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1 Laura Jimenez Dr. Bowlus Chemistry 1A Columbia College 8 December 2010 Respiration: Applied Chemistry External respiration is a summation of pulmonary ventilation and gas exchange through the diffusion of oxygen and carbon dioxide across the respiratory membrane. External respiration is a composition of various chemical phenomena, which the mammalian physiology has evolved to exploit in order to aerobically sustain life. The physical and chemical behaviors of gases within our atmosphere and the interplay of intermolecular forces are particularly important to the physiology of breathing. The dynamics of respiration can be largely understood by applying fundamental scientific laws that have been determined through the studies of chemistry and physics. Boyle’s Law and the Pressure Gradient Air flow is the direct result of a pressure gradient. The direction of the flow is always from high pressure to low pressure. Without a difference in pressure, this air flow will not occur. 2 Boyle’s Law states that the volume of a fixed quantity of gas maintained at constant temperature is inversely proportional to the pressure (Brown et al), and can be mathematically expressed by the following equation; V = constant × 1∕P or PV = constant or P1 V1 = P 2 V2 Boyle’s Law, and the tendency of air to flow with a pressure gradient work together to form the basis for pulmonary ventilation. At the start of inhalation, the intra-alveolar pressure is equal to that of the atmosphere, and there is no air flow either into or out of the lungs. PATM = Ppulmonary When the muscles of the thoracic cavity contract, the two pleural cavities within are expanded. The result is an increase in intrapulmonary volume. This increase in volume causes an inverse decrease in pressure, and the pressure within the alveolar walls falls below atmospheric pressure. ↑Volume = ↓Pressure This pressure gradient causes air to flow from the atmosphere into the lungs and inspiration occurs. PATM > PPulmonary Conversely, when the thoracic muscles relax, the volume of the lungs is compressed and the pressure inside becomes more than that of atmospheric pressure. ↓Volume = ↑Pressure 3 This causes air to be expelled from the lungs into the surrounding atmosphere, resulting in exhalation. PATM < PPulmonary A Solution to Surface Tension At any gas-liquid boundary, the molecules of the liquid are more strongly attracted to each other than they are to the gas molecules, creating surface tension (Marieb, 823). The alveolar walls, which exist as the boundary between the outside world and internal anatomy, are coated with a thin film of serous fluid. While this fluid is necessary in order to facilitate a very rapid exchange of gases (O2 and CO2) across the respiratory membrane, it is also susceptible to the demands of surface tension. Surface tension is a measure of the inward forces that must be overcome in order to expand the surface area of a liquid, and is a direct result of hydrogen bonding. The summation of numerous hydrogen bonds results in the strength of the intermolecular forces between the molecules of a liquid overcoming the attraction of the molecules to any surrounding surfaces (Brown, 448). When the thoracic muscles contract and lung capacity decreases, the alveoli come into very close proximity with one another. Because each alveoli is bathed in serous fluid, the tendency of surface tension would cause the alveoli to stick together, drastically reducing compliance and diminishing the ability of the lungs to inspire once again. The physiological answer to the problematics of surface tension is alveolar surfactant. A complex substance produced by the septal cells of the lung tissue, 4 alveolar surfactant is composed primarily of phospholipids (Martini et al, 634). The anatomy of a phospholipid is such that one end is hydrophilic and the other hydrophobic. The hydrophilic end of the phospholipid orients itself toward the watery serous fluid, creating a dipole-dipole interaction with serous fluid molecules and effectively dispersing hydrogen bonds. The hydrophobic end of the phospholipid is oriented outward toward the fluid/air interface, interrupting the surface tension of the serous fluid. The result is the ability of the individual alveolar sacs to pull away from each other, allowing inspiration. Consequently, this phospholipid composition does not hinder the diffusion of CO2 and O2 across the respiratory membrane because a physical property of gases is lipid solubility. Dalton and Henry Explain Pulmonary Gas Exchange In the lungs, O2 and CO2 are exchanged between the atmosphere and the cardiopulmonary system by way of diffusion. During internal respiration, this same exchange of gases is taking place, also by diffusion, but in the opposite direction (Marieb,826). Two important chemical forces driving this process of gas exchange are; the partial pressures of gases and the diffusion of molecules between a gas and a liquid (Martini et al, 638). John Dalton observed that the total pressure of a mixture of gases equals the sum of the pressures that each would exert if it were present alone. The pressure exerted by a particular component of a mixture of gases is known as the partial pressure of that gas (Brown, 410). The summation of the partial 5 pressures of the individual components represent the total pressure of the gas mixture. Dalton’s law of partial pressures can be represented in the following mathematical equation; Pt = P1 + P2 + P3 + ∙∙∙ This law can be applied to the partial pressures of the atmosphere and the subsequent total pressure exerted on biological life by the gas mixture as a whole, PN2 + P02 + PH2O + PCO2 = 760 mm Hg or 1 atm The physiology of the respiratory system exploits this behavior of partial pressures in its favor as a means of exchanging gas molecules (CO2 and O2) across the respiratory membrane and into and out of the blood stream. Henry’s Law states that at a given temperature the amount of a particular gas in solution is directly proportional to the partial pressure of that gas (Martini, 852). When a gas which is under pressure comes in contact with a liquid, the pressure forces gas molecules into solution. If the pressure of the system remains constant, gas molecules will continue to diffuse into solution until an equilibrium is reached. However, when the partial pressure of the gas later becomes greater in the liquid than in the adjacent gas phase, some of the dissolved gas molecules will exit the solution and re-enter the gas phase (Martini, 852). The rate at which a gas will diffuse into solution, in the case of respiration into the blood plasma, largely depends on the partial pressure exerted on the solution by that particular gas. The physiology of humans and other mammals has exploited this physical 6 property of gas behavior to maximize the efficiency of gas exchange, which must occur very rapidly in order to maintain cellular metabolism. The oxygen of freshly inspired air exerts a partial pressure of 160 mm Hg while intra-alveolar PO2 is 104 mm Hg. This difference in the partial pressure of oxygen at the air-liquid interface (the respiratory membrane) causes O2 molecules to diffuse into the alveolar sacs until equilibrium is reached. Conversely, the partial pressure of CO2 entering the lungs from the atmosphere is 0.3 mm Hg while the PCO2 in the alveolar capillaries is 40 mm Hg. Due to the considerable difference in the partial pressures, as well as the high solubility of CO2 in liquid, carbon dioxide very rapidly diffuses out of the blood, across the alveolar walls and is expired into the atmosphere until an equilibrium is reached at PCO2 = 40 mm Hg on both sides of the respiratory membrane. This large CO2 pressure gradient at the cardiopulmonary interface is so vital because it is important to quickly expel large amounts of CO2, a main byproduct of cellular metabolism, in order to maintain the pH balance of the blood. Meanwhile at the site of internal respiration, the interface between the tissues and the network of cardiovascular capillaries, diffusion of gases is occurring in the opposite direction. PO2 of the systemic arteries is now 100 mm Hg and PCO2 is 40 mm Hg. At the tissues, PO2 > 40 mm Hg and PCO2 < 45 mm Hg. The PO2 gradient forces O2 molecules to dissolve into the extracellular fluid until equilibrium is reached at 40 mm Hg and the PCO2 gradient causes CO2 molecules to dissolve into the capillary blood stream until equilibrium occurs at 45 mm Hg. It can be noticed that the pressure gradient for oxygen diffusion is much 7 greater than that of carbon dioxide. Although this is true, equal amounts of O 2 and CO2 are constantly being exchanged during internal respiration. This is due to the differences in the liquid solubilities of the two gases. Carbon dioxide is much more liquid soluble than oxygen (Marieb, 829). In the time it takes a blood cell to pass through an arteriole, the same amount of CO2 diffuses into the bloodstream as that of O2 diffusing out. In the same respect N2, which is the most abundant atmospheric gas, does not diffuse into the blood stream at altitudes above sea level because its liquid solubility is so very low. Although mammals depend largely on nitrogen, they do not retain the ability to fix it from the atmosphere, and obtain this essential protein component through dietary means. This cycle of the breath, which is the first and last action of life, is dependent on the physical and chemical behavior of the atmosphere and its components. The most stunning aspect of this relationship between living organisms and the terrestrial conditions that support life, is that this has been the way of things since long before scientists such as Dalton and Boyle put it into words. While breathing is usually an unconscious act, a closer look reveals just one example of the wonders of the dynamism between life and the laws of the natural world. 8 Works Cited Brown, Theodore L., H. Eugene LeMay Jr., Bruce E. Bursten, Catherine J. Murphy. Chemistry The Central Science. Upper Saddle River: Prentice Hall, 2009. Marieb, Elaine, Katja Hoehn. Human Anatomy and Physiology. San Francisco: Benjamin Cummings, 2010. Martini, Frederic H. Fundamentals of Anatomy and Physiology. San Francisco: Benjamin Cummings, 2004. Martini, Frederic H., Michael J. Timmons, Michael P. McKinley. Human 9 Anatomy. Upper Saddle River: Prentice Hall, 2000. 10