Partial pressure of gases (PO2 and PCO 2):
* Atmospheric pressure is made up by several gases all of them participate to produce 760 mm hg, and for each gas it has certain percentage by which we can know how much this gas exert pressure (when the percentage increase the partial pressure increase) for example N2 percentage is about 79% so it contribute for 79% X 760 (600 mm hg) and for O2 it’s percentage about 21 % so it contribute for (21 % X 760) i.e. (160 mm hg), and other gases and water vapor contribute for little percentage so they are negligible
* Percentage of CO2 is very little in atmospheric air so its partial pressure is negligible
* Gas diffusion occur from high partial pressure to low partial pressure (simple passive diffusion)
Alveolar partial pressure of gases:
1) PO2 in alveoli is 100 mm hg and that’s because a) the fresh air entering the alveoli that has PO2 160 mm hg will mix with the air in alveoli already present from previous expiration which has low PO2, and b) when air enter to lungs through air ways it will be humidified by adding water vapor to it and by this reducing O2 percentage in the inspired air and resulting reduced PO2
2) We can consider that PO2 in the inspired air is constant 100 mm hg with little variation between inspiration and expiration (that’s because there is always some volume of air remain in alveoli even after forceful expiration called residual volume)
3) Air entering alveoli has very little PCO2 and when mixes with air present in alveoli from previous expiration, which has high PCO2, the resultant PCO2 is 40 mm hg constantly
Partial pressures of gases in pulmonary capillaries:
1) Blood coming through venous system from body tissues will be pumped to lungs and pass through pulmonary capillaries
2) This blood has low PO2 because the tissues used the O2 for energy production so the PO2 in pulmonary blood is low (40 mm hg), and PCO2 is high (46 mm hg)
3) The capillaries come surrounding alveoli, gas exchange will occur from high to low partial pressure and trying to equilibrate
4) Blood leaving pulmonary capillaries has the same PO2 values for alveoli like PO2 is 100 mm hg and PCO 2 is 40 mm hg and this blood will return to heart to be pumped to body tissues
5) Blood coming to capillaries at tissue level will equilibrate with tissue gases which have PO2 40 mm hg and PCO2 46 mm hg, and thus it will deliver O2 to tissues and take CO2 from them and the blood leaving tissues will have PO2 40 mm hg and PCO2 46 mm hg
Lung volumes and capacities:
* When we breathe normally and quietly there is a constant amount air volume of inspired and expired air which is 500 ml and called tidal volume
* When we finish expiration in normal quiet breathing we still able (if we want) to expire more air more than 500 ml by forceful expiration, which is about 1000 ml but, after we finish this expiration of 1000 ml (in addition to 500 ml of tidal volume), can we expire more air? Or is there any more air present in the lung after this forceful expiration? The answer we can’t expire any more although there is still 1200 ml of air found in the lungs and this volume is called (residual volume)
* If we inspired 500 ml (tidal volume) during normal quit breathing, can we inspire more (if we want)? The answer is yes we can inspire about 3000 ml by forceful inspiration
* Now we can predict that maximum air inspired is about 3500 ml and maximum air expired (after tidal volume) is 1000 ml and the volume of air that cannot be expired is 1200 ml, so we can know that lung may capacitate maximum volume of 5700 ml and this called (total lung capacity).
Q. How this residual volume (1200 ml) present?
A. Because when we make forceful expiration, small airways will collapse in some time during expiration and this will prevent full emptying of the alveoli in addition to the presence of negative intrapleural pressure which keeps lungs partially expanded.
Q. What is the wisdom behind the presence of residual volume?
A. 1- to enable gas exchange between blood and alveoli even after full expiration.
2- when the lungs being partially inflated (contain residual volume 1200 ml) it makes inspiration easier cause we know that if alveoli completely empty of air and become very small this will increase the effort to expand them again because there is high collapsing pressure (Laplace’s law)
* We can measure different lung volumes and capacities by using a device called spirometer.
Now lets know the definitions of lung volumes and capacities:
1- Tidal volume (TV): air entered and expired during rest (500 ml).
2- Inspiratory reserve volume (IRV): maximum amount of air can be inspired after tidal volume it is about 3000 ml.
3- Inspiratory capacity (IC): tidal volume + IRV (3500 ml).
4- expiratory reserve volume (ERV): maximum air expired during active forceful expiration after tidal volume (1000ml).
5- Residual volume (RV): amount of air which remains in lungs after forceful expiration (after ERV), it is about 1200 ml, it is not measured directly by spirometer because it does not go in and out during respiration.
6- functional residual capacity (FRC): ERV + RV, it is about (2200 ml).
7- Vital capacity (VC): maximum amount of air that can get in and out, equal to summation of (IRV+TV+ERV).
8- Total lung capacity (TLC): represent all lung volumes (RV, ERV, TV, IRV) it is about 5700 ml.
Pulmonary ventilation and dead space:
* We should remember that there is conducting air ways and its function is only passage of air to reach alveoli where gas exchange occur, i.e. there is no gas exchange present in air ways and the volume of air occupying these passages is about (150 ml).
* From above we can predict that from tidal volume that is inspired (500ml) there is only 350 ml which is available for gas exchange and this volume of air that present in air ways (150 ml) is called dead space.
* We know that respiratory cycle (inspiration and expiration) occur in certain rates per minute, which is in rest about 12/min.
* Then we can measure the volume of air breathed in and out during one minute at rest when we know the respiratory rate (12/min) and amount of air inspired and expired in each cycle (tidal volume) and this is called pulmonary ventilation.
Pulmonary ventilation = tidal volume X respiratory rate
* It is in normal breathing about 6000 ml / min (500 X 12), but, could be increased voluntarily to many folds by increasing respiratory rate and/or depth of inspiration and expiration, but usually increasing depth of breathing is more beneficial than increasing rate because of dead space, i.e. increasing depth of breathing will add more air for gas exchange and dead space is constant 150ml, while increasing rate will not add much new amount of air for gas exchange because dead space is present in each cycle and we can maximally increase the rate to double (24/min.)By this, pulmonary ventilation will increase when we increase the rate but not like when we increase depth of breathing.
* We know that not all air entering lungs will go to the alveoli because some amount will occupy dead space.
* So the amount of air which enter the alveoli / min is called alveolar ventilation, which is equal to:
(Tidal volume – dead space) X respiratory rate = (500 -150) X 12 = 4200 ml.
O2 transport: when O2 diffuse from alveoli to pulmonary capillary blood it could be transported by 2 methods:
I. Dissolved in plasma, which is very little amount about 2-3% of total O2 carried by blood, because O2 is poorly dissolved in plasma and this amount is proportional to (PO2) in blood the more PO2 the more dissolved O2.
Note: this type of transport may be not so important in the process of O2 delivery to the tissues but has very important role for receptors detecting amount of O2 in blood in the process of respiratory regulation.
II. Bound to Hemoglobin (Hb):
* Hb is a large protein containing 4 heme molecules, each one can carry one O2 molecule, and it combines with Hb reversibly.
* When Hb is not bound to O2 it is called deoxyhemoglobin and when bound is called oxyhemoglobin, when first O2 molecule bind Hb it will facilitate the binding of second molecule and the second will facilitate for the third and so on.
* Function of Hb is to pick up O2 at the alveolar level and deliver O2 at the tissue level and this feature is represented in a very important curve which summarize features of Hb take-up and dissociation from O2, this curve is called Oxygen-hemoglobin dissociation curve.
* When 4 molecules of O2 bind to Hb it is called full saturated and the percentage of Hb saturation (% Hb saturation) is determined by PO2
* When PO2 is high (like in alveoli) this will lead to Hb combination with O2 while when PO2 decrease like in tissues the reaction goes with dissociation of oxyhemoglobin to deliver O2 (i.e. reversible reaction).
Oxygen-hemoglobin dissociation curve (saturation curve)
* Hb saturation = amount of O2 bound to Hb, it is related to PO2 amount as shown in the figure.
* O2 – Hb dissociation curve represent the relationship between PO2 and Hb saturation, it is not linear curve but it is S_ shaped curve, has 2 parts; rising part which is called steep portion and flattened part called plateau.
* The steep part represent when PO2 range from (0-60) mmHg, the change in % of Hb saturation is great, from 0 % Hb saturation to nearly 90%, while in the plateau part represent PO2 from (60-100) mmHg, then the change in % Hb saturation is less (from 90% Hb saturation to 100% Hb saturation).
* These two portions have important physiological significance
Significance of plateau:
* This portion represent O2 loading in Hb in PO2 range present in alveoli which is usually 100 mmHg which result in % Hb saturation about 97.5%.
* If there is a fall in alveolar PO2 there is small change in Hb saturation until it reach 60 mmHg and this is because of plateau curve and at 60 mmHg the Hb saturation is still high (90%), thus total O2 content in blood is slightly decreased although there is (40 degree) decrement of PO2 (from 100 to 60 mmHg).
* By this the plateau part of the curve provides good safety margins of O2 carrying capacity of blood in other word when we have pathological condition which may reduce arterial blood PO2 (pulmonary disease, cardiovascular disease, inadequate O2 supply) we still in safety regarding O2 transferred and delivered to tissues as long as the PO2 is not less that 60 mmHg.
1- when we go up in high altitudes like in mountains the PO2 there may be low and thus reducing arterial PO2 but it is ok as long as the arterial PO2 is not below 60 mmHg.
2- notice that in plateau part when we change PO2 40 degree (from 100 to 60) there is only 7.5 change in % of Hb saturation (from 97.5 to 90%)
Significance of steep portion:
* Represent O2 delivery from oxyhemoglobin in systemic capillaries at tissue level where tissue PO2 range from (0 to 60) and the blood coming will equilibrate with tissue PO2 which has PO2 40 mm hg and the blood coming has PO2 100 mm hg
* When blood PO2 equilibrate with tissue PO2 i.e. becomes 40 mm hg, the % of HB saturation is 75% and that means there is 25 % HB saturation reduced to deliver O2 to tissues and the blood leaving venous system still has HB saturation 75%
* If the tissues are consuming large amount of O2 like in increased metabolic activity then the tissue PO2 may fall to 20 mm hg, this will produce HB saturation to 30 % (i.e. reduction in saturation by 45 degree) and that means much of O2 delivery to tissues and this is very important feature of steep portion that means it can deliver more O2 (more change in % HB) to tissues when we need more O2 (in response to relatively small fall in tissue PO2), in apposite to what happen in plateau when we have large change in PO2 (from 100 to 60) and in turn slight change in HB saturation (from 97.5 to 90 %)
1- in plateau portion change in PO2 (from 100 to 60) will not change the HB saturation significantly, only (7.5) and this helps when alveolar PO2 change (like in disease) there is still good amount of O2 carried in blood
2- change in blood PO2 from 100 to 40 mm hg (as occur when oxygenated blood come to tissues) will only change the % of HB saturation by 25 degree (i.e. from 100 % saturation to 75% saturation)
3- change in blood PO2 from 40 to 20 mm hg (when tissues need more O2) will result in large change in HB saturation (40 degree) from 75% to 30% saturation like in exercise, and this happen because change in PO2 is occurring in steep portion
Factors affecting on O2 _ HB dissociation curve:
* HB affinity to O2: when combination oh HB and O2 increase this means increased affinity and in the same time means decreased ability of dissociation between HB and O2
* The curve may be shifted to left or right in response to certain factors, and shifting means change in HB saturation for a given PO2 in the presence of the factor that causes shifting
* Shifting to right: it means less HB affinity to O2 and result in less HB saturation for a given PO2 and in the same time means more O2 dissociation from HB (i.e. more O2 delivery to tissues)
For example in normal curve when the PO2 is 40 mm hg, the saturation is 75%, while in shifting to right curve the PO2 40 mm hg will produce 60 % saturation
* Shifting to left: it means increased HB affinity to O2 and less dissociation ability of HB from O2 (i.e. less O2 delivery to tissues)
Factors that affect the curve:
1- PCO2; when it increase (as in tissue level) it will shift the curve to right, meaning less affinity of HB with O2 and more dissociation from O2 (more O2 delivery to tissues)
2- acidity (H+); when increase it shifts the curve to right as occurs at tissue level when the tissue metabolism release acids (like in exercise)
3- Temperature: when increase it shift curve to right (like in exercise the tissue produce more heat)
4- 2,3 biphsphoglycerate: when it increase it shift the curve to right
* This substance produced in RBC in response to chronic situations which may result in decreased HB saturation and the result will lead to more O2 deliver to tissues (less affinity and more dissociation ability)