Blood Gases

Physiology of Gas Exchange

Blood Gases Details

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  • Respiration and Ventilation

    Definition of Respiration
          Respiration is the total process of delivering oxygen to the cells and carrying away the byproduct of metabolism, carbon dioxide. Respiration includes gas exchange in the lungs, circulation of gases through the blood stream, and transfer of gases at the cellular level.
          Air is drawn into the air sacs of the lungs, where oxygen from the air can enter the blood. Carbon dioxide exits from the blood into the alveolar air. The second half of respiration occurs when the blood reaches the tissues. Oxygen then diffuses into the cells, and carbon dioxide enters the blood. The blood then circulates back to the lung, where the process begins again.

    Definition of Ventilation
          Ventilation is the process of moving gases through the respiratory tract.
          Inspiration (breathing in) occurs when the muscles of the diaphragm and chest wall contract. The contraction of these muscles increases the volume of the chest cavity, lowering the pressure inside. As the pressure in the airways decrease, air rushes in as the chest volume increases.
          Expiration (breathing out) is a passive process. As the muscles relax, the elastic recoil of the lungs puts pressure on the gases inside. The pressure in the chest is now higher than outside pressure, so air rushes out. Expiration stops when the recoil of the lung and the “spring” of the ribs balance each other.
          During quiet breathing, the decrease in pressure in the chest starts about 2.5 mm Hg (compared to the outside pressure), decreasing to around 6 mm Hg towards the end of inspiration. Strong breathing efforts can produce a pressure decrease (vacuum) in the chest as high as 30 mm Hg.
          The muscles of the chest wall, including the diaphragm, contract to expand the volume of the chest. This “vacuum” is transmitted through the fluid-filled pleural space, lowering the pressure in the air sacs of the lung. This draws air in. As the muscles relax, the elastic recoil of the lung pushes air back out. Back to Top

    Lung Anatomy

          Air can enter through either the mouth or nose, merging into a common chamber called the oropharynx. The function of the nose is to humidify and clean the air. From the pharynx, the air enters the larynx, the location of the vocal cords. The larynx is encased in the thyroid cartilage, with the epiglottis protecting the airway from foreign material at the upper margin and the cricoid cartilage providing circular support to the airway below.
          The trachea is formed of semi-circular cartilage rings. The inner membrane of the trachea contains hair cells, mucous cells to continue the job of humidifying and cleaning the air. From the trachea, one major bronchus branches off to each lung. These further divide into smaller bronchi.
          Beyond the bronchi, the smaller airways are called bronchioles. As the smallest bronchioles branch off to enter groups of air sacs, they’re called respiratory bronchioles. Multiple air sacs, called alveoli, form a branching complex at the end of the respiratory bronchiole. In the walls of each alveolus are capillaries. Only a very thin membrane (about 0.3 micrometers thick) separates the air from the red blood cells in the capillaries. Back to Top

    Lung Volumes

          The amount of air that the lungs move in and out with respiration is called the tidal volume. With effort, additional air can be forced in with inspiration, and additional air can be expelled during expiration. The amount of air that can be inspired in excess of the tidal volume is called the inspiratory reserve volume; the air that can be expired after the normal tidal volume has been breathed out is the expiratory reserve volume.
          Tidal volume, and especially the inspiratory and expiratory reserve volumes, are affected by processes that decrease the compliance (the “give” or flexibility) of the chest and lung. After all possible air has been forceably expired, the amount that still remains is called the residual volume. The residual volume increases in diseases that trap air in the chest, such as emphysema. Excess residual volume decreases the efficiency of gas exchange.
          Another “volume” is the respiratory dead space, the amount of air within the chest that is not in contact with alveolar membranes and cannot exchange gases with the blood. The dead space becomes important in certain lung diseases, causing elevation of carbon dioxide levels. Respiratory dead space is NOT the same thing as residual volume. Residual volume includes the respiratory dead space, plus whatever volume is left in the alveoli.
          The vital capacity is often measured clinically. It’s the maximum amount of air that the patient can expire after a full breath — the sum of tidal volume, inspiratory reserve volume, and expiratory reserve volume. The amount of the vital capacity that can be expired in one second (sometimes called “timed vital capacity” or FEV1 — Forced Expiratory Volume in 1 second) gives information about diseases that increase airway resistance such as asthma.
          Peak expiratory flow is a measure of the maximum speed of expiration in volume of gas per second. It provides an easily available (and portable) substitute for the FEV1 in assessing the severity and progress of airway diseases like asthma or chronic bronchitis. Back to Top

    Partial Pressure of Gases

          Dry air is composed of 20.98% oxygen, 0.04% carbon dioxide, 78.06% nitrogen, and 0.92% other gases such as argon and helium. For purposes of blood gas analysis, the amount of a gas present is expressed in terms of “partial pressure.” This is the amount of total gas pressure due to the substance being measured. For example, at sea level the total atmospheric pressure is 760 mm Hg. The amount of this pressure that is due to oxygen is 0.21 x 760 = 160 mm Hg. We would say that the partial pressure of oxygen at sea level in dry air is 160 mm Hg.
          If atmospheric pressure is lower, the partial pressure of a gas will be proportionately decreased. In Salt Lake City, the atmospheric pressure is 647 mm Hg. The partial pressure of oxygen in dry air in Salt Lake is 0.21 x 647 = 136 mm Hg.
          The partial pressure of carbon dioxide in dry air at sea level is 0.03 x 760 = 0.3 mm Hg. However, in the lung carbon dioxide exits the blood to raise the carbon dioxide content of the air. The partial pressure of carbon dioxide in the lung air sacs is around 40 mm Hg. Because this carbon dioxide gas must displace oxygen and nitrogen, the partial pressure of oxygen in the lung air sac will be lower than in outside air.
          Water vapor enters the air when it’s exposed to water. The maximum amount of water vapor in the air varies with temperature. At body temperature (37 centigrade) air can be saturated up to 47 mm Hg. As further water vapor enters the air, other water must condense out — the water content of the air is limited to 47 mm Hg. Therefore in the lung, where air is totally water-saturated, the partial pressure of water vapor would be 47 mm Hg. Back to Top

    Gas Exchange

          During respiration, air becomes saturated with water vapor by the time it enters the alveolar sac. In the alveolus, it also mixes with carbon dioxide.
          At the alveolar membrane, each gas diffuses in the direction where the partial pressure of that gas is less. In other words, oxygen diffuses towards the blood and is taken up by hemoglobin, and carbon dioxide diffuses towards the alveolus and mixes with the air. No “active process” is involved. Oxygen simply diffuses through the membrane and plasma, and is taken up by the red blood cells.
          Although the diffusion occurs very rapidly, the gases do not have time to totally equilibrate. There will be a small pressure difference across the alveolar membrane for each gas. That is, oxygen partial pressure will be somewhat higher in the alveolus than in the blood, and carbon dioxide pressure will be slightly higher in the blood than in the air in the alveolus. In the case of oxygen, this pressure difference is calculated for the lung as a whole as the “arterial-alveolar (Aa) gradient.”
          About 2% of the blood flow through the lungs bypasses the pulmonary capillaries. This blood is not oxygenated, and forms a “physiologic shunt.” Because of this blood that bypasses the alveoli, arterial blood will always contain less oxygen pressure than blood that has equilibrated with the oxygen in the lung alveoli. This “shunt” becomes part of the calculated “Aa gradient.”
          As blood circulates through the body, an opposite change occurs in the capillaries of the systemic circulation. Oxygen diffuses from the area of higher pressure — the blood — into the lower pressure of the cells. Carbon dioxide diffuses from the cells into the blood. Back to Top

    Oxygen Transport

          Hemoglobin is a molecule composed of four subunits. Each subunit is a protein chain attached to a porphyrin ring containing one iron atom. As each iron atom can bind one oxygen (O2) molecule, hemoglobin can carry one, two, three, or four oxygen molecules.
          Normal blood contains about 15-16 grams hemoglobin per 100 ml. Each gram of hemoglobin can carry about 1.34 ml of gaseous oxygen. Fully saturated arterial blood will therefore contain about 20 ml of oxygen per 100 cc. The volume of oxygen in the blood is referred to as the O2 content. Because O2 content is dependent on the hemoglobin concentration, it doesn’t provide a good measure of lung function. The partial pressure of oxygen (PaO2), as measured in arterial blood, does provide an accurate picture of gas exchange in the lung.
          The relative amount of oxygen in the blood compared to the carrying capacity of the hemoglobin is called the oxygen saturation, and is expressed as a percentage. It’s directly proportional to the PaO2 — the partial pressure of oxygen. The hemoglobin in arterial blood is only about 97% saturated with oxygen because of venous blood that passes directly through the lung (physiologic shunt). Venous blood is about 75% saturated. Back to Top

    Effects of Acid on Oxygen Transport

          Oxygen status is affected by acid-base status. Oxygen affects the buffering capacity of hemoglobin through the Bohr effect, but the opposite is also true. At a given oxygen pressure, oxygen saturation in the blood is lowered by increasing either carbon dioxide or hydrogen ion concentrations.
          As the acidity of the serum increases, less oxygen can be bound at a given PaO2. This mechanism assists hemoglobin in unloading oxygen in the capillaries, where acid concentration is higher. Raising the pH, conversely, increases the oxygen binding, allowing more total oxygen to be carried -- a change that occurs in the alveolus as acid is eliminated through CO2. Back to Top

    Carbon Dioxide Transport

          The gas carbon dioxide is transported through the blood stream by conversion to carbonic acid, which dissociates to hydrogen ion and bicarbonate. The hydrogen ion binds to hemoglobin, and is transported to the lungs. In this case, hemoglobin is acting as a buffer for the acid, but also is acting as an effective “transportation vehicle” for ferrying carbon dioxide to the lungs.
          Hemoglobin and bicarbonate act as buffers for the acid produced by metabolism, effectively transporting this acid to the lungs for elimination. Read more about buffers in the “acid-base” section.
          As carbon dioxide is formed in the cells (due to aerobic metabolism) it diffuses into the plasma of the capillary. As it enters the red blood cells (which contain carbonic anhydrase) it’s quickly converted to H2CO3, which breaks down to H+ and HCO3-. About two-thirds of the HCO3- will diffuse out into the plasma (and is replaced by chloride in the red cell). Only small amounts of carbon dioxide remain dissolved or attach to other compounds.
          About 50 ml of CO2 gas are contained in each 100 ml of arterial blood, almost all as HCO3-. As the blood goes through the capillaries, it picks up about 5 ml of additional CO2. With this addition of acidic CO2, the pH drops from 7.4 to 7.36. On reaching lungs, the process is reversed, and 5 ml of CO2 is converted back from H+ and HCO3- and discharged into the alveoli.
          At rest, about 200 ml of CO2 is produced and excreted through the lungs. Over 24 hours, this is the equivalent of 12,500 milliequivalents of acid produced by metabolism and eliminated through CO2. Back to Top

    Chemical Control of Respiration

          Special chemical receptors near the aorta and carotid arteries, called the aortic bodies and carotid bodies, are sensitive to an increase in carbon dioxide or acid concentration, or to a decrease in the pressure of oxygen (PaO2). When these receptors sense acidity or low oxygen, they stimulate the brain respiratory center to increase the speed and depth of breathing.
          The area of the brain stem that controls respiration is directly responsive to increases in acid concentration in the cerebrospinal fluid, producing increased respirations. When acid buildup occurs, such as in diabetic ketoacidosis, strong stimulation of respiration results. The deep rapid breathing mixes alveolar air with increased amounts of low-CO2 air, leading to a decrease in the carbon dioxide in the blood as it passes by the alveolus. The reduction in CO2 raises the pH back towards normal.
          When there is a rise in serum CO2, such as with the increased metabolism of exercise, ventilation is stimulated until the CO2 returns to normal levels.
          Lack of oxygen also acts as a respiratory stimulant, although a weak one. In healthy individuals at normal altitudes, oxygen levels play no role in regulation of ventilation. As arterial oxygen pressure falls, there is not much stimulation of respiration until the level is below 60 mm Hg. Patients suffering from severe chronic bronchitis and emphysema may come to rely on the “hypoxic drive” to stimulate respirations, as they become habituated to high levels of carbon dioxide. Back to Top


          Carbon monoxide binds tightly to hemoglobin, preventing it from accepting oxygen molecules. This CO-hemoglobin complex is called carboxyhemoglobin. Small amounts of carbon monoxide are normally produced by body metabolism. In city dwellers and smokers, the level is much increased. Heavy smokers may have as much as 10% of their hemoglobin bound by carbon monoxide.
          Carbon monoxide reduces the oxygen saturation of hemoglobin at any given PaO2. The presence of carbon monoxide can be suspected, and a rough measure obtained, by comparing a measured oxygen saturation with the oxygen saturation expected for the PaO2 and pH. Carboxyhemoglobin levels (usually expressed as a percentage of total hemoglobin) can also be directly measured. Back to Top

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Copyright 1996 Mad Scientist Software
Argyle, B., Blood Gases Computer Program Manual.
Mad Scientist Software, Alpine UT, 1996.


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