Page 244 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)
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Edemas
       Functional pores in the capillary endothelium  in the lungs (→ p. 80). Possible causes of ede-
       allow largely protein-free plasma fluid to filter  ma are (→ B):
       into the interstitial spaces. About 20 L/d are fil-  ! Blood pressure rise at the arterial end due to
       tered through all capillaries of the body (ex-  precapillary vasodilation (P cap ↑), especially
       cluding the kidneys), of which 90% are imme-  during a simultaneous increase in permeabil-
       diately reabsorbed. The remaining 2 L/d reach  ity to proteins (σ prot ↓ and thus ∆π ↓), for exam-
       the blood compartment only via the lymph  ple, in inflammation or anaphylaxis (hista-
       (→ A).                          mine, bradykinin, etc.).
         The filtration or reabsorption rate Q f is de-  ! Rise in venous pressure (P cap ↑ at the capil-
       termined by the filtration coefficient K f (= wa-  lary end), which may be caused locally by ve-
       ter permeability · exchange area) of the capil-  nous thrombosis or systemically (cardiac ede-
       lary wall, as well as by the effective filtration
                                       ma), for example, by heart failure (→
    Heart and Circulation  between the hydrostatic pressure difference ∆P  cites (→ p.170).
                                       p. 224ff.). Portal vein congestion leads to as-
       pressure P eff (Q f = P eff · K f ). P eff is the difference
                                       ! Reduced plasma concentration of proteins
       and the oncotic (colloidal osmotic) pressure dif-
                                       (especially albumin) causes ∆π to fall exces-
       ference ∆π across the capillary wall (Starling’s
                                       sively. This may be the result of renal loss of
       law), where ∆P = blood pressure in the capil-
                                       proteins (proteinuria; → p.104) or of too little
       laries (P cap ) – interstitial pressure (P int , normal-
                                       liver cirrhosis; → p.172ff.), or of an increased
       centration being higher in plasma than in the
                                       breakdown of plasma proteins to meet amino
       interstitial space by ∆C prot (≈ 1 mmol/L), and it
    7  ly ≈ 0 mmHg). ∆π arises due to the protein con-  hepatic synthesis of plasma proteins (e.g., in
       is the greater, the closer the reflexion coeffi-  acid demand if there is a protein deficiency
       cient for plasma proteins (σ prot ) is to 1.0, i.e.,  (hunger edema).
       the smaller the endothelial permeability for  ! Diminished lymphatic flow may also cause
       plasma proteins (∆π = σ prot · R · T · ∆C prot ). At  local edemas, either by compression (tumors),
       heart level, ∆P at the arterial end of the capil-  transection (operations), fibrosis (radiother-
       laries is ca. 30 mmHg; at the venous end it falls  apy), or occlusion (Bilharziasis) of the lym-
       to ca. 22 mmHg. ∆π (ca. 24 mmHg; → A, right)  phatic vessels.
       counteracts these pressures so that the intially  When edemas form, the interstitial space is
       high filtration (P eff = + 6 mmHg) is turned into  enlarged until a new equilibrium is estab-
       reabsorption when P eff becomes negative. (In  lished (filtration = absorption + lymphatic out-
       the lungs ∆P is only 10 mmHg, so that P eff is  flow). An increased compliance of the intersti-
       very low.)                      tial space encourages edemas to form just as
         Below the level of the heart the hydrostatic  much as a raised hydrostatic pressure in the
       pressure of the column of blood is added to  dependent parts of the body (e.g., ankle ede-
       the pressure in the capillary lumen (at foot lev-  ma) does.
       el ca. + 90 mmHg). It is especially on standing  As edema fluid originates from blood, the
       still that the filtration pressure is very high in  consequence of systemic edema (→ B, bottom)
       the legs. It is compensated by self-regulation  will be a decrease in blood volume, and thus
       in that because of the outflow of water, the  cardiac output. Renal perfusion is reduced not
       protein concentration and thus ∆π is increased  only directly by the fall in CO, but also as a re-
       along the capillaries. It is also part of self-regu-  sult of sympathetic stimulation. The renal fil-
       lation that P int rises when filtation is increased  tration fraction is raised and the renin–angio-
       (limited compliance of the interstitial space),  tensin mechanism is initiated. The resulting
                                        +
       and as a result ∆P decreases.   Na retention raises the extracellular fluid vol-
         If the amount of filtrate exceeds the sum of  ume which, while increasing the blood vol-
                                                                 +
       reabsorbed volume plus lymphatic outflow,  ume, actually makes the edema worse. Na re-
       edemas develop, ascites develop in the region  tention in renal failure also results in edema
  234  of portal vein supply, as do pulmonary edemas  being formed.
       Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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