AR

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

Water Balance

  • Concept: Water balance and its disturbances are determined by osmotic gradients established by extracellular fluid (ECF) and intracellular fluid (ICF) sodium concentrations.

    • Key idea: Water moves to equilibrate osmolarity across cell membranes so that the osmotic gradients are equalized between ECF and ICF.
    • Definitions:
    • ECF = Extracellular fluid
    • ICF = Intracellular fluid (cytoplasm)
    • Important relationship: Na+ concentrations drive osmotic gradients that govern water distribution between ECF and ICF.
    • Notation: [Na^+]{ECF} \quad, [Na^+]{ICF} \quad

  • Regulation of Water Balance

    • Antidiuretic hormone (ADH) effects: Secretion of ADH promotes pure water reabsorption in the renal tubules, influencing water balance without adding solute.
    • This mechanism concentrates the urine and conserves water when needed.

Sodium Balance

  • Major distribution

    • The majority of total body sodium is in the ECF.
    • Sodium distribution ratio: [Na^+]{ECF} : [Na^+]{ICF} \approx 10:1
    • This reflects a much higher Na+ concentration outside cells than inside.
    • Consequence: Sodium gradients drive extracellular osmolarity and, therefore, water movement.

  • Functions of sodium

    • Maintains extracellular osmolarity.
    • Maintains resting membrane potential (RMP) and is required for depolarization of neurons and most muscle cells.
    • Diagrammatic representation: water and Na+ gradients interact to influence membrane potentials and cell excitability.

  • Regulation of plasma sodium

    • Aldosterone effects: Aldosterone secretion increases sodium reabsorption in the renal tubules, increasing Na+ retention.
    • Regulatory mechanism: The secretion of aldosterone is regulated by the renin–angiotensin–aldosterone system (RAAS).

  • RAAS recall

    • Renin–angiotensin–aldosterone system (RAAS) controls aldosterone secretion, which in turn modulates Na+ reabsorption in the kidneys.

Potassium Balance

  • Major distribution

    • The majority of total body potassium is in the cytoplasm (ICF).
    • Potassium distribution ratio: [K^+]{ECF} : [K^+]{ICF} \approx 1:20
    • This means intracellular K+ concentration far exceeds extracellular K+.

  • Regulation of plasma potassium

    • Potassium is normally secreted by renal tubules and excreted in urine.
    • Aldosterone stimulates potassium secretion/excretion by the kidneys.
    • Diagrammatic notes: Glomerulus → Renal tubules → Excretion of K+ in urine.

  • Functions of potassium

    • Maintains resting membrane potential (RMP) and is required for repolarization of excitable cells.
    • Potassium also plays a role in insulin-dependent glucose uptake by most cells.
    • Note: The membrane potential and excitability of neurons and muscles are highly sensitive to extracellular K+ levels.

Test Your Understanding (Concept Overview)

  • Question 1: Where is the majority of the body’s potassium (K+) located?
    • Options (as presented):
    • In the plasma
    • In the cytoplasm of all cells
    • In the kidneys
    • In the tissue fluid
    • Correct emphasis: The majority is in the cytoplasm (ICF).
  • Question 2: Which physiologic effect is associated with increased aldosterone secretion?
    • Options (as presented):
    • Increased urine output
    • Retention of pure water by the kidneys
    • Excretion of Na+ and water by the kidneys
    • Aldosterone secretion
    • Correct emphasis: Aldosterone secretion increases sodium reabsorption; water follows Na+ osmotically, increasing extracellular volume; direct effect on K+ is to promote K+ secretion/excretion.
  • Question 3: What is the physiological effect of increased antidiuretic hormone (ADH) secretion from the posterior pituitary?
    • Answer type anticipated: ADH promotes water reabsorption in the renal tubules, concentrating the urine and conserving free water.

Alterations of Water and Sodium Balance

Isotonic Alterations in Water and Sodium Balance

  • Isotonic Fluid Overload

    • Definition: Excess administration of intravenous normal saline solutions with concurrent aldosterone effects.
    • Mechanism: Increased aldosterone → increased Na+ and H2O reabsorption/retention.
    • Common etiologies: Renal failure; Hypersecretion of aldosterone (hyperaldosteronism).
    • Pathophysiology: Increased blood volume and capillary hydrostatic pressure promote fluid movement into the interstitium (edema).
    • Clinical manifestations: Weight gain; edema; elevated blood pressure (hypertension).

  • Isotonic Fluid Overload – Pathophysiology in depth

    • Increased capillary hydrostatic pressure shifts fluid from the vascular space into the interstitial space, leading to edema.
    • The diagrammatic note illustrates water compartments with multiple H2O units illustrating fluid movement.

  • Isotonic Fluid Overload – Clinical Manifestations (summary)

    • Weight gain
    • Edema
    • Hypertension

  • Isotonic Fluid Deficit (Isotonic Hypovolemia)

    • Causes: Decreased aldosterone; decreased Na+ & H2O reabsorption/retention; loss of Na+ and H2O in sweat; hyposecretion of aldosterone.
    • Mechanisms: Sweating and diuresis lead to isotonic loss of Na+ and water.
    • Clinical manifestations: Weight loss; hypotension (low blood pressure).

  • Isotonic Hypovolemia – clinical relevance

    • Represents a reduction in effective circulating volume without a change in the osmolarity of body fluids.

Alterations of Sodium Balance (Hyponatremia and Hypernatremia)

Hyponatremia

  • Definition: plasma Na+ < 135 mEq/L (normal range 135–145 mEq/L).
  • Common causes
    • Vomiting/gastric suctioning (nasogastric tube suction can remove Na+).
    • Inadequate sodium intake.
    • Excess ADH secretion (syndrome of inappropriate ADH – SIADH).
    • Excess water intake (dilutional hyponatremia).
  • Pathophysiology
    • Early phase: Water shifts from ECF to cytoplasm due to osmotic gradient, causing cellular swelling (notably in neurons).
    • [Na+] in plasma decreases as water dilutes solutes.
    • Cellular swelling of neurons in the brain is life-threatening.
  • Clinical manifestations
    • Neurologic: lethargy, confusion, seizures, coma.
    • Gait disturbances, falls (especially in the elderly).
    • Dilutional features: weight gain and edema can accompany hyponatremia if water gain is substantial.
  • Resting membrane potential (RMP) considerations
    • Early: water shifting results in cytoplasmic swelling; later: RMP becomes more negative, leading to decreased excitability of neurons and muscle cells.
    • Conceptual note: As [Na+] falls, the gradient that maintains normal excitability diminishes, affecting action potential generation.
  • Clinical nuance
    • Dilutional hyponatremia is a key subtype where excess water dilutes plasma Na+.

Hypernatremia

  • Definition: plasma Na+ > 145 mEq/L (normal 135–145).
  • Common causes
    • Pure dietary sodium excess (rare without renal dysfunction).
    • Processed foods high in sodium.
    • Insufficient water intake (dehydration).
    • Decreased ADH secretion (diabetes insipidus).
  • Pathophysiology
    • Early: Shift of water from cytoplasm to plasma, causing cellular dehydration and ↑ [Na+] in plasma.
    • Result: intracellular dehydration and increased serum osmolarity.
  • Resting membrane potential implications
    • RMP becomes more positive over time, increasing cellular excitability.
  • Clinical manifestations
    • Systemic dehydration: thirst, low blood pressure (hypotension), dry mucous membranes, weight loss, decreased urine output with concentrated urine.
    • Neuronal dehydration: restlessness, irritability, seizures.

Alterations of Potassium Balance

Hypokalemia

  • Definition: plasma potassium < 3.5 mEq/L (normal 3.5–5.5 mEq/L).
  • Common causes
    • GI losses (diarrhea).
    • Renal losses (diuresis).
    • Shifts of K+ from ECF to ICF (e.g., insulin administration).
    • Reduced intake (less common; risk higher in elderly or malnourished).
    • Hyperaldosteronism leading to enhanced K+ excretion.
  • Pathophysiology
    • RMP becomes more negative, reducing excitability of muscle and nerve cells.
    • Net effect: decreased muscle function and increased risk of arrhythmias.
  • Clinical manifestations
    • Cardiac: arrhythmias (ECG changes can occur with mild hypokalemia; more serious with larger deficits).
    • Skeletal: weakness, cramps, paralysis (depending on severity).
    • GI: constipation or bowel obstruction.

Hyperkalemia

  • Definition: plasma potassium > 5.5 mEq/L (normal 3.5–5.5 mEq/L).
  • Common causes
    • Renal (kidney) failure → decreased K+ excretion.
    • Increased potassium intake (e.g., IV K+ administration).
    • Cellular breakdown or lysis (e.g., trauma, burns).
    • Insulin deficiency (diabetes mellitus type 1), which impairs cellular K+ uptake.
    • Hypoaldosteronism (reduced K+ excretion).
  • Pathophysiology
    • Mild–moderate hyperkalemia: RMP becomes more positive, increasing excitability of muscle and nerve cells.
    • Severe hyperkalemia: cells depolarize and cannot repolarize, risking life-threatening dysrhythmias.
  • Clinical manifestations
    • Cardiac: arrhythmias, ventricular fibrillation, potential cardiac arrest.
    • Skeletal: muscle weakness, paralysis.
    • Other: can cause restlessness, irritability depending on the degree of hyperkalemia.

Notes on Formulas and Ranges

  • Sodium normal range: 135\,\text{mEq/L} \le [Na^+] \le 145\,\text{mEq/L}
  • Potassium normal range: 3.5\,\text{mEq/L} \le [K^+] \le 5.5\,\text{mEq/L}
  • Sodium gradient driving osmolarity: [Na^+]{ECF} : [Na^+]{ICF} \approx 10:1
  • Potassium gradient driving intracellular dominance: [K^+]{ECF} : [K^+]{ICF} \approx 1 : 20
  • Membrane potential references: typical resting membrane potential (RMP) of neurons/muscle is around -70 mV (depolarization) to -50 mV in various states; shifts in Na+/K+ dramatically alter excitability.

Practical and Ethical/Clinical Implications

  • Isotonic disturbances affect circulating volume and tissue perfusion; management aims to restore normovolemia with appropriate IV fluids and consideration of hormonal regulation (RAAS, ADH).
  • Hyponatremia and hypernatremia require careful correction to avoid osmotic demyelination or cerebral edema, with attention to rate of correction and underlying causes (e.g., SIADH, dehydration).
  • Potassium disorders have immediate cardiovascular implications; rhythm disturbances can be life-threatening; treatment must rapidly address the underlying cause and correct K+ through renal, cellular, or pharmacologic means.
  • Connections to broader physiology: Na+/K+ balance underpins transmembrane potential, neural signaling, muscle contraction, insulin activity, and fluid homeostasis; dysregulation affects multiple organ systems and patient safety.

Real-world relevance

  • In clinical practice, isotonic IV fluids are common; recognizing isotonic overload or deficit helps prevent edema, hypertension, or hypovolemia.
  • Hyponatremia typically results from SIADH or excessive water intake, common in hospital settings (e.g., postoperative patients, psychogenic polydipsia).
  • Hypernatremia often arises from dehydration or diabetes insipidus; monitoring fluid intake and output is essential.
  • Hypokalemia and hyperkalemia frequently emerge in patients with GI losses, renal disease, or endocrine disorders (e.g., aldosterone excess or deficiency); ECG monitoring is essential when potassium levels are abnormal.