Subscribe to RSS
DOI: 10.1055/s-0033-1334092
Calf Pump Activity Influencing Venous Hemodynamics in the Lower Extremity
Publication History
Publication Date:
06 February 2013 (online)
![](https://www.thieme-connect.de/media/ija/201301/lookinside/thumbnails/10.1055-s-0033-1334092-1.jpg)
Abstract
Calf muscle pump is the motive force enhancing return of venous blood from the lower extremity to the heart. It causes displacement of venous blood in both vertical and horizontal directions, generates ambulatory pressure gradient between thigh and lower leg veins, and bidirectional streaming within calf perforators. Ambulatory pressure gradient triggers venous reflux in incompetent veins, which induces ambulatory venous hypertension in the lower leg and foot. Bidirectional flow in calf perforators enables quick pressure equalization between deep and superficial veins of the lower leg; the outward (into the superficial veins) oriented component of the bidirectional flow taking place during calf muscle contraction is no pathological reflux but a physiological centripetal flow streaming via great saphenous vein into the femoral vein. Calf perforators are communicating channels between both systems making them conjoined vessels; they are not involved in the generation of pathological hemodynamic situations, nor do they cause ambulatory venous hypertension. The real cause why recurrences develop has not as yet been cleared. Pressure gradient arising during calf pump activity between the femoral vein and the saphenous remnant after abolition of saphenous reflux triggers biophysical and biochemical events, which might induce recurrence. Thus, abolition of saphenous reflux removes the hemodynamic disturbance, but at the same time it generates precondition for reflux recurrence and for the comeback of the previous pathological situation; this chain of events has been called hemodynamic paradox.
-
References
- 1 Arnoldi CC. Venous pressure in the legs of healthy human subjects at rest and during muscular exercise in nearly erect position. Acta Chir Scand 1965; 130: 530-583
- 2 Bjordal R. Simultaneous pressure and flow recordings in varicose veins of the lower extremity. A haemodynamic study of venous dysfunction. Acta Chir Scand 1970; 136 (4) 309-317
- 3 Trendelenburg F. Ligation of the great saphenous vein in lower leg varicose veins [in German]. Beitr Klin Chir 1891; 7: 195-210
- 4 Ludbrook J, Beale G. Femoral venous valves in relation to varicose veins. Lancet 1962; 1 (7220) 79-81
- 5 Hauser H, Brunner U. New pathophysiological and functional aspects concerning incompetence of small saphenous vein [in German]. Vasa 1993; 22: 338-341
- 6 Recek C, Hammerschlag A. Incompetence of the femoral vein and small saphenous vein: Is there any a causal relationship? [in German]. Phlebologie 1997; 26: 115-119
- 7 Jeanneret C, Labs KH, Aschwanden M, Bollinger A, Hoffmann U, Jäger K. Physiological reflux and venous diameter change in the proximal lower limb veins during a standardised Valsalva manoeuvre. Eur J Vasc Endovasc Surg 1999; 17 (5) 398-403
- 8 Arnoldi CC. Venous pressure in patients with valvular incompetence of the veins of the lower limb. Acta Chir Scand 1966; 132: 628-645
- 9 Recek C, Koudelka V. Effet circulatoire du reflux saphénien dans la varicose essentielle. Phlebologie 1979; 32 (4) 407-414
- 10 Recek C, Koudelka V. Perforating veins of the leg and their role in the pathogenesis of varicose veins. Rozhl Chir 1973; 52 (1) 14-20
- 11 Sarin S, Scurr JH, Smith PD. Medial calf perforators in venous disease: the significance of outward flow. J Vasc Surg 1992; 16 (1) 40-46
- 12 Höjensgard IC, Stürup H. Static and dynamic pressures in superficial and deep veins of the lower extremity in man. Acta Physiol Scand 1952; 27 (1) 49-67
- 13 Recek C, Pojer H. Ambulatory pressure gradient in the veins of the lower extremity. Vasa 2000; 29 (3) 187-190
- 14 Recek C. A critical appraisal of the role of ankle perforators for the genesis of venous ulcers in the lower leg. J Cardiovasc Surg (Torino) 1971; 12 (1) 45-49
- 15 Recek C. Saphenous reflux as a cause of severe hemodynamic disturbance in chronic venous insufficiency [in German]. Acta Chir Austriaca 1998; 30: 76-77
- 16 Recek C, Karisch E, Gruber J. Diameter changes in calf perforators and deep veins of the lower leg after abolition of the saphenous reflux [in German]. Phlebologie 2000; 29: 37-40
- 17 Gohel MS, Barwell JR, Wakely C , et al. The influence of superficial venous surgery and compression on incompetent calf perforators in chronic venous leg ulceration. Eur J Vasc Endovasc Surg 2005; 29 (1) 78-82
- 18 Geier B, Stücker M, Hummel T , et al. Residual stumps associated with inguinal varicose vein recurrences: a multicenter study. Eur J Vasc Endovasc Surg 2008; 36 (2) 207-210
- 19 Dwerryhouse S, Davies B, Harradine K, Earnshaw JJ. Stripping the long saphenous vein reduces the rate of reoperation for recurrent varicose veins: five-year results of a randomized trial. J Vasc Surg 1999; 29 (4) 589-592
- 20 Joshi D, Sinclair A, Tsui J, Sarin S. Incomplete removal of great saphenous vein is the most common cause for recurrent varicose veins. Angiology 2011; 62 (2) 198-201
- 21 Fischer R, Linde N, Duff C, Jeanneret C, Chandler JG, Seeber P. Late recurrent saphenofemoral junction reflux after ligation and stripping of the greater saphenous vein. J Vasc Surg 2001; 34 (2) 236-240
- 22 Allegra C, Antignani PL, Carlizza A. Recurrent varicose veins following surgical treatment: our experience with five years follow-up. Eur J Vasc Endovasc Surg 2007; 33 (6) 751-756
- 23 Glass GM. Neovascularization in recurrence of varices of the great saphenous vein in the groin: phlebography. Angiology 1988; 39 (7, Pt 1) 577-582
- 24 Jones L, Braithwaite BD, Selwyn D, Cooke S, Earnshaw JJ. Neovascularisation is the principal cause of varicose vein recurrence: results of a randomised trial of stripping the long saphenous vein. Eur J Vasc Endovasc Surg 1996; 12 (4) 442-445
- 25 Nyamekye I, Shephard NA, Davies B, Heather BP, Earnshaw JJ. Clinicopathological evidence that neovascularisation is a cause of recurrent varicose veins. Eur J Vasc Endovasc Surg 1998; 15 (5) 412-415
- 26 Winterborn RJ, Earnshaw JJ. Randomised trial of polytetrafluoroethylene patch insertion for recurrent great saphenous varicose veins. Eur J Vasc Endovasc Surg 2007; 34 (3) 367-373
- 27 Bhatti TS, Whitman B, Harradine K, Cooke SG, Heather BP, Earnshaw JJ. Causes of re-recurrence after polytetrafluoroethylene patch saphenoplasty for recurrent varicose veins. Br J Surg 2000; 87 (10) 1356-1360
- 28 Earnshaw JJ, Davies B, Harradine K, Heather BP. Preliminary results of PTFE patch saphenoplasty to prevent neovascularization leading to recurrent varicose veins. Phlebology 1998; 13: 10-13
- 29 Gibbs PJ, Foy DM, Darke SG. Reoperation for recurrent saphenofemoral incompetence: a prospective randomised trial using a reflected flap of pectineus fascia. Eur J Vasc Endovasc Surg 1999; 18 (6) 494-498
- 30 Frings N, Nelle A, Tran VTP , et al. Unavoidable recurrence and neoreflux after correctly performed ligation of the saphenofemoral junction: neovascularization? [in German]. Phlebologie 2003; 32: 96-100
- 31 Turton EP, Scott DJ, Richards SP , et al. Duplex-derived evidence of reflux after varicose vein surgery: neoreflux or neovascularisation?. Eur J Vasc Endovasc Surg 1999; 17 (3) 230-233
- 32 El Wajeh Y, Giannoukas AD, Gulliford CJ, Suvarna SK, Chan P. Saphenofemoral venous channels associated with recurrent varicose veins are not neovascular. Eur J Vasc Endovasc Surg 2004; 28 (6) 590-594
- 33 Recek C. The hemodynamic paradox as a phenomenon triggering recurrent reflux in varicose vein disease. Int J Angiol 2012; 21 (3) 181-185
- 34 Schaper W. Collateral circulation: past and present. Basic Res Cardiol 2009; 104 (1) 5-21
- 35 Pipp F, Boehm S, Cai WJ , et al. Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. Arterioscler Thromb Vasc Biol 2004; 24 (9) 1664-1668
- 36 Schaper W, Scholz D. Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol 2003; 23 (7) 1143-1151
- 37 Resnick N, Gimbrone Jr MA. Hemodynamic forces are complex regulators of endothelial gene expression. FASEB J 1995; 9 (10) 874-882
- 38 Schierling W, Troidl K, Troidl C, Schmitz-Rixen T, Schaper W, Eitenmüller IK. The role of angiogenic growth factors in arteriogenesis. J Vasc Res 2009; 46 (4) 365-374