Disorders of Fluid, Electrolyte, and Acid–Base Balance

Intracellular Fluid (ICF)

Located inside cells; contains about two thirds of body water.

Extracellular Fluid (ECF)

Located outside cells; includes interstitial, intravascular, and transcellular fluid.

Major Intracellular Cation

Potassium (K⁺)

Major Extracellular Cation

Sodium (Na⁺)

Diffusion

Movement of particles from high concentration to low concentration.

Osmosis

Movement of water across a semipermeable membrane toward higher solute concentration.

Hypotonic Solution Effect

Water moves into cells, causing them to swell.

Hypertonic Solution Effect

Water moves out of cells, causing them to shrink.

Isotonic Solution Effect

No major net movement of water; cell volume remains relatively stable.

Antidiuretic Hormone (ADH)

Promotes water conservation by causing kidneys to reabsorb more water.

Renin-Angiotensin-Aldosterone System (RAAS)

Hormones responding to low renal perfusion to restore blood volume and blood pressure.

Aldosterone Function

Promotes sodium reabsorption and potassium excretion in the kidneys.

Natriuretic Peptides

Promote sodium and water excretion and reduce RAAS activity when heart chambers are stretched.

Fluid Volume Deficit Causes

Vomiting, diarrhea, hemorrhage, sweating, diuretics, burns, and poor intake.

Fluid Volume Deficit Pathophysiology

Fluid loss reduces ECF volume, venous return, stroke volume, cardiac output, and tissue perfusion.

Fluid Volume Excess Causes

Heart failure, kidney failure, excessive sodium or IV fluids, and cirrhosis.

Fluid Volume Excess Pathophysiology

Sodium and water retention increase ECF volume and capillary hydrostatic pressure, leading to edema.

Third Spacing

Fluid becomes trapped where it is not readily available for circulation (e.g., ascites, peritonitis).

Sodium Core Concept

Major extracellular cation; primary determinant of ECF osmolality and water balance.

Hyponatremia Pathophysiology

Extracellular Na⁺ decreases, lowering ECF osmolality and causing water to enter cells, leading to brain swelling.

SIADH Mechanism

Excess ADH causes water retention, diluting serum sodium and resulting in concentrated urine.

Hypernatremia Pathophysiology

ECF Na⁺ increases, causing water to leave cells, leading to cellular dehydration and brain cell shrinkage.

Diabetes Insipidus Mechanism

Lack of ADH leads to inability to conserve water, large volume of dilute urine, and hypernatremia.

SIADH vs. Diabetes Insipidus

SIADH causes low serum sodium and concentrated urine; DI causes high serum sodium and dilute urine.

Potassium Core Concept

Major intracellular cation essential for resting membrane potential, nerve conduction, and cardiac conduction.

Hypokalemia Causes & Findings

Caused by diuretics, vomiting, diarrhea, insulin shift; leads to muscle weakness, cramps, and dysrhythmias.

Hyperkalemia Causes & Findings

Caused by kidney failure, acidosis, tissue destruction; leads to weakness, paresthesias, and peaked T waves.

Potassium & Acid-Base Interaction

In acidosis, H⁺ moves into cells and K⁺ moves out (serum K⁺ rises); in alkalosis, K⁺ moves in (serum K⁺ falls).

Calcium Regulation

Regulated by parathyroid hormone (PTH), vitamin D, calcitonin, and kidneys. PTH raises serum calcium.

Hypocalcemia Signs

Increased neuromuscular excitability; classic signs include Chvostek and Trousseau signs, tetany, and seizures.

Hypercalcemia Signs

Decreased neuromuscular activity; findings include weakness, constipation, confusion, and kidney stones.

Magnesium Function

Essential for enzyme activity, neuromuscular function, cardiac conduction, and potassium regulation.

Low vs. High Magnesium Pattern

Low Mg causes neuromuscular excitability (tremors, hyperreflexia); high Mg causes depression (weakness, respiratory depression).

Phosphate Role

Essential for ATP production, bone mineralization, and acid-base buffering; inverse relationship with calcium.

Buffer Systems Speed

Chemical buffers act within seconds; lungs act within minutes; kidneys act within hours to days.

Respiratory Acidosis Cause

Hypoventilation leading to CO₂ retention and increased carbonic acid.

Respiratory Alkalosis Cause

Hyperventilation leading to excessive CO₂ loss and decreased PaCO₂.

Metabolic Acidosis Causes

Bicarbonate loss or acid accumulation, seen in DKA, lactic acidosis, severe diarrhea, and kidney failure.

DKA Mechanism

Insulin deficiency causes increased fat breakdown, ketone production, metabolic acids, and consumption of HCO₃⁻.

Metabolic Alkalosis Causes

Excess acid loss or bicarbonate gain, commonly from vomiting, gastric suction, or diuretics.

ROME Mnemonic

Respiratory Opposite (pH and PaCO₂ move inversely), Metabolic Equal (pH and HCO₃⁻ move in same direction).

Respiratory Acidosis ABG Pattern

Low pH, high PaCO₂ due to hypoventilation.

Respiratory Alkalosis ABG Pattern

High pH, low PaCO₂ due to hyperventilation.

Metabolic Acidosis ABG Pattern

Low pH, low HCO₃⁻ seen in DKA, diarrhea, and renal failure.

Metabolic Alkalosis ABG Pattern

High pH, high HCO₃⁻ seen in vomiting, NG suction, and diuretics.

Compensation Mechanism

Kidneys compensate for respiratory disorders; lungs compensate for metabolic disorders to restore pH toward normal.