Figure 1 (not shown) shows lung ventilation at rest, as a function of the partial pressure of dioxygen (O2) in the arteries, and to get a good model that has kept the CO2 partial pressure constant at 40 mm Hg. As is clearly shown by the curve curvature (hyperbola), is with good approximation talk about an exponential removal. This means that we are extreme on the first axis, with a partial pressure of about 70 to 100 + mm Hg, there is little change in pulmonary ventilation, which will be around. 80-10 liters. minutes. But we are moving more towards the origin, increases lung ventilation more striking, example, if we have a partial pressure in the arteries between 50 mm Hg and 30 mm Hg, there is an increase in lung ventilation in well over 15 (from approx. 15-30, representing a doubling) The reason that this curve looks like it does and that it is not linear, as one might have expected from a simple hypothesis, because the notorious iltbindingskurve (see page 136, fig. 6.6 , Physiology). Curve of arterial blood, as our Figure 1 also dealing with has a characteristic s form. A simplistic conception of iltbindingskurven shows how hemoglobin specific iltbinding affecting oxygen uptake and iltafgivelsen. In lungs exposed to a blood oxygen around. 100 mm Hg, giving an oxygen saturation of approx. 98%, representing almost a 100% saturation. Since the curve is flat at the top, a slight decrease oxygen in the alveoli do not change much on oxygen saturation in the blood. In aerobic tissue oxygen pressure will be significantly lower (20-40 mm Hg), which means that here given oxygen from blood to tissues. Lung ventilation is an expression of how hard and how fast you breathe, put another way:
respiratory depth * breathing frequency = lung ventilation
And it makes that change, our respiratory center located in the extended portion of the spinal cord, medulla oblongata. But to change our Ventilation must be relatively large change ip (O2). For when we know that the pressure of CO2 was constant, the change in pH not be great but so we can see again from the curve's shape, there also must be a pretty big change, in order to increase the ventilation.
Figure 2 (not shown) shows the same as Figure 1 but instead to indicate ventilation as a function of oxygen, is here as a function of carbon dioxide (CO2), and again as in Figure 1, kept the partial pressure of O2 constant at 100 mm Hg. In contrast to Fig. 1, this curve, something that resembles a linear line. That is, to change the pressure of CO2 a bit, modified breathing the same bit, in a special relationship. And one might think, as outlined on the left that this ratio would be 1:1, and it would in itself be if we had not had a carbonated buffer system works as follows: Our blodplasmas pH is almost constant around. 7.4 and the two most important buffers to keep this constant is: bicarbonate: HCO-3 and carbonic acid: H2CO3. Their process can proceed in two places in the blood and in erythrocytes. The only difference is that the process of blood has a very long forløbstid, with constant k = 0.037 s-1, whereas if the process results in red blood cells, accelerated the process of the zinc (II)-containing enzyme: carbonid anhydrase, which accelerates the hydro of external process with approx. 107 (compared to the previously mentioned k). All of this buffer system makes so that the graph is a straight line with equation y = x, but y = 0, n ∙ x.
It is actually seen for ventilation of the lungs to increase due to increased PCO2, due to the same chemo receptors, but is more reactive than CO2 than they are for O2. This gives the straight line. And it is also seen on the graph 1.akse that receptors are more reactive than CO2, because the values are, so to say, closer together, this says that only a small ndring in pressure causes a relatively large change in lung ventilation. The reason for that interval on that axis only goes from 38 to 50, is that we do not naturally want to find occurrences with greater pressures, this would require some form of clean burning of organic material, such as a bonfire of a kind.
b: If the body's working tissues performing a hard work, this tissue cells a strong need for oxygen. And in and they get this large amount of oxygen they produce a lot of CO2, as residue from respirationsprocessen. And all this carbon dioxide your body will want rid of, therefore the pressure of CO2 in the veins, which carry the afiltede blood back to the heart's right atrium where it then forms part of the small circuit (pulmonary circulation), therefore there will be a large amount of CO2 in the venous blood, and there will be a great pressure of O2, since most if not all the oxygen has been used.
The reason that our arterial partial pressure of CO2 and O2 not changed much, is that our body has various mechanisms to control breathing, so that may bear the needed quantity of oxygen and hence carbon dioxide, to the various organs and tissues in the body . The primary system that controls our breathing is the previously mentioned respiratory center which controls the muscles of the diaphragm and around the 12 (on each side) rib. And respiratory center will especially its signals from the H + ions formed as a result of a hydro-lysing activity in the brain. The brain is surrounded by approx. 150 ml (generated daily approx. 500 ml, indicating high activity, and thus high separation), cerebro-spinal fluid (CSF (eng.Cerebrospinal fluid)) and a substance which, however, can diffuse into this fluid is CO2 which is hydrolyzed in fluid, and therefore forms carbonic acid, and hence bicarbonate and free H +, resulting in lower pH. CSF has no buffer system, so a small change in pH, will immediately affect the central chemo receptors in the respiratory center, leading to increased ventilation, and therefore not modified partial pressure.
Sources: Physiology (Routledge)
