it is very essential role in management of body homeostasis mechanism and acid base balance.

1. ELECTROLYTES
Mr.Jagdish Sambad
MSc.Nursing Nephrology
IKDRC-ITS

2. Objectives
 What is electrolyte?
 Which are imp electrolytes in our body?
 What are the functions of particular electrolyte?
 Regulation in body
 Sample collection
 Method of estimation
 Errors which can affect the result
 Pathological alteration

3. What are they??
 Electrolytes are minerals found in body fluids that carry an
electrical charge and are essential to keeping the heart, nerves
and muscles functioning properly.
 As such, it is important to maintain a precise and constant
balance of electrolytes.
CATION - positively charged electrolyte
ANION - negatively charged electrolyte
 Cations = Anions for homeostatsis to exist in each fluid
compartment.
 Commonly measured in mEq/L.

4. Which are they??
Cations Anions
Sodium
Potassium
Calcium
Magnesium
Cations Anions
Sodium (Na+) Chloride(Cl-)
Potassium (K+) Biocarbonate (HCO-)
Calcium (Ca++) Phosphorus (PO4
-)
Magnesium (Mg+)

6. • Most prevalent cation in the ECF.
• Total body Sodium is about 5000 mEq in an adult.
• Daily requirement of sodium is about 100 mEq.
• In normal individuals, the kidney strives to achieve
Na+ balance – that is, to have Na+ excretion equal to
Na+ ingestion.
A. Sodium (Na+)
Introduction

7. Maintain balance of extracellular fluid, thereby it
controls the movements of the water between fluid
compartments.
Transmission of nerve impulses
Neuro muscular and myocardial impulse
transmission
A. Sodium (Na+)
FUNCTIONS

8. A. Hormones increasing sodium reabsorption:
1. Renin:
 Released from the juxtaglomerular apparatus of the kidney
 Release is stimulated by: raised sympathetic tone, falling
plasma volume, and certain prostaglandins, such as PGE2
 No direct effects promoting Na+ retention, it controls the renin-
angiotensin-aldosterone axis
2. Angiotensin II:
 Levels rise as result of renin release
 In turn, it stimulates the release of aldosterone
 Also increases tone in the efferent glomerular arteriole. The net
effect is to enhance Na+ reabsorption from the proximal tubule.
A. Sodium (Na+)
REGULATION

9. 3. Aldosterone:
 Steroid hormone released from the adrenal cortex
 End product of the RAAS system
 Acts on the distal tubule and collecting duct to increase Na+ and
water reabsorption (proportionately more Na+ than water)
4. Arginine vasopressin (AVP), anti-diuretic hormone (ADH):
 Neuron cell bodies in supra-optic and paraventricular nuclei of the
Hypothalamus,
 Stored in posterior pituitary.
 Passive absorption of water from the collecting ducts along with a
small degree of Na+ re-absorption, concentrating the urine
A. Sodium (Na+)
REGULATION

10. RAAS SYSTEM
A. Sodium (Na+)
RAAS SYSTEM

11. B.Hormones increasing sodium excretion:
1.Atrial Natriuretic Peptide (ANP):
 A small peptide produced from the atrial wall as
a result of atrial stretching.
 Increase Na (and hence water) excretion by
increasing GFR and blocking Na reabsorption in
PCT
2.Brain Natriuretic Peptide (ANP):
 secreted by the hypothalamus, termed brain
natriuretic peptides (BNP)
 Have a similar roles.
A. Sodium (Na+)
REGULATION

12.  Serum: venous blood sample in gel vaccutainer
 Urine:
 24 hrs urine collection
 No preservative is required
 Store at 2-8 degree
Sample collection
Method of estimation
 Ions selective electrode
A. Sodium (Na+)

13. Ion selective
electrode

14. Potentiometric measurements:
Potentio-metry is to determine the difference in potential between
a working (an indicator) electrode and a counter (a reference)
electrode.
- Cathode is the working / indicator electrode.
- Anode is the counter / reference electrode.
Indicator Electrode:
Electrode that responds to analyte and donates / accepts electrons
Reference Electrode:
Second ½ cell at a constant potential
ell voltage is difference between the indicator and reference
electrode
Ecell = Ec ─ Ea
Where : Ec is the reduction potential at the cathode.
: Ea is the reduction potential at the anode.

16.  Serum: 135 – 145 mEq/L
 Urine:
24 hr urine sample: 40-220 mEq/day
Note: For random, it is better to do FeNa .
Also used in calculation of Anion gap & Osmolality
Biological reference range
Panic value
 Serum level >160 and <120 mEq/L
A. Sodium (Na+)

17. Errors affecting Na+ result
A. Pseudohyponatraemia :
1. Sample collection from IV site, thus the sample is diluted by the
hypotonic fluid (5% dextrose).- confirmed by dilution effect on
other parameters
2. High plasma glucose level: increase 100 mg/dl – lowering Na
1.6 mmol/L, after 400 mg/dl, every 100 mg/dl lowering 2.4
mmol/L
Corrected Sodium = [0.016 x (serum glucose – 100)] + serum
Na
3. Increased viscosity due to the Hyperproteinemia,
Hyperlipidemia due subsequent decreased watery portion of
plasma can thus cause false low sodium concentrations
A. Sodium (Na+)

18. B. Pseudohypernatraemia :
1. Sample collection from IV site - confirmed by measurements
of CL- and K+
2. Drugs – SSRI, sodium valproate etc.
Errors affecting Na+ result
A. Sodium (Na+)

19. S. Sodium level < 135 mEq/L
< 280 mOsm/Kg > 280 mOsm/Kg
(N or increase)
True Hyponatremia
Pseudohyponatremia
Hypo-
volemic
Eu-
volemic
Hyper-
volemic
Cause Investigation
Paraproteinemia s. protein,
electrophoresis
Hyperlipidemia S. Cholestrol,TG
Hyperglycemia S. Glucose
A. HyponatremiaA. Sodium (Na+)

20. < 20 mEq/L
Extrarenal causes
vomiting
Diarrhea
Third spacing of fluid
Burns
Decrease total body water
Decrease total body sodium (more deficit)
Measure urinary sodium
>20 mEq/L
Renal causes
Diuretics
Salt losing nephropathy
Mineralocorticoids Def.
Osmotic diuresis
Note : In vomiting, to compensate metabolic alkalosis urinary Na > 20
mEq/L, and urinary cl- < 10 mmol/L
A. HyponatremiaA. Sodium (Na+)
A. Hypovolemic hyponatremia

21. Increase total body water
No change in total body sodium
Urinary sodium > 20 mEq/L
Urine osmolality>100 moSm/Kg
Causes
Glucocorticoids deficiency
SIADH
Hypothyroidism
Drugs
A. Sodium (Na+)
B. Euvolemic hyponatremia
A. Hyponatremia

22. Increase total body water (More)
Increase total body sodium
Measure urinary sodium
< 20 mEq/L
Other causes
Cirrhosis
Cardiac failure
>20 mEq/L
Renal causes
AKI
CKD
A. Sodium (Na+) A. Hyponatremia
C. Hypervolemic hyponatremia

23. A. Sodium (Na+) B. Hypernatremia
S. Sodium level > 145 mEq/L

24. Hypo-volemic Eu-volemic Hyper-volemic
Hypo-
natremia
Na - Na - N Na -
H2O - H2O- H2O -
Hyper-
natremia
Na - Na – N Na -
H2O - H2O H2O -
Sumarry of Natremic disorders

26. • Major intracellular cation.
• Total body K+ content in a normal adult 3000-
4000mEq.
• 98% Intracellular , 2% in ECF
B. Potassium (K+)
Introduction

27. Regulates neuromuscular excitability and
muscle contraction
As coenzyme - glycogen & protein synthesis
Correction of acid base imbalances
FUNCTIONS
B. Potassium (K+)

28. The primary mechanism maintaining this balance : the
Na-K – ATP phase pump
Na-K ATPhase pump actively transports Na+ out of the
cell and K+ into the cell in a 3:2 ratio
Renal excretion – Major route of excess K+
Approx 90% of K+ excretion occurs in the urine
less than 10% excreted through sweat or stool.
Regulation
B. Potassium (K+)

29. B. Potassium (K+)

30.  Serum: venous blood sample in gel vaccutainer
 Urine:
 24 hrs urine collection
 No preservative is required
 Store at 2-8 degree
Sample collection
Method of estimation
 Ions Selective Electrode
B. Potassium (K+)

31.  Serum: 3.5 – 5.5 mEq/L
 Urine:
• 24 hr urine sample: 25-125 mEq/day
• Random urine: 13-101 mmol/g creat
Note: Also used in calculation of anion gap
Biological reference range
Panic value
 Serum level <2.0 and >7.0 mEq/L
B. Potassium (K+)

32. Errors affecting K+ result
A. Pseudohyperkalemia :
1. Cleaning of puncture site:
The site for venipuncture is to be cleaned with povidone
iodine.
2. Tourniquet application:
• It should be released once the first blood flow was
established.
• More than 1 min of tourniquet : haemo-concentration
3. Clenching fist for longer time causes elevation potassium.
B. Potassium (K+)

33. B. Potassium (K+)
4. Needle or syringe:
Size of syringe / pushing of blood in vaccutainer.
5. Order of drawing tubes:
The blood collected in a specific order avoids cross
contamination of additives.
Examples of the common carryover problems observed
are the EDTA which is easily determined by marked
hyperkalemia, hypocalcemia, hypomagnesemia and
hypozincanemia.
6. Centrifugation and vigorous shaking of sample.

34. 1. Sterile-blood culture
2. Coagulation (light blue)/ Citrate
3. Non-additive (red top)/ Plain
4. Gel separator tube (red or gold)/ Plain
5. Heparin tube (green top)
6. EDTA (lavender/purple top)
7. fluoride tube (grey top)
8. All other tubes
Order of blood collection by CLSI

35. 7. Storage : store after separation of serum
8. Lymphocytosis and thrombocytosis: Hyper cellularity
9. Fluid containing potassium
B. Potassium (K+)

36. B. Pseudohypokalemia :
1. Sample collection from IV site, thus the sample is diluted by
the hypotonic fluid (5% dextrose).- confirmed by dilutional
effect on other parameters
2. High plasma glucose level: Dilution effect
3. Increased viscosity
Errors affecting K+ result
B. Potassium (K+)

37. A. hypokalemiaB. Potassium (K+)
S. Potassium level < 3.5 mEq/L

38. 1. Decreased intake:
 Food is the main source of potassium
A. hypokalemiaB. Potassium (K+)

39. 2. Excessive loss :
a. GIT loss:
• Persistent vomiting
• Diarrhea
• Gastric suction and Fistula
b. Hypovolemia: Increased aldosterone Hypo-K+
A. hypokalemiaB. Potassium (K+)

40. c. Renal loss:
I. Hyperaldosteronism:
 Primary hyperaldosteronism : Adrenal tumors
 Secondary hyperaldosteronism:
 Reduced effective arterial volume in CCF
 Liver cirrhosis
 Nephrotic syndrome
A. HypokalemiaB. Potassium (K+)

41. A. hypokalemiaB. Potassium (K+)
II. Diuretics :
 Thiazines, Furosemide

42. A. hypokalemiaB. Potassium (K+)
III. Renal Tubular Acidosis type-1/2:
 Type 1: dRTA : Decreased H+ Excretion in DCT
 Type 2: pRTA: Decreased reabsorption of HCO3
-

43. 3. Shifting of K+ from ECF to ICF
A. hypokalemiaB. Potassium (K+)
a. In alkalosis,
H+ moves out of the cells, at the same time, K+ moves into the
cells.
For each 0.1 unit increase of pH in ECF, the [K+] of serum
decreases 0.7 mmol/L.
b. Insulin: stimulates Na+-K+ ATPase.
c. Hyperthyroidism: Over-dose thyroxin stimulates Na+-K+ ATPase.

44. Serum potassium level of >5.5 mEq/L
• Common Causes:
1. Intra- to extracellular shift:
 Acidosis – Uptake of H+, efflux of K+
 Hyperosmolality- Hypertonic dextrose, mannitol, - Solvent Drag effect
 β2-Adrenergic antagonists (non-cardioselective agents): Suppresses
catecholamine stimulated renin release- in turn aldosterone synthesis
Digoxin and related glycosides : Inhibits Na/K ATPase
Succinylcholine: Depolarizes Muscle cells, Efflux of K
Rapid tumor lysis / Rhabdomyolysis
B. HyperkalemiaB. Potassium (K+)

45. 2. Inhibition of the renin-angiotensin-aldosterone axis:
(↑ risk of hyperkalemia when these drugs are used in combination)
Angiotensin-converting enzyme (ACE) inhibitors
 Renin inhibitors; aliskiren
Angiotensin receptor blockers (ARBs)
Blockade of the mineralocorticoid receptor: spironolactone
 Blockade of the epithelial sodium channel (ENaC): amiloride,
triamterene
B. HyperkalemiaB. Potassium (K+)

46. 4. Renal resistance to mineralocorticoids:
Tubulointerstitial diseases:
SLE, amyloidosis, sickle cell anemia, obstructive uropathy, post–
acute tubular necrosis
Hereditary:
pseudohypoaldosteronism type I; defects in the mineralocorticoid
receptor or the epithelial sodium channel (ENaC)
5. Advanced renal insufficiency:
 Chronic kidney disease
 End-stage renal disease
 Acute oliguric kidney injury
B. HyperkalemiaB. Potassium (K+)

48.  Most abundant mineral in human beings.
 Total calcium in an average adult is about 1,000 gm :
 99% in bones & teeth.
 Rest in various tissues and body fluids.
 Calcium is present in bones mainly in the form of
calcium phosphate.
C. Calcium (Ca++)
Introduction

49.  About 50% of this is bound to protein (protein-bound or
non-diffusible calcium).
 About 5% with organic anions e.g. citrate, (diffusible)
 The remaining 45%: free ionized calcium (freely
diffusible)
 Ionized calcium: Active form
C. Calcium (Ca++)

50. Functions
Formation of bones and teeth
Excitability and conductivity of nerves
Neuromuscular transmission
Excitability and contractility of myocardium
Coagulation of blood
Action of hormones
C. Calcium

51. Calcium regulating factors
Vitamin D
PTH
Phosphorus level
EMB-RCG
C. Calcium

52. Cholecalciferol
Hydroxylase
25-Hydroxycholecalciferol
Parathormone Parathyroid
glands
1, 25-Dihydroxycholecalciferol
Induction
Calcium-binding protein
Ca -dependent ATPase
Alkaline phosphatase
++
Calcium absorption
Release into circulation
Plasma calcium
LIVER
KIDNEY
INTESTINAL
MUCOSA
Hydroxylase
INTESTINAL
MUCOSA

–
C. Calcium

53.  Serum: venous blood sample in gel vaccutainer
 Urine:
 24 hrs urine collection
 No preservative is required
 Store at 2-8 degree
Sample collection
Method of estimation
C. Calcium
1. T. Calcium: Arsenzo- III Spectrophotometric method
2. Ionized Calcium: ISE
Ca+ + + Arsenazo III Ca- Arsenazo III complex (purple)

54. T. Serum: 8.5-10.5 mg/dL
Ionized Calcium: 0.9 – 1.3 mmol/L
Urine:
24 hr urine sample: 100-250 mg/day
Biological reference range
C. Calcium

55.  Free calcium is useful index - provides the better indication
of calcium biologically active and tightly regulated by
calcium binding hormones.
 Calcium is predominantly transported bound to serum
proteins, total calcium levels are greatly influenced by protein
concentration especially albumin.
 Earlier no proper technique to measure. This problem is
now solved due to availability of ion-selective electrodes, for
free calcium measurements .
What is better Ionized or Total ???

56. Corrected calcium : Total calcium + 0.8 (4.0 – S. Alb)
For this patient = 8.1 + 0.8 (4 – 3.2) = 8.1 + 0.64=8.75
Corrected total calcium ? ?

57. A. Pseudohypercalcemia:
1. Cleaning the venipuncture site:
2. Tourniquet application:
3. Clenching fist
4. Needle or syringe:
5. Order of drawing tubes:
6. Centrifugation and vigorous shaking of sample
Errors affecting Ca++ level
C. Calcium

58. 7. Storage:
8. Sample type:
9. Lymphocytosis and thrombocytosis
Errors affecting Ca++ level
C. Calcium
B. Pseudohypocalcemia:
1. Sample collection from IV site
2. High plasma glucose level
3. Increased viscosity

59.  Hyperparathyroidism
 Hypervitaminosis D
 Bone cancer
 Multiple myeloma
 Leukaemia
 Polycythaemia
 Milk-alkali syndrome
 Sarcoidosis
 Idiopathic infantile
hypercalcaemia
A. Hypercalcemia
C. Calcium
B. Hypocalcemia
 Hypoparathyroidism
 Rickets
 Osteomalacia
 Chronic renal failure
 Nephrotic syndrome

61. The total amount of chlorine in an average
adult is about 80 gm
Chlorine, in the form of chloride ions, is the
chief anion of extracellular compartment
Normal serum chloride level is 98-107 mEq/L
(355-375 mg/dl)
D. Chloride

62. The chloride content of cerebrospinal fluid is 120
to 130 mEq/L
The interstitial fluid contains about 110 mEq/L
The intracellular fluid contains only about 4
mEq/L
D. Chloride

63. Functions
Maintenance of osmotic pressure
Maintenance of pH
Formation of hydrochloric acid
D. Chloride

64. Serum: venous blood sample in gel vaccutainer
Urine:
 24 hrs urine collection
 No preservative is required
 Store at 2-8 degree
Sample collection
D. Chloride
Method of estimation
By Ion Selective Electrode

65. Abnormal serum chloride levels
 Changes in serum chloride level are parallel to those in
serum sodium level.
 Serum chloride level is raised (hyperchloraemia) in
dehydration, respiratory alkalosis, metabolic acidosis
and adrenocortical hyperactivity.
 Serum chloride level is decreased (hypochloraemia) in
severe vomiting, prolonged gastric suction, respiratory
acidosis, metabolic alkalosis and Addison’s disease.
D. Chloride

66. DIURETICS AND ELECTROLYTE

67. Classification of Diuretics
(According to the site of action)
DRUGS USED IN RENAL DISORDERS
Drugs that modify Drugs that modify
salt excretion water excretion
PCT TAL DCT CCT Osmotic diuretics ADH ADH
agonist antagonist
K+-sparing
diuretics
Thiazides
Loop
diuretics
Carbonic
anhydrase
inhibitors

68. PROXIMAL
CONVULATED
TUBULE

69. 1. PROXIMAL CONVULATED TUBULE
1. Direct entry of Na+
2. Na+/ K+ pump @ BL membrane : Transfer of Na+
and K+ along with glucose, amino acids and other
organic anions & PO4
-3
3. Exchange of H+ @ Luminal Membrane:
Proximal tubule cells secrete H+ with the help of
carbonic anhydrase.
4. Large amount of HCO3
-, amino acid, acetate
along with Cl-

70. Hypo Na
Hypo HCO3
Metabolic
Acidosis

71. Diuretic acting on PCT
1. Carbonic anhydrase inhibitors:
Acetazolamide
 Mechanism : Inhibit CAH enzyme in
tubular cell & lumen
 Effects on serum electrolytes:
• Hypo Na+
• Low HCO3
- Metabolic acidosis

72. Loop of Henle

73. 2a. LOOP OF HENLE
(DESCEDING LOOP OF HENLE)
• The filtrate entering: isotonic
• Water absorption thereafter
• Tubular fluid becomes concentrated (Hypertonic)
(Three fold increase in salt concentration).
2b. LOOP OF HENLE
(ASCENDING LOOP OF HENLE)
1. ASCENDING LOOP OF HENLE (Medullary part lined by
cuboidal cells).
• Unique, Impermeable to water

74. • Active reabsorption of Na+, K+ & Cl- is mediated by
a Na+/K+/2Cl- Cotransporter.
• Mg++ and Ca++ enter the interstitial fluid.
• 25% to 30% of tubular NaCl returns to the Fluid
(blood).
2. ASCENDING LOOP OF HENLE (Cortical part lined by
flattened cells).
• Impermeable to water
• Salt reabsorption continues through Na+
electrochemical gradient transport

76. Diuretic acting on Thick Asc. Loop Henle
1. Na+ K+/ 2CL- symporter inhibitor
Furosemide
 Effects on electrolytes:
• Hypo Na +
• Hypo K +
• Hypo Cl- -Hypochloremic Alkalosis
• Hypo Mg ++
• Hypo Ca++
Note: Magnesium and Calcium reabsorption in the thick
ascending limb is dependent on the positive lumen voltage
gradient set up by potassium recycling through renal outer
medullary potassium channel, loop diuretics also inhibit
their reabsorption

77. Hypo
Na+
Hypo
K+
Hypo
Cl-
Hypo
Ca/Mg

78. DISTAL
CONVULATED
TUBULE

79. 3. DISTAL CONVULATED TUBULE
• Impermeable to water.
• 10% of NaCl is reabsorbed
• Na+/Cl- transporter (inhibited by Thiazide)
• Calcium reabsorption: Na+/Ca++ exchanger into
the interstitial fluid.
• Ca++ excretion: PTH

80. Diuretic acting on DCT
1. Na+/ CL- Symporter
Thiazide
 Effects on electrolytes:
• Hypo Na +
• Hypo Cl- -Hypochloremic Alkalosis
• Hyper Ca++
Note: By lowering the sodium concentration within the
epithelial cells, thiazides increase the activity of the Na+/Ca2+
anti-porter on the basolateral membrane to transport more
Ca2+ into the interstitium. This, in turn, decreases the
intracellular Ca2+.

81. Thiazides
Hypo
Na+
Hyper
Ca++
Hypo
Cl-
Hypo H+
Metabolic Alkalosis
Slow down

82. COLLECTING
TUBULES
&
DUCT

83. 4. COLLECTING TUBULE & DUCT
• Aquaporins: Water Absorption – ADH dependent
• Na+ absorption @ Luminal membrane:
aldosterone dependent (inhibited by amiloride)
• Na+/K+-ATPase @ BL membrane: aldosterone
dependent

85. A. PCT
1. Na+: Direct entry
Na+/ K+ pump @ BL membrane
2. Glucose, amino acids, PO4
-3 & organic anions :
Active transport along with sodium
3. HCO3
-, acetate, Cl-: Passive diffusion
B. Loop of Henle:
a. Descending loop:
1. Water
b. Ascending loop:
1. Active reabsorption of Na+, K+ & Cl- :
Na+/K+/2Cl- Cotransporter.
2. Mg++ and Ca++: Gradient
3. Na+ electrochemical gradient transport
Summary of sites of renal reabsorption of filtrate

86. C. DCT
1. Na+/Cl- transporter (inhibited by Thiazide)
2. Calcium reabsorption: Na+/Ca++ exchanger
into the interstitial fluid.
D. Collecting Duct
1. Aquaporins: Water Absorption – ADH
dependent
2. Na+ absorption @ Luminal membrane:
aldosterone dependent (inhibited by
amiloride)
3. Na+/ K+-ATPase @ BL membrane: aldosterone
dependent