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ELECTROLYTES
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ELECTROLYTES
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ELECTROLYTE FUNCTIONS
• Volume and osmotic regulation
• Myocardial rhythm and contractility
• Cofactors in enzyme activation
• Regulation of ATPase ion pumps
• Acid-base balance
• Blood coagulation
• Neuromuscular excitability
• Production of ATP from glucose
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ELECTROLYTE PANEL
• Panel consists of:
● sodium (Na)
● potassium (K)
● chloride (Cl)
● bicarbonate CO2 (in its ion form = HCO3- )
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ANALYTES OF THE ELECTROLYTE
PANEL
• Sodium (Na)–
● the major cation of extracellular fluid
● Most abundant (90 %) extracellular cation
● Diet
• Easily absorbed from many foods
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FUNCTION: SODIUM
• Neuromuscular excitability
● extremes in concentration can result in neuromuscular
symptoms
• Na-K ATP-ase Pump
● pumps Na out and K into cells
● Without this active transport pump, the cells would fill
with Na+ and subsequent osmotic pressure would rupture
the cells
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REGULATION OF SODIUM
• Concentration depends on:
● intake of water in response to thirst
● excretion of water due to blood volume or osmolality
changes
• Renal regulation of sodium
● Kidneys can conserve or excrete Na+ depending on ECF
and blood volume
• by aldosterone
• Serum
● 136-145 mEq/L or mmol/L
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SODIUM
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DISORDERS OF SODIUM
HOMEOSTASIS
• Hyponatremia: < 136 mmol/L
● Causes of:
• Increased Na+ loss
• Water imbalance
• Increased intake/retention
● hypoadrenalism
• Diabetes mellitus
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HYPONATREMIA
• Renal failure
• Nephrotic syndrome
• Hepatic cirrhosis
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HYPONATREMIA
• Chronic condition
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SODIUM
Note:
• Increased lipids or proteins may cause false
decrease in results. This would be classified as
artifactual/pseudo-hyponatremia
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CLINICAL SYMPTOMS OF
HYPONATREMIA
• Neurological
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HYPERNATREMIA
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HYPERNATREMIA
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CLINICAL SYMPTOMS OF
HYPERNATREMIA
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SPECIMEN COLLECTION: SODIUM
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ANALYTES OF THE ELECTROLYTE
PANEL
• Potassium (K+)
● the major cation of intracellular fluid
• Only 2 % of potassium is in the plasma
• exchanges 3 Na for 1 K
● Diet
• easily consumed by food products such as
bananas 22
FUNCTION: POTASSIUM
• Critically important to the functions of
neuromuscular cells
● Acid-base balance
● Intracellular fluid volume
● Controls heart muscle contraction
● Promotes muscular excitability
• Decreased potassium decreases
excitability (paralysis and
arrhythmias)
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REGULATION OF
POTASSIUM
• Kidneys
● Responsible for regulation. Potassium is readily
excreted, but gets reabsorbed in the proximal tubule -
under the control of ALDOSTERONE
• Diet
• Cell Uptake/Exchange
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REFERENCE RANGES:
POTASSIUM
• Serum (adults)
● 3.5 - 5.1 mEq/L or mmol/L
• Newborns
● 3.7 - 5.9 mEq/L
• Urine (24 hour collection)
● 25 - 125 mEq/L
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DISORDERS OF POTASSIUM
HOMEOSTASIS
• Hypokalemia
● < 3.5 mmol/L
● Causes of:
• Non-renal loss
• Renal Loss
• Cellular Shift
• Decreased intake
• Hyperkalemia
● >5.1 mmol/L
● Causes of
• Decreased renal excretion
• Cellular shift
• Increased intake
• Artifactual/False elevations
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HYPOKALEMIA
1. Non-renal loss
● Excessive fluid loss ( diarrhea,
vomiting, diuretics )
● Increased Aldosterone promote Na
reabsorption … K is excreted in
its place
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HYPOKALEMIA
2. Renal Loss
● Nephritis, renal tubular acidosis,
hyperaldosteronism, Cushing’s
Syndrome
3. Cellular Shift
● Alkalosis, insulin overdose
4. Decreased intake
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MECHANISM OF
HYPOKALEMIA
• Increased plasma pH ( decreased Hydrogen ion )
RB
C H
+
K
+
• Neuromuscular weakness
• Cardiac arrhythmia
• Constipation
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HYPERKALEMIA
1. Decreased renal excretion
● Renal disease
● Addison’s disease
● Hypoaldosteronism
2. Cellular Shift
● Such as acidosis, chemotherapy, leukemia,
muscle/cellular injury
● Hydrogen ions compete with potassium to get into
the cells
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HYPERKALEMIA
3. Increased intake
• Insulin IVs promote rapid cellular potassium
uptake
4. Artifactual
• Sample hemolysis
• Prolonged tourniquet use
• Excessive fist clenching
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CLINICAL SYMPTOMS OF
HYPERKALEMIA
• Muscle weakness
• Tingling
• Numbness
• Mental confusion
• Cardiac arrhythmias
• Cardiac arrest
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SPECIMEN COLLECTION:
POTASSIUM
• Non-hemolyzed serum
• heparinized plasma
• 24 hr urine
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ANALYTES OF THE ELECTROLYTE
PANEL
• Chloride (Cl-)
● The major anion of extracellular fluid
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FUNCTION: CHLORIDE
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REGULATION OF
CHLORIDE
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REFERENCE RANGES: CHLORIDE
• Serum
● 98 -107 mEq/L or mmol/L
• 24 hour urine
● 110-250 mEq/L
● varies with intake
• CSF
● 120 - 132 mEq/L
● Often CSF Cl is decreased when CSF protein is
increased, as often occurs in bacterial meningitis.
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DETERMINATION: CHLORIDE
• Specimen type
● Serum
● Plasma
● 24 hour urine
● CSF
● Sweat
• Sweat Chloride Test
• Used to identify cystic fibrosis patients
• Hyperchloremia
● Increased blood chloride
● Causes of:
• Conditions where input exceeds output
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HYPOCHLOREMIA
• Decreased serum Cl
● loss of gastric HCl
● salt loosing renal diseases
● metabolic alkalosis/compensated respiratory acidosis
• increased HCO3- and decreased Cl-
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HYPERCHLOREMIA
• Increased serum Cl
● dehydration (relative increase)
● excessive intake (IV)
● congestive heart failure
● renal tubular disease
● metabolic acidosis
• decreased HCO3- & increased Cl-
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ANALYTES OF THE ELECTROLYTE
PANEL
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FUNCTION:
BICARBONATE ION
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REGULATION OF
BICARBONATE ION
● Bicarbonate is regulated by
secretion / reabsorption of the renal
tubules
● Acidosis: decreased renal excretion
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REGULATION OF
BICARBONATE ION
• Kidney regulation requires the enzyme carbonic
anhydrase - which is present in renal tubular cells &
RBCs
carbonic anhydrase
Pulmonary Control
Renal
Control 46
REFERENCE RANGE:
BICARBONATE ION
• Total Carbon dioxide (venous)
● 23-29 mEq/L or mmol/L
• includes bicarb, dissolved and undissociated H2CO3 -
carbonic acid (bicarbonate)
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SPECIMEN COLLECTION:
BICARBONATE ION
● heparinized plasma
● arterial whole blood
● fresh serum
● Anaerobic collection preferred
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ELECTROLYTE BALANCE
• Aniongap (AG)
• Difference between unmeasured anions and cations
• Useful to detect instrument issues
• Clinical Applications
• Increased AG –
• uncontrolled diabetes (due to lactic & keto acids)
• severe renal disorders
• Hypernatremia
• lab error
• Decreased AG -
• a decrease AG is rare, more often it occurs when
one test/instrument error
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ANION GAP
• Anion Gap Calculations
Or
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REFERENCES
• Bishop, M., Fody, E., & Schoeff, l. (2010). Clinical
Chemistry: Techniques, principles, Correlations. Baltimore:
Wolters Kluwer Lippincott Williams & Wilkins.
• http://thejunction.net/2009/04/11/the-how-to-authority-for-
donating-blood-plasma/
• http://www.nlm.nih.gov/medlineplus/ency/article/002350.ht
m
• Sunheimer, R., & Graves, L. (2010). Clinical Laboratory
Chemistry. Upper Saddle River: Pearson .
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