Fluid & Electrolyte Imbalances: Alterations of Water, Sodium & Potassium Balance

Vocabulary flashcards covering water, sodium, and potassium balance concepts from the lecture notes.

Extracellular fluid (ECF)

Fluid outside cells (including plasma and interstitial fluid) that determines extracellular osmolarity.

Intracellular fluid (ICF)

Fluid inside cells; major reservoir for potassium and site of many cellular processes.

Osmotic gradient

Difference in solute concentration between ECF and ICF that drives water movement.

Sodium (Na+) balance

Regulation of extracellular Na+; main determinant of extracellular osmolarity and fluid volume.

Water balance

Regulation of total body water, mediated by ADH and renal reabsorption.

Antidiuretic hormone (ADH)

Posterior pituitary hormone that promotes water reabsorption in renal tubules, concentrating urine.

Effects of ADH on water reabsorption

ADH promotes reabsorption of free water in the kidneys (collecting ducts).

Aldosterone

Mineralocorticoid that increases Na+ reabsorption (and water retention) in renal tubules and promotes K+ excretion.

Renin–angiotensin–aldosterone system (RAAS)

Hormonal cascade regulating blood pressure, Na+ and water balance; stimulates aldosterone release.

Isotonic fluid overload

Excess IV normal saline or increased Na+/H2O reabsorption causing expanded extracellular fluid and edema.

Pathophysiology of isotonic fluid overload

Increased capillary hydrostatic pressure raises fluid leakage into interstitial spaces (edema).

Clinical manifestations of isotonic fluid overload

Weight gain, edema, and hypertension.

Isotonic fluid deficit (isotonic hypovolemia)

Loss of Na+ and water with decreased aldosterone or sweating/diuresis, causing hypovolemia.

Causes of isotonic fluid deficit

Decreased aldosterone, sweating, diuresis leading to Na+ and water loss.

Hyponatremia

Plasma Na+ < 135 mEq/L; dilutional or due to excess water or SIADH.

Common causes of hyponatremia

Vomiting/gastric suctioning, inadequate Na+ intake, excessive water intake, SIADH.

Pathophysiology of hyponatremia

Water moves from ECF into ICF causing cellular swelling, especially brain cells.

Clinical manifestations of hyponatremia

Lethargy, confusion, seizures, coma; gait disturbances; edema in dilutional forms.

Hypernatremia

Plasma Na+ > 145 mEq/L; usually from dehydration or excess Na+ intake.

Common causes of hypernatremia

Inadequate water intake, decreased ADH (diabetes insipidus), excess Na+ intake.

Pathophysiology of hypernatremia

Water shifts from intracellular space to the plasma, causing cellular dehydration.

Clinical manifestations of hypernatremia

Thirst, hypotension, dry mucous membranes, decreased skin turgor, weight loss, oliguria.

Potassium balance

Major intracellular cation; most K+ is inside cells (ICF); small amount in the ECF.

Potassium distribution (ECF/ICF ratio)

Approximately 1:20 (ECF:ICF); higher K+ inside cells.

Regulation of plasma potassium

Kidneys excrete K+; aldosterone increases K+ secretion by renal tubules.

Potassium functions

Maintains resting membrane potential; essential for depolarization and repolarization; supports insulin-mediated glucose uptake.

Hypokalemia

Plasma K+ < 3.5 mEq/L; causes include GI losses, renal losses, and shifts of K+ into cells.

Pathophysiology of hypokalemia

RMP becomes more negative, decreasing muscle/cardiac excitability.

Clinical manifestations of hypokalemia

Cardiac arrhythmias, muscle weakness, cramps, constipation.

Hyperkalemia

Plasma K+ > 5.5 mEq/L; causes include renal failure, excess intake, and cell lysis.

Pathophysiology of hyperkalemia

RMP becomes more positive; mild/moderate causes increased excitability; severe impairs repolarization and can cause arrest.

Clinical manifestations of hyperkalemia

Cardiac arrhythmias, ventricular fibrillation, cardiac arrest; muscle weakness or paralysis.

ADH effect on renal water reabsorption

ADH increases water reabsorption in collecting ducts, concentrating urine.

Insulin and potassium uptake

Insulin stimulates uptake of potassium into cells, affecting serum K+ levels.