Fluids, Electrolytes, and Acid-Base Balance

Flashcards for reviewing lecture notes on fluid, electrolytes, and acid-base balance.

Sodium (Na+)

The primary ECF cation, regulates osmosis, acid-base balance, cellular reactions, transport, and electrical excitability; regulated by aldosterone and natriuretic peptides.

Chloride (Cl-)

The primary ECF anion, in balance with sodium; involved in neuron inhibition.

Aldosterone

Increases excretion of potassium by the distal tubule of the kidney.

Natriuretic peptides

Decrease tubular resorption, promoting urinary excretion of sodium. Examples include atrial natriuretic peptide, brain natriuretic peptide, and urodilatin.

Antidiuretic hormone (ADH)

Regulates water balance by increasing water reabsorption in the kidneys; release stimulated by osmolality receptors and baroreceptors.

Potassium (K+)

The major intracellular cation; important for electrotransmission in neurons and muscle cells; regulates ICF osmolality.

Calcium (Ca2+)

Mostly stored in bone as hydroxyapatite; important for bone/teeth structure, blood clotting, hormone and neurotransmitter secretion, cell metabolism, and muscle contractions.

Phosphate

Mostly in bone; important for high-energy bonds (ATP), acts as an anion buffer, and is needed for muscle contraction; rigidly inversely controlled with calcium.

Magnesium

An intracellular cation stored mostly in muscle and bone; interacts with calcium, is a cofactor in intracellular reactions, protein synthesis, nucleic acid stability, and neuromuscular excitability.

Hypernatremia

Serum sodium >145 mEq/L, due to sodium gain or water loss; causes water to move out of cells, leading to intracellular dehydration. Treat with isotonic salt-free fluids.

Hyponatremia

Serum sodium level <135 mEq/L, plasma hypoosmolality, cellular swelling.

Hypokalemia

Potassium level <3.5 mEq/L, caused by reduced potassium intake, increased potassium entry into cell, or increased potassium loss; leads to decreased neuromuscular excitability and cardiac dysrhythmias. Treated by K+ replacement.

Hyperkalemia

Potassium level >5.0 mEq/L, causes include increased intake, shift to ECF, decreased renal excretion, hypoxia, acidosis, insulin deficiency, cell trauma, or digitalis overdose; can cause tingling, restlessness, paresis, hypotonia, and paralysis. Treatment involves calcium gluconate, insulin and/or glucose, buffered solutions, or dialysis.

Hypocalcemia

Calcium level <9.0 mg/dL, caused by inadequate intake or absorption, decreased PTH and vitamin D, or blood transfusions; leads to increased neuromuscular excitability, muscle spasms, Chvostek and Trousseau signs, and convulsions. Treated with calcium gluconate, calcium replacement, and decreased phosphate intake.

Hypercalcemia

Calcium level >10.5 mg/dL, caused by hyperparathyroidism, bone metastasis, excess vitamin D, or immobilization; leads to decreased neuromuscular excitability, weakness, kidney stones, constipation, and heart block. Treated with oral phosphate, IV normal saline, bisphosphonates, calcitonin, or denosumab.

Hypophosphatemia

Phosphate level <2.0 mg/dL, causes include intestinal malabsorption and renal excretion, vitamin D deficiency, antacid use, alcohol abuse, or refeeding syndromes; leads to diminished release of oxygen, osteomalacia, muscle weakness, and bleeding disorders.

Hyperphosphatemia

Phosphate level >4.7 mg/dL, causes include addition of phosphate to ECF, chemotherapy, long-term use of phosphate enemas or laxatives, or renal failure; leads to manifestations similar to hypocalcemia with possible calcification of soft tissue.

Hypomagnesemia

From malabsorption, associated with hypocalcemia and hypokalemia; leads to neuromuscular irritability, tetany, and convulsions.

Hypermagnesemia

From renal failure; leads to skeletal muscle depression, muscle weakness, hypotension, respiratory depression, and bradycardia.

Acidosis

pH is less than 7.35; systemic increase in H+ concentration.

Alkalosis

pH is greater than 7.45; systemic decrease in H+ concentration or excess of base.

Respiratory acidosis

Elevation of pCO2 as a result of ventilation depression.

Respiratory alkalosis

Depression of pCO2 as a result of hyperventilation.

Metabolic acidosis

Depression of HCO3− or an increase in noncarbonic acids.

Metabolic alkalosis

Elevation of HCO3− , usually as a result of an excessive loss of metabolic acids.

Lactic acidosis

A cause of metabolic acidosis.

Diabetic ketoacidosis

A cause of metabolic acidosis.

Kussmaul respirations

A manifestation of metabolic acidosis.

Hyperventilation

A compensation mechanism that occurs with Metabolic acidosis as well as anxiety/panic disorders and high altitudes with respiratory alkalosis.

Hypoventilation

Causes CO2 levels to increase and pH to drop which results in Respiratory Acidosis.

Anion gap

Used to distinguish different types of metabolic acidosis.

Respiratory Rate and depth

Controlled in the brainstem's respiratory center and affects the amount of CO2 given off which has an effect on the pH.

Bicarbonate

Can be reabsorbed or regenerated by the kidneys but the kidneys do not act as fast as the lungs related to compensation.

Buffer

Chemical that can bind excessive H+ or OH− without a significant change in pH.

H+ ions number relationship within blood

If H+ is high in number, pH is low (acidic). If H+ is low in number, pH is high (alkaline).

Metabolic Acidosis Manifestations

Headache, Lethargy, Kussmaul respirations

Metabolic Alkalosis Manifestations

Weakness, muscle cramps, and hyperactive reflexes with signs of hypocalcemia

Respiratory Acidosis Manifestations

Headache, restlessness, blurred vision, apprehension, lethargy, muscle twitching, tremors, convulsions, coma

Respiratory Alkalosis Manifestations

Dizziness, confusion, tingling of extremities (paresthesias), convulsions, and coma with signs of hypocalcemia