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Respiration can be broken up conceptually into three phases:
external, internal, and cellular respiration.
External respiration is about the mechanics of breathing, moving gases
(air) in and out of the lungs.
Internal respiration is about ensuring the transport of oxygen in the
blood from the lungs to tissue cells, and then the transport of metabolic CO2
from tissue cells to the lungs for both its excretion and its reallocation to
systemic circulation for acid-base regulation. Cellular respiration is the utilization of
oxygen in mitochondria for the synthesis of adenosine triphosphate (ATP),
molecules that cells ultimately break down for their energy. Basic to external respiration is the subject of gas
exchange. Gases are measured by virtue
of the pressures that they exert. When
gases are mixed, e.g., air, they each contribute to a total pressure. Each gas contributes a partial pressure
(P). Total atmospheric air pressure at
sea level, at 15 degrees C and zero humidity, is 760 mmHg (millimeters of
mercury). At sea level partial
pressure oxygen, written PO2, is 159 mmHg (20.93%), and partial
pressure carbon dioxide, written PCO2, is 0.3 mmHg (less than
0.04%). Most of the gas exchange, O2
and CO2, takes place in the fundamental alveolar-capillary unit,
the alveolus. There are about 300
million alveoli in the lungs, surrounded by about 280 billion pulmonary
capillaries. Capnography is about
measurement of average alveolar PCO2, which is observed/measured
in the final portion of exhalation when gases are presumably 100 percent
alveolar (not mixed with anatomical dead space gases); this measurement is known
as End Tidal CO2, or ETCO2, or PCO2 at the
“end of the tides of air,” that is, when the “tide is out.” The Henderson-Hasselbach (H-H) equation is central to
understanding internal respiration, which describes pH regulation in
extracellular fluids: pH = [HCO3‾]
÷ PCO2 (in its simplified conceptual format), wherein PCO2
is regulated by breathing, and bicarbonate concentration [HCO3‾]
is regulated by the kidneys. These
fluids include blood plasma, interstitial (fluids that surround tissue
cells), lymph, and cerebrospinal fluids.
Changes in the numerator of the equation, bicarbonate concentration,
are generally slow (8 hours to 5 days), whereas changes in the denominator,
partial pressure carbon dioxide (PCO2), are immediate. This places breathing center stage in
moment-to-moment acid-base regulation.
Arterial levels of PCO2, known as PaCO2, remain
between 35 and 45 mmHg to keep plasma pH within its normal range (7.35 to
7.45). In normal healthy lungs, when
perfusion (blood) and ventilation (air) are matched, alveolar PCO2
(and hence, ETCO2) is approximately equivalent to PaCO2.
Balancing the Henderson-Hasselbach (H-H) equation is achieved
through the presence of receptor sites in (1) the brainstem that are
sensitive to interstitial pH and PCO2, and (2) the arterial system
(aorta and carotid arteries) that are sensitive to plasma pH and PCO2. Changes in pH and PCO2 in both
locations together drive the respiratory centers in the brainstem, along with
partial pressure oxygen (PO2) changes detected also at arterial
receptor sites. If pH is too low (<
7.35), or too high (>7.45), PaCO2 is reduced or increased by
altering breathing rate and depth (minute volume). Brainstem reflex-regulated breathing, under
normal circumstances, maintains alveolar PCO2 at 35 to 45 mmHg,
wherein rapid diffusion from alveolus to pulmonary capillary provides for
almost immediate equilibration, thus ensuring a PaCO2 of about the
same value. Actual quantities of carbon dioxide generated by the body vary
considerably based on metabolism, e.g., meditation vs. exercise, although the
PaCO2 values required for maintaining acid-base balance remain the
same. At rest, for example, only about
15 percent of the CO2 arriving in the lungs is actually excreted;
the balance is reallocated to systemic circulation. Capnograph instrumentation does not
indicate how much CO2 is being exhaled, rather it indicates the
alveolar PCO2 being maintained, and thus the approximate PaCO2. Levitzky, M. G. Pulmonary Physiology. New York: McGraw Hill, 2007 (7th edition). Thomson, W. S. T., Adams, J. F., & Cowan, R. A. Clinical
Acid-Base Balance. New York:
Oxford University Press, 1997. Copyrighted by Behavioral Physiology
Institute, Santa Fe, New Mexico USA |