Electrolytes and body fluids
By
Maysa Ibrahim mohamed
Lecturer of clinical pathology
Electrolyte composition of ICF and ECF is
different: ECF, Na is predominant and ICF, K is
predominant
This difference is maintained by membrane
transport pumps (energy consuming ATPases)
Distribution of water between different body spaces is
dependent on permeability of the relevant membranes
and the quantity of the solute within each space
ECF and Na
• Na content is 55- 65 mmol/Kg body wt
• In plasma ~140 mmol/L
• Phys. control of ECF volume is through control of
effective plasma volume (actively perfusing tissues)
Renal control of Na output
Intrinsic renal control of
tubular absorption of Na
Approx. 80% of Na in glomerular filtrate is reabsorbed
in proximal tubule
Renin-angiotensin-aldosterone axis
Na appetite
Natriuritc Peptides
ANP
BNP
Na Deficiency
Causes
1. Extrarenal
GIT: vomiting, aspiration, fistula, blood loss
Pancreatic and biliary fistulae, diarrhea, bleeding,
excess mucous production
Skin: sweating, burns, exudative skin disease
Sequestration: ileus, intestinal obstruction, peritonitis,
pleural effusion
Primary renal
Acute: diuretic phase of ARF (polyuria, natriuresis and
kaliuresis)
Post renal transplantation (transient tubular
dysfunction), following relief or UT
obstruction (prostatic enlargement), acute interstitial
nephritis
Chronic: CRF, salt losing nephropathy (chronic
pyelonephritis, medullary cystic disease, toxic
nephropathies
Secondary renal (hormonal or diuretic)
1- Addison: ↓aldosterone→ Na wasDng
2- Congenital adrenal hyperplasia: Na wasting
(mineralocorticoid synthesis impairment) more
commonly seen with 21 hydroxylase deficiency (2/3 of
cases)
3- Hyporeninaemic hypoaldosteronism
4- Pseudohypoaldosteronism (rare congenital; end organ
failure of response to aldosterone.
5- Infants present with dehydraDon, ↓Na, ↑K, metabolic
acidosis and failure to thrive
6- Diuretic abuse
Lab investigation of Na deficiency
• No single lab finding is diagnostic of Na deficiency and
it remains primarily a clinical diagnosis.
• There may be uremia, particularly in prerenal
pattern (urea disproportionately elevated
compared to creatinine)
Serum Na may be normal, decreased (uremia), or even
increased (when Na deficit is less than the water
deficit)
• Hematocrit may help establish degree of reduction of
ECF
Serum ptn may suggest ECF contraction
• Urine electrolytes: if urine Na is low (< 10 mmol/L
i.e. kidneys properly retaining Na) the loss is
Extra-renal. If urine Na is elevated (> 20 mmol/L)
renal loss is suspected.
Lab investigation of Na deficiency
• Serum osmolality are of no value in DD. (creatinine,
urea, Na)When renal loss of Na is present without
evidence of renal impairment, secondary hormonal or
diureticrelated
Na depletion considered
• Hypoaldosterone related disorders are associated with
↑K
Hypernatermia
Causes
1. Na excess with edema
2. Na excess without edema
a) Congestive heart failure: ↓circulaDng vol→ acDvaDon
of reninangiotensin-aldosterone, release of AVP
b) Nephrotic syndrome (severe glomerular ptnuria,
hypoalbuminemia and edema, 2ndry Na retention)
c) Liver disease→ Na retenDon (↓glomerular filtraDon,
activation of reninangiotensin- aldosterone, enhanced
proximal tubular reabsorption
d) Pregnancy (↑ Na retention, ↑ renin- angiotensin-
aldosterone stimulation, ↑ estrogens)
e) Excess Na retention in preeclampsia
f) Menstrual cycle plasma aldosterone and renin are ↑ in
luteal phase, but is coupled with ↑ progesterone
(antagonize renal acDons of
aldosterone)
g) Idiopathic edema
Na excess without edema
a) Acute Na loading
Acute hypernatremia ++ thirst thus to maintain the
condition, the intake of luid must be prevented by
inability.
b) Renal Na retention
Potassium
ECF, ICF and K
In health, plasma K conc ranges between 3.1-
4.6 mmol/L with serum levels about 0.3- 0.4
higher due to release of K during clotting.
98% of total body K is in the ICF (160 mmol/kg)
IC and EC distribution of K
K content of a cell is determined by a balance of
activity between active uptake of K due to:
membrane bound Na-K-ATPase and the passive loss or
leakage from the cell.
Factors affecting distribution of K
1. Acid base balance
2. Hormones
3. Osmolality
4. Cellular content of K
Acid base status
Association between hypokalemia and alkalosis and
hyperkalemia and acidosis
Insulin
Promotes active uptake of K by cells by direct
stimulation of the Na-K-ATPase.
Catecholamine
Promote cellular uptake of K which explains the
transient ↓K observed in acutely ill patients.
↑ tonicity: Following hyperosmotic infusions of saline,
manitol or with hyperglycemia →↑plasma K due to
leakage as a result of cellular dehydration
Factors regulating distal tubular K secretion
• Intake of Na and K.
• Water flow rate in the DT.
• Mineralocorticoids.
• Acid base balance.
Total body K in a 70 Kg individual 40- 59
mmol/kg, of which 1.5- 2% are present in the
ECF.
Hypokalemia
Plasma K < 3.5 mmol/L
Signs and symptoms of hypokalemia
Cardiovascular , Neuromuscular and Renal/electrolyte
Causes
I. Redistribution
II. True K deficit
In vivo
Initial insulin therapy for diabetic hyperglycemia.
Cells
must take up K along with glucose.
Alkalosis
1.K moves into the ECF while H+ move in opposite
direction
2. renal conservation of H in distal tubules at the expense
of K ions.
3.On the other hand severe IC K depletion → alkalosis
due to intracellular H shift.
•Pseudohypokalemia (intracellular redistribution) due to a
time dependent transport of K into cells after the blood
sample is drawn.
Laboratory Investigation of Hypokalemia
• Lab provides monitoring service
• Fresh sample for Na, K, renal function, acid-base
status
• Differentiate between renal and extrarenal causes: a 24h
urine <25mmol and random sample <20mmol/L or
2mmol/mmol creatinine provide strong evidence of
extrarenal loss
• K not conserved by kidneys, presence of metabolic
acidosis would suggest the cause (RTA, DM, UTI)
Hypokalemia with metabolic alkalosis can be further
differentiated by urine Cl. Random
urine Cl <20mmol/L indicates renal Cl retention and
implies Cl depletion, if Laboratory Investigation of
Hypokalemia >20mmol/L, then Bartter’s syndrome,
Gitelman’s syndrome or diuretic abuse.
In presence of hypertension, glucocorticoid,
mineralocorticoid excess should by considered
Unexplained hypokalemia →Mg to exclude
concomitant Mg depletion
Specimen collection for K
• Serum, heparinized plasma, whole blood,
sweat, urine, feces or GIT fluid.
• Plasma, serum or urine are stored at 2- 4˚C or
frozen for later analysis.
• Hemolysis: if not severe therefore less error as
RBCs contain 1/10 of serum Na.
• Lipaemic samples are ultracentrifuged.
• Fecal and GIT samples are prepared by
filtration and centrifugation.
K levels in plasma and whole blood are 0.1- 0.7
mmol/L lower than serum depending of platelet count
• Minimize hemolysis as an ↑ in K of 0.6% to every
10mg/dl of plasma Hb.
Pre-analytical errors
– Storage: chilling of whole blood → inhibition of Na-K-
ATPase pump, therefore causing a false ↑ in K due to
leakage from RBC.
On the other hand false ↓ K if un-separated sample is
stored at 37˚C
– Leukocytosis: false ↓ K (count, temp., glucose content).
Biphasic: inital ↓ K → glycolysis. ↑K → glucose
exhaustion.
– Muscular activity due to anaerobic glycolysis therefore
decreased ATP production. Prolonged tourniquet
application
Thank you
