WATER AND
ELECTROLYTES
BALANCE
WATER BALANCE
• Water constitutes about 60% of body
weight in men and 50% in women.
• 2/3rd of water is in ICF (about 28L).
• 1/3rd is in ECF (about 14L) Blood plasma,
interstitial fluids, lymph and transcellular
fluids (free fluid in pleural, pericardial and
peritoneal cavities CSF and digestive
secretions).
• 93% of plasma volume is water and 7% is
proteins.
TOTAL BODY WATER AND ITS
COMPONENTS
TOTAL BODY
WATER IN 70
Kg
42 – 45 L
(60 %)
INTRACELLULAR
24 – 26 L
EXTRA CELLULAR
18 – 19 L
INTERSTITIAL:13–14 L
PLASMA : 5 – 5.5 L
WATER BALANCE IN THE ADULTS
IN TAKE
OUT PUT
BEVERAGES
= 1500 mL
URINE
= 1500 mL
WATER IN FOOD = 600 mL
SKIN LOSS
= 500 mL
METABOLIC WATER= 400 mL (SWEAT / INSENSIBLE)
LUNGS
= 400 mL
TOTAL
= 2500 mL
FECES
= 100 mL
TOTAL
= 2500 mL
WATER BALANCE
• Water balance is maintained by the
electrolyte balance and is controlled by
the Antidiuretic Hormone (ADH)
secreted from posterior pituitary by
acting on renal tubules for the control of
water reabsorption in response to body
water intake / loss.
WATER BALANCE
• Proximal Renal Convoluted Tubules &
Collecting Ducts membranes have
small integral proteins with hydrophilic
Aquaporin Channels AQP1, AQP2,
AQP3, AQP4 & AQP6 which open
under the influence of ADH to
facilitate water reabsorption in order to
maintain water balance.
WATER BALANCE
• Water content of ICF and ECF is
controlled by differences in the
osmotic pressure across the cell
membrane plasma which are very
permeable to water but the osmolality
between the two must be equal other
wise the water will move from lower
osmolality to high osmolality until new
equilibrium is attained.
WATER BALANCE
• WATER DEPLETION : occurs in variety
of diseases like diarrhea, vomiting, fever,
burns etc.
• The loss of water increases plasma
osmolality and causes dehydration of ICF
specially of
• CNS tissues as water moves from ICF to
ECF which more dangerous than ECF
dehydration & may result in coma and
death in severe cases.
WATER BALANCE
• Body responds with stimulation of
thirst which increases the intake of
water and stimulation of ADH release
which increases water reabsorption
from kidneys thereby restoring the
water balance.
HOMEOSTATIC CORRECTION OF
WATER DEPLETION
8
ADH
+
THIRST
+
A
7
HYPOTHALAMIC +
OSMOLALITY
RENIN
B
6
[ Na+ ]
+
H2O VOLUME
1
RENAL BLOOD FLOW
2
+
RELEASE
3
+
ANGIOTENSIN II
+
ALDOSTERONE
4
5
LOSS OF BODY WATER
HEMOCONCENTRATION
RELEASE OF ADH
INCREASED REABSORPTION
OF WATER IN THE
RENAL TUBULES
THIRST
INCREASED
WATER INTAKE
PLASMA TONICITY/VOLUME RESTORED
WATER BALANCE
• WATER EXCESS : occurs rarely
specially in those patients who are on
Intravenous(IV) fluids and in some
Psychiatric diseases.
• The excess of water decreases plasma
osmolality and causes over hydration.
WATER BALANCE
• Body responds with inhibition of
thirst which decreases the intake of
water and inhibition of ADH release
which decreases water reabsorption
from kidneys thereby restoring the
water balance.
HOMEOSTATIC CORECTION OF
WATER EXCESS
8
ADH
-
+
THIRST
-
H2O VOLUME
1
+
RENAL BLOOD FLOW
2
A
-
7
HYPOTHALAMIC OSMOLALITY
B
-
6
[ Na+ ]
-
RENIN
3
ANGIOTENSIN
-
4
ALDOSTERONE
5
EXCESSIVE WATER DRINKING
HEMODILUTION
INHIBITION OF ADH
INHIBITION OF THIRST
DECREASED TUBULAR
REABSORPTION OF WATER;
GREATER WATER LOSS
LESS WATER INTAKE
PLASMA TONICITY/VOLUME RESTORED
WATER BALANCE
ABNORMALITY OF ADH DIABETES
INSIPIDUS:
Rare disease of posterior pituitary resulting
in loss of ADH secretion.
• The loss of water increases plasma
osmolality and causes dehydration of ICF.
WATER BALANCE
• Body tries to respond with
stimulation of thirst which increases
the intake of water but due to
disease of ADH there is no increase
reabsorption of water from the
kidneys so the balance is not
restored and patient continues to
excrete a large amount of urine
although he is dehydrated.
RESULTS OF ADH DEFECIENCY
8
ADH
-
BLOCK
THIRST
+
A
H2O VOLUME
1
RENAL BLOOD FLOW
2
+
7
HYPOTHALAMIC +
OSMOLALITY
B
+
6
[ Na+ ]
+
RENIN
3
+
ANGIOTENSIN
+
4
ALDOSTERONE
5
COMPOSITION OF THE BODY FLUIDS
EXTRA CELLULAR FLUIDS
ANIONS
CATIONS
Cl ˉ =100 mmol/L
HCO3=26mmol/L
ORGANIC
IONS =3 mmol/L
PHOSPHATE = 1
mmol/L
SULPHATE = 0.5
mmol/L
PLASMA PROTEINS=
16 mmol/L
SODIUM = 140
mmol/L
K+ = 4.5 mmol/L
Ca 2+ = 1.3
mmol/L
Mg 2+ =
0.7mmol/L
INTRACELLULAR FLUIDS
ANIONS
PHOSPHATE = 126
HCO3 = 10
SULPHATE = 10
ORGANIC IONS = 05
PROTEINATE = 40
As mmol / Kg of
WATER
CATIONS
K+ = 165
Mg+ = 14
Na+ = 12
Ca+ = very less
As mmol / Kg
of WATER
SODIUM
THE MOST ABUNDANT ‘CATION’ OF
ECF, 140-142 mmol/L REPRESENTING
HALF OF OSMOTIC STRENGTH OF
PLASMA AND THEREFORE PLAYS
IMPORTANT ROLE IN DISTRIBUTION
OF WATER AND MAINTAINANCE OF
OSMOTIC PRESSURE IN ECF, WHERE
AS IN ICF IT IS ONLY 10-20 mmol/L.
1/3rd IS PRESENT IN SKELETON AS
INORGANIC PORTION.
SODIUM
NORMAL DAILY INTAKE IS 130-260
mmol (8-15 gm) WHERE AS BODY
REQUIRES ONLY 2-5 mmol. THE
REST IS EXCRETED IN URINE ,
SWEAT, GIT SECRETIONS ETC.
EXCESS INTAKE:
HYPERTENTION.
SODIUM
IT ENTERS THE CELLS
THROUGH ATP DEPENDENT
‘SODIUM POTASSIUM ATPase’
PUMP.
IT IS REABSORBED FROM
RENAL TUBULES UNDER THE
EFFECT OF ALDOSTERONE, A
HORMONE SECRETED BY
ADRENAL CORTEX. ACTH AND
DEOXYCORTICOSTERONE MAY
ALSO CAUSE RENAL
REABSORPTION TO SOME
EXTENT.
SODIUM
FUNCTIONS
MAINTAINANCE OF PLASMA
OSMOTIC PRESSURE AND VOLUME.
DECREASED Na+ RESULTS IN
DECREASED PLASMA VOLUME
LEADING TO DECREASED CARDIAC
OUT PUT AND HYPOTENSION.
PLAYS IN IMPORTANT ROLE IN
REGULATION OF NERVE
EXCITABILITY.
SODIUM
DUE TO ITS ASSOCIATION WITH
CHLORIDE, IT SERVES AS AN
IMPORTANT SOURCE OF Cl- FOR
FORMATION OF HCl IN GASTRIC
JUICE AND IN TRANSPORT OF
CARBON DIOXIDE FROM TISSUES TO
THE LUNGS.
INVOLVED IN EXCHANGE FOR H ION
EXCRETION FROM KIDNEYS
THEREFORE HELPS IN THE
REGULATION OF BLOOD pH AND
NORMAL ACID BASE BALANCE OF
BODY.
RENIN-ANGIOTENSIN SYSTEM
• ‘RENIN’ IS A PROTEOLYTIC ENZYME
SECRETED BY ‘JUXTAGLOMERULAR
APPARATUS’ ADJACENT TO RENAL
GLOMERULI.
• IT SPLITS A DECAPEPTIDE,
‘ANGIOTENSIN-I’ FROM α-2 GLOBULIN.
• ANOTHER PEPTIDASE ‘ANGIOTENSIN
CONVERTING ENZYME (ACE)’ PRESENT
MOSTLY IN LUNGS CONVERTS IT INTO A
HORMONE ‘ANGIOTENSIN-II’ WHICH
HAS 2 IMPORTANT SYSTEMIC
FUNCTIONS.
RENIN-ANGIOTENSIN SYSTEM
• 1.ACTS DIRECTLY ON CAPPILARY WALLS
CAUSING VASOCONSTRICTION THERE
BY MAINTAINS BLOOD PRESSURE.
• 2.STIMULATES CELLS OF ZONA
GLOMERULOSA IN ADRENAL CORTEX TO
SYNTHESIZE AND SECRET
MINERALOCORTICOID HORMONE
ALDOSTERONE.
ALDOSTERONE
NORMAL PLASMA LEVELS –
SUPINE 2 – 9 mg / dL.
URINARY EXCREATION = 20 – 26
mg / dL.
FUNCTIONS
INCREASE RETENTION /
REABSORPTION OF Na+ THROUGH
DECREASED EXCRETION FROM
KIDNEYS.
ALDOSTERONE
INCREASE EXCRETION OF K+ , H+ ,
NH4.
SIMILAR EFFECTS ON IONIC
TRANSPORT IN SWEAT GLANDS,
SALIVARY GLANDS AND
INTESTINAL MUCOSA.
DEOXYCORTICOSTERONE ALSO
AFFECTS BUT 30 - 50 TIMES LESS
POTENT THAN ALDOSTERONE.
SODIUM
ABNORMALITIES
1. HYPONATRAEMIA: DECREASE IN
PLASMA SODIUM DUE TO ACUTE
URAEMIA, VOLUME DEPLETION,
DIURETIC TREATMENT, ADRENAL
INSUFFICENCY (ADDISON ,S
DISEASE), ADH ABNORMALITIES,
INCREASED ECF VOLUME WITH
OEDEMA, CONGESTIVE CARDIAC
FAILURE AND RENAL DISEASES.
SODIUM
• CLINICAL FEATURES:
CELLULAR OVERHYDRATION
SPECIALLY OF CNS LEADING TO
HEADACHE, CONFUSION,
FITS,DECREASED CARDIAC
OUTPUT, HYPOTENSION AND EVEN
DEATH MAY OCCUR.
SODIUM
2. HYPERNATRAEMIA:
EXCESS OF PLASMA SODIUM
CAUSED BY DECREASED INTAKE
OF WATER, UNCONSCIOUSNESS,
DAMAGE TO THIRST CENTRE,
EXCESSIVE WATER LOSS AS IN
DIABETES INSIPIDUS,
GLYCOSURIA, EXCESSIVE INTAKE
OF Na+ IN DIET OR IN DRUGS,
EXCESSIVE RETENTION OF Na+ AS
IN CUSHING,S SYNDROME AND
CONN,S SYNDROME.
SODIUM
CLINICAL FEATURES:
 ‘HYPERVOLAEMIA’ LEADING TO
MILD- MODERATE TO SEVERE
HYPERTENSION WITH OEDEMA
AND IN SEVERE CASES
‘HEADACHE (THROBING)’
‘DYSPNOEA’ AND OTHER EFFECTS
ON CVS LIKE ‘CONGESTIVE
CARDIAC FAILURE(CCF)’.
DISORDERS OF ALDOSTERONE
PRIMARY ALDOSTERONISM
‘(CONN,S SYNDROME)’.
‘ADENOMAS ‘OF GLOMERULOSA
CELLS.
CLINICAL FEATURES
Na+ RETENTION AND
‘HYPERTENTION’
K+ LOSS AND ‘ALKALOSIS’.
DISORDERS OF
ALDOSTERONE
MUSCLES PARASTHESIAS’,
WEAKNESS, ‘PARALYSIS’.
‘POLYDIPSIA’, ‘POLYURIA’ AND
‘TETANY’.
TREATMENT
REMOVAL OF ‘TUMOUR’ AND
‘SPIRANOLACTONE ‘(ALDECTONE)
THERAPY.
SECONDARY ALDOSTERONISM
‘RENAL ARTERY STENOSIS’ :
HYPERPLASIA AND HYPERFUNCTION OF
‘JUXTAGLOMERULAR CELLS’.
‘CIRRHOSIS OF LIVER’, ‘CARDIAC
FAILURE’, ‘NEPHROTIC SYNDROME’.
‘RENIN AND ANGIOTENSIN – II’.
SIGNS AND SYMPTOMS SAME AS IN
‘PRIMARY’.
CHLORIDE
PRESENT IN CLOSE ASSOCIATION WITH
SODIUM AND THEREFORE FUNCTIONS
SIMILAR TO IT I.E
 MAINTAINANCE OF ‘WATER AND
ELECTROLYTES BALANCE’.
 ‘PLASMA OSMOTIC PRESSURE’.
‘ACID BASE BALANCE’: IN TRANSPORT OF
CO2 FROM TISSUE TO LUNGS IN ALSO IN
THE EXCRETION OF NH4 IONS.
CHLORIDE
FORMATION OF HCl IN THE
GASTRIC JUICE
THE MAIN SOURCE IS DRINKING
WATER & TO SOME EXTENT
VEGETABLES AND FRUITS
IN VOMITING THERE IS MORE
LOSS OF CHLORIDE AND
COMPENSATORY INCREASE IN
HCO3- : ‘HYPOCHLOREMIC
ALKALOSIS’.
POTASSIUM
THE MOST ABUNDANT CATION OF ICF.
DAILY REQUIREMENT IS 2-4 gm
PRESENT IN FRUITS, VEGETABLES,
MEATS, GRAINS & MILK.
FOUND MOSTLY INSIDE THE CELL, LIKE
MUSCLE CELLS.
POTASSIUM
FUNCTIONS
NERVE ACTIVITY IN SKLETAL &
CARDIAC MUSCLE.
PART OF Na+ / K+ ATPASE OF
SODIUM PUMP IN TISSUES.
REQUIRED FOR MANY ENZYME
REACTIONS LIKE GLCOGEN
SYNTHASE.
COMPETES WITH H+ FOR
EXCHANGE WITH Na+ IN KIDNEYS.
POTASSIUM
ABNORMALITIES
HYPERKALEMIA ; NORMALLY THE
EFFICIENT RENAL EXCREATION DOES
NOT RESULT IN HYPERKALEMIA, BUT
MAY BE SEEN IN FOLLOWING CONDITION
RENAL FAILURE.
FEVERS ; EXCESSIVE BREAK DOWN OF
BODY PROTEINS AN RELEASE OF K+.
INJURY OR INFECTION OF THE MUSCLES.
LYSIS OF TUMOURS.
ADDISON,S DISEASE.
POTASSIUM
CLINICAL FEATURE
WEAKNES AND NUMBNESS OF
MUSCLES TINGLING OF
EXTREMITIES.
BROAD QRS COMPLEX WITH
PEAKED “T” WAVE AND NO “P”
WAVE. ARRHYTHMIAS LIKE
BRADYCARDIA APPEAR AND
HEART MAY STOCK DIASTOLE.
POTASSIUM
HYPOKALEMIA: NORMALLY NOT
OBSERVED BUT MAY BE PRESENT IN
DECREASED INTAKE , PROLONG
INFUSION OF K+ FREE IV FLUIDS.
INCREASED RENAL LOSS LIKE IN
RENAL DISEASES , DIURETICS ,
METABOLIC ALKALOSIS AND EXCESS
OF ALDOSTERONE.
LOSS FROM GIT AS IN VOMITING
DIARRHEA.
2.
POTASSIUM
CLINICAL FEATURE
ANOREXIA , NAUSEA AND MAY BE
PARALYTIC ILEUS.
MUSCLE WEAKNES MENTAL
DEPRESSION.
ECG CHANGES LIKE INVERSION OF
“T” WAVE.
RAPID IRREGULAR PULSE AND
HYPOTENSION.
ANDROGENS
DHEA AND ANDROSTENEDIONE
WEAKER ANDROGENS.
ANABOLIC EFFECTS IN
RETENSION OF Na+ , P , K , Cl
AND PROTEINS.
INCREASE SECRETION MAY
CAUSE MUSCULINIZATION IN
FEMALES AND FEMINIZATION
IN MALES.
LAB DIAGNOSIS
INCREASE PLASMA CORTISOL,
ACTH.
LOSS OF DIURNAL RHYTHM.
INCREASE URINARY CORTISOL.
GLUCORTCOID SUPPRESSION.
+ IN CUSHING,S DISEASE.
- IN CUSHING,S SYNDROM.
TREATMENT
REMOVAL OF TUMOUR TISSUE.
METYRAPONE AND
AMINOGLUTETHIMIDE, TO
BLOCK CORTISOL SYNTHESIS.
K+ REPLACEMENT.