Complexity of human circulation design: tips for students.

MEDICAL STUDENTS are faced with a challenge to comprehend the enormous complexity of our circulatory systems. There is a gap between courses of anatomy, with detailed description of all normally present macroscopic vessels, and histology, which is focused on microscopic tissue architecture. Both courses leave arterioles, capillaries, and venules almost marginal and are not used to consider the hydrostatic pressure changes that continuously alter tissue perfusion. Often this knowledge gap is left for teachers of medical physiology. It is typically addressed during teaching about blood volumes in different circulatory segments, as a good occasion to explain the complex structure of the entire circulatory system. This article is intended to help teachers clarify the complexity of the human circulatory system in a short and digested form based on data from contemporary textbooks (1, 2). The same data were used in Table 1 to calculate some volumes and values (blood volume, number of vessels, and average length) and ratios (number of arterioles per 1 artery, number of capillaries per 1 arteriole, number of capillaries per 1 venule, and number of venules per 1 vein) that can be used to illustrate some unique circulatory features. The number of vessels and their length are calculated for an adult with 6 liters of blood in circulation to make a simplified description of the human circulation. This model shows that while the aorta divides in 160 arteries, each artery branches in 0.356 million arterioles. Each arteriole divides into almost 400 capillaries. The venous part of the circulation starts when 18 capillaries unite in 1 venule, whereas it takes the joining of 6 millions venules to make a single vein. The need for so many vessels can be explained through the fact that our circulatory system functions due to well-defined pressure drops along the arterial tree. If we look at the data shown in Table 1 more carefully, arterioles on average may be 1.5 mm long and 30 m wide, whereas capillaries are just 5 m wide and 0.7 mm long. Their limited dimensions define flow resistance and pressure drop along individual vessels. If we accept that, as described by the Hagen-Poiseuille law, only narrow arterioles can sufficiently reduce the arterial pressure before reaching capillaries, it is understandable that any changes in arteriolar or capillary dimensions (longer, shorter, wider, or more narrow) would make their pressure profiles less suitable for tissue perfusion. In other words, to meet tissue needs, our body is forced to multiply vessels of optimal resistance without altering their dimensions. High perfusion rates in peripheral tissue require parallel blood flow through many narrow arterioles. The same can be said for kidneys. Pressure drops along the narrow vascular nephron structure are required for adequate glomerular filtration and absorption in peritubular capillaries. Larger vascular structures would not be suitable for this purpose, and we can assume that functiondetermined hydrostatic pressures in different nephron segments limit nephron dimensions. The consequence is that sufficient function of human kidneys depends on the simultaneous work of nearly 2 millions nephrons. Knowing pressure drops along arterioles (from 87 to 37 mmHg, a difference of 50 mmHg) and capillaries (from 37 to 17 mmHg, a difference of only 20 mmHg), the overall resistance of all arterioles might be 2.5 times the overall capillary resistance (50/20 2.5). On the other hand, overall venous resistance might be some 15% lower than the overall capillary resistence (17/20 0.85). Table 2 shows that changes in relative flows ranging from 25% to 185% require changes in arteriolar diameters from 19 to 45 m. These changes also affect the capillary pressure gradient with increased filtration rates in cases of arteriolar dilatation, due to increased arteriolar end pressure. As expected, arteriolar constriction reduces blood flow and almost stops filtration since pressures along capillaries become lower than the plasma oncotic pressure. Vasodilation and constriction of arterioles, respectively, can explain skeletal muscle edema after heavy exercise or high resistance of inactive subcutaneous tissue.