Chapter 25
Water and Fluid Compartments in the Body
Water content differences by age and size
Adults have more total fluid than babies; babies are smaller but metabolically active with rapid fluid turnover.
As you age, your percentage of body fluid decreases even though absolute volume may grow; organs still require fluid to function.
Kidneys and brain, liver, kidneys depend on adequate fluid for function.
Why fluid balance matters medically
All organs need fluid to function properly; imbalances can affect organ performance, mental status, and perfusion.
Body Fluid Compartments and Distribution
Major compartments
Intracellular fluid (ICF): fluid inside cells; makes up the majority of total body fluid.
Extracellular fluid (ECF): fluid outside cells; includes interstitial fluid and plasma.
Intracellular fluid specifics
Cytosol vs cytoplasm
Cytosol: the fluid portion inside cells, without organelles.
Cytoplasm: cytosol plus organelles; jelly-like substance inside the cell.
Intracellular fluid (ICF) is mainly cytosol; it accounts for about two-thirds of total body fluid:
Extracellular fluid specifics
Fluid outside the cells; includes plasma (fluid in blood) and interstitial fluid (fluid between cells).
Examples of extracellular fluids:
Cerebrospinal fluid (CSF): extracellular fluid in the CNS.
Synovial fluid: in joints.
Tears and saliva: extracellular fluids.
Fluids associated with specific body regions:
Eye fluids: aqueous humor (anterior chamber) and vitreous humor (posterior chamber).
Aqueous humor is in the anterior chamber; anterior chamber is smaller than posterior.
Vitreous humor is more jelly-like.
Inner ear fluids contribute to equilibrium.
Serous fluids in body cavities: pleural (between lung and pleura), pericardial (around the heart), peritoneal/ascites (in abdominal cavity).
Fluid in body cavities and edema terminology
Edema: extracellular fluid accumulation, usually extracellular and often localized.
Fluid sequestration: fluid is in the wrong spaces but total body fluid may be normal.
Localized edema conditions include:
Ascites: fluid in the peritoneal cavity (abdominal fluid).
Pericardial effusion: fluid around the heart.
Pleural effusion: fluid in the pleural cavity around the lungs.
Lymphedema: edema due to impaired lymphatic drainage or surgical removal/blockage of lymph vessels.
Fluid assessment techniques (clinical cues)
Ultrasound can be used to assess abdominal or other fluid accumulations.
Percussion and auscultation are used to evaluate fluid status and organ involvement; percussion to assess fluid pockets; auscultation to listen for organ function and effusions.
Osmolarity and Fluid Movement
Key concepts
Osmolarity: the concentration of solutes in a fluid; higher osmolarity means more solutes per unit of water.
Fluid movement between compartments responds to osmotic gradients; two major systems drive fluid movement:
Cardiovascular system (blood flow and capillary exchange)
Urinary/renal system (kidneys) and lymphatic system (fluid balance and return to circulation)
What contributes to osmolarity in the body
Major solutes: sodium and other electrolytes, proteins, and other charged particles.
Higher solute content = higher osmolarity. Conversely, more water dilutes solutes and lowers osmolarity.
How drinking water affects osmolarity
Drinking water increases total body water and plasma water, which tends to decrease plasma osmolarity:
Practical examples of osmolarity changes
In a desert marathon scenario with salty snacks and no water:
Plasma osmolarity increases due to higher solute-to-water ratio; this prompts thirst and renal adjustments.
Fluids entering the body from food, especially foods with water content, typically increase total body fluid; salty foods can modulate osmolarity very slightly via salt load.
Effects of kidney function on osmolarity
Kidney failure complicates osmolarity balance because the kidney’s ability to filter and excrete solutes and water is impaired.
In-class discussion highlighted a nuanced point: kidney failure can lead to either increased or decreased osmolarity depending on the balance of total body water retention and solute retention; the instructor emphasized that many patients with kidney failure end up with decreased osmolarity due to fluid retention, though this can vary in specific contexts.
Sodium, Water, and Hormonal Regulation of Fluid Balance
Sodium as the principal extracellular solute
The principal solute of the extracellular fluid is , crucial for neuromuscular function and renal (kidney) function.
Sodium exerts the strongest osmotic pull on water; water follows sodium during movement between compartments (osmosis).
High extracellular sodium increases plasma osmolality and drives water retention in the vascular compartment, contributing to higher blood pressure.
Key regulatory hormones and their actions
Atrial natriuretic peptide (ANP/ANP-like peptide in lecture noted as AMP):
Made in the atria of the heart.
Promotes excretion of sodium and water by the kidneys; lowers blood volume and pressure.
Antidiuretic hormone (ADH, vasopressin):
Made in the hypothalamus; stored and released from the posterior pituitary.
In the brain, ADH stimulates thirst; in the kidneys, it increases water reabsorption (water retention) to raise circulating fluid volume.
Aldosterone (a mineralocorticoid):
Made in the adrenal cortex, specifically the zona glomerulosa.
Increases sodium and water reabsorption in the kidney tubules and promotes potassium excretion.
Triggered by low blood pressure and/or low plasma sodium levels; part of the renin-angiotensin-aldosterone system (RAAS).
Renin-angiotensin-aldosterone system (RAAS)
Angiotensinogen is produced by the liver.
Renin is produced by the juxtaglomerular (JG) apparatus in the kidneys and converts angiotensinogen to angiotensin I.
Angiotensin-converting enzyme (ACE), mainly in the lungs, converts angiotensin I to angiotensin II.
Angiotensin II causes vasoconstriction and stimulates aldosterone release.
Major components of the RAAS pathway (summary)
Liver: angiotensinogen production.
Kidney JG apparatus: renin release; macula densa and granular (JG) cells participate in renin regulation.
Lungs: ACE converts angiotensin I to angiotensin II.
Adrenal cortex (zona glomerulosa): aldosterone release in response to angiotensin II and other signals.
Effects of angiotensin II: vasoconstriction, stimulates aldosterone release, increases blood pressure and maintains blood volume.
Pharmacology and clinical notes
ACE inhibitors reduce conversion of angiotensin I to angiotensin II, lowering blood pressure.
A common side effect of ACE inhibitors is a dry cough, due to bradykinin accumulation when ACE is inhibited.
Potassium-sparing diuretics and loop diuretics oppose aldosterone’s actions and affect electrolyte balance (sodium and potassium) and water reabsorption.
Acid-Base Balance and Respiratory vs Metabolic Disorders
Normal blood gas ranges and buffers
Normal blood pH: 7.35-7.45
Target center (often memorized as around)
Carbon dioxide and bicarbonate reference values (typical teaching cues):
Acid-base categories and compensation
Acidosis: pH < 7.35; alkalosis: pH > 7.45.
If a primary metabolic disorder occurs, the respiratory system compensates via altered ventilation (hyperventilation to blow off CO2 in metabolic acidosis; hypoventilation to retain CO2 in metabolic alkalosis).
If a primary respiratory disorder occurs, the kidneys compensate by adjusting bicarbonate excretion/retention (to balance the acid-base state).
Common scenarios and diagnoses discussed
Respiratory acidosis: decreased ventilation leading to CO2 retention (e.g., emphysema, COPD).
Respiratory alkalosis: hyperventilation (e.g., high altitude exposure, anxiety leading to rapid breathing).
Metabolic acidosis: excess fixed acids or bicarbonate loss (e.g., ketoacidosis in diabetes, severe diarrhea, renal failure with acid retention).
Metabolic alkalosis: loss of acid (e.g., profuse vomiting) or gain of bicarbonate (less common in this lecture context).
Practical examples from the lecture
Emphysema/COPD: respiratory acidosis due to impaired CO2 exhalation.
High altitude exposure: respiratory alkalosis due to hyperventilation driven by low oxygen leading to excessive CO2 loss.
Clues from vomiting and diarrhea:
Vomiting tends to cause metabolic alkalosis (loss of stomach acid).
Severe diarrhea tends to cause metabolic acidosis (loss of bicarbonate and fluids elsewhere in the body).
Diabetes and ketoacidosis:
Ketoacidosis represents metabolic acidosis driven by excess keto acids.
Renal compensation will increase bicarbonate excretion or retention to counterbalance acidity; respiratory compensation may also occur via altered breathing patterns.
Practical mental model to remember acid-base changes
A simple mnemonic: things that come out the top raise pH (vomiting - metabolic alkalosis), things that come out the bottom lower pH (diarrhea or renal failure with acid – metabolic acidosis).
Respiratory disorders affect PaCO2 and are considered respiratory acidosis/alkalosis; metabolic disorders affect HCO3- and are metabolic acidosis/alkalosis.
Diabetic ketoacidosis and urine pH
In metabolic acidosis from ketoacidosis, renal compensation increases acid excretion and lowers urine pH; bicarbonate may be depleted in blood as it buffers excess acid.
Blood bicarbonate (HCO3^-) tends to be lower in metabolic acidosis due to buffering and renal excretion of H^+ with bicarbonate loss.
Quick Recap: Key Connections and Takeaways
Water in the body is mainly in:
Intracellular fluid (ICF): primarily cytosol; about two-thirds of TBW.
Extracellular fluid (ECF): includes plasma and interstitial fluid; important for nutrient/waste exchange and circulation.
Osmolarity and fluid shifts depend on solute concentration; water moves toward higher solute concentration.
Sodium is the principal extracellular solute and drives water movement; many regulatory pathways center on maintaining Na^+ balance to control fluid volume and BP.
Major regulatory systems:
RAAS (renin-angiotensin-aldosterone system) controls Na^+ and water retention and vascular tone; RAAS components are produced in kidney (renin), liver (angiotensinogen), lungs (ACE), and adrenal cortex (aldosterone).
ADH (vasopressin) controls water reabsorption in kidneys and thirst; ANP/atrial natriuretic peptide promotes Na^+ and water excretion to lower blood volume.
Common clinical fluid disturbances:
Edema (extracellular fluid excess) and fluid sequestration (fluid in wrong places).
Ascites, pericardial effusion, and pleural effusion as examples of fluid in body cavities.
Lymphedema from lymphatic obstruction.
Acid-base balance and gas exchange:
Normal pH range: , often summarized as around .
Normal values: {PaCO}2=40 mmHg,{HCO}3=24mEq/L.
Distinguish respiratory vs metabolic etiologies and understand compensatory mechanisms.
Examples discussed: emphysema/COPD (respiratory acidosis), high altitude (respiratory alkalosis), vomiting (metabolic alkalosis), diarrhea (metabolic acidosis), ketoacidosis (metabolic acidosis).
Practical clinical notes
Hypernatremia/hyponatremia impact on osmolality and cell volume; high salt can raise BP due to increased extracellular volume and vascular resistance.
Diuretics (loop or potassium-sparing) affect kidneys’ handling of Na^+ and water, and can influence K^+ balance and acid-base status.
When assessing fluid status, consider intake (water and food), losses (urine, stool, sweat), and distribution (ICF vs ECF), plus the hormonal state (ADH, aldosterone, ANP).
Important Quantities and Formulas to Remember (LaTeX)
Normal pH range:
Typical reference values:
{PaCO2=35-45 mmHg
HCO_3=22-26
Hemodynamic and osmotic relationships discussed include:
Higher solute concentration increases osmolarity; water moves toward higher osmolarity via osmosis.
Sodium drives extracellular osmolality and water retention; ANP reduces Na^+ and water and lowers blood volume.
RAAS cascade (summary):
Angiotensinogen (liver) --(Renin)--> Angiotensin I --(ACE in lungs)--> Angiotensin II
Angiotensin II stimulates aldosterone release (adrenal cortex, zona glomerulosa) and causes vasoconstriction.
Aldosterone promotes Na^+ and water reabsorption and K^+ excretion in the kidneys.