An electrolyte disorder is an imbalance of certain
(i.e., bicarbonate, calcium, chloride, magnesium, phos
phate, potassium, and sodium) in the blood.
Electrolytes are ionized molecules found throughout
the blood, tissues, and cells of the body.
General Functions of Electrolytes
Help to balance pH and acid-base levels in the body.
Facilitate the passage of fluid between and within
cells through osmosis
• Play a part in regulating the function of the
neuromuscular, endocrine, and excretory systems.
Specific Electrolytes – Functions
• Helps to balance fluid levels in the body and
• Facilitates neuromuscular functioning.
• Potassium (K)
• Main component of cellular fluid
• Helps to regulate neuromuscular function and
Affects neuromuscular performance and
Contributes to skeletal growth
Influences muscle contractions and
Regulates blood pressure.
Impacts metabolism and
regulates acid-base balance and
Assists in the regulation of blood pH levels
Treatment of Hypernatremia
Acute Hypernatremia can be corrected rapidly
Chronic Hypernatremia (more than 48 hours) should
be corrected slowly.
If hypernatremia is rapidly corrected, the osmotic
imbalance may cause cerebral edema and potentially
severe neurologic impairment.
Aim for serum sodium correction of approximately 12
mol/L/24h (0.5 mmol/L/h)
Volume in (L) to be replaced = Current TBW × [Na] – 140
where TBW is typically 50% of total mass in women and
55% of total mass in men.
Hypernatremia with hypovolemia
Patients should receive isotonic 0.9% normal saline to
restore euvolemia and to treat hyperosmolality
After adequate volume resuscitation with normal
saline, 0.45% saline or 5% dextrose (or both) can be
used to replace any remaining free water deficit.
Hypernatremia with euvolemia
Water ingestion or intravenous 5% dextrose will result
in the excretion of excess sodium in the urine.
Hypernatremia with hypervolemia
Furosemide (1mg/kg) to get rid of sodium + Free water
replacement as 5% D/W
• (* furosemide alone will aggravate the
• Dialysis may be required for patients with oliguric
(Serum sodium less than 135
mEq/L)of all hospitalized patients develop
Up to 1%
hyponatremia, making it one of the most common
Hyponatremia usually reflects excess water retention
relative to sodium rather than sodium deficiency.
The clinician should be wary about hyponatremia
since mismanagement can result in neurologic
catastrophes from cerebral osmotic demyelination.
Symptoms andis Signs depends on its
Whether hyponatremia symptomatic
severity and acuity.
Chronic disease can be severe (sodium concentration <
110 mEq/L), yet remarkably asymptomatic because the
brain has adapted by decreasing its tonicity over weeks
Acute disease that has developed over hours to days
can be severely symptomatic with relatively modest
The most serious complication of hyponatremia is
iatrogenic cerebral osmotic demyelination from overly
rapid sodium correction.
Also called central pontine myelinolysis.
Demyelination may occur days after sodium
correction or initial neurologic recovery from
The neurologic effects are generally catastrophic and
Correction of Hyponatremia
Treatment depends on:
Etiology and types of hyponatremia
Serum Na level
Regardless of the patient’s volume status, another
common feature is to restrict free water and hypotonic
fluid intake, since these solutions will exacerbate
Free water intake from oral intake and intravenous
fluids should generally be < 1–1.5 L/d.
Require adequate fluid resuscitation from isotonic
fluids (either normal saline or lactated Ringer
solution) to suppress the hypovolemic stimulus for
Patients with cerebral salt wasting may require
hypertonic saline to prevent circulatory collapse; some
may respond to fludrocortisone.
May require loop diuretics or dialysis, or both, to
correct increased total body water and sodium.
To treat the basic CAUSE.
May respond to free water restriction alone.
a non edematous, severely symptomatic 70 kg woman
with a serum sodium of 122 mEq/L should have her
serum sodium corrected to approximately 132 mEq/L
in the first 24 hours. Her sodium deficit is calculated
3% hypertonic saline has a sodium concentration of
514 mEq/1000 mL. The delivery rate for hypertonic
saline can be calculated as:
Hypertonic saline in hyper-volemic patients can be
hazardous, resulting in worsening volume
overload, pulmonary edema, and ascites.
• Normal : 3.5-5.5 mEq/L
Main component of cellular fluid
Helps to regulate neuromuscular function and
S. Potassium > 5.5 m Eq/L
Signs and Symptoms
Tingling, numbness, or other unusual sensations
ECG changes in hyperkalemia include bradycardia, PR
interval prolongation, peaked T waves, QRS
widening, and biphasic QRS–T complexes.
Conduction disturbances, such as bundle branch block
and atrioventricular block, may occur.
Ventricular fibrillation and cardiac arrest are terminal
Hyperkalemia - Etiology
What Causes It?
Inadequate Excretion :
• Renal failure
• Addison’s disease
• Excessive intake
• Diet high in potassium
(bananas, oranges, tomatoes, dates, high protein
diets, salt substitutes, potassium supplements)
Shifting of potassium from tissues
• Trauma, especially crush injuries or burns
• Insulin deficiency
• Digoxin, scuuinyl choline, beta agonists, potassium
Treatment of Hyperkalemia
Mild: (Serum K+ = 5.5 to 6.0 m Eq/L)
Stop intake of potassium
• Stop offending drugs
Restrict potassium rich diet
Moderate to Severe: (in addition to above..)
(Serum K+ = 6.0 to 8.0 m Eq/L or peaked T
• Glucose Insulin Infusion : (0.5g/kg with 0.3 U
regular insulin / g of glucose)
• Sodabicarb infusion (2 mEq/kg of NaHCO3 over 5
– 10 min)
IV Calcium gluconate 0.5 mEq/kg – to reverse cardiac
• Dialysis in cases of resistant hyperkalemia
• Nebulized salbutamol
• Sodium polyesterene sulphate - ion exchange resin
for long term management
Symptoms and Signs
Muscular weakness, fatigue, and muscle cramps are
frequent complaints in mild to moderate hypokalemia.
Gastrointestinal smooth muscle involvement may
result in constipation or ileus.
paralysis, hyporeflexia, hypercapnia, tetany, and
rhabdomyolysis may be seen with severe hypokalemia
(< 2.5 mEq/L).
Urinary potassium concentration is low (< 20 mEq/L)
as a result of extrarenal loss (eg, diarrhea, vomiting)
and inappropriately high (> 40 mEq/L) with renal
loss (eg, mineralocorticoid excess, Bartter
syndrome, Liddle syndrome)
The electrocardiogram (ECG) shows decreased
amplitude and broadening of T waves, prominent U
waves, premature ventricular contractions, and
depressed ST segments.
Treatment of Hypokalemia
Oral potassium supplementation is the safest and
easiest treatment for mild to moderate deficiency.
Intravenous potassium is indicated for patients with
severe hypokalemia and for those who cannot take oral
For severe deficiency, potassium may be given through
a peripheral intravenous line in a concentration up to
40 mEq/L and at rates up to 10 mEq/h.
Concentrations of up to 20 mEq/h may be given
through a central venous catheter.
Continuous ECG monitoring is indicated, and the
serum potassium level should be checked every 3–6
Magnesium deficiency should be
corrected, particularly in refractory hypokalemia.
Formula for correction of
Required K+ in mmol = 0.3 × Weight × [ Desired K+
level – Measured K+ level]
Deficit corrected over 24 hour period.
Multiple bone fractures,
• Milk-alkali syndrome, and
• Paget's disease.
• Excessive use of calcium-containing supplements
• Certain over-the-counter medications
(i.e., Antacids) may also cause hypercalcemia.
HYPERCALCEMIA - Management
Forced saline diuresis with fruesemide
Treat primary cause
Bisphosphonates are the treatment of choice for
hypercalcemia of malignancy. Although they are safe,
effective, and normalize calcium in > 70% of patients,
bisphosphonates may require up to 48–72 hours before
reaching full therapeutic effect.
Calcitonin may be helpful in the short-term until
bisphosphonates reach therapeutic levels.
In emergency cases, dialysis with low calcium dialysate
may be needed.
Exogenous sources of magnesium should be
Calcium antagonizes Mg2+ and may be given
intravenously as calcium chloride, 500 mg or more at a
rate of 100 mg (4.1 mmol) per minute.
Hemodialysis or peritoneal dialysis may be necessary
to remove magnesium, particularly with severe kidney