Electrolyte Imbalance Disorders

GNUR 293: Pathophysiology

Sodium Normal Range

135-145 mEq/L

Potassium Normal Range

3.5-5.0 mEq/L

Total Calcium Normal Range

8.5-10.5 mEq/L

Ionized Calcium Normal Range

4.5-5.6 mEq/L

Magnesium Normal Range

1.8-3.0 mEq/L

Chloride Normal Range

95-105 mEq/L

Phosphate Normal Range

2.5-4.5 mEq/L

Cations

Positively charged ions

Anions

Negatively charged ions

-emia

“in the blood”

What hormones influence Electrolyte Distribution?

Insulin and the Parathyroid hormone

Paracentesis

Medical procedure of using a needle/catheter to drain ascites from the peritoneal cavity in the abdomen - Way of electrolyte loss

Ascites

Abnormal buildup of excess fluid inside the abdominal cavity

Hemodialysis

Medical procedure using an artificial machine and filter to clean the blood when kidneys fail - Way of electrolyte loss

Fistula

An abnormal tunnel or hollow connection that forms between two body parts

Hyponatremia

Excess of water in proportion to salt (Decreased sodium) due to LOSS of sodium or GAIN of water. Cells SWELL

Hypernatremia

Excess of salt in proportion to water (Increased sodium) due to LOSS of water or GAIN of sodium. Cells SHRINK

Hyponatremia Clinical Manifestations

Malaise (weakness), Anorexia, Nausea, Vomiting, Headaches, Confusion, Lethargy, Seizures, Coma, Cerebral herniation

Hypernatremia Clinical Manifestations

Thirst, Oliguria, Confusion, Lethargy, Seizures, Coma, Death

Potassium (K+) function

-Nerve, skeletal, smooth & cardiac muscle transmission and conduction.

-Resting membrane potential

-Normal cardiac rhythms

-Cell growth and function

-Acid-base balance

Hypokalemia

Decreased K+ in ECF due to decreased INTAKE, increased EXCRETION, EXCESS INSULIN (pushing K+ from ECF into cell)

Hypokalemia Clinical Manifestations

-Altered muscle function and weakness

-Arrythmias & Ectopic cardiac rhythms

-Diminished GI/GU symptoms

Hyperkalemia

Increased K+ in the ECF due to increased INTAKE, decreased EXCRETION, shifts of potassium into the ECF

Hyperkalemia Clinical Manifestations

-Intestinal cramping

-Diarrhea

-Muscle weakness

-Cardiac dysrhythmias

-Cardiac arrest

Hypokalemia Excitability Imbalance

Low excitement, harder to reach threshold.

Hyperkalemia Excitability Imbalance

Chronically activated, easily excitable to reach threshold.

Serum Calcium Forms

1. Bound to Plasma Proteins

2. Bound to Small organic ions

3. Unbound

Serum Calcium Regulating hosts

Parathyroid hormone and Calcitriol (Active VitD)

Serum Calcium functions

-Transmission of nerve impulses

-Myocardial contractions

-Blood clotting

-Bone and teeth formation

-Muscle contractions

Hypocalcemia

Low IONIZED calcium levels, PTH secretion (release calcium from bones, increase absorption). Caused by decreased INTAKE, ABSORPTION, AVALIABILITY, or increased EXCRETION.

Hypocalcemia Clinical Manifestations

Increased excitability of neuromuscular cells (hyperactive reflexes, paresthesia’s, twitching, cramping, laryngospasm, seizures, dysrhythmias, secondary hyperthyroidism)

Hypercalcemia

Elevation of calcium CONCENTRATION in ECF. PTH suppressed, decrease calcium release from bone and increase excretion. Caused by increased ABSORPTION or INTAKE, decreased EXCRETION, or extracellular shift of calcium from bone to ECF.

Hypercalcemia Clinical Manifestations

Causes decreased neuromuscular excitability (muscle weakness, hypoactive reflexes, cardiac dysrhythmias, anorexia, nausea, vomiting, fatigue, constipation, headaches, confusion, lethargy, personality change, pathological fractures, Renal Calculi (kidney stones))

Serum Magnesium (Mg²+)

Magnesium ions bound or unbound. Metabolizes protein and carbs, regulate muscle/nerve/BP function, balance neuromuscular junction)

Hypomagnesemia

Decreased level of Magnesium in ECF. Due to decreased INTAKE/ABSORPTION, increased EXCRETION, loss by abnormal route (vomiting)

Hypomagnesemia Clinical Manifestations

Increased neuromuscular excitability due to increased ACH release.

-Hypertension

-Insomnia

-Hyperactive reflexes

-Cramps/twitching

-Nystagmus

-Dysphagia

-Ataxia

-Tetany

-Seizures

-Cardiac Dysrhythmias

Hypermagnesemia

Elevation of Magnesium in the ECF, decreases ACH release from the neuromuscular junction. Caused by increased INTAKE/ABSORPTION, and decreased EXCRETION.

Hypermagnesemia Clinical Manifestations

Reduced neuromuscular excitability/reflexes

-Flaccid paralysis

-Hypotension

-Bradycardia

-Dysrhythmias

-Cardiac arrest

-Lethargy

-Flushing

-Diaphoresis

-Drowsiness

-Respiratory depression

Preeclampsia

Condition in pregnancy with high BP. Give magnesium to treat/lower BP.

Laxative/Antacid Warning

Some contain high amounts of magnesium—assess levels when administrating.

Serum Phosphate

Inverse of Calcium. Aids in bone and teeth formation. Building block for energy, membranes, DNA

Hypophosphatemia

Decreased level of phosphate in ECF, caused by decreased INTAKE/ABSORPTION, increased EXCRETION, intracellular shifts into cells

Hypophosphatemia Clinical Manifestations

-Malaise

-Confusion

-Stupor

-Coma

-Hemolysis

-Muscle aches, weakness

-Respiratory failure

-Impaired cardiac function

-Impaired bone mineralization

Hyperphosphatemia

Elevated levels of phosphate in ECF. Due to increased INTAKE/ABSORPTION, decreased EXCRETION, or extracellular shift into cells

Hyperphosphatemia Clinical Manifestations

-Increased neuromuscular excitability (hyperactive reflexes)

-Compensatory increased PTH

-Phosphate salt deposits

-Joint pain/stiffness

-Severe itching

-Eye irritation/Conjunctivitis