Download File - Laura L. Jimenez, RN, BSN

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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.
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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
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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,
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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
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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
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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
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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.
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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
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Anatomy.
Upper Saddle River: Prentice Hall, 2000.
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