VENOUS RETURN 



I 127 



to or perhaps considerably greater than those on 

 the outside of the veins. In these instances the vein 

 become distended and the venous resistance becomes 

 automatically reduced. This turns out to be an im- 

 portant safety factor in venous return, for often an 

 elevated right atrial pressure results from a damaged 

 heart, in which case return of blood to the heart 

 would become inadequate if the venous resistance 

 should remain as high under these conditions as it 

 is in the normal circulation. Fortunately, however, 

 the reduced resistance of the veins allows the existing 

 pressure gradient from the periphery to the heart to 

 force blood toward the heart almost equally as well 

 as it occurs normally. For this reason, the peripheral 

 pressures ordinarily do not rise significantly until 

 the right atrial pressure has risen above approxi- 

 mately + 4 to +6 mm Hg (74). Above this point, 

 the veins by then will have become distended, and 

 any additional rise in right atrial pressure is there- 

 after reflected by a similar increase in peripheral 

 venous pressure (83). 



parts of the body and creates negative pressure in 

 areas above the heart. The collapse factor and the 

 venous pump that modify these pressures were 

 described earlier in the chapter. Particularly impor- 

 tant is the fact that the veins of the neck collapse and 

 their resistances automatically become greatly ele- 

 vated. Therefore, venous pressure in the neck almost 

 never falls below atmospheric pressure unless un- 

 usual circumstances prevent the veins from collaps- 

 ing. 



Because of the importance of the hydrostatic fac- 

 tor in all venous pressure measurements, two very- 

 similar methods have been suggested for determin- 

 ing a "physiological zero" pressure in the venous 

 system (93, 1 1 1 ). The second of these, which was 

 presented from our laboratory, depends on rotating 

 a dog about two different axes. It was found that 

 venous pressures referred to a point barely inside 

 the right ventricle at the tricuspid valve did not 

 vary a measurable amount regardless of the position 

 of the animal. 



EFFECT OF VENOUS FLOW ON PERIPHERAL VENOUS 



pressures. An increase in the volume of venous 

 blood flowing toward the heart theoretically would 

 cause essentially the same effects on peripheral 

 venous pressures as would an increase in venous 

 resistance. However, from a practical point of view 

 this is not true, because an increase in volume of flow 

 normally simply distends the collapsed veins to a 

 greater degree, thus reducing the resistance to flow. 

 The flow and decreased resistance ordinarily com- 

 pensate for each other so that increasing the flow- 

 has relatively minor effect in increasing the peripheral 

 venous pressures rather than a major effect as might 

 be expected (88). This has been demonstrated es- 

 pecially in the case of blood flowing from the periph- 

 eral limbs through the abdominal cavity when the 

 intra-abdominal pressure is elevated. For instance, 

 if the intra-abdominal pressure is +10 mm Hg, 

 whether the flow from the leg to the right heart 

 is 0.5 ml per min or 200 ml per min, the pressure 

 in the femoral vein leading into the abdominal cavity 

 still remains only 1 mm Hg or so greater than the 

 10 mm Hg intra-abdominal pressure. 



EFFECT OF HYDROSTATIC PRESSURE ON PERIPHERAL 



venous pressures. Finally, we have the well-known 

 effect of hydrostatic forces on peripheral venous 

 pressures. That is, the simple weight of the blood 

 increases the venous pressures in the dependent 



SUMMARY 



To summarize this entire chapter, its important 

 point has been that one cannot analyze venous re- 

 turn separately from a simultaneous analysis of 

 many other factors in the circulation. However, 

 relatively simplified analyses, based principally on 

 four major segments of the circulation, the right 

 heart, the pulmonary circulation, the left heart, 

 and the systemic circulation, can provide an almost 

 complete understanding of the interrelationships 

 between a) venous return, /;) cardiac output, c) 

 right atrial pressure, d) left atrial pressure, e) mean 

 systemic pressure, /) mean pulmonary pressure, g) 

 mean pulmonary volume, and /() mean systemic blood 

 volume. 



If we should choose any single factor that might 

 be the primary regulator of venous return, and 

 hence also the primary regulator of cardiac output, 

 it might be the tissue utilization of oxygen. Cer- 

 tainly, in over half of the tissues of the body if not 

 in the entire body, local blood flow seems to be 

 controlled by the local utilization of oxygen, and 

 the summated value of all the local flows is the venous 

 return. Therefore, oxygen utilization by the tissues 

 might well be, in the final analysis, the primary 

 regulator of venous return. 



