Starling Forces - The Great Exchange
- Fluid movement across capillaries is governed by Starling forces, balancing hydrostatic (push) and oncotic (pull) pressures. Net movement determines filtration or absorption.
- Net Filtration Pressure Equation: $J_v = K_f [ (P_c - P_i) - \sigma (\pi_c - \pi_i) ]$
- $P_c$ (Capillary hydrostatic): Pushes fluid out.
- $\pi_c$ (Capillary oncotic): Pulls fluid in.
- $P_i$ (Interstitial hydrostatic): Pushes fluid in.
- $\pi_i$ (Interstitial oncotic): Pulls fluid out.
- 📌 Mnemonic: 'Push out, Pull in'. P for Hydrostatic Pressure Pushes; π for Oncotic Pressure Pulls.

⭐ The reflection coefficient (σ) indicates the effectiveness of the capillary wall in preventing protein passage. A value of 1 implies impermeability, while 0 implies free passage.
| Capillary Type | Structure & Permeability | Key Locations |
|---|---|---|
| Continuous | Least permeable; tight junctions. | Muscle, skin, lungs, CNS. |
| Fenestrated | Moderate permeability; pores. | Kidneys (glomeruli), endocrine glands. |
| Sinusoidal | Most permeable; large gaps. | Liver, spleen, bone marrow. |
Flow Regulation - Local Traffic Control
Autoregulation is the intrinsic ability of an organ to maintain constant blood flow despite changes in perfusion pressure. Key mechanisms:
- Myogenic Mechanism: Smooth muscle contracts in response to ↑ stretch (↑ pressure) and relaxes with ↓ stretch.
- Metabolic Mechanism: Tissue metabolism dictates local blood flow.
Hyperemia:
- Active Hyperemia: Blood flow increases to meet metabolic demand (e.g., exercise).
- Reactive Hyperemia: A transient increase in blood flow following a period of ischemia.

Local Vaso-regulators:
- Vasodilators:
- Nitric Oxide (NO)
- Adenosine
- $K^+$
- $CO_2$
- $H^+$
- Vasoconstrictors:
- Endothelin
- Myogenic response
⭐ In the heart, adenosine is the most critical local vasodilator linking coronary blood flow to myocardial oxygen demand.
Lymphatics & Edema - The Drainage System
Lymphatic capillaries drain excess interstitial fluid, protein, and macromolecules, returning it to circulation. Failure of this system results in edema-fluid accumulation in the interstitium.
-
Pathophysiology (Altered Starling Forces):
- ↑ $P_c$ (Capillary Hydrostatic Pressure): Pushes excess fluid out (e.g., heart failure, DVT).
- ↓ $\pi_c$ (Plasma Oncotic Pressure): Fails to pull fluid in (e.g., liver failure, nephrotic syndrome).
- ↑ $K_f$ (Capillary Permeability): Allows protein and fluid to leak out (e.g., inflammation, burns).
- Lymphatic Obstruction: Impairs fluid return (e.g., post-surgery, filariasis).
-
Types: Pitting edema (low-protein fluid) vs. Non-pitting edema (protein-rich fluid).
⭐ Lymphedema, caused by lymphatic obstruction (e.g., post-mastectomy, filariasis), is a classic cause of non-pitting edema due to the high protein content of the interstitial fluid.

- Starling forces (hydrostatic & oncotic pressures) dictate fluid flux across the capillary wall.
- Capillary hydrostatic pressure (Pc) is the main force driving filtration (fluid out).
- Plasma oncotic pressure (πc) is the main force driving reabsorption (fluid in).
- Arterioles are the primary site of vascular resistance, regulating blood flow into the capillary bed.
- Lymphatics are essential for draining excess interstitial fluid, preventing edema.
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