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Starling equation

PhysiologyCardiovascularRenalRespiratoryLymphaticHepatic

Summary

The Starling equation describes net fluid movement across a capillary wall: Jv = Kf[(Pc − Pi) − σ(πc − πi)]. Hydrostatic pressure pushes fluid out of capillaries, while plasma oncotic pressure (mainly albumin) pulls it back in. Disruption of these forces causes edema (e.g., heart failure, nephrotic syndrome, cirrhosis, sepsis).

Detail

**Equation:** Net filtration (Jv) = Kf [(Pc − Pi) − σ(πc − πi)]

- **Pc** = capillary hydrostatic pressure (favors filtration; higher at the arteriolar end, ~30–35 mmHg, falling to ~15 mmHg at the venular end) - **Pi** = interstitial hydrostatic pressure (normally ~0 or slightly negative) - **πc** = capillary oncotic (colloid osmotic) pressure (~25–28 mmHg; mostly albumin; favors reabsorption) - **πi** = interstitial oncotic pressure (~0–5 mmHg) - **Kf** = filtration coefficient = hydraulic conductance × surface area (the capillary's permeability to water) - **σ** = reflection coefficient (0 = freely permeable to protein, 1 = impermeable)

**Physiology:** - Fluid is filtered at the arteriolar end, where Pc exceeds πc. Net filtration is positive there. - Classic teaching says fluid is reabsorbed at the venular end, where Pc falls below πc. The revised Starling principle says this is mostly wrong. Most capillaries show net filtration along their entire length. The endothelial glycocalyx and subglycocalyx oncotic pressure matter more than πi, and the lymphatics return the filtered fluid (~2–4 L/day) to the circulation. - The Pc − πc balance is determined by pre- vs post-capillary resistance. Arteriolar constriction lowers Pc and favors reabsorption. Arteriolar dilation or venous constriction raises Pc and favors filtration.

**Clinical correlates (causes of edema):** - **↑ Pc:** heart failure, volume overload, venous obstruction (DVT), pregnancy, and the dependent edema of prolonged standing. Pulmonary edema in left heart failure follows the same principle. - **↓ πc:** nephrotic syndrome (urinary albumin loss), cirrhosis (↓ albumin synthesis), malnutrition (kwashiorkor), and protein-losing enteropathy. - **↑ Kf or ↓ σ (↑ capillary permeability):** sepsis, burns, anaphylaxis/histamine, ARDS, and other inflammatory states, with protein-rich exudate. - **↑ πi / impaired lymphatic drainage:** lymphedema (filariasis, post-mastectomy or lymph node dissection, malignancy), myxedema (hypothyroidism, due to glycosaminoglycans).

**Exam tips:** - Transudate (↓ protein; due to altered Starling forces) vs exudate (↑ protein; due to ↑ permeability) is a classic distinction. - Starling forces also apply to the **glomerulus**: GFR = Kf[(PGC − PBS) − (πGC − πBS)]. πBS is normally ~0. Afferent constriction ↓ PGC, ↓ GFR. Efferent constriction ↑ PGC, ↑ GFR, and ↑ filtration fraction. Ureteral obstruction ↑ PBS, ↓ GFR. ↑ plasma protein (e.g., dehydration) ↑ πGC, ↓ GFR. - Edema formation is limited by safety factors: ↑ lymph flow, ↓ interstitial oncotic pressure from washout of protein, and ↑ Pi. - Pulmonary capillaries follow the same principles. Left atrial pressure elevation ↑ Pc and causes cardiogenic pulmonary edema, whereas ARDS is a permeability (↑ Kf, ↓ σ) edema. - Ascites in cirrhosis combines portal hypertension (↑ Pc in splanchnic capillaries) with hypoalbuminemia (↓ πc). The SAAG ≥1.1 g/dL indicates portal hypertension.

Sources

  • Guyton and Hall Textbook of Medical Physiology (Capillary fluid exchange, interstitial fluid, and lymph flow)
  • Costanzo Physiology (Cardiovascular Physiology: Microcirculation and Lymph)
  • Levick JR, Michel CC. Microvascular fluid exchange and the revised Starling principle. Cardiovasc Res. 2010;87(2):198-210
  • First Aid for the USMLE Step 1 (Cardiovascular and Renal Physiology: Starling forces)
  • Boron and Boulpaep Medical Physiology

Reviewed by Medusa editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.