Diffusing capacity
Diffusing capacity | |
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codes | CPT: 94720 |
Diffusing capacity of the lung (DL) (also known as Transfer factor) measures the transfer of gas from air in the lung, to the
In
The term may be considered a misnomer as it represents neither
The diffusing capacity does not directly measure the primary cause of hypoxemia, or low blood oxygen, namely mismatch of ventilation to perfusion:[2]
- Not all pulmonary arterial blood goes to areas of the lung where gas exchange can occur (the anatomic or physiologic shunts), and this poorly oxygenated blood rejoins the well oxygenated blood from healthy lung in the pulmonary vein. Together, the mixture has less oxygen than that blood from the healthy lung alone, and so is hypoxemic.
- Similarly, not all inspired air goes to areas of the lung where gas exchange can occur (the anatomic and the physiological dead spaces), and so is wasted.
Testing
The single-breath diffusing capacity test is the most common way to determine . are two such gasses. The test gas is held in the lung for about 10 seconds during which time the CO (but not the tracer gas) continuously moves from the alveoli into the blood. Then the subject exhales.
The anatomy of the airways means inspired air must pass through the mouth, trachea, bronchi and bronchioles (
-
.
(4)
-
- The pulmonary function equipment monitors the change in the concentration of CO that occurred during the breath hold, , and also records the time .
- The volume of the alveoli, , is determined by the degree to which the tracer gas has been diluted by inhaling it into the lung.
Similarly,
-
.
(5)
-
where
- is the initial alveolar fractional CO concentration, as calculated by the dilution of the tracer gas.
- is the barometric pressure
Other methods that are not so widely used at present can measure the diffusing capacity. These include the steady state diffusing capacity that is performed during regular tidal breathing, or the rebreathing method that requires rebreathing from a reservoir of gas mixtures.
Calculation
The diffusion capacity for oxygen is the proportionality factor relating the rate of oxygen uptake into the lung to the oxygen gradient between the capillary blood and the alveoli (per
-
(1)
-
- (For , say "V dot". This is the notation of Isaac Newton for a first derivative (or rate) and is commonly used in respiratory physiology for this purpose.)
- is the rate that oxygen is taken up by the lung (ml/min).
- is the partial pressure of oxygen in the alveoli.
- is the partial pressure of oxygen in the pulmonary artery.
- is the partial pressure of oxygen in the systemic veins (where it can actually be measured).
Thus, the higher the diffusing capacity , the more gas will be transferred into the lung per unit time for a given gradient in partial pressure (or concentration) of the gas. Since it can be possible to know the alveolar oxygen concentration and the rate of oxygen uptake - but not the oxygen concentration in the pulmonary artery - it is the venous oxygen concentration that is generally employed as a useful approximation in a clinical setting.
Sampling the oxygen concentration in the pulmonary artery is a highly invasive procedure, but fortunately another similar gas can be used instead that obviates this need (
-
.
(2)
-
Interpretation
In general, a healthy individual has a value of between 75% and 125% of the average.[4] However, individuals vary according to age, sex, height and a variety of other parameters. For this reason, reference values have been published, based on populations of healthy subjects[5][6][7] as well as measurements made at altitude,[8] for children[9] and some specific population groups.[10][11][12]
Blood CO levels may not be negligible
In heavy smokers, blood CO is great enough to influence the measurement of , and requires an adjustment of the calculation when COHb is greater than 2% of the whole.
While is of great practical importance, being the overall measure of gas transport, the interpretation of this measurement is complicated by the fact that it does not measure any one part of a multi-step process. So as a conceptual aid in interpreting the results of this test, the time needed to transfer CO from the air to the blood can be divided into two parts. First CO crosses the alveolar capillary membrane (represented by ) and then CO combines with the hemoglobin in capillary red blood cells at a rate times the volume of capillary blood present ().[13] Since the steps are in series, the conductances add as the sum of the reciprocals:
-
.
(3)
-
The volume of blood in the lung capillaries, , changes appreciably during ordinary activities such as
In disease, hemorrhage into the lung will increase the number of haemoglobin molecules in contact with air, and so measured will increase. In this case, the carbon monoxide used in the test will bind to haemoglobin that has bled into the lung. This does not reflect an increase in diffusing capacity of the lung to transfer oxygen to the systemic circulation.
Finally, is increased in obesity and when the subject lies down, both of which increase the blood in the lung by compression and by gravity and thus both increase .
The rate of CO uptake into the blood, , depends on the concentration of hemoglobin in that blood, abbreviated
The lung blood volume is also reduced when blood flow is interrupted by blood clots (
.Varying the ambient concentration of oxygen also alters . At high altitude, inspired oxygen is low and more of the blood's hemoglobin is free to bind CO; thus is increased and appears to be increased. Conversely, supplemental oxygen increases Hb saturation, decreasing and .
Diseases that alter lung tissue reduce both and to a variable extent, and so decrease .
- Loss of lung parenchyma in diseases like emphysema.
- Diseases that scar the lung (the interstitial lung disease), such as idiopathic pulmonary fibrosis, or sarcoidosis
- Swelling of lung tissue (pulmonary edema) due to heart failure, or due to an acute inflammatory response to allergens (acute interstitial pneumonitis).
- Diseases of the blood vessels in the lung, either inflammatory (pulmonary vasculitis) or hypertrophic (pulmonary hypertension).
- Alveolar hemorrhage due increase in volume of blood exposed to inspired gas.
- Asthma due to better perfusion of apices of lung. This is caused by increase in pulmonary arterial pressure and/or due to more negative pleural pressure generated during inspiration due to bronchial narrowing.[17]
History
In one sense, it is remarkable that DLCO has retained such clinical utility. The technique was invented to settle one of the great controversies of pulmonary physiology a century ago, namely the question of whether oxygen and the other gases were actively transported into and out of the blood by the lung, or whether gas molecules diffused passively.[18] Remarkable too is the fact that both sides used the technique to gain evidence for their respective hypotheses. To begin with, Christian Bohr invented the technique, using a protocol analogous to the steady state diffusion capacity for carbon monoxide, and concluded that oxygen was actively transported into the lung. His student, August Krogh developed the single breath diffusion capacity technique along with his wife Marie, and convincingly demonstrated that gasses diffuse passively,[19][20][21][22][23][24][25] a finding that led to the demonstration that capillaries in the blood were recruited into use as needed – a Nobel Prize–winning idea.[26]
See also
- DLCO
References
- ^ S2CID 18177228.
- ISBN 978-1-60913-640-6
- PMID 7298468.
- ^ LUNGFUNKTION - Practice compendium for semester 6. Department of Medical Sciences, Clinical Physiology, Academic Hospital, Uppsala, Sweden. Retrieved 2010.
- PMID 6830050.)
{{cite journal}}
: CS1 maint: DOI inactive as of January 2024 (link - PMID 3565929.
- S2CID 54555111.
- PMID 6927541.
- PMID 20889322. Erratum in Respir. Med. 2011 Dec;105(12):1970-1.
- S2CID 31037816.
- S2CID 22302973.
- S2CID 5897844.
- PMID 13475180.
- PMID 7249536.
- PMID 14016987.
- S2CID 27264342.
- PMID 8181330.
- S2CID 31010852.
- ^ Krogh A. 1910 On the oxygen metabolism of the blood. Skand Arch Physiol 23: 193–199
- ^ Krogh A. 1910 On the mechanism of the gas-exchange in the lungs of the tortoise. Skand Arch Physiol 23: 200–216.
- ^ Krogh A. 1910 On the combination of hæmoglobin with mixtures of oxygen and carbonic acid. Skand Arch Physiol 23: 217–223.
- ^ Krogh A. 1910 Some experiments on the invasion of oxygen and carbonic oxide into water. Skand Arch Physiol 23: 224–235
- ^ Krogh A. 1910 On the mechanism of gas exchange in the lungs. Skand Arch Physiol 23: 248–278
- ^ Krogh A, Krogh M. 1910 On the tensions of gases in arterial blood. Skand Arch Physiol 23: 179–192.
- ^ Krogh A, Krogh M. 1910 Rate of diffusion into lungs of man. Skand Arch Physiol 23: 236–247
- ^ "The Nobel Prize in Physiology or Medicine 1920".
Further reading
- Mason RJ, Broaddus VC, Martin T, King T Jr., Schraufnagel D, Murray JF, Nadel JA. (2010) Textbook of Respiratory Medicine. 5e. ISBN 978-1-4160-4710-0.
- Ruppel, G. L. (2008) Manual of Pulmonary Function Testing. 9e. ISBN 978-0-323-05212-2.
- West, J. (2011) Respiratory Physiology: The Essentials. 9e. ISBN 978-1-60913-640-6.
- West, J. (2012) Pulmonary Pathophysiology: The Essentials. 8e. ISBN 978-1-4511-0713-5.
External links
- Pulmonary+diffusing+capacity at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
- MedlinePlus Encyclopedia: 003854
- American Association for Respiratory Care Clinical Practice Guidelines
- The American Physiological Society home page
- The American Thoracic Society home page
- The European Respiratory Society home page