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Is there gas exchange in the fingers?

Is there gas exchange in the fingers?


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I saw A documentary many years ago that said that hemoglobin will take in O2 in the fingers and toes. I have Not been able to find any information on this. But it would seem that being so close to the surface some gas exchange would occur, and more so in the fingers and toes than the teunk.


At first I was skeptical about this question but then I did some researching and apparently, a certain amount of oxygen is indeed taken up from the surroundings through the upper layers of our skin. In fact, the paper titled "The cutaneous uptake of atmospheric oxygen contributes significantly to the oxygen supply of human dermis and epidermis. states that

the upper skin layers to a depth of of 0.25-0.40 mm are almost exclusively supplied by external oxygen, whereas the oxygen transport of the blood has a minor influence.

Here is another paper that you would find interesting. In short, I would say that its not just the fingers but O2 diffusion into cells take place over the whole body.


Extremes of Temperature and Hydration

Yoram Epstein , Daniel S. Moran , in Travel Medicine (Fourth Edition) , 2019

Dry Heat Exchange

Dry heat exchange occurs through conduction, convection, and radiation. Conduction is heat exchange between two surfaces in direct contact. Usually heat exchange by conduction is relatively low. It becomes significant when one lies uninsulated on cold ground, especially if under the influence of vasodilating drugs or alcohol. Convection refers to heat transferred from a surface to a gas or liquid environment. This is significant during cold water immersion because of the much higher heat capacity and the higher thermal conductivity of water as opposed to air. Radiation refers to the transfer of heat by electromagnetic waves (at the spectrum of infrared wavelength). Radiant heat transfer is very much dependent on the insulation from the environment. A major source of heat gain in hot climates is solar load, which can be significantly reduced (by >50%) by wearing light clothing. Radiation is the major way of losing heat in the cold.


Describe how the lungs are adapted for gas exchange (6 marks)

-There are a large number of alveoli, increasing the surface area available for gas exchange. The alveoli have many infoldings, further increasing the surface area.- The walls of the alveoli are thin, they are one cell thick. This reduces the diffusion distance for gases, increasing the rate of gas exchange.- The alveoli are surrounded by a dense capillary network. This means gases diffuse into the blood, where they are rapidly removed from the alveoli, helping to maintain a concentration gradient for the diffusion of gases.- The alveoli are moist, which also aids the diffusion of gases.Key themes large surface area, short diffusion distance, moist surfaces, capillary network


Three weeks ago, 20-year-old Sacheen came down with symptoms typical of the common cold. She had a runny nose, fatigue, and a mild cough. Her symptoms had been starting to improve, but recently her cough has been getting worse. She coughs up a lot of thick mucus, her throat is sore from frequent coughing, and her chest feels very congested. According to her wife, Sacheen has a &ldquochest cold.&rdquo Sacheen is a smoker and wonders if her habit is making her cough worse. She decides that it is time to see a doctor.

Figure (PageIndex<1>): Coughing

Dr. Tsosie examines Sacheen and asks about her symptoms and health history. She checks the level of oxygen in Sacheen&rsquos blood by attaching a device called a pulse oximeter to Sacheen&rsquos finger (Figure (PageIndex<2>)). Dr. Tsosie concludes that Sacheen has bronchitis, an infection that commonly occurs after a person has a cold or flu. Bronchitis is sometimes referred to as a &ldquochest cold,&rdquo so Sacheen&rsquos wife was right! Bronchitis causes inflammation and a build-up of mucus in the bronchial tubes in the chest.

Figure (PageIndex<2>): A pulse oximeter, used to measure blood oxygen levels.

Because viruses, and not bacteria, usually cause bronchitis, Dr. Tsosie tells Sacheen that antibiotics are not likely to help. Instead, she recommends that Sacheen try to thin and remove the mucus by drinking plenty of fluids and using a humidifier, or spending time in a steamy shower. She also recommends that Sacheen get plenty of rest.

Dr. Tsosie also tells Sacheen some things not to do&mdashmost importantly, not to smoke while she is sick and to try to quit smoking in the long term. She explains that smoking can make people more susceptible to bronchitis and can hinder recovery. She also advises Sacheen not to take over-the-counter cough suppressant medication.

As you read this chapter on the respiratory system, you will better understand what bronchitis is and why Dr. Tsosie made the treatment recommendations that she did. At the end of the chapter, you will learn more about acute bronchitis, which is the type that Sacheen has. This information may come in handy to you personally because the chances are high that you will get this common infection at some point in your life&mdashthere are millions of bronchitis cases every year!


Abnormal gas exchange

Lung disease can lead to severe abnormalities in blood gas composition. Because of the differences in oxygen and carbon dioxide transport, impaired oxygen exchange is far more common than impaired carbon dioxide exchange. Mechanisms of abnormal gas exchange are grouped into four categories— hypoventilation, shunting, ventilation–blood flow imbalance, and limitations of diffusion.

If the quantity of inspired air entering the lungs is less than is needed to maintain normal exchange—a condition known as hypoventilation—the alveolar partial pressure of carbon dioxide rises and the partial pressure of oxygen falls almost reciprocally. Similar changes occur in arterial blood partial pressures because the composition of alveolar gas determines gas partial pressures in blood perfusing the lungs. This abnormality leads to parallel changes in both gas and blood and is the only abnormality in gas exchange that does not cause an increase in the normally small difference between arterial and alveolar partial pressures of oxygen.

In shunting, venous blood enters the bloodstream without passing through functioning lung tissue. Shunting of blood may result from abnormal vascular (blood vessel) communications or from blood flowing through unventilated portions of the lung (e.g., alveoli filled with fluid or inflammatory material). A reduction in arterial blood oxygenation is seen with shunting, but the level of carbon dioxide in arterial blood is not elevated even though the shunted blood contains more carbon dioxide than arterial blood.

The differing effects of shunting on oxygen and carbon dioxide partial pressures are the result of the different configurations of the blood-dissociation curves of the two gases. As noted above, the oxygen-dissociation curve is S-shaped and plateaus near the normal alveolar oxygen partial pressure, but the carbon dioxide-dissociation curve is steeper and does not plateau as the partial pressure of carbon dioxide increases. When blood perfusing the collapsed, unventilated area of the lung leaves the lung without exchanging oxygen or carbon dioxide, the content of carbon dioxide is greater than the normal carbon dioxide content. The remaining healthy portion of the lung receives both its usual ventilation and the ventilation that normally would be directed to the abnormal lung. This lowers the partial pressure of carbon dioxide in the alveoli of the normal area of the lung. As a result, blood leaving the healthy portion of the lung has a lower carbon dioxide content than normal. The lower carbon dioxide content in this blood counteracts the addition of blood with a higher carbon dioxide content from the abnormal area, and the composite arterial blood carbon dioxide content remains normal. This compensatory mechanism is less efficient than normal carbon dioxide exchange and requires a modest increase in overall ventilation, which is usually achieved without difficulty. Because the carbon dioxide-dissociation curve is steep and relatively linear, compensation for decreased carbon dioxide exchange in one portion of the lung can be counterbalanced by increased excretion of carbon dioxide in another area of the lung.

In contrast, shunting of venous blood has a substantial effect on arterial blood oxygen content and partial pressure. Blood leaving an unventilated area of the lung has an oxygen content that is less than the normal content (indicated by the square). In the healthy area of the lung, the increase in ventilation above normal raises the partial pressure of oxygen in the alveolar gas and, therefore, in the arterial blood. The oxygen-dissociation curve, however, reaches a plateau at the normal alveolar partial pressure, and an increase in blood partial pressure results in a negligible increase in oxygen content. Mixture of blood from this healthy portion of the lung (with normal oxygen content) and blood from the abnormal area of the lung (with decreased oxygen content) produces a composite arterial oxygen content that is less than the normal level. Thus, an area of healthy lung cannot counterbalance the effect of an abnormal portion of the lung on blood oxygenation because the oxygen-dissociation curve reaches a plateau at a normal alveolar partial pressure of oxygen. This effect on blood oxygenation is seen not only in shunting but in any abnormality that results in a localized reduction in blood oxygen content.

Mismatching of ventilation and blood flow is by far the most common cause of a decrease in partial pressure of oxygen in blood. There are minimal changes in blood carbon dioxide content unless the degree of mismatch is extremely severe. Inspired air and blood flow normally are distributed uniformly, and each alveolus receives approximately equal quantities of both. As matching of inspired air and blood flow deviates from the normal ratio of 1 to 1, alveoli become either overventilated or underventilated in relation to their blood flow. In alveoli that are overventilated, the amount of carbon dioxide eliminated is increased, which counteracts the fact that there is less carbon dioxide eliminated in the alveoli that are relatively underventilated. Overventilated alveoli, however, cannot compensate in terms of greater oxygenation for underventilated alveoli because, as is shown in the oxygen-dissociation curve, a plateau is reached at the alveolar partial pressure of oxygen, and increased ventilation will not increase blood oxygen content. In healthy lungs there is a narrow distribution of the ratio of ventilation to blood flow throughout the lung that is centred around a ratio of 1 to 1. In disease, this distribution can broaden substantially so that individual alveoli can have ratios that markedly deviate from the ratio of 1 to 1. Any deviation from the usual clustering around the ratio of 1 to 1 leads to decreased blood oxygenation—the more disparate the deviation, the greater the reduction in blood oxygenation. Carbon dioxide exchange, on the other hand, is not affected by an abnormal ratio of ventilation and blood flow as long as the increase in ventilation that is required to maintain carbon dioxide excretion in overventilated alveoli can be achieved.

A fourth category of abnormal gas exchange involves limitation of diffusion of gases across the thin membrane separating the alveoli from the pulmonary capillaries. A variety of processes can interfere with this orderly exchange for oxygen, these include increased thickness of the alveolar–capillary membrane, loss of surface area available for diffusion of oxygen, a reduction in the alveolar partial pressure of oxygen required for diffusion, and decreased time available for exchange due to increased velocity of flow. These factors are usually grouped under the broad description of “diffusion limitation,” and any can cause incomplete transfer of oxygen with a resultant reduction in blood oxygen content. There is no diffusion limitation of the exchange of carbon dioxide because this gas is more soluble than oxygen in the alveolar–capillary membrane, which facilitates carbon dioxide exchange. The complex reactions involved in carbon dioxide transport proceed with sufficient rapidity to avoid being a significant limiting factor in exchange.


BREATHING AIR OR WATER

Terrestrial vertebrates use lungs to perform gas exchange. While our aquatic ancestors breathed using gills, these are of no use on land, as gravity would collapse them and cause them to lose their form. As lungs are found inside the body, they can keep their form in a habitat with much higher gravity. Both gills and lungs have highly branched structures to increase their diffusion surface, and this way facilitate gas exchange (in a larger surface there’s more exchange).

We can find a third form of gas exchange in vertebrates. Even if it’s not as widespread as gills or lungs, cutaneous respiration is found in several groups of animals, such as lunged fish and some marine reptiles (turtles and sea snakes). Yet the lissamphibians are the group that has brought their specialization in cutaneous respiration to the ultimate level.


Central Control of Breathing

The rate of cellular respiration (and hence oxygen consumption and carbon dioxide production) varies with level of activity. Vigorous exercise can increase by 20&ndash25 times the demand of the tissues for oxygen. This is met by increasing the rate and depth of breathing.

It is a rising concentration of carbon dioxide &mdash not a declining concentration of oxygen &mdash that plays the major role in regulating the ventilation of the lungs. Certain cells in the medulla oblongata are very sensitive to a drop in pH. As the CO2 content of the blood rises above normal levels, the pH drops
[CO2 + H2O &rarr HCO3 &minus + H + ],
and the medulla oblongata responds by increasing the number and rate of nerve impulses that control the action of the intercostal muscles and diaphragm. This produces an increase in the rate of lung ventilation, which quickly brings the CO2 concentration of the alveolar air, and then of the blood, back to normal levels.

However, the carotid body in the carotid arteries does have receptors that respond to a drop in oxygen. Their activation is important in situations (e.g., at high altitude in the unpressurized cabin of an aircraft) where oxygen supply is inadequate but there has been no increase in the production of CO2. People who live at high altitudes, e.g., in the Andes, have enlarged carotid bodies.


Respiratory Physiology: Structure, Function, and Integrative Responses to Intervention with Special Emphasis on the Ventilatory Pump

Determinants of Gas Exchange

Gas exchange takes place in the alveolus by a process of diffusion. Diffusion is the random movement of molecules down their concentration gradient. The term partial pressure can be substituted for concentration when speaking of gas mixtures, because the contribution of each gas to the total pressure of a gas mixture is directly proportional to the concentration of that gas in the mixture (Dalton's law). If the fractional concentration (F) of oxygen in a dry gas mixture is 21%, the partial pressure exerted by the oxygen is 21% of the total pressure. The total pressure of ambient (atmospheric) air is the barometric pressure. At sea level, this is 1 atmosphere, or 760 mm Hg. The barometric pressure determines the total pressure of the air in the respiratory passages and the alveoli when the respiratory system is at rest.

Alveolar air is a mixture of nitrogen, oxygen, carbon dioxide, and water vapor ( Fig. 2-27 ). The concentrations and consequently the partial pressures of these gases in the alveolar air differ considerably from their concentrations in the ambient air. In ambient air, the water vapor content (humidity) is variable. As the inspired air moves through the respiratory passages into the alveoli, it becomes fully saturated with water, and it is warmed to body temperature (37° C). Such air has a water vapor pressure of 47 mm Hg. The concentration of oxygen in the alveoli (approximately 14%) is much less than in ambient air (21%). Although the oxygen supply to the alveolus is periodically renewed during inspiration, oxygen is constantly removed from the alveolar air by the blood. The average partial pressure of oxygen in alveolar air (P AO 2) at sea level is approximately 100 mm Hg. There is a negligible amount of carbon dioxide in ambient air and significant amounts (approximately 5.6%) in alveolar air, because carbon dioxide is constantly being added to the alveolar air by the blood. During normal breathing, the average partial pressure of alveolar carbon dioxide (P aco 2) is 40 mm Hg. If the carbon dioxide production by the tissues remains constant, a decrease in alveolar ventilation will result in an accumulation of carbon dioxide in the alveolus with an increase in its partial pressure. This is termed hypoventilation. Conversely, an increase in alveolar ventilation will produce a decreased alveolar partial pressure of carbon dioxide.

When a liquid is exposed to a gas mixture, as pulmonary capillary blood is to alveolar air, the molecules of each gas diffuse between air and liquid until the pressure of the dissolved molecules equals the partial pressure of that gas in the gas mixture ( Fig. 2-28 ). When equilibrium is achieved in the alveolus, the gas tensions in the end-pulmonary capillary blood are the same as the partial pressures of the gases in the alveolar air.


Metabolism, Gas Exchange, and Carbon Spiraling in Rivers

Ecosystem metabolism, that is, gross primary productivity (GPP) and ecosystem respiration (ER), controls organic carbon (OC) cycling in stream and river networks and is expected to vary predictably with network position. However, estimates of metabolism in small streams outnumber those from rivers such that there are limited empirical data comparing metabolism across a range of stream and river sizes. We measured metabolism in 14 rivers (discharge range 14–84 m 3 s −1 ) in the Western and Midwestern United States (US). We estimated GPP, ER, and gas exchange rates using a Lagrangian, 2-station oxygen model solved in a Bayesian framework. GPP ranged from 0.6–22 g O2 m −2 d −1 and ER tracked GPP, suggesting that autotrophic production supports much of riverine ER in summer. Net ecosystem production, the balance between GPP and ER was 0 or greater in 4 rivers showing autotrophy on that day. River velocity and slope predicted gas exchange estimates from these 14 rivers in agreement with empirical models. Carbon turnover lengths (that is, the distance traveled before OC is mineralized to CO2) ranged from 38 to 1190 km, with the longest turnover lengths in high-sediment, arid-land rivers. We also compared estimated turnover lengths with the relative length of the river segment between major tributaries or lakes the mean ratio of carbon turnover length to river length was 1.6, demonstrating that rivers can mineralize much of the OC load along their length at baseflow. Carbon mineralization velocities ranged from 0.05 to 0.81 m d −1 , and were not different than measurements from small streams. Given high GPP relative to ER, combined with generally short OC spiraling lengths, rivers can be highly reactive with regard to OC cycling.

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What makes the sound when we crack our knuckles?

To understand what happens when you "crack" your knuckles, or any other joint, first you need a little background about the nature of the joints of the body. The type of joints that you can most easily "pop" or "crack" are the diarthrodial joints. These are your most typical joints. They consist of two bones that contact each other at their cartilage surfaces the cartilage surfaces are surrounded by a joint capsule. Inside the joint capsule is a lubricant, known as synovial fluid, which also serves as a source of nutrients for the cells that maintain the joint cartilage. In addition, the synovial fluid contains dissolved gases, including oxygen, nitrogen and carbon dioxide.

The easiest joints to pop are the ones in your fingers (the interphalangeal and the metacarpophalangeal joints). As the joint capsule stretches, its expansion is limited by a number of factors. When small forces are applied to the joint, one factor that limits the motion is the volume of the joint. That volume is set by the amount of synovial fluid contained in the joint. The synovial fluid cannot expand unless the pressure inside the capsule drops to a point at which the dissolved gases can escape the solution when the gases come out of solution, they increase the volume and hence the mobility of the joint.

The cracking or popping sound is thought to be caused by the gases rapidly coming out of solution, allowing the capsule to stretch a little further. The stretching of the joint is soon thereafter limited by the length of the capsule. If you take an x-ray of the joint after cracking, you can see a gas bubble inside the joint. This gas increases the joint volume by 15 to 20 percent it consists mostly (about 80 percent) of carbon dioxide. The joint cannot be cracked again until the gases have dissolved back into the synovial fluid, which explains why you cannot crack the same knuckle repeatedly.

But how can releasing such a small quantity of gas cause so much noise? There is no good answer for this question. Researchers have estimated the energy levels of the sound by using accelerometers to measure the vibrations caused during joint popping. The amounts of energy involved are very small, on the order of 0.1 milli-joule per cubic millimeter. Studies have also shown that there are two sound peaks during knuckle cracking, but the causes of these peaks are unknown. It is likely that the first sound is related to the gas dissolving out of solution, whereas the second sound is caused by the capsule reaching its length limit.

A common, related question is, Does popping a joint cause any damage? There are actually few scientific data available on this topic. One study found no correlation between knuckle cracking and osteoarthritis in the finger joints. Another study, however, showed that repetitive knuckle cracking may affect the soft tissue surrounding the joint. Also, the habit tends to cause an increase in hand swelling and a decrease in the grip strength of the hand.

Another source of popping and cracking sounds is the tendons and ligaments near the joint. Tendons must cross at least one joint in order to cause motion. But when a joint moves, the tendon's position with respect to the joint is forced to change. It is not uncommon for a tendon to shift to a slightly different position, followed by a sudden snap as the tendon returns to its original location with respect to the joint. These noises are often heard in the knee and ankle joints when standing up from a seated position or when walking up or down the stairs.