemia
 hypervolemia
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16. SALT AND WATER
Plasma Osmolality
280-290mOsm/Kg
Decrease Increase
 Thirst  ADH
Dilute Urine
Disorder
involving
urine dilution
with water intake
HYPONATRAEMIA
 Thirst  ADH
Concentrated Urine
HYPERNATRAEMIA
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17. HYPONATREMIA
 Normal plasma sodium concentration ranges
from 135 mmol/L to145 mmol/L.
 Hyponatremia is defined as a plasma sodium
concentrationof <135 mmol/L.
 Severe hyponatremia is defined as a plasma
sodium concentration of <115 mmol/L
 Acute hyponatremia is development of
hyponatremia in <36–48 hours.
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18. Mechanism of Development of Hyponatremia
 In normal humans, plasma sodium concentration is
quite stable and varies by only about 1% .
 This is due to the fact that a 1% change in plasma
osmolality brings about changes in plasma
vasopressin level and thirst.
 Hyponatremia can be due to a gain of water, a loss
of sodium, or both.
 A water gain in excess of sodium gain or loss of
sodium in excess of the water loss
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19. Hyponatremia
relative excess of extracellular water compared to
extracellular sodium
Total extracellular sodium can be
low
normal
high
hypovolemia
normal/slightly expanded volume
hypervolemia/overload
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20. HYPONATRAEMIA
Assess volume status
Hypovolaemia
TBW 
Total body Na+  
Euvolaemia
TBW no change
No change Total body Na+
Measure urinary
Na+
Renal Losses
Diuretic
Steroid def
Osmotic Diuresis
Extrarenal
losses
Vomiting
Diarrhoea
Burns
Hypervolaemia
TBW  
Total body Na+ 
Glucocorticoid def
Hypothyroid
SIADH
Measure urinary
Na+
ARF/CRF
Nephrotic snyndrome
Cirrhosis
Cardiac failure
>20mmol/l >20mmol/l<20mmol/l <20mmol/l
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21. Clinical features of hyponatremia
Mild Moderate Severe
Anorexia Personality change Drowsiness
Headache Muscle cramps Diminished reflexes
Nausea Muscle weakness Convulsions
Vomiting Confusion Coma
Lethargy Ataxia Death
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22. Hyponatremia + hypovolemia
deficit of total body water, larger deficit of extracellular
Na+
Renal loss Non-renal loss
Aetiology Diuretics Vomiting
Mineralocorticoid
deficiency
Diarrhoea
Sodium losing
nephropathy
Burns,
excessive
sweating
Urinary
sodium
> 20 < 10
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23. Hyponatremia + hypervolemia
excess of extracellular Na+ , larger excess of total body water
• Cardiac failure
• Renal failure
• Cirrhosis
• Nephrotic syndrome
• Inappropriate IV therapy
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24. Hyponatremia + normovolemia
normal or slight excess of total body water
• syndrome of inappropriate ADH
• glucocorticoid deficiency
• inappropriate iv fluids
• hypothyroidism
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25. SYMPTOMATIC HYPONATREMIA MX
Severe
Hyponatremia
<115mmol/l
Asymptomatic Symptomatic
Chronic
Rarely <48hrs
No Immediate action
Long term Management
Acute
<48hrs
Chronic
>48hrs
Emergency
correction
Hypertonic saline
Furosemide
Some immediate
correction
Hypertonic saline
Furosemide
Change to water restrict when
Na increase 10%
Freq serum tests
No more than 1.0-1.5mmol/h
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26. HYPERNATREMIA
 Hypernatremia is defined as a plasma sodium
concentration of>145 mmol/L.
 Severe hypernatremia is defined as a plasma
sodium value of >160 mmol
 Commonly seen in critically ill patients.
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27. Mechanism of Development
 Hypernatremia can be due to loss of water,
gain of sodium, or both.
 Loss of water is the more common
denominator.
 Many patients with hypernatremia have an
inability to access water, as hyperosmolality is
a very a strong stimulus for thirst
 Plasma sodium concentration determines
intracellular fluid volume.Hypernatremia leads
to shrinkage of brain cell volume and
secondary neurological symptoms.
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28. CAUSES OF HYPERNATRAEMIA
• Lack of water
– Reduced access
• coma
• stroke
• immobility
– Excessive loss
• burns
• diarrhoea
• osmotic diuresis
– Neurological hypodypsia
• Too much sodium
– iatrogenic
– accidental
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29. ASSESSMENT OF HYPERNATREMIA
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30. CLINICAL FEATURES OF HYPERNATREMIA
 Mostly relate to CNS
 Lethargy
 Restlessness
 Seizures
 Irritability
 Mortality
- Very high in acute
hypernatremia
-Chronic hypernatremia
10% mortality
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31. TREATMENT OF HYPERNATREMIA
 General Therapeutic Recommendations
• Whenever possible, water deficit should be treated with water
administered via the oral or gastric route.
 In acute hypernatremia (hypernatremia developing within hours),
reducing the plasma sodium is recommended
 The correction rate should still be at a slower rate of 0.5 mmol/L/h over
48–72 hours
 Patients with intravascular volume depletion manifestating as
hypotension or orthostasis may require normal saline infusion to
replenish the volume deficit first. The water deficit can be addressed
after the ECF volume has been restored
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32. DISORDERS OF POTASSIUM BALANCE-
HYPOKALEMIA
 K+ less than
3.5mmol/l
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33.  Clinical Features
❏ often have no symptoms, particularly when mild (3.0 – 3.5
mmol/L)
❏ with more severe hypokalemia, may see fatigue, generalized
weakness, myalgia, constipation
 ❏ as hypokalemia becomes more severe, muscle necrosis,
arrhythmias can occur and rarely paralysis can develop with
eventual respiratory impairment
❏ arrhythmias occur at variable level of [K+]
❏ ECG changes are more predictive of clinical picture than K+
levels
❏ ECG changes
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34.  Treatment
❏ serum levels do not correlate well with deficit
❏ risk of hyperkalemia secondary to K+ supplements is
especially high in elderly and with decreased renal
function
❏ if urine output and renal function are impaired,
correct with extreme caution
❏ oral sources - food, tablets, KCl liquid solutions
❏ IV - usually KCl
• initially use saline solutions to mix
• maximum 60 mmol/L via peripheral vein
❏ K+ - sparing diuretics
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35. HYPERKALEMIA - K+> 5-5MMOL/L
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36.  Clinical Features
❏ usually asymptomatic but may develop muscle
weakness, paresthesias, areflexia, ascending
paralysis,and hypoventilation
❏ impaired renal ammoniagenesis and metabolic
acidosis
❏ if severe, ECG changes and cardiotoxicity (do
not correlate well with K+ concentration)
• peaked and narrow T waves
• decreased amplitude widening of QRS and
eventual merging with T wave (sine-wave pattern)
• AV block
• ventricular fibrillation, asystole
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37.  Treatment
❏ acute therapy is warranted if K+ high, symptoms present, ECG
changes
❏ general measures
• perform ECG, repeat blood test, r/o pseudohyperkalemia (i.e.
hemolyzed specimen)
• hold exogenous K+ and K+ - retaining meds
1. Protect Heart
❏ Ca2+ gluconate 1-2 amps ONLY (10 mL of 10% solution) IV
(cardioprotectant); giving more can result in
calcium toxicity and death!
2. Shift K+ into Cells
❏ regular insulin (Insulin R) 10-20 units IV, with 1/2 to 1 amp D50W: must
monitor blood glucose q1h
❏ NaHCO3 1-3 amps (given as 3 amps of 7.5% or 8.4% NaHCO3 in 1L
D5W)
❏ ß2-agonist (ventolin) in nebulized form
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38. 3.Enhance K+ Removal from Body
A.via urine - try furosemide, may need IV NS to avoid
hyperkalemia
• try fludrocortisone (synthetic mineral corticoid) if
suspect aldosterone deficiency
B. via gut
• cation-exchange resins: Calcium Resonium or
Kayexalate
C. dialysis (renal failure, life threatening hyperK+
unresponsive to therapy
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