Electrolyte
Dr. Samira Ferdous
Assistant Professor
Biochemistry
SMAMC
ELECTROLYTE
A substance that breaks up into ions that means
particles with electrical charges when it is
dissolved in water or body fluids. Some
examples are sodium (Na+), potassium (K+),
calcium (Ca2+), chloride (Cl-) phosphate (PO4-),
magnessium (Mg2+), and bicarbonate (HCO3-).
These electrolytes are distributed in different
body fluid compartments mainly in ECF and ICF.
These ions help to move nutrients into
cells, waste out of cell, conduction of nerve
impulse and muscle functions, play critical
role in balancing body fluids and regulating
heart rhythm.
Electrolytes of ECF and ICF with the normal values:
Electrolyt Normal
es
Symbol Total
Range
Na+ 135-145 meq/l
K+ 3.5-5 meq/l
Cations 2.4 meq/l or 9-11 150
EC Ca2+ mg%
Mg2+ 3 meq/l
F Cl- 98-107 meq /l
HCO3- 22-28 meq/l
Anions 150
Protein 16 meq /l
Others 10 meq /l
K+ 150 meq /l
Cations Na+ 10 meq /l 200
Mg2+ 40 meq/l
ICF Phosphate 140 meq/l
Protein 40 meq/l
Anions HCO3- 10 meq/l
200
Cl- & Others 10 meq/l
Serum electrolytes with their normal
value:
Serum Na+ 135 - 145 mmol/L
Serum K+ 3.5 – 5 mmol/L
Serum Cl- 95-105mmol/L
Serum HCO3- 22-28 mmol/L
Serum Mg++ 0.6- 1.1 mmol/L
Serum Ca++ 2.2- 2.6 mmol/L
Functions of electrolytes:
Maintains body fluid volume and osmolarity .
Move nutrients into cell.
Remove waste product from cells .
Allow nerves to send signals.
Enable muscles to relax and contract effectively.
Maintains brain and heart function.
Regulation of sodium balance
(Volume regulation)
Regulation of sodium balance
( ECF volume Regulation)
Afferent limb Efferent limb
(sensor or sensing (effector organ)
mechanism)
Baroreceptors present in kidney act as
atria, carotid sinus, aortic arch, effector organ to
great veins and afferent the volume status
arteriole of kidney act (body sodium content)
as afferent limb. by renal Nacl retention or
excretion & its regulation.
Baroreceptors are stimulated by volume expansion (increased
sodium content.)
Baroreceptors are inhibited by volume contraction (Decreased
sodium content.)
Biochemical events of sodium balance
(volume regulation) following excess NaCl
intake
Increased NaCl intake or
hypernatremia
Hypervolemia
SNS inhibition Stimulation of barorecptors
GFR increased RAAS inhibited ANP increased
Aldosterone Decreased renin SNS- sympathetic
Escape nervous system
Decreased angiotensin II RAAS- renin -
angiotensin -
aldosterone system
Decreased aldosterone
Salt and water excretion Normal
ECF
volume
Biochemical events of sodium balance (volume regulation)
following decrease NaCl intake
Decreased NaCl intake or hyponatremia
Hypovolemia
SNS stimulation Inhibition of barorecptors
GFR Decreased RAAS stimulated ANP decreased
No Aldosterone Increased renin
Escape
Increased angiotensin II
Increased aldosterone
salt and water retention
normalise ECF vol
Hyponatremia
Hyponatremia is defined as an decreased serum
sodium concentration <135mmol/ L.
Causes
Acute renal failure.
Nephrotic syndrome
CCF
Cirrhosis of liver
Addison’s disease
Syndrome of inappropriate ADH secretion (SIADH)
All causes at a glance:
Consequences of hyponatremia
Hyponatremia
Decreased ECF osmolarity
Cerebral edema
Gradually decreased the conscious level
Drowsiness
Disorientation
Convulsion
Coma
Death
Hypernatremia
Hypernatremia is defined as an increased
serum sodium concentration above
145mmol/L.
Causes :
Hypertonic saline infusion (Iatrogenic)
Diabetes insipidus
Severe diarrhea, vomiting
Profuse sweating, severe burn
Cushing syndrome
Conn’s syndrome (increased aldosterone)
Consequences of hypernatremia
Hypernatremia
Increased ECF osmolarity
Cerebral dehydration
Gradually deterioration of cerebral function
Dizziness
Disorientation
Convulsion
Coma
Death
Hormones regulating sodium balance
(ECF volume regulation)
Aldosterone :
It increases NaCl reabsorption from distal nephron
(CD)
Renin : It increases the synthesis of angiotensin
II which increases NaCl reabsorption from PCT.
Catecholamine : It increases NaCl reabsorption
from PCT.
Atrial natriuretic peptide (ANP) :
It decreases NaCl reabsorption from CD.
Regulation of plasma potassium
concentration or potassium balance
Short term regulation ( internal potassium
balance):
Done by insulin, aldosterone, catecholamine
by transmembrane potassium flux.
Long term regulation (external potassium
balance ) :
Done by aldosterone by tuning renal K+
excretion / retention.
Short term regulation
In case of potassium overload,
potassium immediately moves in to the
cell (K+ influx) and in case of potassium
deficit, potassium immediately comes
out of the cell (K+ efflux) to keep the
serum potassium concentration normal.
Hormonal control of short term
regulation :
It is done by insulin, aldosterone and
catecholamine.
Hyperkalemia stimulates the release of
insulin, aldosterone and catecholamines . All
these hormones quickly cause k+ influx
into the cells to keep serum K+
concentration within normal range.
Factors regulating transmembrane potassium
flux :
Factor Function Effect on serum
K+
Insulin
Aldosterone,
epinephrine
Acute potassium influx hypokalemia
excess
Alkalosis
β-agonist
α-blocker
Factor Function Effect on serum K+
Glucagon,
norepinephrine
ECF hyperosmolarity
efflux hyperkalemia
Acute potassium
deficit
Acidosis
α-agonist
β-blocker
Long term regulation :
Done by aldosterone by tuning renal K + excretion /
retention.
Renal response starts late and takes time to be
completed.
In hyperkalemia, aldosterone increases renal
excretion.
And in hypokalemia, there is reduction of renal K +
excretion.
This gradually brings the serum K+ concentration
back to normal.
Hyperkalemia :
It is the clinical condition when serum K+ > 5.0
mmol /L .
Causes:
1. Impaired renal excretion of K+ ( It is
the commonest cause).
2. Tissue breakdown.
3. Redistribution of K+ by K+ efflux from
cells.
4. Increase K+ intake.
Consequences:
1. Cardiac Arrhythmia.
2. Cardiac Arrest.
3. Tingling and Paresthesia.
4. Paresis and Paralysis
5. Respiratory muscle paralysis.
6. Paralytic Ileus.
Hypokalemia
It is the clinical condition when serum
K+ < 3.5 mmol/L.
Causes:
[Link] K+ loss.
[Link] K+ loss.
3. Redistribution of K+ by K+ influx
into cell.
Hypokalemia
Consequences:
1. Cardiac Arrhythmia.
2. Cardiac Arrest.
3. Muscle cramps, myalgia, fatigue.
4. Paresis, paralysis, Paralytic ileus.
5. Respiratory muscle paralysis.
6. Renal disfunction.
Calcium
Total plasma calcium concentration :
9 -11 mg % or 2.2-2.6 mmol/L
Forms of plasma calcium :
Free ionized calcium---- 50%
Protein (mainly albumin)bound calcium-
---- 45%
soluble calcium complex with anions
(citrate, phosphate)-------- 5%
45%
50%
37
C)Calcium Balance
►Intake -1000 mg/day
(milk, milk products, fish, meat, vegetables)
►output -1000mg/day
(Urine 200 mg/day & Feces 800 mg/day)
Balance is related to
-Intestinal absorption of calcium
-Renal excretion of calcium
38
Function of calcium –
[Link] function : helps in
bone mineralization.
[Link] function
►muscle contraction
►control of neuromuscular
excitability :
-CNS depression(act as
neurosedative)
-increased excitability
►release of neurotransmitters.
[Link] in coagulation & release
of hormone (PTH).
[Link] as intracellular 2nd
messenger in transmembrane
39
signaling.
Regulation of Calcium Balance:
►First line defense-
Done by calcium buffer activity of labile calcium pool of bone in case
of acute calcium excess or deficit
►Second line defense-
By 3 hormones: active vit D( calcitriol),PTH,Calcitonin
40
Hormonal regulation of calcium
balance:
It is done by three hormones :
Active vitamin D( calcitriol)
Parathyroid hormone
Calcitonin
Parathyroid hormone (PTH) : stimulated by
hypocalcemia and it increases the blood
calcium level by
Increase bone resorption and release of calcium
Increase calcium reabsorption from distal
nephron
Indirectly Increase the intestinal absorption of
calcium by stimulating the Calcitriol .
Calcitriol : stimulated by hypocalcemia and
PTH. It increases the blood calcium level by:
Increases the intestinal absorption of
calcium
Facilitates PTH induced bone resorption and
release of calcium.
Facilitates PTH induced calcium
reabsorption from distal nephron.
Calcitonin: Decreases the blood calcium
level by
Inhibit bone resorption thereby decrease the
plasma calcium level.
Increase the renal clearance of calcium.
Hypocalcemia
Increased PTH
Increased Calcitriol
Bone Intestine kidney
Increased calcium absorption
Bone resorption
and release of calcium Increased calcium
reabsorption
Serum calcium comes back to normal
Reverse effect occur in hypercalcemia
Hypercalcemia : Ca >2.6 mmol / L or
>10.2mg%
Cause:
1. Hyperparathyroidism
[Link] D intoxication 3. Endocrinopathies
(Thyrotoxicosis, Pheochromocytoma)
[Link]
46
47
Effects of Hypercalcemia:
[Link] depression
[Link] tissue calcification(metastatic
calcification)
[Link] arrythmia & cardiac arrest
[Link] kidney disease :
►renal stone formation, polyuria, polydipsia
►nephrocalcinosis, tubular function impairment
►loss of conc. power with resistance to ADH
►salt & water loss with hypovolemia,
dehydration, coma.
[Link] complication-
psychosis, neurosis, lethargy.
[Link] complication-PUD, acute
pancreatitis
48
Hypocalcemia:
Ca < 2.1mmol/L or <8.4mg%
Cause :
1. Hypoparathyroidism
2. Vit D deficiency
3. Vit D resistance
4. Pseudohypoparathyroidism
5. Chronic renal failure
6. Acute pancreatitis
7. Alkalosis
49
Effects of Hypocalcemia-
[Link] excitement ( Tetany, seizure, bronchospasm,
muscle cramp)
[Link] irritability, arrythmia , bradycardia, hypotension
[Link] disturbance.
51
Tetany:
Clinical manifestation of
neuromuscular hyper
excitability due to
hypocalcemia
Symptom: ►Carpopedal
spasm
►laryngeal stridor
►convulsion
Sign: ● Trousseau’s sign
● Chvostek’s sign
52
Magnesium
Recommended dietary allowance:300-400 mg/day.
Normal level :1.8-3.6 mg %.
53
Function:
1. Component of bone & teeth.
2. Regulate neuromuscular function.
3. Act as a cofactor of enzymes eg: CPK,
hexokinase.
Hypomagnesemia :
causes convulsion.
Hypermagnesemia:
causes CNS depression.
55
Bicarbonate
Normal level : In arterial blood 22-28
mmol /L.
Bicarbonate buffer system:
►PCO2 in plasma determines the
dissolved CO2 amount which later on give
rise to H2CO3 that immediately
dissociates into bicarbonate ion &
hydrogen ion.
►If PCO2 increases ,the reaction
proceeds to right increasing serum
56 bicarbonate conc.
Following mechanisms regulate the acid
base balance by renal system:
1) Excretion of H+
2) Production of HCO3-
3) Reabsorption of filtered HCO3-
4) Elimination of titratable acid
5) Excretion of ammonium
58
Role of KIDNEY played in normal
condition:
Normally urine is acidic by excretion H+ ion in the form of
NH4+ & H2PO4-.
This task is accomplished by 2 mechanisms-
►Proximal acidification mechanism :
Done by complete reabsorption of filtered HCO3- from
PCT
►Distal acidification mechanism :
Done by total excretion of endogenously produced non
volatile acid with resultant generation of new HCO3- & its
absorption to blood .
59
Normal Acid Base Composition of
Blood :
Parameter Arterial blood Venous blood
pH 7.4 7.38
PCO2 40 mmHg (34–45) 46 mmHg
Serum HCO3- 24 mmol /L (22- 26 mmol /L
28)
Plasma Anion 8 -16 meq / L 8 -16 meq /L
gap
Base excess ± 2 mmol / L ± 2 mmol /L
PO2 95 mmHg (85– 40 mmHg
100)
Oxygen saturation > 95 % 60-85 %
Comprehensive view of simple acid base
disorder :
Types Primary defect Compensation Mechanism of
compensation
Metabolic Decreased PCO2 Hyperventilation
acidosis HCO3-
Metabolic Increased PCO2 Hypoventilation
alkalosis HCO3-
Respiratory Increased PCO2 HCO3- Renal HCO3
acidosis generation
Respiratory Decreased HCO3- Renal HCO3
alkalosis PCO2 excretion
