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Partial pressures of different gas in human blood and how they are calculated?

Partial pressures of different gas in human blood and how they are calculated?



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In Respiratory Physiology, we use the $P_x{O_2}$ and $P_x{CO_2}$ in blood at different regions of the peripheral circulation. From my Chemistry knowledge I know that $P_x$ of a gas in a solution is the fraction of total pressure caused due to the gas dissolved. But in blood $O_2$ is present mostly as $OxyHb$ and $CO_2$ is also present as $CarbaminoHb$ & $HCO_3^-$. In blood their dissolved state fraction is very low. Now my question is how do we measure the $P_x$ of any gas ($O_2$ or $CO_2$) in blood and what is the logic here? [x means either arterial blood or venous blood]

Here is the data I'm talking about.(https://i.stack.imgur.com/lA1M5.jpg">


As a notation note, I never seen your $P_a{O_2}$ notation used except for referring to arterial partial pressure ($P_v{O_2}$ would be venous). Generically, partial pressures are usually noted as, for example, $P_{O_2}$.

When we talk about partial pressures in biology, we literally mean the partial pressures: that caused by dissolved gas.

Hemoglobin-bound oxygen is not the same as gaseous oxygen, nor is carbonic acid the same as carbon dioxide. Neither contribute to the partial pressure. They do relate to the total oxygen/carbon dioxide carrying capacity of blood, but this cannot be measured directly through partial pressures.

See this Q&A for a situation this comes up: Why is arterial pO2 normal in carbon monoxide poisoning?

In medicine, it is common to use oxygen saturation as an alternative measure of blood oxygen concentration; this refers to the percentage of oxygen binding sites of Hb that are saturated.

It is important to realize that the partial pressures of dissolved gases will eventually reach equilibrium with the surrounding atmosphere; the lungs are a great gas exchange organ (that's their entire job), so blood leaving the lungs should have partial pressures that approximate those inspired air (in practice, there is some discrepancy because the lungs are very humid and also are constantly refilled with $CO_2$ from blood, so water vapor and carbon dioxide contribute a substantial gas pressure that pushes out other gases: see the similarity between arterial blood and alveolar gas in your data table and the differences between atmospheric gas and alveolar gas).

Clinically/in a lab, we measure these things with a machine that just magically gives the numbers. I looked for a simple description of how these machines actually function, and found https://acutecaretesting.org/en/articles/understanding-the-principles-behind-blood-gas-sensor-technology to be useful. In summary, $CO_2$is measured by exposing a captive solution to the gas and measuring the pH, giving an indirect (but accurate) measure of $CO_2$. $O_2$ is measured with a reducing current. It's also possible to measure concentrations of arbitrary compounds more directly with gas chromatography - colleagues of mine have used this for anesthetic gases, for example.


What Is the Partial Pressure of Oxygen (PaO2) Test?

Sanja Jelic, MD, is board-certified in sleep medicine, critical care medicine, pulmonary disease, and internal medicine.

The partial pressure of oxygen, also known as PaO2, is a measurement of oxygen pressure in arterial blood. It reflects how well oxygen is able to move from the lungs to the blood, and it is often altered by severe illnesses.

The PaO2 is one of the components measured in an arterial blood gas (ABG) test—which also reports oxygen (O2) saturation, bicarbonate (HCO3), the partial pressure of carbon dioxide (CO2), and the pH level in red blood cells.


Lung Volumes and Capacities

Different animals have different lung capacities based on their activities. Cheetahs have evolved a much higher lung capacity than humans it helps provide oxygen to all the muscles in the body and allows them to run very fast. Elephants also have a high lung capacity. In this case, it is not because they run fast but because they have a large body and must be able to take up oxygen in accordance with their body size.

Human lung size is determined by genetics, sex, and height. At maximal capacity, an average lung can hold almost six liters of air, but lungs do not usually operate at maximal capacity. Air in the lungs is measured in terms of lung volumes and lung capacities ([Figure 1] and [Table 1]). Volume measures the amount of air for one function (such as inhalation or exhalation). Capacity is any two or more volumes (for example, how much can be inhaled from the end of a maximal exhalation).

Figure 1: Human lung volumes and capacities are shown. The total lung capacity of the adult male is six liters. Tidal volume is the volume of air inhaled in a single, normal breath. Inspiratory capacity is the amount of air taken in during a deep breath, and residual volume is the amount of air left in the lungs after forceful respiration.

The volume in the lung can be divided into four units: tidal volume, expiratory reserve volume, inspiratory reserve volume, and residual volume. Tidal volume (TV) measures the amount of air that is inspired and expired during a normal breath. On average, this volume is around one-half liter, which is a little less than the capacity of a 20-ounce drink bottle. The expiratory reserve volume (ERV) is the additional amount of air that can be exhaled after a normal exhalation. It is the reserve amount that can be exhaled beyond what is normal. Conversely, the inspiratory reserve volume (IRV) is the additional amount of air that can be inhaled after a normal inhalation. The residual volume (RV) is the amount of air that is left after expiratory reserve volume is exhaled. The lungs are never completely empty: There is always some air left in the lungs after a maximal exhalation. If this residual volume did not exist and the lungs emptied completely, the lung tissues would stick together and the energy necessary to re-inflate the lung could be too great to overcome. Therefore, there is always some air remaining in the lungs. Residual volume is also important for preventing large fluctuations in respiratory gases (O2 and CO2). The residual volume is the only lung volume that cannot be measured directly because it is impossible to completely empty the lung of air. This volume can only be calculated rather than measured.

Capacities are measurements of two or more volumes. The vital capacity (VC) measures the maximum amount of air that can be inhaled or exhaled during a respiratory cycle. It is the sum of the expiratory reserve volume, tidal volume, and inspiratory reserve volume. The inspiratory capacity (IC) is the amount of air that can be inhaled after the end of a normal expiration. It is, therefore, the sum of the tidal volume and inspiratory reserve volume. The functional residual capacity (FRC) includes the expiratory reserve volume and the residual volume. The FRC measures the amount of additional air that can be exhaled after a normal exhalation. Lastly, the total lung capacity (TLC) is a measurement of the total amount of air that the lung can hold. It is the sum of the residual volume, expiratory reserve volume, tidal volume, and inspiratory reserve volume.

Lung volumes are measured by a technique called spirometry . An important measurement taken during spirometry is the forced expiratory volume (FEV) , which measures how much air can be forced out of the lung over a specific period, usually one second (FEV1). In addition, the forced vital capacity (FVC), which is the total amount of air that can be forcibly exhaled, is measured. The ratio of these values ( FEV1/FVC ratio ) is used to diagnose lung diseases including asthma, emphysema, and fibrosis. If the FEV1/FVC ratio is high, the lungs are not compliant (meaning they are stiff and unable to bend properly), and the patient most likely has lung fibrosis. Patients exhale most of the lung volume very quickly. Conversely, when the FEV1/FVC ratio is low, there is resistance in the lung that is characteristic of asthma. In this instance, it is hard for the patient to get the air out of his or her lungs, and it takes a long time to reach the maximal exhalation volume. In either case, breathing is difficult and complications arise.


Lung Volumes and Capacities

Different animals have different lung capacities based on their activities. Cheetahs have evolved a much higher lung capacity than humans it helps provide oxygen to all the muscles in the body and allows them to run very fast. Elephants also have a high lung capacity. In this case, it is not because they run fast but because they have a large body and must be able to take up oxygen in accordance with their body size.

Figure (PageIndex<1>): Human lung volumes and capacities are shown. The total lung capacity of the adult male is six liters. Tidal volume is the volume of air inhaled in a single, normal breath. Inspiratory capacity is the amount of air taken in during a deep breath, and residual volume is the amount of air left in the lungs after forceful respiration.

Human lung size is determined by genetics, gender, and height. At maximal capacity, an average lung can hold almost six liters of air, but lungs do not usually operate at maximal capacity. Air in the lungs is measured in terms of lung volumes and lung capacities (Figure (PageIndex<1>) and Table (PageIndex<1>)). Volume measures the amount of air for one function (such as inhalation or exhalation). Capacity is any two or more volumes (for example, how much can be inhaled from the end of a maximal exhalation).

Table (PageIndex<1>): Lung Volumes and Capacities (Avg Adult Male)

Volume/Capacity Definition Volume (liters) Equations Tidal volume (TV) Amount of air inhaled during a normal breath 0.5 - Expiratory reserve volume (ERV) Amount of air that can be exhaled after a normal exhalation 1.2 - Inspiratory reserve volume (IRV) Amount of air that can be further inhaled after a normal inhalation 3.1 - Residual volume (RV) Air left in the lungs after a forced exhalation 1.2 - Vital capacity (VC) Maximum amount of air that can be moved in or out of the lungs in a single respiratory cycle 4.8 ERV+TV+IRV Inspiratory capacity (IC) Volume of air that can be inhaled in addition to a normal exhalation 3.6 TV+IRV Functional residual capacity (FRC) Volume of air remaining after a normal exhalation 2.4 ERV+RV Total lung capacity (TLC) Total volume of air in the lungs after a maximal inspiration 6.0 RV+ERV+TV+IRV Forced expiratory volume (FEV1) How much air can be forced out of the lungs over a specific time period, usually one second

The volume in the lung can be divided into four units: tidal volume, expiratory reserve volume, inspiratory reserve volume, and residual volume. Tidal volume (TV) measures the amount of air that is inspired and expired during a normal breath. On average, this volume is around one-half liter, which is a little less than the capacity of a 20-ounce drink bottle. The expiratory reserve volume (ERV) is the additional amount of air that can be exhaled after a normal exhalation. It is the reserve amount that can be exhaled beyond what is normal. Conversely, the inspiratory reserve volume (IRV) is the additional amount of air that can be inhaled after a normal inhalation. The residual volume (RV) is the amount of air that is left after expiratory reserve volume is exhaled. The lungs are never completely empty: There is always some air left in the lungs after a maximal exhalation. If this residual volume did not exist and the lungs emptied completely, the lung tissues would stick together and the energy necessary to re-inflate the lung could be too great to overcome. Therefore, there is always some air remaining in the lungs. Residual volume is also important for preventing large fluctuations in respiratory gases (O2 and CO2). The residual volume is the only lung volume that cannot be measured directly because it is impossible to completely empty the lung of air. This volume can only be calculated rather than measured.

Capacities are measurements of two or more volumes. The vital capacity (VC) measures the maximum amount of air that can be inhaled or exhaled during a respiratory cycle. It is the sum of the expiratory reserve volume, tidal volume, and inspiratory reserve volume. The inspiratory capacity (IC) is the amount of air that can be inhaled after the end of a normal expiration. It is, therefore, the sum of the tidal volume and inspiratory reserve volume. The functional residual capacity (FRC) includes the expiratory reserve volume and the residual volume. The FRC measures the amount of additional air that can be exhaled after a normal exhalation. Lastly, the total lung capacity (TLC) is a measurement of the total amount of air that the lung can hold. It is the sum of the residual volume, expiratory reserve volume, tidal volume, and inspiratory reserve volume.

Lung volumes are measured by a technique called spirometry . An important measurement taken during spirometry is the forced expiratory volume (FEV) , which measures how much air can be forced out of the lung over a specific period, usually one second (FEV1). In addition, the forced vital capacity (FVC), which is the total amount of air that can be forcibly exhaled, is measured. The ratio of these values ( FEV1/FVC ratio ) is used to diagnose lung diseases including asthma, emphysema, and fibrosis. If the FEV1/FVC ratio is high, the lungs are not compliant (meaning they are stiff and unable to bend properly), and the patient most likely has lung fibrosis. Patients exhale most of the lung volume very quickly. Conversely, when the FEV1/FVC ratio is low, there is resistance in the lung that is characteristic of asthma. In this instance, it is hard for the patient to get the air out of his or her lungs, and it takes a long time to reach the maximal exhalation volume. In either case, breathing is difficult and complications arise.

Respiratory therapists or respiratory practitioners evaluate and treat patients with lung and cardiovascular diseases. They work as part of a medical team to develop treatment plans for patients. Respiratory therapists may treat premature babies with underdeveloped lungs, patients with chronic conditions such as asthma, or older patients suffering from lung disease such as emphysema and chronic obstructive pulmonary disease (COPD). They may operate advanced equipment such as compressed gas delivery systems, ventilators, blood gas analyzers, and resuscitators. Specialized programs to become a respiratory therapist generally lead to a bachelor&rsquos degree with a respiratory therapist specialty. Because of a growing aging population, career opportunities as a respiratory therapist are expected to remain strong.


Partial pressure - liquids

In our discussion of pressure in dilute (nearly ideal) gases, we learned that each molecule in the gas that bounced off a wall felt a force from the wall, and therefore, by Newton's 3rd law, exerted a force on the wall. The pressure (force on the wall per unit area) was proportional to the concentration &mdash the number of molecules per unit volume hitting the wall. At constant T, the pressure could therefore be used as a stand-in for concentration (= number density).

When there is a mixture of gases, each molecule of each gas contributes the same amount to the pressure, so the total pressure is the sum of the partial pressures created by each gas separately.

Gases can also be dissolved in liquids. In order to make contact with the way concentrations are described in gases, we would like to use the same language. But a problem arises that can lead to confusion. The key physics that makes the ideal gas law work is that it is dilute. Molecules are far apart, collide rarely, and mostly travel in straight lines (ignoring gravity). This leads to the ideal gas law: $p=nk_BT$where $n$ is the concentration.

But in liquids, molecules are close to each other. Basically they touching and interact with each other all the time. This means the the ideal gas law does NOT hold for liquids &mdash not even for gases dissolved in liquids.

We might say, well, let's just use the same equation anyway. This would say the partial pressure is the concentration the gas would have if there were no liquid . I've struck this through since this is NOT what is done. Rather, a somewhat more sophisticated choice is made. It is defined as follows.

The partial pressure of a gas dissolved in a liquid is taken to be that partial pressure of gas that would be in equilibrium when that gas is in contact with the liquid.

Although this sounds a bit confusing, it makes sense if you consider that one way to measure the concentration of dissolved gas in a liquid is to let it come to equilibrium with a small open space above the liquid and then measure the concentration (partial pressure) in the gas. It's much harder to measure the actual concentration of gas inside a liquid directly.

This image of lung alvaeoli
by Unknown
Author is licensed
under CC BY-SA

But besides being reasonable from a measurement point of view it makes a lot of sense biologically. A critical point in many places in biology is exchanging gases between a gas (air) and a liquid (water). Animals need to take in oxygen from the air into their fluids and put out carbon dioxides. Complex structures such as lungs, alveoli, and gills are evolved to facilitate this.

Let's consider an example. Consider oxygen (O2) dissolved in water. In the picture at the right, we show a container of water with a surface open to the air above the water. The dissolved oxygen has a concentration of $n_$ molecules per cm 3 and the air has a concentration of $n_$ molecules per cm 3 . Only the oxygen molecules are shown (but the water is shown as blue.)

The partial pressure of the oxygen in the air ($n_$) is, by our discussion of gases, proportional to the number density of oxygen molecules by

[Careful! Since we are only talking about the oxygen pressure on this page we won't bother to write $p_$ or $n_$. That just seems to cumbersome. But don't confuse $p_$ with the total air pressure. Throughout, we are always talking about the pressure and density of only the oxygen.]

Molecules of oxygen are continually crossing the surface from both sides. The equilibrium value occurs (the numbers stabilize) when equal numbers leave and enter the water. But because the molecules of oxygen interact strongly with the water molecules (but not strongly with the molecules of air, the equilibrium value does NOT occur when the two concentrations are the same.

Let's define the ratio of the two concentrations at equilibrium at $H$. (Note that $H$ is dimensionless since it is the ratio of two of the same kinds of quantities.) It will depend on the properties of the liquid and what gas we are considering. The equilibrium concentrations determine H by

It's not trivial to figure this ratio out. It basically has to be measured.

We define the partial pressure of the oxygen in water to be

Note that this is the amount of oxygen in the air that would be in equilibrium with the oxygen in the water. This is NOT equal to the concentration of oxygen in air that produces this pressure. To relate this to the actual concentration of the oxygen in the water, we have to substitute for $n_$

This relates the partial pressure of the oxygen above the water to the concentration (number density) of oxygen in the water.

Chemists (and biologists) tend to prefer to use molar concentration rather than number of molecules. To convert the number of molecules to the number of moles we have to divide by Avogadro's number, NA. The number of moles per cubic centimeter is called the molar concentration and is typically written c. We therefore have

$c_ = n_ / N_A quad mathrm quad n_ = N_A c_$

Note that changing from number density ($n$) to molar density ($c$) just changes $k_B$ into $k_BN_A = R$, the familiar gas constant from chemistry. The combination $HRT$ is referred to as Henry's constant, $k_H$.

The final result typically quoted in chemistry is

that is, what we define to be the partial pressure of oxygen in water is proportional to the molar concentration of oxygen in water. This is called Henry's law. Of course this is easily generalized to any liquid and any dissolved gas. Note also that although it's called "Henry's constant", it actually depends on what dissolved gas we are talking about, the temperature, and the properties of the liquid. This is not easily calculated. It has to be looked up in a table obtained from measured values.

The discussion of Henry's law and the Henry constant is somewhat confused by the fact that different communities measure pressure in different units and different communities measure concentrations in different units. As a result, there are lots of different values for a single "Henry constant." Although the (unitless) constant "$H$" we defined above is not commonly used, the relation $n_ = Hn_$ is probably a good way to think about what Henry's law is telling you.

While the "concentration" meaning of partial pressure is the primary biological consideration for dissolved gases, there are contexts in which the "leads to a force" meaning of partial pressure also can have biological implications.

Image courtesy of Payal Razdan.

When divers descend deep below the water the pressure of the gases they are inhaling has to be increased to match the increased pressure from the water. As a result the concentration of dissolved gases in the blood (particularly nitrogen) can become much higher than those concentrations that are in equilibrium with air at normal pressure. If the pressure is not dropped slowly so that the nitrogen in the blood can be expressed to the air through the lungs, bubbles of nitrogen can form in the blood.

Now, partial pressure is not just concentration! Inside a gas bubble, the pressure of the gas exerts forces on the walls of the bubble and, as the bubble expands, on the walls of the blood vessels, doing physical damage ("the bends")!


Physiological factors which affect the haemoglobin-oxygen dissociation curve

The relation between blood oxygen saturation (or content) and partial pressure is not constant, even within an individual. Classically the factors recognised to influence the oxygen dissociation curve (ODC) include the local prevailing CO2 partial pressure (PCO2), pH and temperature. The curve is shifted to the right (i.e. lower saturation for a given PO2) by higher PCO2, greater acidity (lower pH) and higher temperature. The effect of PCO2 (known as the 𠇋ohr effect”) is mediated largely by the accompanying change in acidity in vitro studies have shown that PCO2 itself also has an independent effect, which becomes most evident under more acidic and severely hypoxic conditions [4].

The factors which shift the ODC to the right (lower pH, higher temperature and PCO2) are directly relevant to the conditions which prevail in metabolising tissues and consequently, as blood flows through the tissues, the ODC shifts to the right. This implies a reduction in the affinity of the blood for oxygen (for a given PO2, venous blood contains less oxygen than arterial blood), which is advantageous as it facilitates the unloading of oxygen from haemoglobin in the tissues. The converse occurs during passage through the pulmonary capillaries, with the greater affinity accompanying a shift of the ODC to the left aiding the uptake of oxygen.

A further compensatory mechanism which aids oxygen delivery by altering the position of the ODC is the concentration in the red cells of 2,3-biphosphoglycerate (also known as diphosphoglycerate (DPG)), an intermediate metabolite in the glycolytic pathway which binds to deoxyhaemoglobin. Higher concentrations of 2,3-DPG, seen, for example, with chronic hypoxia, shift the curve to the right, again facilitating the extraction of oxygen by metabolising tissues.


Small molecules and hypoxia

Chemotherapeutic drugs

Tumour cells are highly unresponsive to most anticancer drugs [31]. Tumour blood vessels are chaotic, leaky and disorganized. This results in a poor perfusion efficacy, reduced oxygen delivery to tumour cells and induction of chronic hypoxia. This lack of O2 in tumours tends to select cells with stronger malignant phenotype. Moreover increased DNA mutations in tumour cells activate genes that influence the uptake, metabolism and export of drugs, in favour of tumour survival. For example, in tumour cells P-glycoprotein expression and multidrug resistance receptors are enhanced [32]. Furthermore, modifications in sensitivity to p53-mediated apoptosis and in DNA mismatch repair make cells resistant to platinum-based chemotherapeutic agents (as carboplatin or cisplatin) [33, 34]. Transient hypoxia can also disturb protein folding in the endoplasmic reticulum, which confers to tumour cells resistance to topoisomerase II-targeted drugs [35] as etoposide, doxorubicin, etc.

The abnormal structure and function of tumour vasculature make it inefficient for red blood cells mediated oxygen supply as well as blood-borne drug delivery. The distribution of many drugs within tumours is also heterogeneous therefore only a portion of the target tumour cells is exposed to a potentially lethal concentration of the cytotoxic agent.

Moreover cell proliferation decreases as a function of its distance from blood vessels, an effect that is at least partially due to hypoxia [36]. This relatively low rate of cell proliferation in hypoxia limits the effectiveness of chemotherapeutic drugs active mainly against highly proliferative cells. Thus, many anticancer agents such as methotrexate, 5-fluorouracil, doxorubicin, carboplatin, melphalan, bleomycin, etoposide, etc. have reduced in vitro cytotoxicity in experimental hypoxic conditions.

Radiation sensitizers: the nitroimidazoles

Nevertheless, by its specificity and its major role in drug resistance, tumour hypoxia represents a unique and attractive target to develop strategies for cancer therapy. For this reason studies were conducted on drugs that are selectively toxic against hypoxic cells. For example, nitroimidazoles could mimic the effects of oxygen and thereby sensitize hypoxic cells to radiation. In clinical trials, radiotherapy added to nitroimidazoles (metronidazole, misonidazole and etanidazole) did not result in significant improvements over radiotherapy alone, mainly because the overall toxicity of these derivatives prevented them from being given at high enough doses [37].

Hypoxia prodrugs: tirapazimine and anthraquinone

Another strategy uses hypoxia-activated prodrugs. Tirapazimine is the first compound to be developed specifically as a hypoxic cytotoxin and whose clinical development has been the most important [38] ( Table 1 ). This benzotriazine di-N-oxide is selectively activated by multiple reductases to form free radicals in hypoxic cells thereby resulting in radical damage directly to the topoisomerase II enzyme [39] or to DNA. Despite the very promising results obtained in various preclinical studies, survival benefit is not clearly demonstrated in clinical trials [40, 41].

Table 1

Examples of small molecules targeting or mimicking hypoxia: their chemical structure and mechanism.

Small molecules
StructureMechanismReferences
pO2 modulator
myo-inositol trispyrophosphate (ITPP)Allosteric effector of haemoglobin[43�]
Hypoxia-activated prodrugs
TirapazimineForms free radicals when activated[38�]
anthraquinone (AQ4N)Cytotoxic when reduced to AQ4[42]
Hypoxia mimetics
Dimethyloxallyl glycine (DMOG)Inhibition of prolyl-4-hydroxylase by competition with the substrate[48, 49]
DesferrioxamineInhibition of prolyl hydroxylase by Fe 2+ chelation of the catalytic core[50, 51]
Metal ions (for example, Co 2+ and Cu 2+ ) Inhibition of prolyl hydroxylase by substitution for Fe 2+ of the catalytic core[51, 52]

The only other hypoxia-activated prodrug now in clinical trials is the anthraquinone AQ4N ( Table 1 ). AQ4N is a prodrug of a potent DNA intercalator/topoisomerase poison, AQ4. AQ4N has substantial activity against hypoxic cells in various transplanted tumours [42] and has recently completed a Phase I clinical trial.

PO2 modulator: myo-inositol trispyrophosphate (ITPP)

At the opposite of these drugs whose activity is modified by hypoxia, ITPP is, as we know, the only compound able to directly modulate pO2. ITPP acts as an allosteric effector, by enhancing the capacity of haemoglobin to release bound oxygen [43]. This leads to higher oxygen tension in the hypoxic environment, and thus inhibits hypoxia-induced angiogenesis. ITPP is a promising molecule for cancer [44] as well as heart failure [45] therapies, by restoring physiological level of oxygenation in hypoxic tissues ( Table 1 ). Such a molecule could be beneficially used to combine and potentialize drugs that preferentially induce apoptosis of endothelial cells in the tumour as 5,6-dimethylxanthenone-4-acetic acid (DMXAA) [46] and that was recently shown to act through the redox pathway [47].

Hypoxia mimetics: dimethyloxallyl glycine, desferrioxamine and metal ions

For tumour hypoxia modelling in vitro, the use of a hypoxia chamber, in which 95% N2/5% CO2 gas mixture was introduced up to obtain the desired pO2, was the technique of choice. Small molecules mimicking the hypoxic signal were also attractive tools. Dimethyloxallyl glycine [48, 49], desferrioxamine [50, 51] and metal ions [51, 52] were commonly used as hypoxia mimetics ( Table 1 ). In general, these molecules block the catalytic activity of prolyl-hydroxylases, an oxygen sensor able to inactivate hypoxia inducible factor (HIF)-1α activity in normoxic conditions.

This shows how meaningful the knowledge of the oxygen status in normal compared to pathological tissues can be for the design of diagnosis settings, on the one hand, and for therapeutic strategies, on the other hand. This led us to define the physioxia concept.


Lung Volumes and Capacities

Lung volumes measure the amount of air for a specific function, while lung capacities are the sum of two or more volumes.

Learning Objectives

Distinguish between lung volume and lung capacity

Key Takeaways

Key Points

  • The lung volumes that can be measured using a spirometer include tidal volume (TV), expiratory reserve volume (ERV), and inspiratory reserve volume (IRV).
  • Residual volume (RV) is a lung volume representing the amount of air left in the lungs after a forced exhalation this volume cannot be measured, only calculated.
  • The lung capacities that can be calculated include vital capacity (ERV+TV+IRV), inspiratory capacity (TV+IRV), functional residual capacity (ERV+RV), and total lung capacity (RV+ERV+TV+IRV).

Key Terms

  • tidal volume: the amount of air breathed in or out during normal respiration
  • residual volume: the volume of unexpended air that remains in the lungs following maximum expiration
  • spirometry: the measurement of the volume of air that a person can move into and out of the lungs

Lung Volumes and Capacities

Different animals exhibit different lung capacities based on their activities. For example, cheetahs have evolved a much higher lung capacity than humans in order to provide oxygen to all the muscles in the body, allowing them to run very fast. Elephants also have a high lung capacity due to their large body and their need to take up oxygen in accordance with their body size.

Human lung size is determined by genetics, gender, and height. At maximal capacity, an average lung can hold almost six liters of air however, lungs do not usually operate at maximal capacity. Air in the lungs is measured in terms of lung volumes and lung capacities. Volume measures the amount of air for one function (such as inhalation or exhalation) and capacity is any two or more volumes (for example, how much can be inhaled from the end of a maximal exhalation).

Human lung volumes and capacities: The total lung capacity of the adult male is six liters. Tidal volume is the volume of air inhaled in a single, normal breath. Inspiratory capacity is the amount of air taken in during a deep breath, while residual volume is the amount of air left in the lungs after forceful respiration.

Lung Volumes

The volume in the lung can be divided into four units: tidal volume, expiratory reserve volume, inspiratory reserve volume, and residual volume. Tidal volume (TV) measures the amount of air that is inspired and expired during a normal breath. On average, this volume is around one-half liter, which is a little less than the capacity of a 20-ounce drink bottle. The expiratory reserve volume (ERV) is the additional amount of air that can be exhaled after a normal exhalation. It is the reserve amount that can be exhaled beyond what is normal. Conversely, the inspiratory reserve volume (IRV) is the additional amount of air that can be inhaled after a normal inhalation. The residual volume (RV) is the amount of air that is left after expiratory reserve volume is exhaled. The lungs are never completely empty there is always some air left in the lungs after a maximal exhalation. If this residual volume did not exist and the lungs emptied completely, the lung tissues would stick together. The energy necessary to re-inflate the lung could be too great to overcome. Therefore, there is always some air remaining in the lungs. Residual volume is also important for preventing large fluctuations in respiratory gases (O2 and CO2). The residual volume is the only lung volume that cannot be measured directly because it is impossible to completely empty the lung of air. This volume can only be calculated rather than measured..

Lung volumes are measured by a technique called spirometry. An important measurement taken during spirometry is the forced expiratory volume (FEV), which measures how much air can be forced out of the lung over a specific period, usually one second (FEV1). In addition, the forced vital capacity (FVC), which is the total amount of air that can be forcibly exhaled, is measured. The ratio of these values (FEV1/FVC ratio) is used to diagnose lung diseases including asthma, emphysema, and fibrosis. If the FEV1/FVC ratio is high, the lungs are not compliant (meaning they are stiff and unable to bend properly) the patient probably has lung fibrosis. Patients exhale most of the lung volume very quickly. Conversely, when the FEV1/FVC ratio is low, there is resistance in the lung that is characteristic of asthma. In this instance, it is difficult for the patient to get the air out of his or her lungs. It takes a long time to reach the maximal exhalation volume. In either case, breathing is difficult and complications arise.

Lung Capacities

The lung capacities are measurements of two or more volumes. The vital capacity (VC) measures the maximum amount of air that can be inhaled or exhaled during a respiratory cycle. It is the sum of the expiratory reserve volume, tidal volume, and inspiratory reserve volume. The inspiratory capacity (IC) is the amount of air that can be inhaled after the end of a normal expiration. It is, therefore, the sum of the tidal volume and inspiratory reserve volume. The functional residual capacity (FRC) includes the expiratory reserve volume and the residual volume. The FRC measures the amount of additional air that can be exhaled after a normal exhalation. The total lung capacity (TLC) is a measurement of the total amount of air that the lung can hold. It is the sum of the residual volume, expiratory reserve volume, tidal volume, and inspiratory reserve volume..


A VBG on the other hand, tests the venous blood and can accurately determine pH and CO2 but is unable to provide reliable O2 data. For this reason, arterial testing has become the gold standard in sick patients who are at risk for sudden decompensation or those with a respiratory component.

ABGs are drawn for a variety of reasons. These may include concern for:

  • Lung Failure
  • Kidney Failure
  • Shock
  • Trauma
  • Uncontrolled diabetes
  • Asthma
  • Chronic Obstructive Pulmonary Disease (COPD)
  • Hemorrhage
  • Drug Overdose
  • Metabolic Disease
  • Chemical Poisoning
  • To check if lung condition treatments are working

Contents

In medicine, oxygen saturation, commonly referred to as "sats", measures the percentage of hemoglobin binding sites in the bloodstream occupied by oxygen. [2] At low partial pressures of oxygen, most hemoglobin is deoxygenated. At around 90% (the value varies according to the clinical context) oxygen saturation increases according to an oxygen-hemoglobin dissociation curve and approaches 100% at partial oxygen pressures of >11 kPa. A pulse oximeter relies on the light absorption characteristics of saturated hemoglobin to give an indication of oxygen saturation.

The body maintains a stable level of oxygen saturation for the most part by chemical processes of aerobic metabolism associated with breathing. Using the respiratory system, red blood cells, specifically the hemoglobin, gather oxygen in the lungs and distribute it to the rest of the body. The needs of the body's blood oxygen may fluctuate such as during exercise when more oxygen is required [3] or when living at higher altitudes. A blood cell is said to be "saturated" when carrying a normal amount of oxygen. [4] Both too high and too low levels can have adverse effects on the body. [5]

An SaO2 (arterial oxygen saturation, as determined by an arterial blood gas test [6] ) value below 90% indicates hypoxemia (which can also be caused by anemia). Hypoxemia due to low SaO2 is indicated by cyanosis. Oxygen saturation can be measured in different tissues: [6]

  • Venous oxygen saturation (SvO2) is the percentage of oxygenated hemoglobin returning to the right side of the heart. It can be measured to see if oxygen delivery meets the tissues' demands. SvO2 typically varies between 60% and 80%. [7] A lower value indicates that the body is in lack of oxygen, and ischemic diseases occur. This measurement is often used under treatment with a heart lung machine (extracorporeal circulation), and can give the perfusionist an idea of how much flow the patient needs to stay healthy.
  • Tissue oxygen saturation (StO2) can be measured by near infrared spectroscopy. Although the measurements are still widely discussed, they give an idea of tissue oxygenation in various conditions.
  • Peripheral oxygen saturation (SpO2) is an estimation of the oxygen saturation level usually measured with a pulse oximeter device. It can be calculated with pulse oximetry according to the formula [6] where HbO2 is oxygenated hemoglobin (oxyhemoglobin) and Hb is deoxygenated hemoglobin.

Pulse oximetry is a method used to estimate the percentage of oxygen bound to hemoglobin in the blood. [8] This approximation to SaO2 is designated SpO2 (peripheral oxygen saturation). The pulse oximeter consists of a small device that clips to the body (typically a finger, an earlobe or an infant's foot) and transfers its readings to a reading meter by wire or wirelessly. The device uses light-emitting diodes of different colours in conjunction with a light-sensitive sensor to measure the absorption of red and infrared light in the extremity. The difference in absorption between oxygenated and deoxygenated hemoglobin makes the calculation possible. [6]

Healthy individuals at sea level usually exhibit oxygen saturation values between 96% and 99%, and should be above 94%. At 1,600 meters' altitude (about one mile high) oxygen saturation should be above 92%. [9]