It is absurdly obvious that complex multicellular organisms are lumbered with a circulatory system (and all its accompanying ills) because it must be there to provide nutrients and oxygen to distant cells, and to remove waste products. Extending our trite teleological argument a bit, it makes absolutely no sense for the normal heart to be anything other than a subservient pump, pumping to meet the needs of the periphery! Thus we must look to the periphery, and the demands of the organs, in order to establish the normal regulatory mechanisms that govern the output of the heart. A vast amount of experimental evidence supports this contention (See for example Guyton et al.). To understand circulatory physiology we must first appreciate that we are looking at a system. We cannot hope to grasp what is going on if we simply observe isolated components without consideration of the whole. Unfortunately there are literally hundreds of factors that influence circulatory function. Even complex computer simulations hardly come up to scratch in modelling the cardiovascular system.
We have already looked at myocardial function and its regulation - we must now consider this in the context of the whole system and how it functions. We should not regard the roles of the periphery and of the heart as antagonistic, but rather as complementary. Also bear in mind that the heart has finite resources - in circumstances where it is grossly overloaded or diseased, it may well become a potent limiting factor in circulatory performance.
In a similar analogy, we can define the capacitance as the change in volume per unit pressure.
V /
P
Armed with these simple definitions, let's consider what will happen if we vary them (again, only considering the systemic section, moving blood from the left heart to the right heart). Let us pretend for a moment that all the normal complex mechanisms regulating the circulation are paralysed. The following are intuitively clear:
In our simple model, we have already found two potent factors that regulate flow through the system - alterations in resistance and in "capacitance". It is clear that we can alter the effective "capacitance" in two ways - lowering the blood volume, or increasing the true capacitance of the system. Note that changes in resistance and/or capacitance can be made to both the venous and arterial limbs.
What effect will this have on the heart? From our previous discussion of myocardial function, we know that generally the more preload is applied to the heart, the more vigorously it will pump, and the greater the volume that will be ejected (afterload remaining constant). This is the simplest way we can integrate venous return and cardiac output. The peripheral tissues, and indeed all factors that control myocardial function have three powerful mechanisms for controlling cardiac output - they could modulate peripheral resistance, peripheral capacitance, or intravascular volume. It is the delicate interplay between these factors that governs cardiovascular function!
Clearly, certain portions of the circulation may be more amenable to certain modifications - the venous capacitance is far greater than arterial, so if we wish to alter capacitance it is 'logical' to alter it on the venous limb; likewise the principle source of resistance in the systemic circulation is in the arterioles, so it is there that a change in resistance will usually have maximal effect.
It is also apparent that should we artificially oppose the pressure driving blood towards the heart, that at a certain level of pressure, flow towards the heart will cease. Classically, this concept has been made very confusing, with the driving force being called "vis a tergo", and almost any opposing force being termed "vis a fronte".
Guyton has fortunately examined factors governing venous return in immense detail. He has even provided quantitation, where previously there was only confusion. Before we examine his work, however, we need to establish one more point..
{ As an aside, in dogs, the physiological pressure reference point is midway between the sides of the chest transversely, 61.4% of the thickest part of the chest anterior to the back, and 76.7% of the distance from the suprasternal notch moving down to the tip of the xiphoid. What are the corresponding coordinates in man? }
What this means practically is that a pressure of 7mmHg is sufficient to entirely stop venous return, provided no compensatory reflexes are allowed to come into play!
| Date of First Publication: 2000 | Date of Last Update: 2006/10/24 | Web page author: Click here |