7 Heart and Circulation Edemas Functional pores in the capillary endothelium allow largely protein-free plasma fluid to filter into the interstitial spaces. About 20 L/d are fil- tered through all capillaries of the body (ex- cluding the kidneys), of which 90% are imme- diately reabsorbed. The remaining 2 L/d reach the blood compartment only via the lymph (5a). The filtration or reabsorption rate Q, is de- termined by the filtration coefficient K; (= wa- ter permeability - exchange area) of the capil- lary wall, as well as by the effective filtration pressure Puy (Q;= Poy - K;). Pow is the difference between the hydrostatic pressure difference AP and the oncotic (colloidal osmotic) pressure dif- (ference Ax across the capillary wall (Starling's law), where AP=blood pressure in the capil- laries (Pip) - interstitial pressure (Pjq., normal- ly =OmmHg). Anarises due to the protein con- centration being higher in plasma than in the interstitial space by AC,,.¢ (= 1 mmol/L), and it is the greater, the closer the reflexion coeffi- cient for plasma proteins (6j:) iS to 1.0, ie, the smaller the endothelial permeability for plasma proteins (Am=Opre*R-T-ACprot). At heart level, AP at the arterial end of the capil- laries is ca. 30 mmHg; at the venous end it falls to ca, 22 mmHg. Ax (ca. 24 mmHg; = A, right) counteracts these pressures so that the intially high filtration (P,y=+6 mmHg) is turned into reabsorption when P. becomes negative. (In the lungs AP is only 10mmHsg, so that Py» is very low.) Below the level of the heart the hydrostatic pressure of the column of blood is added to the pressure in the capillary lumen (at foot lev- el ca. +90 mmHg). It is especially on standing still that the filtration pressure is very high in the legs. It is compensated by self-regulation in that because of the outflow of water, the protein concentration and thus Ax is increased along the capillaries. Itis also part of self-regu- lation that Pi rises when filtation is increased (limited compliance of the interstitial space), and asa result AP decreases. Ifthe amount of filtrate exceeds the sum of reabsorbed volume plus lymphatic outflow, edemas develop, ascites develop in the region of portal vein supply, as do pulmonary edemas Silbernag/Lan Color Atlas of Pathophysiology in the lungs (+ p. 80). Possible causes of ede- ma are (—B): Blood pressure rise at the arterial end due to precapillary vasodilation (P..)1), especially during a simultaneous increase in permeabil- ity to proteins (ojj.¢/ and thus 7-1), for exam- ple, in inflammation or anaphylaxis (hista- mine, bradykinin, etc.). Rise in venous pressure (P,4y 7 at the capil- lary end), which may be caused locally by ve- nous thrombosis or systemically (cardiac ede- ma), for example, by heart failure (> p.224ff.). Portal vein congestion leads to as- cites (— p.170). Reduced plasma concentration of proteins (especially albumin) causes Ax to fall exces- sively. This may be the result of renal loss of proteins (proteinuria; — p. 104) or of too little hepatic synthesis of plasma proteins (e.g,, in liver cirrhosis; — p.172ff.), or of an increased breakdown of plasma proteins to meet amino acid demand if there is a protein deficiency (hunger edema), Diminished lymphatic flow may also cause local edemas, either by compression (tumors), transection (operations), fibrosis (radiother- apy), or occlusion (Bilharziasis) of the lym- phatic vessels. When edemas form, the interstitial space is enlarged until a new equilibrium is estab- lished (filtration = absorption + lymphatic out- flow). An increased compliance of the intersti- tial space encourages edemas to form just as much as a raised hydrostatic pressure in the dependent parts of the body (e.g,, ankle ede- ma) does. ‘As edema fluid originates from blood, the consequence of systemic edema (->B, bottom) will be a decrease in blood volume, and thus cardiac output, Renal perfusion is reduced not only directly by the fall in CO, but also as a re- sult of sympathetic stimulation. The renal fil- tration fraction is raised and the renin-angio- tensin mechanism is initiated. The resulting Nat retention raises the extracellular fluid vol- ume which, while increasing the blood vol- ume, actually makes the edema worse. Na* re- tention in renal failure also results in edema being formed. © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.— A. Fluid Exchange at Capillaries Arteriole Vein kPa mmHg 30 \ tmen C= 40 [10% ca. 90% > | 35 El El eo post 3.0 race Lathan I 2S as ‘0 ance (00%) \ 20 5 , oy 7\A\ — pe PacP)-a: RT SC Filtration = Reabsorption + Lymphatic drainage = AP— An (kPa, mmHg) — B. Edema Formation Circulation” Capillaries Kidney > | | Liver — an cell ~ ' ) ats | / (AZ 4 € FF | r (AF / | / ‘Systemic: Systemic: Glomerular | Liver damage heart failure anaphylaxia, damage ' (e.g. cirrhosis) ete. sepsis, etc. (nephrotic Local Local syndrome) v venous thrombosis, inflammation ete ’ v Local: iene ee Protein Protein (portal vein) Histamine et. loss formation y uM Congestion Venous congestion Precapilary vasodilation Plasma proteins 71 Ascite Peas t cay —>Mcay) See Na’ metabolism J Nat uptake high, Pt > dP —> Na’ retention 4 (e.g. renal failure) \ —An An += Keene u ko Lymphatic Nat balance positive —> ECVt \ ery sae Compression of lymphatic vessels wl FON ad ot] LIN Obliteration x * “ (cadiotherapy) Rein Angiotensin Ese nite, (1 owen yy * Lymph ee Renal blood flow Plate 7.31 Edemas 235