E L E C T RO LY T E S

JUDI TH MAYE G. BOLIC O, RM T

 Ions capable of carrying an electric
charge

ELECTROLYTES
Cations = Anions Electroneurality
E L E C T R O LY T E S
• 40-75% average water content of the
human body
• Age
• Weight
• 60% of the body’s water is inside the cell
• The rest is in the bloodstream or tissue
fluids
 Extracellular Fluid (ECF)

• 1/3 of the total body water

• 16L

ELECTR OLYTES Intracellular Fluid (ICF)

• 2/3 of the total body water

• 24L
PLASMA

• Composed of
• 93% - water
• 12% higher than in WB
• 7% - Solute
 EDEMA

RETEN TIO N OF 3L OF
F L U I D I N T HE
TISSUES
DEFICIENCY OF
VA S O P R E S S I N
• 10-20L of water excretion daily
 • Predominant cation in ECF:
Sodium
• Predominant cation in ICF:
Potassium

MBER!
• Predominant anion in ICF:
Phosphates and proteins
• Predominant anion in ECF:
Chloride and bicarbonate
FUNCTIONS OF
E L E C T R O LY T E S
1. For volume and osmotic regulation
2. For myocardial rhythm and contractility
3. Important cofactors in enzyme activation
4. For the regulation of ATP ion pumps
5. For neuromuscular excitability
6. For the production and use of ATP from glucose
7. Maintenance of acid-base balance
8. Replication of DNA and the translation of mRNA
S A LT
•Main determinant of the
ECF volume.
 SO DI UM

JUDI TH MAYE G. BOLIC O, RM T

 SODIUM

A.K.A = Natrium
Major extracellular CATION

Major contributor of OSMOLALITY

Principal osmotic particle outside the cell

Plasma concentration depends on the intake and excretion of water

Reference Value:

• 135-145 mmol/L

Threshold CriticalValue

• 160 mmol/L Hypernatremia

• 120 mmol/L Hyponatremia
SODIUM

CSF Sodium

• 136-150 mmol/L
HORMONES AFFECTING SODIUM

• Absorption of Na in the distal tubule

Aldosterone
• Sodium retention
• Potassium excretion

• Endogenous antihypertensive agent

Atrial • Secreted from cardiac atria
Natriuretic • Block aldosterone and renin secretion
Factor (ANF) • Inhibits action of Angiotensin II and vasopressin
• Causes natriuresis
 H Y P E R N AT R E M I A

EXCESS WATER LOSS DECREASED WATER INCREASED INTAKE OF

INTAKE SODIUM OR RETENTION
H Y P O N AT R E M I A

Increased sodium loss Increased water retention

 Increased sodium concentration in plasma water

Diagnosed at serum sodium levels >145 mmol/L

Usually results due to excessive water loss

Water deficit of 1-2% leads to severe thirst

H Y P E R N AT R E M I A

Serum levels of 150-160 mEq/L – moderate deficit of water

>165 mEq/L – severe deficit of water

H Y P E R N AT R E M I A

Rapid intake of water

• Venous Na is 4 mmol/L > Arterial blood

20 mL/kg of water in 15 minutes

• Reduced arterial serum sodium by 8mmol/L

Thirst

• Major defense against hyperosmolality and hypernatremia

 Most common electrolyte disorder

Reduced plasma sodium concentration

HYPONATREMIA

<135 mmol/L

Clinical concern :
130 mmol/L
 H Y P O N AT R E M I A
• KidneyfailsKidneyscan’tconcentratetheurine=Hyponatremia

• Urine sodium >20mmol/day = ongoing renal loss of sodium and water

• In Diabetes Mellitus, sodium loss occurs with ketonuria
• Sodium <125 mmol/L = severe neuropsychiatric symptoms
 P S E U D O H Y P O N AT R E M I A

Reduction in serum concentration Most common – in vitro hemolysis Marked hemolysis  dilutional effect 
– systematic error in measurement decreased Na
 H Y P O N AT R E M I A W I T H N O R M A L
RENAL FUNCTION

Cause Serum Na Urine Na 24hr UNa Urine Serum K

Osmolality
Overhydration Low Low Low Low Normal or Low

Diuretics Low Low High Low Low

SIADH Low High High High Normal or Low

Adrenal failure Mildly elevated Normal High High

Bartter’s Syndrome Low Low High Low Low

Diabetic Low Normal Normal Normal High
Hyperosmolarity
 P OTA S S I U M

JUDI TH MAYE G. BOLIC O, RM T

RM T
 P O TA S S I U M

A.K.A “Kalium”
Major intracellular cation
2% : total potassium circulates in plasma
Concentration in RBC : 105 mmol/L
P O TA S S I U M

Ascending Loop of
Proximal Tubule:
Henle: K+ is reabsorbed
reabsorbed by active and
Glomeruli : Filtered together with Na and Cl
passive mechanisms (70-
by the K-Cl
80%)
cotransporter
P O TA S S I U M

Singlemostimportantanalyte If there’san abnormality : life

threatening
Heart Contraction

Neuromuscular excitability

FUNCTIONS ICF Volume Regulation

Hydrogen Ion Concentration

VA L U E S

Reference Values: Threshold critical value

3.5-5.2 mmol/L 6.5 mmol/L – Hyperkalemia
2.5 mmol/L - Hypokalemia
S P E C I M E N C O N S I D E R AT I O N
• Hemolysis
• 0.5% RBC can increase levels by 0.5 mmol/L (30% increase in gross hemolysis)
• Plasma level > Serum level
• Release of platelets into serum on clot formation
• Muscular activity (exercise, prolonged standing): 10-20% increase
• Prolonged contact of serum and red cell
• Prolonged tourniquet application
 1. Decreased renal excretion
• Acuteorchronicrenalfailure

• Severe dehydration
• Addison’s disease
2. Extracellular Shift
• Acidosis
• Muscle/Cellular injury
• Chemotherapy
HYPERKALEMIA
• Vigorous Exercise
• Digitalis intoxication
3. Increased intake – oral or IV infusion
4. Useofimmunosuppressivedrugs–

Tacrolimus andcyclosporine
 1. Gastrointestinal Loss
• Gastric suction and laxative abuse
• Intestinal tumor and malabsorption
• Cancer and radio therapy
• Vomiting and diarrhea
2. Renal Loss
• Diuretics use
• Hyperaldosteronism
• Cushing syndrome
HYPOKALEMIA • Leukemia
• Bartter’s syndrome
• Gitelman’s syndrome
• Liddle’s syndrome
• Malignant hypertension
3. Intracellular shift
• Alkalosis and insulin overdose
HYPERKALEMIA

Almost ALWAYS due to impaired renal excretions.

Elevations in serum potassium can directly stimulate the adrenal

cortex to release aldosterone.
 MECHANISMS OF DIMINIS HED
R E N A L P O TA S S I U M E X C R E T I O N

Reducedaldosterone RenalFailure ReduceddistaldeliveryofNa

 Most common cause of chronic
hyperkalemia among non-dialysis patient

Caused by chronic renal insufficiency of

primary tubulointerstitial disease.
H Y P O R E N I N E M I C
H Y PO ALD O S T E R O N I S M

Most common cause of aldosterone

deficiency
• Severehyperkalemia canultimatelycausealackofmuscleexcitability:8mmol/L

• Plasma potassium levels of 6-7 mmol/L may alter ECG

• Plasma potassium levels of 10 mmol/L is fatal (cardiac arrest)
• The heart may experience cessation of contraction in either hyperkalemia ang
hypokalemia

EFFECTS TO C ARDIAC M U S C L E
• Low insulin level cause high serum potassium
• Therapeutic potassium administration – most common
cause of hyperkalemia among hospitalized patients.
• Hyperkalemic drugs
• Catopril
• Spironolactone
• Digoxin
• Cyclosporine
• Heparin Therapy N OT E S TO
• Digitalis inhibits the sodium-potassium ATPase pump REMEMBER
PSEUDOHYPERKALEMIA
Caused by

• Sample hemolysis
• Thrombocytosis
• Prolonged tourniquet application
• Fist clenching
• Blood stored in ice
• IV fluid and high blast counts
HYPOKALEMIA

Plasma level : 3.0-3.4 mmol/L : Hypokalemia

Hypomagnesemia leads to hypokalemia by promoting urinary loss of

potassium
I M PA I R E D R E N A L F U N C T I O N

Most common cause of hypokalemia

 • Most common cause of extra renal loss of potassium
• Low urine anion gap

DIARRHEA
C H LO R I D E
METHODS
• Heparinized plasma is preferred over serum
• Platelets contain potassium that is released into serum on clot formation
1. Emission Flame Photometry
2. Ion Selective Electrode
3. ASS
4. Colorimetry (Lockhead and Purcell)
 Major extracellular anion
Promotes maintenance of water balance and osmotic pressure in conjunction with sodium

Only anion to serve as an enzyme activator

Excreted in the urine and sweat

Disorders of chloride are the same as sodium since they both are extracellular cations

Chloride usually follows Na (if one is abnormal, so is the other)

FUNCTIONS

Maintains
Maintains Maintains
electric
osmolality blood volume
neutrality
 Cl- ions are almost completely absorbed from the intestinal tract.

They are filtered from plasma at the glomeruli and are passively reabsorbed,
along with Na+ , in the proximal tubules.

In the thick ascending limb of the loop of Henle, Cl− is actively reabsorbed
by the Cl− pump, which promotes passive reabsorption of Na+.

C H LO R I D E
C H LO R I D E S H I F T
• Chloride shift is also called hamburger phenomenon because the plasma is surrounded by the
cell.
• This is done in order to resent how metabolism is taken place and how carbon dioxide is
generated
• Carbon dioxide + water bicarbonates hydrogen ion + bicarbonate
• HCO3 accumulates inside RBC as they pick up CO2
• Some diffuses out into plasma
• To balance the loss of negative ions, chloride moves into RBC from plasma
• Important in Maintenance of electrical neutrality
 Mercuric Titration (Schales and Schales)

Spectrophotometric Methods

• Mercuric Thiocyanate (Whitehorn Titration

Method)
• Ferric Phosphate
METHODS OF
D E T E R M I N A T I ON Colorimetric Amperometric Titration

• Cotlove Chloridometer

Ion Selective Electrode

 METHO D S OF
D E T E R M I N AT I O N
 SPECIMENS

SERUM SWEAT HEPARINIZED 24 HOUR

PLASMA SWEAT
 S W E AT C H L O R I D E
• Need fresh sweat to accurately measure true Cl concentration
• Testing procedure : to identify cystic fibrosis patients by the increase salt concentration
in their sweat
• Pilocarpine iontophoresis
• Pilocarpine = the chemical used to stimulate sweat production (usually at the back of
the baby)
• Iontophoresis = mild electrical current that stimulates sweat production
R E F E R E N C E VA L U E
 Renal tubular acidosis

Diabetes insipidus

HYP E RC HLO R E MI A
Salicylate intoxication

Primary hyperparathyroidism

Metabolic Acidosis

Prolonged diarrhea
H Y P O C HLO R E M I A

Prolonged Aldosterone Metabolic Salt-losing

vomiting deficiency acidosis nephritis
Most abundantcation

5th common inorganic element in the body

99% - found in the skeleton as hydroxyapatite crystal together with
phosphate
1% in the blood
I M P O R TA N T I N

Blood Muscle Membrane

coagulation contraction permeability
C A LC I U M

60% - free calcium or ionized form which is the 40% - bound to albumin
physiologically active form of the calcium
 Dairy Products (Milk, Cheese,
Yoghurt)

IN T
H E DI
E T, Seafood
 C A LC I U M

Absorbed in the duodenum by means of calcium

lowering protein called calmodullin

Kidneys excrete the excess calcium when the blood

level exceeds 10 mg/dL. Mostly lost in the feces
REFERENCE VA L U E S

8.6-10 mg/dL (adult) 4.6-5.3 mg/dL (adult)

8.8-10.8 mg/dL (child) 4.8-5.5 mg/dL (child)
 Ionized calcium 50%

Protein-bound
FORMS OF Calcium
40%

C A LC I U M

Complete with anions 10%

S E N S I T I V E A N D S P E C I FI C MARKER
F O R C A L C IU M D I S O R D E R S .

IONIZED
C A LC I U M
HORMONES

Active vitamin D3 (1,25- dihydroxycholecalciferol)

PTH

Calcitonin
H Y P E RC A LC E M I A H Y P O C A LC E M I A
• Primary hyperparathyroidism – main cause • Vitamin D deficiency
• Cancer (lungs and mammary)O • Primary hypothyroidism
• Increased Vitamin D • Acute pancreatitis
• Multiple Myeloma • Hypomagnesemia
• Sarcoidosis • Renal Tubular Failure
METHODS
• Clark Collip Precipitation
Precipitation • Ferro Ham Chloranilic Acid Precipitation

Ortho-Cresolphtalein • Dye : Arzeno III

Complexone Dyes • Mg+ inhibitor: 8-hydroxyquinoline (chelator)

EDTA Titration Method • Bachra, Dawer, and Sobel

Ion-selective Electrode • Liquid-membrane

 AAS - Reference method
A
 BICARBONATE
Second most abundant anion in the ECF

Accounts for 90% of the total CO2 at physiologic pH

Buffers excess hydrogen ion by containing with acid

Maintenance of high plasma bicarbonate concentration occurs in advanced renal failure or when the renal
threshold for bicarbonate is increased
 Function

• Major component of the

buffering system in blood
BICARBONAT E

Specimen

• Blood anaerobically collected

R E F E R E N C E VA L U E

21-28 mEq/L
 METHODS

Enzymatic
ISE
methods
 MAG N ESIUM

JUDI TH MAYE G. BOLIC O, RM T

 M AG N E S I U M

Second most abundant intracellular cation

Majority is stored in bones with calcium and phosphate

Essential cofactors of several enzymes

Influences neuromuscular excitability

M AG N E S I U M

70% free or ionized form

30% protein bound

 Specimen consideration 10x more concentrated in the
RBC and the ECF

Maybe erroneously low of blow is obtained after

administration of IV calcium gluconate

Increased in women treated with Mg salts for eclampsia (occurs

MAGNESIUM near delivery week; women developing hypertension)

Samples should be drawn without venous stasis

F A CT O RS

AFFECTING
MG PTH

Aldosterone and Thyroxine

CLINICAL SIGNIFICANCE

Hypermagnesemia

• Addison's disease
• Acute or chronic renal failure
• Untreated diabetic coma
• Oliguria
CLINICAL SIGNIFICANCE
Hypomagnesemia

• Malabsorption syndrome
• Cushing's syndrome
• Chronic alcoholism
• Toxemia of pregnancy
• Chronic diarrhea
• After administration of insulin - decrease levels of magnesium in the blood
• Acute pancreatitis
• Hypercalcemia
NORM A L V A LUE

0.65-1.05 mmol/L
 METHODS

Dye lake (Titan Fluorometric and Xylidyll blue reaction AAS (most
Yellow) by Basinski Complexometric (Mann and yoe) recommended)
M E T H O DS

Dye lake (Titan Yellow) by Basinski

• Titan yellow in alkaline solution is adsorbed unto colloidal

particles of Mg(OH)2 when the
• Mg in serum encounters a strong alkaline solution
• The dye lake produced is red in color and is stabilized by the
addition of PVA
METHODS

Fluorometric and Complexometric

• Hydroxyquinoline sulfuric acid forms a

chelate CPD with Mg that has a fluorescent
property of excited at 380-410 nm
METHODS

Xylidyll blue reaction (Mann and yoe)

• Mg produce a red chelate when combined with

xylidyll blue in aqueous alcoholic solution
METHODS
AAS (most recommended)

• Mg is first released from proteins by treatment with acid such as

trichloroacetic acid or hypochlorite acid
• Lanthanum or strontium is added to bind the phosphates in the
sample.
• After that it is analyzed in AAS, where Mg is at maximum abs at
285 nm
PHOSPHORUS

JUDI TH MAYE G. BOLIC O, RM T

 PHOSPHORUS

Important in the transfer of energy in the intermediary metabolism of food

stocks
Acts as a buffer to maintain the pH

Important constituent of the bones because it binds with calcium to form

crystals (hydroxyapatite crystals)
Majority of these is excreted in the urine
PHOSPHORUS

Inversely related to calcium

Maximally absorbed in the jejunum

PHOSPHORUS

85% in the bones

15% in the ECF

 Free or unbound – 55%

FORMS OF

PHOSPHORUS Complexed with ions – 35%

Protein-bound – 10%
PHOSPHORUS

70% of the total phosphorus is organic 30% is inorganic phosphorus

I N O RG A N I C P H O S P H O RU S EXISTS
A S:

ORGANIC PHOSPHATE INORGANIC PHOSPHATE

FA C TO R S PTH
AFFECTING
P H O S P H AT E
C O N C E N T R AT I O N
Calcitonin

Growth Hormone
 N O R M A L VA L U E S

At Birth • 1.34-3.36 mmol/L

Children • 1.28-2.24 mmol/L
Adults • 0.96 - 1.44 mmol/L
 S P E C I M E N C O N S I D E R AT I O N

Non fasting specimen decrease the inorganic phosphorus level because carbohydrate will depress
the serum IP levels by cellular intake and by the formation of phosphate esterase

Hemolysis: False increase because red cells are rich in phosphate

Heparinized plasma must not be used because of the presence of phosphate on commercially prepared
heparin

IP should be processed at once because there is the action of phosphatases during clot formation

Contains diurnal variations (increase values during the day hence it is preferred to collect samples in the
morning)
CLINICAL SIGNIFICANCE

Hyperphosphatemia

• Hypoparathyroidism
• Chromic glomerulonephritis
• Uremia
• Hypervitaminosis D
• Hypersecretion of growthhormone

Hypophosphatemia

• Hyperparathyroidism
• Ricketts
• Osteomalacia
METHOD
• Fiske Subbarow Method
• Ammonium molybdate method
• Most commonly used method to
measure serum Inorganic PO4
• Most common reducing agent: pictol
• End product: ammonium-molybdate complex