Electrolytes: Chapter 8 & Acid-Base Balance Intro

Introduction to Electrolytes

• Focus should be on completing the Electrolytes chapter (Chapter 8) and the introduction to acid-base imbalance (Chapter 9).
• Arterial Blood Gas (ABG) problems are likely to appear on the test.
• Attending study sessions improves understanding.

Anions and Cations

• Anions are negatively charged ions.
• Cations are positively charged ions.
• Focus on electrolytes outside the cell (ECF), intracellular values are not required for testing purposes.

Key Electrolyte Values

• Potassium normal range is 3.5–5.0 mEq/L.
• Sodium normal range is 135–145 mEq/L.
• Calcium normal range is 8.2–10.2 mg/dL.
• Chloride normal range is 98–106 mEq/L (97–107 mEq/L in nursing).
• Phosphate normal range is 2.5–4.5 mg/dL.
• Bicarbonate normal range is 22–26 mEq/L.
• Values above normal ranges are "hyper" conditions (e.g., hyperkalemia).
• Values below normal ranges are "hypo" conditions (e.g., hypokalemia).

Regulation of Sodium

• Thirst receptors trigger fluid intake based on osmotic pressure.
• Kidneys filter and reabsorb sodium as needed.
• Renin is released by kidneys in response to low blood volume or pressure as part of the Renin-Angiotensin-Aldosterone System (RAAS).
• Angiotensin II increases sympathetic activity and causes vasoconstriction.
• Aldosterone promotes sodium and water reabsorption and excretes potassium.
• Antidiuretic Hormone (ADH) retains fluids by reducing excretion.

Hyponatremia vs. Hypernatremia

• Hyponatremia occurs when serum sodium levels are less than 135 mEq/L.
• Hyponatremia can be caused by increased water intake, diuretic use, heart failure, renal failure, Addison's disease, or SIADH (Syndrome of Inappropriate ADH).
• Manifestations of hyponatremia include muscle weakness, cramps, seizures (if <110 mEq/L), and nausea.
• Hyponatremia is diagnosed by serum sodium <135 mEq/L, serum osmolality <275 mOsm/kg, and urine osmolality >1.030.
• Treatment for hyponatremia involves fluid restriction, diuretics, and sodium chloride supplementation for extremely low levels.
• Hypernatremia occurs when serum sodium is greater than 145 mEq/L.
• Hypernatremia can be caused by Diabetes Insipidus (DI), excessive salt intake, or dehydration.
• Manifestations of hypernatremia include extreme thirst, increased body temperature, central nervous system disturbances, seizures, and increased blood pressure.
• Hypernatremia is diagnosed by serum sodium >145 mEq/L, serum osmolality >295 mOsm/kg, and urine osmolality <1.005.
• Treatment for hypernatremia involves fluid replacement (oral or IV isotonic/hypotonic solutions).

Diuretics

• Loop diuretics have primo effectiveness.
• Thiazides are next in effectiveness.
• Potassium-sparing diuretics are the least effective.
• All diuretics increase diuresis by releasing sodium, which causes water to follow.
• Loop and Thiazide diuretics can cause hypovolemia and may lead to hypokalemia
• Potassium-sparing diuretics can cause hyperkalemia.
• Thiazides can hold onto calcium, potentially causing hypercalcemia.

SIADH and DI (Diabetes Insipidus)

• SIADH (Syndrome of Inappropriate ADH) is characterized by increased ADH levels, fluid retention leading to dilutional hyponatremia, serum osmolality <275 mOsm/kg, and urine specific gravity >1.030.
• SIADH is treated with fluid restriction, diuretics, and sodium supplementation in severe cases.
• Diabetes Insipidus (DI) is characterized by decreased ADH levels, excessive urination leading to hypernatremia, serum osmolality >295 mOsm/kg, and urine specific gravity <1.005.
• DI is treated with fluid replacement (oral or IV isotonic/hypotonic solutions).

Potassium Regulation

• Potassium functions include heart function, acid-base balance, and neuromuscular excitability.
• Aldosterone promotes potassium excretion, regulated by the RAAS.
• In hyperkalemia, potassium moves into cells, and hydrogen ions move out, potentially causing acidosis.
• In hypokalemia, potassium moves out of cells, and hydrogen ions move in, potentially causing alkalosis.

Hyperkalemia

• Hyperkalemia can be caused by kidney failure, potassium-sparing diuretics, IV potassium overdose, or cell lysis (e.g., crush injuries).
• Manifestations of hyperkalemia include bradycardia, dysrhythmias, and cardiac arrest.
• Hyperkalemia is diagnosed by serum potassium >5.0 mEq/L.
• Treatment for hyperkalemia includes reducing intake, discontinuing potassium-sparing diuretics, administering insulin and glucose, and using calcium to stabilize cardiac cells.

Hypokalemia

• Hypokalemia can be caused by diuretic use (loop and thiazides), vomiting, diarrhea, laxative abuse, or inadequate dietary intake.
• Symptoms of hypokalemia include muscle weakness, cramps, dysrhythmias, and hypokalemia-induced alkalosis.
• Hypokalemia is diagnosed by serum potassium <3.5 mEq/L.
• Increase potassium intake and administer potassium chloride to treat hypokalemia while addressing the underlying causes.

Cushing's and Addison's Diseases

• Cushing's disease is characterized by excess cortisol and aldosterone.
• Effects of Cushing's disease include increased sodium and water retention, potassium excretion leading to hypokalemia, and increased blood pressure.
• Addison's disease is characterized by insufficient cortisol and aldosterone.
• Addison's disease leads to decreased sodium retention, potassium retention resulting in hyperkalemia, and hypotension.

Kidney Failure and Electrolyte Imbalances

• Electrolyte disturbances in kidney failure include hyperkalemia and hyperphosphatemia.
• Additional electrolyte imbalances in kidney failure include hyperchloremia, hypocalcemia, and acidosis.
• Kidney failure can impair RAAS function, reduce Vitamin D activation, and decrease erythropoietin production.
• Treatment considerations for kidney failure include phosphate binders, calcium supplements, and addressing acidosis through bicarbonate administration.

Calcium Regulation

• Calcium functions in bone and teeth health, blood clotting, and neuromuscular excitability.
• Hypocalcemia can be regulated by increased Vitamin D activation in the kidneys and the release of Parathyroid Hormone (PTH) to resorb calcium from bones.
• Hypercalcemia can be regulated by increased release of Calcitonin from the thyroid gland to decrease bone resorption.

Hypocalcemia

• Hypocalcemia can be caused by hypoparathyroidism, malabsorption, kidney failure, or alkalosis.
• Manifestations of hypocalcemia include tingling, muscle cramps, seizures, and positive Trousseau's and Chvostek's signs.
• Hypocalcemia is diagnosed by serum calcium <8.5 mg/dL, serum phosphate >4.5 mg/dL, serum osmolality <275 mOsm/kg.
• Treatment for hypocalcemia includes calcium supplements, Vitamin D supplementation, along with IV calcium chloride in severe cases.

Hypercalcemia

• Hypercalcemia can be caused by hyperparathyroidism, excessive intake of calcium or Vitamin D, or thiazide diuretics.
• Manifestations of hypercalcemia include decreased neuromuscular excitability, constipation, and decreased deep tendon reflexes.
• Hypercalcemia is diagnosed by serum calcium >10.5 mg/dL, serum phosphate <2.5 mg/dL, and serum osmolality >295 mOsm/kg.
• Treatment for hypercalcemia involves reducing calcium intake, discontinuing calcium supplements or thiazides, administering diuretics, or using calcitonin.

Phosphate Regulation

• Phosphate functions in bone health and energy metabolism.
• Hypophosphatemia can be caused by hyperparathyroidism, malabsorption, or excessive phosphate excretion.
• Manifestations of hypophosphatemia include muscle weakness, respiratory failure, and hemolytic anemia.
• Hypophosphatemia is diagnosed by serum phosphate <2.5 mg/dL.
• Hypophosphatemia is treated with phosphate supplements and a dietary phosphate increase.

Hyperphosphatemia

• Hyperphosphatemia can be caused by kidney failure, excessive dietary intake, or cell lysis.
• Manifestations of hyperphosphatemia are often associated with hypocalcemia.
• Hyperphosphatemia is diagnosed by serum phosphate >4.5 mg/dL.
• Treatment for hyperphosphatemia includes phosphate binders and dietary phosphate restriction.