Starling forces

**Starling equation:** Net filtration (J_v) = K_f [(P_c − P_i) − σ(π_c − π_i)]

- **P_c** = capillary hydrostatic pressure (favors filtration/out of capillary). Highest at the arteriolar end (~35 mmHg), falling to ~15 mmHg at the venular end. - **P_i** = interstitial hydrostatic pressure (normally ~0 or slightly negative; favors filtration when negative). - **π_c** = capillary oncotic pressure (~25–28 mmHg; mainly albumin; pulls fluid INTO the capillary). - **π_i** = interstitial oncotic pressure (~0–5 mmHg; pulls fluid out). - **K_f** = filtration coefficient = hydraulic conductivity × surface area (increased in inflammation/burns). - **σ** = reflection coefficient (0–1; 1 = completely impermeable to protein, 0 = freely permeable). Decreased in inflammation, so protein leaks and fluid follows.

**Net result:** Slight net filtration overall (~2–4 L/day). The excess is returned to circulation by lymphatics.

**Clinical correlations (causes of edema):** 1. **↑ Capillary hydrostatic pressure (P_c):** Heart failure (especially right-sided → peripheral edema, left-sided → pulmonary edema), venous obstruction (DVT, cirrhosis with portal hypertension → ascites), volume overload (renal failure), prolonged standing, pregnancy. 2. **↓ Plasma oncotic pressure (π_c):** Nephrotic syndrome (protein loss in urine), cirrhosis/liver failure (↓ albumin synthesis), malnutrition (kwashiorkor), protein-losing enteropathy. Gives generalized pitting edema; periorbital edema in nephrotic syndrome. 3. **↑ Capillary permeability (↑ K_f, ↓ σ):** Sepsis, burns, inflammation, anaphylaxis (histamine, bradykinin, leukotrienes), ARDS. Leads to protein-rich exudate. 4. **↑ Interstitial oncotic pressure / impaired lymphatic drainage:** Lymphatic obstruction (filariasis, malignancy, surgery/radiation, e.g., post-mastectomy lymphedema) gives non-pitting edema.

**Transudate vs exudate:** Altered Starling forces (↑ hydrostatic, ↓ oncotic) produce a **transudate** (low protein, specific gravity <1.012). Increased permeability produces an **exudate** (high protein). Light's criteria are used to distinguish pleural effusions.

**Pulmonary circulation:** Same principles apply; pulmonary capillary hydrostatic pressure is lower (~8–10 mmHg), so the lung stays relatively dry. A pulmonary capillary wedge pressure above ~18–20 mmHg predisposes to cardiogenic pulmonary edema. In ARDS, permeability is increased (non-cardiogenic edema with normal wedge pressure).

**Renal application:** In the glomerulus, the same forces determine GFR: GFR = K_f [(P_GC − P_BS) − π_GC]. π_BS is ~0. Because π_GC rises along the capillary (filtration concentrates protein) and there is no reabsorption, filtration equilibrium may be reached. Effects: afferent arteriole constriction ↓ P_GC → ↓ GFR and ↓ RPF (filtration fraction unchanged/↔); efferent constriction ↑ P_GC → ↑ GFR, ↓ RPF, ↑ FF; ureteral obstruction ↑ P_BS → ↓ GFR; ↑ plasma protein (dehydration) ↑ π_GC → ↓ GFR; ↓ plasma protein ↓ π_GC → ↑ GFR. Peritubular capillaries use the same forces: ↑ FF raises π in peritubular capillaries, which promotes proximal tubule reabsorption.

**High-yield pearls:** - Albumin is the main contributor to plasma oncotic pressure; the Gibbs-Donnan effect adds a small contribution. - Pitting edema = increased fluid in interstitium (hydrostatic/oncotic/permeability causes); non-pitting = lymphedema, myxedema (hypothyroidism: glycosaminoglycan deposition), lipedema. - Treatment is aimed at the cause: diuretics (↓ P_c via ↓ volume), albumin infusion in select settings (SBP, large-volume paracentesis), compression stockings (↑ P_i), ACE inhibitors/ARBs and glucocorticoids for proteinuria. - Cerebral capillaries (tight junctions, blood–brain barrier) have σ near 1; vasogenic edema results from BBB breakdown, while cytotoxic edema reflects cell swelling (e.g., ischemia, Na/K-ATPase failure).