Fluid, Electrolyte, and Acid-Base Imbalances

Comprehensive vocabulary flashcards covering fluid compartments, Starling forces, electrolyte imbalances, and acid-base disturbances based on the lecture notes.

60-40-20 Rule

A clinical guideline describing total body water ($\text{TBW}$) distribution in adult males: total body water comprises $60\%$ of total body weight, intracellular fluid ($\text{ICF}$) constitutes $40\%$ ($2/3$ of $\text{TBW}$), and extracellular fluid ($\text{ECF}$) constitutes $20\%$ ($1/3$ of $\text{TBW}$).

Intracellular Compartment (ICF)

The fluid compartment located inside the body's cells, comprising approximately $40\%$ of body weight ($2/3$ of total body water), where potassium ($\text{K}^+$) serves as the primary cation and organic phosphates and proteins serve as the primary anions.

Extracellular Compartment (ECF)

The fluid compartment situated outside of cells, comprising approximately $20\%$ of body weight ($1/3$ of total body water), where sodium ($\text{Na}^+$) is the primary cation and chloride ($\text{Cl}^-$) and bicarbonate ($\text{HCO}_3^-$) are the primary anions.

Interstitial Fluid (ISF)

The intercellular fluid that surrounds tissue cells outside of the vascular system, accounting for approximately $75\%$ of the extracellular fluid ($\text{ECF}$).

Intravascular Fluid (IVF)

The fluid portion of the blood (plasma volume) contained inside the vascular tree, representing roughly $25\%$ of the extracellular fluid ($\text{ECF}$).

Transcellular Fluid

Specialized extracellular fluids located in epithelial-lined cavities, such as cerebrospinal fluid ($\text{CSF}$), synovial fluid, pleural fluid, and pericardial fluid; normally accounts for $< 1\%$ of body fluid, but can expand dramatically in disease states like ascites.

Antidiuretic Hormone (ADH)

A hormone synthesized by the hypothalamus and released by the posterior pituitary in response to increased plasma osmolarity or decreased blood volume; it increases water reabsorption by increasing the permeability of the distal convoluted tubule ($\text{DCT}$) and collecting duct ($\text{CD}$) in the nephron.

Aldosterone

A mineralocorticoid hormone synthesized and released by the adrenal cortex that acts on renal principal cells in the distal convoluted tubule ($\text{DCT}$) to increase $\text{Na}^+$ and $\text{H}_2\text{O}$ reabsorption while promoting $\text{K}^+$ excretion and $\text{H}^+$ secretion.

Atrial Natriuretic Peptide (ANP)

A peptide hormone synthesized and released by atrial cardiac myocytes in response to high blood volume or high atrial pressure; it increases glomerular filtration rate ($\text{GFR}$), inhibits $\text{ADH}$ and the $\text{RAAS}$, promotes renal $\text{Na}^+$ and water excretion, and causes vasodilation to lower blood pressure.

Capillary Hydrostatic Pressure ($P_c$)

The outward 'push' force generated by fluid pressure within the capillary lumen that filters water and small permeable solutes out of the vascular compartment into the interstitial fluid space.

Capillary Oncotic Pressure ($\pi_c$)

The inward 'pull' osmotic force generated by large, impermeable plasma proteins (primarily albumin) in the blood that draws water out of the interstitial space and back into the capillary lumen.

Starling Law of the Capillary

The physiological principle governing trans-capillary fluid exchange, where net filtration pressure ($\text{NFP}$) is determined by the balance between hydrostatic and oncotic pressures: $\text{NFP} = K_f \times [(P_c - P_i) - (\pi_c - \pi_i)]$.

Edema

The abnormal accumulation of an excessive volume of fluid in the interstitial compartment, resulting in localized or generalized tissue enlargement and swelling.

Pitting Edema

A form of soft edema caused by excess mobile free fluid in the interstitial space, clinically demonstrated when firm thumb pressure for $5\text{--}10\text{ seconds}$ produces a persistent visible indentation.

Non-Pitting Edema

A form of firm or rubbery tissue swelling caused by increased tissue solids or lymphatic obstruction (e.g., lymphedema, myxedema, lipedema) where sustained mechanical pressure does not leave a visible pit.

Osmolality

The concentration of all solute particles per kilogram of solvent ($\text{Osm/kg}\,\text{H}_2\text{O}$), which is temperature independent and represents the primary clinical measure of body fluid solute concentration.

Osmolarity

The concentration of solute particles per liter of solution ($\text{Osm/L}$), which varies depending on ambient temperature.

Osmolar Gap

The difference between measured serum osmolality and calculated serum osmolality ($\text{Measured Osmolality} - \text{Calculated Osmolality}$), elevated in the presence of unmeasured low-molecular-weight solutes such as toxic alcohols (methanol, ethylene glycol) or medication infusions (propofol, lorazepam).

Third Spacing

The pathological shift of fluid out of the intravascular compartment into a body cavity or interstitial compartment (such as peritonitis or ascites) where it is physiologically sequestered and unavailable as circulating blood volume.

Hyponatremia

A serum sodium concentration below $135\,\text{mEq/L}$, which causes decreased extracellular osmotic pressure, cell swelling (cerebral edema), fatigue, nausea, vomiting, muscle cramps, and potential seizures.

Hypernatremia

A serum sodium concentration above $145\,\text{mEq/L}$, which causes an osmotic shift of water out of body cells leading to cellular dehydration, intense thirst, flushed skin, restlessness, and neurological dysfunction.

Hypokalemia

A serum potassium concentration below $3.5\,\text{mEq/L}$, typically caused by GI losses, diuretic therapy, or alkalosis, and characterized by cardiac dysrhythmias, prominent U waves on an ECG, muscle weakness, and cramps.

Hyperkalemia

A serum potassium concentration above $5.0\,\text{mEq/L}$, caused by tissue trauma, acidosis, or renal failure, and characterized by neuromuscular weakness, small/absent P waves, tall peaked T-waves, and potential cardiac arrest.

Chvostek’s Sign

A clinical indicator of hypocalcemia and latent tetany, elicited by tapping cranial nerve VII (facial nerve) anterior to the tragus of the ear, resulting in ipsilateral twitching or spasm of the facial muscles.

Trousseau’s Sign

A diagnostic sign of hypocalcemia characterized by carpopedal spasm of the hand and wrist induced by inflating a sphygmomanometer cuff above the patient's systolic blood pressure for three minutes.

Hypocalcemia

A serum total calcium level below $4\,\text{mEq/L}$, which increases nerve membrane permeability and excitability, causing spontaneous neuromuscular stimulation, tetany, carpopedal spasms, and cardiac conduction delays.

Hypercalcemia

A serum calcium level exceeding $5\,\text{mEq/L}$, commonly caused by hyperparathyroidism or malignancy, manifesting clinically with 'stones, moans, bones, and groans' (renal calculi, muscle weakness, bone pain, constipation, and cognitive impairment).

Chloride Shift

The reciprocal exchange of chloride ($\text{Cl}^-$) and bicarbonate ($\text{HCO}_3^-$) ions across red blood cell membranes to maintain systemic electroneutrality during acid-base shifts and carbon dioxide transport.

Anion Gap

A mathematical calculation of unmeasured anions in the blood plasma, determined by the formula: $\text{AG} = [\text{Na}^+] - ([\text{Cl}^-] + [\text{HCO}_3^-])$, with a normal physiological reference range of $12 \pm 4\,\text{mEq/L}$.

High Anion Gap Metabolic Acidosis (HAGMA)

A metabolic acidosis characterized by an elevated anion gap ($> 16\,\text{mEq/L}$) due to the accumulation of unmeasured fixed organic acids, categorized by the mnemonic GOLDMARK (glycols, oxoproline, L-lactate, D-lactate, methanol, aspirin, renal failure, ketoacidosis).

Normal Anion Gap Metabolic Acidosis (NAGMA)

A hyperchloremic metabolic acidosis with an anion gap within normal limits ($12 \pm 4\,\text{mEq/L}$), caused by direct loss of bicarbonate (e.g., severe diarrhea, acetazolamide, renal tubular acidosis) or excessive infusions of normal saline ($0.9\%\,\text{NaCl}$).

Metabolic Acidosis

An acid-base disturbance defined by an arterial $\text{pH} < 7.35$ and serum $\text{HCO}_3^- < 22\,\text{mEq/L}$, which elicits compensatory respiratory hyperventilation (Kussmaul breathing) to eliminate $\text{CO}_2$.

Metabolic Alkalosis

An acid-base disturbance characterized by an arterial $\text{pH} > 7.45$ and serum $\text{HCO}_3^- > 26\,\text{mEq/L}$, compensated for by respiratory hypoventilation to retain volatile $\text{CO}_2$.

Respiratory Acidosis

A primary acid-base disorder caused by alveolar hypoventilation, presenting with an arterial $\text{pH} < 7.35$ and $\text{PaCO}_2 > 45\,\text{mmHg}$, compensated chronically over $2\text{--}5\text{ days}$ by renal bicarbonate retention and hydrogen ion excretion.

Respiratory Alkalosis

A primary acid-base disorder caused by alveolar hyperventilation, defined by an arterial $\text{pH} > 7.45$ and $\text{PaCO}_2 < 35\,\text{mmHg}$, compensated by renal excretion of $\text{HCO}_3^-$ and retention of $\text{H}^+$.

Mixed Acid-Base Disorder

A clinical state where two or more independent primary acid-base disturbances coexist simultaneously, causing laboratory $\text{PaCO}_2$ and $\text{HCO}_3^-$ values to deviate from standard mathematical compensation formulas.