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Body water (~60% of body weight) is distributed between intracellular fluid (ICF, ~67%) and extracellular fluid (ECF, ~33%, split between interstitial fluid and plasma). Osmolarity is maintained near 290 mOsm/kg by ADH and thirst mechanisms; electrolyte imbalances (hyponatremia, hyperkalemia, etc.) have serious neuromuscular and cardiac consequences. Blood pH is tightly maintained at 7.35–7.45 by three systems with different time constants: chemical buffer systems (bicarbonate, phosphate, protein — seconds), respiratory compensation (minutes), and renal compensation (hours to days). Acid-base disorders are classified as metabolic or respiratory and as acidosis or alkalosis, each with predictable compensatory responses.
Use the 'tic-tac-toe' ABG interpretation method on real arterial blood gas cases. Map out each fluid compartment's ionic composition to understand why IV fluids must be isotonic and why K⁺ disorders affect cardiac rhythm.
The human body is roughly 60% water by weight, but that water is not uniformly distributed. About two-thirds resides *inside* cells as intracellular fluid (ICF), where it participates in metabolism and maintains cell volume. The remaining third is extracellular fluid (ECF), split between the interstitial fluid bathing cells and the plasma circulating in blood. Each compartment has a distinct ionic composition: the ICF is rich in K⁺, Mg²⁺, and phosphate, while the ECF is dominated by Na⁺ and Cl⁻. These gradients are not accidents — they are actively maintained by ion pumps and are essential for generating membrane potentials and supporting neural and muscular function.
Water moves between compartments by osmosis — always toward the compartment with higher solute concentration. Osmolarity (the total concentration of solutes) is normally held near 290 mOsm/kg in all compartments; deviations are detected by osmoreceptors in the hypothalamus, which trigger ADH release or thirst. ADH tells the kidney collecting ducts to reabsorb more water, concentrating urine and diluting plasma back toward normal. When you drink too much plain water, you dilute plasma Na⁺ faster than ADH can adjust, producing hyponatremia. When you are severely dehydrated, the priority is restoring isotonic volume — so IV fluids matched to plasma osmolarity are preferred over plain water.
Electrolyte imbalances have clinical consequences that follow directly from membrane physiology. Sodium sets the ECF osmolarity and cell volume; hyponatremia causes cells to swell (cerebral edema), while hypernatremia causes them to shrink. Potassium governs the resting membrane potential of excitable cells; hyperkalemia depolarizes cardiac myocytes, disrupting conduction and risking fatal arrhythmia. Calcium affects neuromuscular excitability; hypocalcemia causes tetany, while hypercalcemia causes muscle weakness and kidney stones.
Blood pH is maintained at 7.35–7.45 by three buffer systems that operate on very different timescales. Chemical buffers (primarily bicarbonate/carbonic acid, but also phosphate and plasma proteins) respond in seconds by accepting or donating H⁺. The respiratory system responds in minutes by adjusting ventilation: hyperventilating blows off CO2, reducing carbonic acid and raising pH; hypoventilating retains CO2, lowering pH. The kidneys respond over hours to days by adjusting bicarbonate reabsorption, H⁺ secretion, and ammonia synthesis.
A critical clinical distinction: compensation is not correction. A patient with metabolic acidosis (e.g., from diabetic ketoacidosis) will hyperventilate to blow off CO2, raising pH somewhat — but pH will not return to 7.40 until the underlying ketoacidosis is treated. Compensation limits the pH change; only treating the root cause resolves the disorder. Arterial blood gas interpretation relies on this framework: identify whether the primary problem is metabolic or respiratory, then assess whether appropriate compensation is present.