Fluid, Electrolyte, and Acid-Base Imbalances (Chapter 2)

Fluid Imbalance: Overview

• Water is the major component of the body and exists inside and outside cells. It is essential for homeostasis, acts as the medium for metabolic reactions, and serves as the transport system (nutrients into cells, wastes out, enzymes in secretions, blood cell movement). Adequate fluid is necessary for cell function and survival.
• Major learning objectives include understanding water movement between compartments, edema vs dehydration, third-spacing, hyponatremia/hypernatremia, potassium/calcium imbalances, acid-base balance, and compensation/decompensation mechanisms.

Key Concepts and Numbers

• Total body water (adult): ~60% of body weight; infant ~70%. Female bodies have lower percent water than males due to higher fat content; elderly and obese have lower water content.
• Fluid compartments (ECF vs ICF): intracellular fluid (ICF) is inside cells; extracellular fluid (ECF) includes plasma (intravascular), interstitial fluid (ISF), cerebrospinal fluid (CSF), and transcellular fluids (secretions in pericardial, synovial cavities, etc.). In an adult male: blood ~4% body weight, ISF ~15%, transcellular fluids ~1%.
• Movement between compartments depends on membrane permeability and the forces of filtration and osmosis. Water moves from areas of higher hydrostatic pressure to lower hydrostatic pressure, and across membranes driven by osmotic gradients.
• Thirst mechanism: hypothalamus osmoreceptors sense volume and concentration of body fluids; ADH (antidiuretic hormone) promotes water reabsorption in kidneys to conserve water.
• Aldosterone: reabsorbs sodium (and water) in the kidney tubules, conserving fluid during deficits.
• Natriuretic peptides (ANP and BNP): released when atrial pressure/volume increases; promote water and sodium excretion to reduce volume and BP; ANP reduces renin secretion and inhibits the renin–angiotensin system; aldosterone secretion is reduced; elevated ANP observed in congestive heart failure with high atrial volume.
• Fluid balance is achieved by intake (fluid and foods; metabolic water) and losses (urine, feces, insensible losses via skin and lungs).

Fluid Compartments and Water Movement

• Fluid compartments and percentages (adult male example):
  • Intracellular fluid (ICF): ~28% of body weight (cellular content varies with age/sex)
  • Extracellular fluid (ECF): ~15% of body weight, including plasma (~4%) and interstitial fluid (~15%)
  • Transcellular fluids: ~1%
• Movement mechanisms:
  • Filtration: movement of water/solutes from blood (high hydrostatic pressure) to ISF (low pressure) across semipermeable membranes; at arteriolar end, capillary hydrostatic pressure > ISF hydrostatic pressure and plasma oncotic pressure, driving fluid out of capillaries. At venous end, hydrostatic pressure is lower and oncotic pressure draws fluid back in.
  • Diffusion: solutes move from high concentration to low concentration.
  • Osmosis: water moves from low solute concentration (ISF) to high solute concentration (blood) to equalize osmolality.
  • Lymphatics return excess ISF to circulation.
• Interplay of hydrostatic pressure and osmotic pressure governs fluid shifts; proteins and electrolytes contribute to osmotic (oncotic) pressure, maintaining fluid balance.

Edema: Fluid Excess in the Extracellular Space

• Edema definition: excessive fluid in the interstitial compartment causing tissue swelling.
• Extent can be localized or generalized; often more pronounced in dependent areas due to gravity (e.g., feet/ankles when upright).
• Functional consequences: impaired venous return, arterial circulation, and cellular function in the affected area.
• Signs of edema can include pitting edema (a finger depresses tissue and a pit remains)
• Generalized edema often accompanies detectable weight gain; edema can impair organ function (e.g., intestinal edema affecting digestion/absorption; cardiac/respiratory organ edema impairing function).
• Causes of edema (four main categories): 1) Increased capillary hydrostatic pressure (elevated blood pressure or hypervolemia) causing excessive filtration into ISF.
  • Examples: kidney failure with fluid retention, pregnancy with venous compression, congestive heart failure, iatrogenic fluid administration; ascites in severe edema due to venous congestion.
    2) Loss of plasma proteins (especially albumin) reducing plasma oncotic pressure, leading to more fluid leaving capillaries and less returning to venous end.
  • Causes: nephrotic syndrome, liver disease, malnutrition/malabsorption, burns with protein loss.
    3) Obstruction of lymphatic drainage, causing localized edema (excess fluid/protein not returned to circulation).
    4) Increased capillary permeability due to inflammation or infection; mediators (e.g., histamine) increase permeability, causing localized edema. In severe cases, generalized capillary permeability can cause hypovolemia/shock.
• Effects and signs: local swelling, possible color changes; pitting vs non-pitting edema; dependent edema common; can interfere with joints and organ function; in severe cases, tissue necrosis/ulcers due to impaired blood flow.
• Edema vs dehydration comparison: edema involves excess ISF; dehydration involves loss of extracellular/intravascular fluids with later cellular dehydration in severe cases.
• Think About prompts (example questions): mechanisms by which edema occurs; effects of kidney disease; why edema in a leg on a chair leads to weakness/skin breakdown; ascites from malnutrition; edema in varicose veins.

Fluid Deficit: Dehydration

• Dehydration: insufficient body fluid due to inadequate intake or excessive loss; losses primarily affect the extracellular compartment first; fluid can shift between extracellular compartments.
• Assessment indicators:
  • Weight loss as a measure of extracellular fluid loss: mild deficit ≈ 2% body weight loss; moderate ≈ 5%; severe ≈ 8% (adjust for age/body size).
  • In infants and elderly, fluid reserves are lower and dehydration is more dangerous; infants show decreased urine output, lethargy, and dry mucous membranes.
• Causes of dehydration: vomiting/diarrhea (GI losses of water and electrolytes), excessive sweating, diabetic ketoacidosis, insufficient water intake, concentrated formula in infants.
• Types of dehydration (based on electrolytes):
  • Isotonic dehydration: proportional loss of fluid and electrolytes.
  • Hypotonic (hypoosmolar) dehydration: loss of more electrolytes than water (lower osmolarity).
  • Hypertonic (hyperosmolar) dehydration: loss of more water than electrolytes (higher osmolarity).
• Effects: early decreases in ISF and intravascular fluid; signs include dry mucous membranes, poor skin turgor, hypotension, tachycardia, fatigue; CNS effects with brain cell dehydration (confusion, stupor).
• Compensatory responses to dehydration:
  • Thirst increase, tachycardia, peripheral vasoconstriction (pale, cool skin).
  • Renal responses: ADH and aldosterone increase, concentrating urine and reducing urine volume.
• Third-spacing: a related concept where fluid shifts out of the vasculature into a body cavity or tissue (e.g., burns edema) and is not available for circulating volume; requires additional assessment (hematocrit/electrolyes) to identify.
• Signs/Think About prompts for dehydration: poor skin turgor; dry mucous membranes; dry eyes; confusion or lethargy; thirst; weight loss indicators; how to distinguish dehydration from edema clinically.

第三空间: Fluid Deficit and Fluid Excess

• Third-spacing refers to fluid shifting out of blood into body cavities or tissues where it’s not circulating, causing hypovolemia (vascular space deficit) and interstitial (third-space) fluid excess. Weighing the patient may not reflect this shift; labs like hematocrit/electrolyte changes help identify third-spacing. Burns cause edema in wound areas (third-spacing).

Electrolyte Imbalances: Sodium

• Sodium (Na+) basics:
  • Primary extracellular cation; maintains extracellular fluid volume via osmotic pressure (~90% of extracellular solute).
  • Important for nerve impulse conduction and muscle contraction; ingested in food/drinks; lost in urine, feces, and sweat; regulated by kidneys via aldosterone.
  • In intracellular fluid (low Na+) and in extracellular fluid (high Na+).
• Hyponatremia (<135 mEq/L or as stated in materials: below 3.8–5 mmol/L, 135 mEq/L):
  • Causes: excessive sweating, vomiting, diarrhea; diuretics with low-salt diets; hormonal issues (low aldosterone, adrenal insufficiency, SIADH); early renal failure; excessive water intake.
  • Effects: fatigue, lethargy, muscle cramps, headaches, confusion; seizures in severe cases; decreased blood pressure; cells may swell due to reduced extracellular osmotic pressure.
• Hypernatremia (>145 mEq/L):
  • Causes: excessive Na+ intake without enough water, or water loss faster than Na+ loss (e.g., insufficient ADH, diabetes insipidus, watery diarrhea, prolonged rapid respiration).
  • Effects: fluid shift from cells to extracellular space causing cell dehydration; signs include thirst, dry mucous membranes, firm tissues, agitation; decreased urine output in some cases depending on cause (e.g., dehydration with intact ADH can reduce urine output).
• Sodium distribution and balance: changes in serum Na+ affect fluid distribution between compartments; high Na+ tends to pull water into the extracellular space; low Na+ can cause water to move into cells.
• Illustrative figure/notes: Na+ transport involves diffusion across membranes; the Na+/K+ pump maintains extracellular Na+ high relative to intracellular Na+.
• Practical note: hyponatremia and hypernatremia share some signs (thirst, mental status changes) but differ in edema/volume status and urine output patterns; sodium imbalances can affect cardiac function and brain function.

Potassium Imbalance

• Potassium (K+) basics:
  • Major intracellular cation; serum K+ is relatively low (approx. 3.5–5 mEq/L or 3.5–5 mmol/L) compared with intracellular levels (~160 mEq/L).
  • Regulated mainly by the kidneys under aldosterone influence; insulin promotes cellular uptake of potassium; dietary sources include bananas, citrus, tomatoes, lentils; also present in medications like potassium chloride.
  • Acid-base balance modulates K+: acidosis shifts K+ out of cells into extracellular fluid (hyperkalemia risk); alkalosis drives K+ into cells (hypokalemia risk). Hydrogen ions can displace K+ during acidosis.
• Role in physiology: intracellular pH regulation, intracellular fluid volume, nerve conduction, muscle contraction; critical in cardiac muscle conduction; small changes in K+ have major cardiac effects (ECG changes, risk of arrest).
• Hypokalemia (K+ < 3.5 mmol/L or <2 mmol/L depending on source):
  • Causes: excessive GI losses (diarrhea, vomiting), diuretic therapy (e.g., loop diuretics like furosemide), elevated aldosterone or glucocorticoids (Cushing syndrome), poor dietary intake (alcoholism, eating disorders), treatment of diabetic ketoacidosis with insulin.
  • Effects: cardiac dysrhythmias (ECG changes; risk of arrest), fatigue, muscle weakness, paresthesias, decreased GI motility, shallow respiration, polyuria with impaired concentrating ability in severe cases.
• Hyperkalemia (K+ > 5 mEq/L or >5 mmol/L):
  • Causes: renal failure, aldosterone deficiency, potassium-sparing diuretics, tissue breakdown (crush injuries, burns) releasing intracellular K+, acidosis-driven K+ shift from cells to extracellular space.
  • Effects: cardiac dysrhythmias, potential arrest; muscle weakness, fatigue, paresthesias, nausea, diarrhea; respiratory difficulties in severe cases; ECG changes vary with degree of elevation.
• ECG and clinical signs: hypokalemia shows flattened or inverted T waves and prominent U waves; hyperkalemia shows tall peaked T waves, widened QRS complex, and possible sine-wave patterns; these ECG changes reflect changes in membrane excitability and conduction.
• Interplay with acid-base: acidosis tends to raise extracellular K+; alkalosis lowers extracellular K+.

Calcium Imbalance

• Calcium basics:
  • Extracellular cation; essential for bones/teeth, nerve membrane stability, muscle contraction, blood clotting; balance controlled by parathyroid hormone (PTH), calcitonin, vitamin D, and phosphate levels.
  • Vitamin D activation (in kidneys) promotes calcium absorption in gut; lack of vitamin D decreases calcium absorption; sun exposure affects vitamin D synthesis; dietary sources important in low-sun climates.
  • Calcium and phosphate have a reciprocal relationship; the product of their concentrations is maintained at a consistent level; high calcium often means low phosphate and vice versa.
• Hypocalcemia (Ca2+ < ~2.2 mmol/L or <4 mEq/L):
  • Causes: hypoparathyroidism (low PTH), malabsorption, deficient serum albumin, alkalosis; renal failure with phosphate retention and poor vitamin D activation can also cause hypocalcemia.
  • Effects: increased nerve membrane permeability/excitability leading to spontaneous muscle activity (tetany); signs include carpopedal spasm, Chvostek sign (facial twitch on tapping), Trousseau sign (carpopedal spasm with BP cuff); laryngospasm in severe cases; paresthesias and abdominal cramps; cardiac contractions may be weak due to decreased extracellular calcium.
• Hypercalcemia (Ca2+ > ~2.5 mmol/L or >5 mEq/L):
  • Causes: PTH-related hypercalcemia from paraneoplastic PTH secretion, hyperparathyroidism, immobility with bone demineralization, excessive calcium or vitamin D intake, milk-alkali syndrome.
  • Effects: depressed neuromuscular activity with weakness and lethargy; polyuria with potential dehydration; constipation and decreased mental status; heart contractions may be stronger and arrhythmias can occur; possible kidney stone formation; bone density changes depend on etiology (bone resorption vs deposition).
• Interactions: PTH increases bone resorption and intestinal calcium absorption; calcitonin lowers calcium; vitamin D supports calcium absorption; phosphate handling interacts with calcium in kidneys.
• Think About prompts outline differential signs (e.g., skeletal vs cardiac impact of calcium imbalance) and relationships to bone health and vitamin D.

Other Electrolytes

• Magnesium (Mg2+): intracellular; normal serum range ~0.7–1.1 mmol/L. About 50% stored in bone. Influences potassium and calcium balance; essential for enzyme reactions, protein/DNA synthesis. Hypomagnesemia often accompanies alcoholism, malnutrition; diuretic use; hyperparathyroidism; hyperaldosteronism. Hypermagnesemia usually due to renal failure.
• Phosphate (PO4^3-): primarily in bone; normal serum ~0.85–1.45 mmol/L. Involved in bone mineralization, energy metabolism (ATP), buffering system, cell membranes. Reciprocal relationship with calcium.
  • Hypophosphatemia: malabsorption, diarrhea, antacid overuse, alkalosis, hyperparathyroidism; signs include tremors, weak reflexes, paresthesias, confusion, anemia-related symptoms, dyssphagia.
  • Hyperphosphatemia: often from renal failure; can accompany tissue damage/cancer chemotherapy; manifestations mirror hypocalcemia due to calcium-phosphate interactions.
• Chloride (Cl-): major extracellular anion; normal serum ~98–106 mmol/L. Follows Na+ due to electrochemical neutrality. Exchange with bicarbonate in the chloride shift; helps maintain acid-base balance. Vomiting can cause hypochloremia; excessive NaCl intake or hypernatremia can cause hyperchloremia with edema.
• Acid-Base Balance: Chloride-bicarbonate exchange and shifts affect pH. Vomiting causes loss of HCl and can lead to metabolic alkalosis; chloride shifts can replace lost chloride by shifting bicarbonate into serum.

Acid-Base Imbalance: Concepts and Processes

• Normal serum pH range: 7.35–7.45. Death can occur if pH < 6.8 or > 7.8. Acidosis occurs with increased H+ or decreased bicarbonate; alkalosis with decreased H+ or increased bicarbonate.
• Buffers in the blood: four major buffer systems maintain pH
  1) Sodium bicarbonate-carbonic acid system (major extracellular buffer)
  2) Phosphate system
  3) Hemoglobin system
  4) Protein system
• Bicarbonate-carbonic acid buffer specifics:
  • Carbonic acid H2CO3 forms from CO2 + H2O via carbonic anhydrase; bicarbonate HCO3- is the conjugate base.
  • In the lungs, CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3- can be shifted to remove CO2 (exhale) reducing acid; in the kidneys, acids are excreted and bicarbonate is reabsorbed to replenish buffer.
  • The ratio [HCO3^-] : [H2CO3] (or CO2 in solution) must remain approximately 20:1 to keep pH near 7.40. If one component changes, the other must adjust to preserve the 20:1 ratio.
  • This ratio concept is used to understand metabolic vs respiratory disturbances and their compensation.
• Respiratory system: changes in CO2 control acidity (carbonic acid). If CO2 increases, pH falls (acidosis); if CO2 decreases, pH rises (alkalosis). The respiratory system can rapidly respond but has limited scope (only CO2/pCO2 affects buffer system).
• Renal system: kidneys can excrete acids, reabsorb or generate bicarbonate, and thus adjust HCO3- levels; slower but more comprehensive in correcting chronic imbalances.
• Compensation and decompensation:
  • Compensation refers to physiological adjustments that restore pH toward normal without correcting the underlying problem. Example: metabolic acidosis triggers increased ventilation to blow off CO2; kidneys increase bicarbonate reabsorption to balance pH.
  • Decompensation occurs when compensation is insufficient: serum pH moves outside the normal range and cellular function is impaired; requires medical intervention.
• Types of acid-base imbalances (table references in the text):
  • Respiratory acidosis: increased CO2 due to impaired ventilation; kidneys compensate by increasing bicarbonate reabsorption and H+ excretion; may show elevated bicarbonate and pCO2; stages from compensation to decompensation with rising CO2 and acid levels.
  • Respiratory alkalosis: decreased CO2 due to hyperventilation; kidneys compensate by decreasing bicarbonate reabsorption and increasing H+ excretion; can be compensated with a maintained ratio; if prolonged, decompensation occurs.
  • Metabolic acidosis: decreased bicarbonate due to loss of bicarbonate or accumulation of acids (e.g., ketoacids, lactic acid); respiratory compensation via increased ventilation to blow off CO2; kidneys attempt to excrete acids and reabsorb bicarbonate; decompensation occurs if kidneys cannot compensate.
  • Metabolic alkalosis: increased bicarbonate (e.g., from vomiting HCl loss or excessive bicarbonate intake); respiratory compensation via hypoventilation to retain CO2; chloride-containing solutions and renal adjustments occur to restore balance.
• Practical diagnostic tools: arterial blood gases, base excess/deficit, anion gap; typical best-practice assessment uses the 20:1 bicarbonate-to-CO2 ratio concept and compensatory responses.
• Think About prompts for acid-base: predict how control of serum pH could be impaired; how bicarbonate loss affects carbonic acid; how to distinguish compensated from decompensated states; how different disease states affect buffer systems.

Case Studies and Practice Scenarios

• Case Study 2.1 Vomiting (Mr. K.B., 81 years): presents with gastritis and severe vomiting; dehydration with hypernatremia; decreased serum bicarbonate; pH 7.35; high hematocrit; high urine specific gravity; signs show fluid/electrolyte imbalance and developing metabolic alkalosis early, with later metabolic acidosis in progression due to bicarbonate loss and ketoacid formation; questions focus on compartment involvement, sodium loss, early dehydration signs, expected serum pH after vomiting, and compensatory mechanisms; older age implies reduced compensatory ability.
  • Part A (early stage): fluid loss from gastric secretions; alkalosis develops due to H+ loss and Cl- loss; chloride shifts to maintain electrical neutrality; bicarbonate increases in serum.
  • Part B (days 2–3): continued losses include Na+, K+, bicarbonate; elevated serum Na+; intracellular fluid shifts; ongoing dehydration impacts blood volume, cellular function, kidney function; potassium disturbances become more dangerous.
  • Part C (admission to hospital): prolonged vomiting leads to metabolic acidosis from bicarbonate loss, ketoacid production, dehydration and reduced kidney function; lactic acid rise due to hypoperfusion. Treatment involves careful fluid and electrolyte restoration with attention to Na+ and K+ balance.
• Case Study 2.2 Diarrhea (Baby C., 3 months): viral gastroenteritis with severe watery diarrhea and fever; dehydration in infant risks high due to larger body surface area and higher metabolic rate; major losses include water, electrolytes, and nutrients; infant dehydration can progress rapidly; questions address major losses, signs, and reasons for rapid dehydration.

Chapter Summary (Key Takeaways)

• Water/electrolyte/acid-base homeostasis relies on distribution across intracellular and extracellular compartments and controlled movement between compartments via osmosis, diffusion, and filtration.
• Edema results from increased capillary hydrostatic pressure, decreased plasma osmotic pressure (hypoalbuminemia), lymphatic obstruction, or increased capillary permeability. Edema has localized and systemic implications and may indicate underlying pathophysiology (e.g., heart failure, liver disease, nephrotic syndrome).
• Dehydration results from inadequate intake or excessive loss; infants and elderly are at higher risk. Evaluate with weight changes and clinical signs, plus differentiate isotonic, hypotonic, and hypertonic dehydration.
• Sodium imbalances (hyponatremia/hypernatremia) impact extracellular fluid volume, intracellular osmolality, and neurological function; signs range from lethargy and confusion to seizures and coma.
• Potassium imbalances (hypokalemia/hyperkalemia) profoundly affect neuromuscular function and cardiac conduction; ECG changes reflect membrane potential alterations and can lead to arrhythmias or arrest.
• Calcium imbalances (hypocalcemia/hypercalcemia) affect nerve excitability, muscle function (tetany vs weakness), cardiac function, and bone health; PTH, calcitonin, vitamin D, and phosphate regulate calcium homeostasis.
• Magnesium and phosphate play critical roles in enzymatic reactions and energy metabolism; imbalances affect neuromuscular and cardiac function.
• Chloride and bicarbonate shifts are central to acid-base balance; vomiting and diarrhea drive alkalosis or acidosis via loss of H+ or bicarbonate and shifts in chloride.
• Acid-base balance is regulated by buffers (bicarbonate, phosphate, hemoglobin, proteins), respiratory control of CO2, and renal control of H+ and HCO3-; compensation vs decompensation depends on whether the ratio of bicarbonate to carbonic acid (CO2) remains near ~20:1.
• Common patterns include respiratory acidosis/alkalosis and metabolic acidosis/alkalosis with variable compensation and potential decompensation requiring clinical intervention.
• Practical clinical reasoning involves recognizing edema vs dehydration, monitoring fluid/electrolyte balance, and restoring homeostasis while addressing underlying causes (e.g., diuresis, GI losses, renal failure, endocrine disorders).

Think About and Practice Questions (Representative Examples)

• 2.1 Predict changes in three factors that could alter normal movement of fluid in the body (capillary pressure, plasma proteins, lymphatic drainage).
• 2.2 Explain three ways control of serum pH could be impaired and how compensation occurs.
• 2.3 Describe how ANP/BNP participate in homeostasis and how elevated ANP might be observed in congestive heart failure.
• 2.4 Explain the effects of a high venous end hydrostatic pressure on fluid shifts; how hypoalbuminemia changes capillary filtration; how hypernatremia/hyponatremia influence intracellular fluid.
• 2.5 Discuss signs of edema and dehydration in various anatomical sites; how third-spacing presents in burns and peritoneal infections.
• 2.6 Compare signs of local edema (e.g., knee) and implications of persistent edema on function and tissue integrity.
• 2.7 Explain infant vulnerability to fluid loss and how electrolyte losses accompany dehydration.
• 2.8 List three signs of dehydration and three compensatory signs.
• 2.9 Describe three signs and symptoms of third-spacing related to a large burn area.
• 2.10 Identify causes of hyponatremia and list signs/effects; discuss how hyponatremia alters osmotic balance and brain function.
• 2.11 Describe hypernatremia causes and effects, including thirst and urine output patterns.
• 2.12 Compare signs and symptoms of hyponatremia vs hypernatremia and how each affects cardiac function.
• 2.13 Compare manifestations of hypokalemia vs hyperkalemia and why small potassium changes are dangerous.
• 2.14 Explain how low calcium affects skeletal vs cardiac muscle and neuromuscular excitability.
• 2.15 Explain how hypocalcemia affects skeletal muscle tetany and cardiac function; distinguish actions of calcium on nerves vs cardiac contraction.
• 2.16 Describe how hypercalcemia affects neuromuscular activity, ADH function, and kidney function; discuss bone density and kidney stones.
• 2.17 Explain interactions of calcium with phosphate; discuss how low phosphate affects calcium and bone interactions.
• 2.18 Summarize acid-base imbalance categories and list typical compensations; describe the approach to treat imbalances while considering underlying causes.
• CASE STUDY 2.1 Vomiting (conceptual questions about compartments, dehydration signs, pH expectations, compensation, age-related factors).
• CASE STUDY 2.2 Diarrhea (infant dehydration; major losses; rapid progression; electrolyte and acid-base implications).

Formulas and Key Ratios (LaTeX)

• Buffer ratio (bicarbonate system):
  \frac{[\mathrm{HCO3^-}]}{[\mathrm{H2CO_3}]} \approx 20:1
  where H2CO3 is in equilibrium with CO2 in blood (carbonic acid). In practice, the ratio is often expressed in terms of CO2 as the dissolved CO2 concentration, i.e., CO2 relates to H2CO3 via carbonic anhydrase.
• Normal pH range: 7.35 \leq \mathrm{pH} \leq 7.45.
• Normal serum pH and bicarbonate-CO2 balance: when pH remains near 7.40, the 20:1 ratio is maintained; deviations require compensation (respiratory or renal changes).
• Normal body water content variances: adults ~60% body weight; infants ~70%; elderly and obese have lower percentages.
• Sodium distribution references: extracellular Na+ makes up a large portion of extracellular osmolarity; normal serum Na+ ~135–145 mmol/L (hyponatremia
• Potassium distribution: intracellular ~160 mEq/L vs extracellular ~3.5–5 mEq/L; severe shifts across membranes have major cardiac implications.

Notes on Figures and Tables (referenced concepts)

• Fig. 2.1 Movement of water and electrolytes between compartments: shows filtration, diffusion, and osmosis across capillary membranes and the role of hydrostatic and osmotic pressures.
• Fig. 2.2 Causes of edema: A–E diagrams illustrating normal capillary filtration vs edema due to increased hydrostatic pressure, decreased plasma oncotic pressure, lymphatic obstruction, and increased capillary permeability.
• Fig. 2.3 Pitting edema visual reference.
• Fig. 2.5 Role of Na+ and K+ in nerve impulse conduction (membrane potentials).
• Fig. 2.6 Hyponatremia and intracellular fluid shifts due to osmotic changes.
• Fig. 2.7 Relationship of hydrogen and potassium ions (H+ shifts with acidosis/alkalosis affect K+ distribution).
• Fig. 2.8 ECG changes with potassium imbalance.
• Fig. 2.9 Chloride-bicarbonate shift during vomiting (hypochloremic alkalosis).
• Fig. 2.11 Buffer system and acid-base balance changes with CO2 and HCO3- adjustments.
• Fig. 2.12 Metabolic acidosis schematic; Fig. 2.13 Metabolic alkalosis schematic; Fig. 2.14 Respiratory acidosis schematic; Fig. 2.15 Respiratory alkalosis schematic.

End of Notes