CLINICAL CHEMISTRY

ELECTROLYTES
K Y L A L E I Z Y L L A N G - A Y M AY O S , R M T
ELECTROLYTES
THE ELECTROLYTES
• Na, K, Cl, HCO3, Ca, Mg, PO4

BASIC LIFE FUNCTIONING

• Electrical neutrality
• Blood volume
• Osmotic regulation
• Generation and conduction of action
potentials in nerves and muscles
• Myocardial rhythm and contractility
• Acid-base balance
• Blood coagulation
• Production and use of ATP from glucose
MODULE 3
UNIT 1: Blood volume
regulation; Water and TABLE
Sodium
UNIT 2:
OF CONTENTS
UNIT 1:
BLOOD VOLUME REGULATION;
WATER AND SODIUM
FLUID AND ELECTROLYTES BALANCE

WATER IN PHYSIOLOGICAL PROCESSES

–TRANSPORT NUTRIENTS ; DETERMINES CELL VOLUME
–REMOVES WASTE PRODUCTS
–THERMOREGULATION
–PROTECTION
–DIGESTION; REGULATION OF BODY WEIGHT
FUNCTION OF COMPOUNDS
–COMPOUNDS NEED AQUEOUS MEDIUM
–INTRACELLULAR & EXTRACELLULAR COMPARTMENT
FLUID AND ELECTROLYTE
BALANCE
MAINTENANCE OF ELECTROLYTES TOTAL BODY WATER
- ACTIVE TRANSPORT - INTRACELLULAR WATER
REQUIRES ENERGY 2/3 OR 60%
- DIFFUSION - EXTRACELLULAR WATER
PASSIVE MOVEMENT 1/3 OR 40%
- FACTORS INFLUENCING PROCESSES
VARIABLE
BALANCE B/W ELECTROLYTES
PROTEINS
COMPOSITION OF THE EXTRACELLULAR AND
INTRACELLULAR COMPARTMENTS
FLUID AND ELECTROLYTES BALANCE

ISF
Physiological
EC water
Extracellular
Plasma water
water
Total body Transcellular
water water
Intracellular
water
FLUID AND ELECTROLYTES BALANCE

WHAT IS THE CONCEPT OF ELECTRONEUTRALITY?

THE EXTRACELLULAR FLUID VOLUME IN RELATION TO ELECTROLYTES
–RELATIVE INCREASE;RELATIVE DECREASE

WATER DISTRIBUTION
- INFANTS: 75% WATER BY MASS
- ADULTS: 50-60% WATER
AVERAGE WATER CONTENT: 40-75%
EXTRACELLULAR= 1/3 / 16L
INTRACELLULAR= 2/3 / 24L
FLUID AND ELECTROLYTES BALANCE

EDEMA: RETENTION OF 3L OF FLUID IN THE TISSUES

DEFICIENCY OF AVP: 10-20 L WATER EXCRETED DAILY

ELECTRONEUTRALITY & MOVEMENT OF SUBSTANCES

FLUID AND ELECTROLYTES BALANCE
FLUID AND ELECTROLYTES BALANCE

SODIUM/ NATRIUM
–major extracellular cation, hence the major contributor of osmolality
–principal osmotic particle outside the celL
–Plasma conc. depends on water intake
–Extracellular volume depends primarily on plasma Na, (regulated by AVP)
and aldosterone
–monitored together with urine Na and osmolality & UA
–Na*/K+-ATPase ion pump
• Out: 3 Na
• In : 2 K
FLUID AND ELECTROLYTES BALANCE

- 60%-75% of filteredsodium is reabsorbed in PCT

- blood volume regulated by Na balance
Reference ranges
- 24 hr urine
- CSF sodium
- Serum critical level
SODIUM

ALDOSTERONE
- ENHANCES ABSORPTION OF Na at DCT
- promotes Na retention ; K excretion
- Na retention in renal tubules = conservation of water

ATRIAL NATRIURETIC FACTOR

- Blocks aldosterone and renin secretion; blocks angiotensin II and
vasopressin
- Causes natriuresis
FLUID AND ELECTROLYTES BALANCE

URODILANTIN
- From renal tubules
- belongs to group of natriuretic peptides
- promotes natriuresis

ANGIOTENSIN II & CATECHOLAMINES

- influence the renal tubular reabsorption of sodium
- Catecholamines affect the renal blood flow
SODIUM
SODIUM
 SODIUM

HYPERNATREMIA
- characterized by increased plasma sodium
- loss of water, gain of sodium (excess solutes), or both
- does not occur unless the thirst mechanism is impaired
- water deficit of 1%-2% leads to a severe thirst
- Thirst is the major defense against hyperosmolality and
hypernatremia
CORRELATIONS
- Hypovolemia
- CNS involvement
 SODIUM

PATIENT MANAGEMENT
- corrected gradually (0.5 mmol/L/h plasma sodium).
- Too rapid decline may cause cerebral edema and death.
- Too rapid rise may develop osmotic demyelination
 SODIUM

HYPONATREMIA
- most common electrolyte disorder encountered in clinical
practice
- Classified acc to osmolality
- Decreased osmolality is the most common cause of hyponatremia
either due to sodium loss or water retention
 SODIUM

CLINICAL CORRELATION
- RENAL FAILURE
- NEPHROTIC SYNDROME, HEPATIC CIRRHOSIS
- POTASSIUM DEFICIENCY
- BARTTER SYNDROME
- CYSTIC FIBROSIS
- TRANSLOCATIONAL HYPONATREMIA
- DILUTIONAL HYPONATREMIA
- ALDOSTERONE DEFICIENCY
 SODIUM

PLASMA SODIUM IN THE CONTEXT OF HYPERGLYCEMIA

- glucose is osmotically active and moves water from the cells to the
ECF, diluting its is electrolytes
- Accumulation of glucose or mannitol in the EC

FOR EVERY 100 mg/dL INC in blood glucose, serum Na will INC by
1.6mmol/L
 SODIUM
Syndrome of Inappropriate ADH Secretion (SIADH)
– continuous secretion of ADH in the absence of a stimulus
–euvolemic hypoosmolar hyponatremia associated with hyperosmolar
urine
–excessive free water retention coupled with hypoosmotic volume
expansion
–Excess free water reabsorption in the distal renal tubule leading to a
decreased osmolality of the ECF
- Increased AVP secretion equals increased water retention
 SODIUM
PATIENT MANAGEMENT
– FLUID ADMINISTRATION
• TOO RAPID
• TOO SLOW

–CENTRAL PONTINE MYELINOLYSIS

PSEUDOHYPONATREMIA
–reduction in serum sodium concentration caused by a systematic error in
measurement
 SODIUM
FRACTIONAL EXCRETION
–quantity of a substance excreted in the urine expressed as a fraction of
the filtered load of the same substance
 POTASSIUM
KALIUM
–major intracellular cation, and only 2% of the body's total potassium circulates
in plasma
–single most important analytein terms of an abnormality being immediately
life-threatening
–concentration in the red blood cells is 105 mmol/L or 23x its concentration in
plasma
–In the ascending limb, it is reabsorbed w/ Na and Cl
–Filtered at the glomeruli & is (70-80%) mostly reabsorbed by active and passive
mechanism at the PCT
• Functions: cardiac contraction, neuromuscular excitability, ICF volume regulation,
and hydrogen ion
• concentration Kt has a major effect on the contraction of skeletal and cardiac
muscles
 POTASSIUM
HORMONES AFFECTING PLASMA POTASSIUM LEVELS
1. ALDOSTERONE
• Regulatesurinary loss of potassium in the cortical collecting duct
2. EPINEPHRINE
• Channel for the cellular entry of potassium
3. INSULIN
• Promotes entry of potassium into skeletal muscles and hepatic
 POTASSIUM
SPECIMEN CONSIDERATIONS
–Slight hemolysis (50g/dL of Hgb)
• K inc by 0.5 mmol/L or 3%
–Severe hemolysis (>500 mg/dL Hgb)
• K inc by 30%
–Muscular activity
–Prolonged serum and red cell: INC
–Prolonged tourniquet application: INC
–Forearm exercise and fist clenching: INC
–Release of plt in the serum during clot formation: INC
POTASSIUM
POTASSIUM
 POTASSIUM
HYPERKALEMIA
–almost always due to impaired renal excretion
–Major mechanisms of diminished renal potassium excretion: Reduced
aldosterone or aldosterone responsiveness renalfailure, and reduced
distal delivery of sodium
–Elevations in seruin k' can directlystimulate the adrenalcortex torelease
aldosterone
–Inhibits NaCl reabsorption in the DCT
 POTASSIUM
REDUCED ALDOSTERONE
- Hyporeninemic hypoaldosteronism
MUSCLE/ CELLULAR INJURY
- rhabdomyolysis & hemolytic disorders
- muscle trauma, massive blood transfusion, and tumor lysis
syndrome
RENAL FAILURE & DIABETES MELLITUS
- reduced GFR & decreased tubular secretion
- insulin deficiency
 POTASSIUM
HYPERKALEMIA IN THE CONTEXT OF CARDIAC MUSCLE FUNCTION
– RESTING MEMBRANE POTENTIAL
–ALTERATION OF ECG
–LACK OF MUSCLE EXCITABILITY
–CARDIAC ARREST: 10mmol/L

pH IMBALANCE (ACIDOSIS) AND DRUGS

- diuretics and K+ administration
- Hyperkalemic drugs:Captopril, spironolactone (K* sparing-diuretic),
digoxin, cyclosporine, and heparin therapy
 POTASSIUM
PSEUDOHYPERKALEMIA
–Sample hemolysis, thrombocytosis, prolongedtourniquet application,fist
clenching, blood stored in ice, IVfluid, and high blast count in acute or
accelerated phase leukemias (blast may lyse during standard
phlebotomy releasing K*)
–THROMBOCYTOSIS
–HIGHER BLAST COUNTS
–RECENTRIFUGATION OF SST
 POTASSIUM
END OF LECTURE AS OF 10/12/2023