10.1 Alterations in Fluid, Electrolyte, and Acid-Base Balance

The body's intricate regulatory mechanisms maintain fluid, electrolyte, and acid-base balance. These systems work together to keep our internal environment stable, allowing cells to function properly. When imbalances occur, they can lead to various disorders with wide-ranging effects on the body.

Electrolyte disorders like hyponatremia and hyperkalemia can cause symptoms from mild nausea to life-threatening arrhythmias. Acid-base imbalances, whether metabolic or respiratory in origin, disrupt the body's pH, affecting everything from enzyme function to oxygen delivery.

Regulatory Mechanisms and Imbalances

Regulation of body fluid balance

• Fluid regulation
  • Antidiuretic hormone (ADH) regulates water reabsorption in kidneys
  • Renin-angiotensin-aldosterone system (RAAS) controls blood pressure and sodium retention
  • Atrial natriuretic peptide (ANP) promotes sodium and water excretion
• Electrolyte regulation
  • Hormonal control maintains electrolyte balance (aldosterone for sodium/potassium, parathyroid hormone for calcium)
  • Renal mechanisms filter and reabsorb electrolytes
  • Cellular transport systems move ions across cell membranes (sodium-potassium pump)
• Acid-base balance
  • Buffer systems neutralize excess acids or bases
    • Bicarbonate buffer system most important extracellular buffer
    • Phosphate buffer system crucial in urine and intracellular fluid
    • Protein buffer system helps in blood and cells
  • Respiratory regulation eliminates CO2 through lungs adjusting breathing rate
  • Renal regulation excretes H+ and reabsorbs/regenerates HCO3- in kidneys

Causes of fluid imbalances

• Dehydration
  • Causes
    • Insufficient fluid intake leads to negative fluid balance
    • Excessive fluid loss through vomiting, diarrhea, or sweating depletes body water
    • Certain medications increase urine output (loop diuretics)
  • Consequences
    • Decreased blood volume reduces cardiac output
    • Electrolyte imbalances disrupt cellular functions
    • Reduced organ perfusion impairs tissue oxygenation
    • Increased risk of blood clots due to blood concentration
• Overhydration
  • Causes
    • Excessive fluid intake overwhelms excretion capacity
    • Impaired fluid excretion in heart failure or kidney disease
    • Inappropriate ADH secretion retains excess water (SIADH)
  • Consequences
    • Edema causes tissue swelling (peripheral, pulmonary)
    • Hyponatremia dilutes sodium concentration
    • Increased intracranial pressure from cerebral edema
    • Pulmonary edema impairs gas exchange

Electrolyte and Acid-Base Disorders

Electrolyte disorders and manifestations

• Hyponatremia (low sodium)
  • Pathophysiology
    • Excess water relative to sodium dilutes serum concentration
    • Dilutional effect from water retention or sodium loss from sweating
  • Clinical manifestations
    • Nausea and headache from cellular swelling
    • Confusion and seizures in severe cases
    • Muscle cramps from altered nerve conduction
• Hypernatremia (high sodium)
  • Pathophysiology
    • Water loss exceeds sodium loss concentrating serum
    • Excessive sodium intake from IV fluids or salt ingestion
  • Clinical manifestations
    • Thirst and dry mucous membranes from cellular dehydration
    • Altered mental status ranging from irritability to coma
    • Muscle twitching and seizures from neuronal irritability
• Hypokalemia (low potassium)
  • Pathophysiology
    • Inadequate intake or excessive loss through GI tract or kidneys
    • Shift of potassium into cells (insulin administration)
  • Clinical manifestations
    • Muscle weakness affecting skeletal and smooth muscles
    • Cardiac arrhythmias (U waves on ECG)
    • Paralytic ileus from impaired intestinal motility
• Hyperkalemia (high potassium)
  • Pathophysiology
    • Reduced renal excretion in kidney disease
    • Excessive intake or cell damage releasing intracellular potassium
  • Clinical manifestations
    • Muscle weakness from altered membrane potential
    • Cardiac conduction abnormalities (peaked T waves)
    • Paresthesias in extremities

Metabolic vs respiratory acid-base disorders

• Metabolic acidosis
  • Causes: increased acid production (lactic acidosis), bicarbonate loss (diarrhea)
  • Primary change: decreased HCO3- in blood
  • Compensatory mechanism: increased respiratory rate to blow off CO2
• Metabolic alkalosis
  • Causes: loss of H+ ions (vomiting), excess bicarbonate (antacid overuse)
  • Primary change: increased HCO3- in blood
  • Compensatory mechanism: decreased respiratory rate to retain CO2
• Respiratory acidosis
  • Causes: hypoventilation (opioid overdose), CO2 retention (COPD)
  • Primary change: increased PaCO2 in blood
  • Compensatory mechanism: increased renal HCO3- reabsorption to buffer acid
• Respiratory alkalosis
  • Causes: hyperventilation (anxiety), excessive CO2 loss (mechanical ventilation)
  • Primary change: decreased PaCO2 in blood
  • Compensatory mechanism: increased renal HCO3- excretion to balance pH
• Anion gap
  • Formula calculates unmeasured anions $AG = [Na+] - ([Cl-] + [HCO3-])$
  • Normal range 8-12 mEq/L indicates balanced electrolytes
  • Elevated in certain types of metabolic acidosis (ketoacidosis, lactic acidosis)