Dead space (physiology)

Blood gas, acid-base, and gas exchange terms
PaO2Arterial oxygen tension, or partial pressure
PAO2Alveolar oxygen tension, or partial pressure
PaCO2Arterial carbon dioxide tension, or partial pressure
PACO2Alveolar carbon dioxide tension, or partial pressure
PvO2Oxygen tension of mixed venous blood
P(A-a)O2Alveolar-arterial oxygen tension difference. The term formerly used (A-a DO2) is discouraged.
P(a/A)O2Alveolar-arterial tension ratio; PaO2:PAO2 The term oxygen exchange index describes this ratio.
C(a-v)O2Arteriovenous oxygen content difference
SaO2Oxygen saturation of the hemoglobin of arterial blood
SpO2Oxygen saturation as measured by pulse oximetry
CaO2Oxygen content of arterial blood
pHSymbol relating the hydrogen ion concentration or activity of a solution to that of a standard solution; approximately equal to the negative logarithm of the hydrogen ion concentration. pH is an indicator of the relative acidity or alkalinity of a solution

Dead space is the volume of air that is inhaled that does not take part in the gas exchange, because it either remains in the conducting airways or reaches alveoli that are not perfused or poorly perfused. It means that not all the air in each breath is available for the exchange of oxygen and carbon dioxide. Mammals breathe in and out of their lungs, wasting that part of the inhalation which remains in the conducting airways where no gas exchange can occur.

Components

Total dead space (also known as physiological dead space) is the sum of the anatomical dead space plus the alveolar dead space.

Benefits do accrue to a seemingly wasteful design for ventilation that includes dead space.[1]

  1. Carbon dioxide is retained, making a bicarbonate-buffered blood and interstitium possible.
  2. Inspired air is brought to body temperature, increasing the affinity of hemoglobin for oxygen, improving O2 uptake.[2]
  3. Particulate matter is trapped on the mucus that lines the conducting airways, allowing its removal by mucociliary transport.
  4. Inspired air is humidified, improving the quality of airway mucus.[2]

In humans, about a third of every resting breath has no change in O2 and CO2 levels. In adults, it is usually in the range of 150 mL.[3]

Dead space can be increased (and better envisioned) by breathing through a long tube, such as a snorkel. Although one end of the snorkel is open to the air, when the wearer breathes in, they inhale a significant quantity of air that remained in the snorkel from the previous exhalation. Therefore, a snorkel increases the person's dead space by adding even more airway that does not participate in gas exchange.

Anatomical dead space

Anatomical dead space is that portion of the airways (such as the mouth and trachea to the bronchioles) which conducts gas to the alveoli. No gas exchange is possible in these spaces. In healthy lungs where the alveolar dead space is small, Fowler's method accurately measures the anatomic dead space by a nitrogen washout technique.[4][5]

The normal value for dead space volume (in mL) is approximately the lean mass of the body (in pounds), and averages about a third of the resting tidal volume (450-500 mL). In Fowler's original study, the anatomic dead space was 156 ± 28 mL (n=45 males) or 26% of their tidal volume.[4] Despite the flexibility of the trachea and smaller conducting airways, their overall volume (i.e. the anatomic dead space) changes little with bronchoconstriction or when breathing hard during exercise.[4][6]

As birds have a longer and wider trachea than mammals the same size, they have a disproportionately large anatomic dead space, reducing the airway resistance. This adaptation does not impact gas exchange because birds flow air through their lungs - they do not breathe in and out like mammals.[7]

Alveolar dead space

Alveolar dead space is sum of the volumes of those alveoli which have little or no blood flowing through their adjacent pulmonary capillaries, i.e., alveoli that are ventilated but not perfused, and where, as a result, no gas exchange can occur.[1] Alveolar dead space is negligible in healthy individuals, but it can increase dramatically in some lung diseases due to ventilation-perfusion mismatch.

Calculating

Just as dead space wastes a fraction of the inhaled breath, dead space dilutes alveolar air during exhalation. By quantifying this dilution, it is possible to measure anatomical and alveolar dead space, employing the concept of mass balance, as expressed by Bohr equation.[8][9]

where is the dead space volume and is the tidal volume;
is the partial pressure of carbon dioxide in the arterial blood, and
is the partial pressure of carbon dioxide in the expired (exhaled) air.

Physiological dead space

The concentration of carbon dioxide (CO2) in healthy alveoli is known. It is equal to its concentration in arterial blood since CO2 rapidly equilibrates across the alveolar–capillary membrane. The quantity of CO2 exhaled from the healthy alveoli will be diluted by the air in the conducting airways and by air from alveoli that are poorly perfused. This dilution factor can be calculated once the CO2 in the exhaled breath is determined (either by electronically monitoring the exhaled breath or by collecting the exhaled breath in a gas impermeant bag (a Douglas bag) and then measuring the mixed gas in the collection bag). Algebraically, this dilution factor will give us the physiological dead space as calculated by the Bohr equation:

Alveolar dead space

When the poorly perfused alveoli empty at the same rate as the normal alveoli, it is possible to measure the alveolar dead space. In this case, the end-tidal sample of gas (measured by capnography) contains CO2 at a concentration that is less than that found in the normal alveoli (i.e. in the blood):[10]

Caution: The end tidal CO2 concentration may not be a well defined number.
  1. Poorly ventilated alveoli do not generally empty at the same rate as healthy alveoli. Particularly in emphysematous lungs, diseased alveoli empty slowly, and so the CO2 concentration of the exhaled air increases progressively throughout the expiration.[1]
  2. Monitoring alveolar dead space during a surgical operation is a sensitive and important tool in monitoring airway function.[11]
  3. During strenuous exercise, CO2 will rise throughout the exhalation and may not be easily matched to a blood gas determination, which led to serious errors of interpretation early in the history of dead space determinations.[8]
Example: For a tidal volume of 500 mL, an arterial carbon dioxide of 42 mm Hg, and an end-expired carbon dioxide of 40 mm Hg:
and so

Anatomic dead space

A different maneuver is employed in measuring anatomic dead space: the test subject breathes all the way out, inhales deeply from a 0% nitrogen gas mixture (usually 100% oxygen) and then breathes out into equipment that measures nitrogen and gas volume. This final exhalation occurs in three phases. The first phase has no nitrogen, and is the air that entered the lung only as far as the conducting airways. The nitrogen concentration then rapidly increases during the brief second phase and finally reaches a plateau, the third phase. The anatomic dead space is equal to the volume exhaled during the first phase plus half that exhaled during the second phase. The Bohr equation is used to justify the inclusion of half the second phase in this calculation.[4]

Ventilated patient

The depth and frequency of our breathing is determined by chemoreceptors and the brainstem, as modified by a number of subjective sensations. When mechanically ventilated using a mandatory mode, the patient breathes at a rate and tidal volume that is dictated by the machine. Because of dead space, taking deep breaths more slowly (e.g. ten 500 ml breaths per minute) is more effective than taking shallow breaths quickly (e.g. twenty 250 ml breaths per minute). Although the amount of gas per minute is the same (5 L/min), a large proportion of the shallow breaths is dead space, and does not allow oxygen to get into the blood.

Mechanical dead space

Mechanical dead space is dead space in an apparatus in which the breathing gas must flow in both directions as the user breathes in and out, increasing the necessary respiratory effort to get the same amount of usable air or breathing gas, and risking accumulation of carbon dioxide from shallow breaths. It is in effect an external extension of the physiological dead space.

It can be reduced by:

  • Using separate intake and exhaust passages with one-way valves placed in the mouthpiece. This limits the dead space to between the non return valves and the user's mouth or nose. The additional dead space can be minimized by keeping the volume of this external dead space as small as possible, but this should not unduly increase work of breathing.
  • With a full face mask or demand diving helmet:
    • Keeping the inside volume small
    • Having a small internal orinasal mask inside the main mask, which separates the external respiratory passage from the rest of the mask interior.
    • In a few models of full face mask a mouthpiece like those used on diving regulators is fitted, which has the same function as an orinasal mask, but can further reduce the volume of the external dead space, at the cost of forcing mouth-breathing (and acting like a gag, preventing clear talking).

See also

  • Bohr equation – Equation describing the amount of physiological dead space in a person's lungs
  • Christian Bohr – Danish physician and professor of physiology
  • Multiple inert gas elimination technique – Medical technique for measuring the concentrations of various infused, inert gases in mixed venous blood, arterial blood, and expired gas
  • Respiratory system – Biological system in animals and plants for gas exchange

References

  1. 1 2 3 West, John B. (2011). Respiratory physiology : the essentials (9th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-1-60913-640-6.
  2. 1 2 Williams, R; Rankin, N; Smith, T; Galler, D; Seakins, P (November 1996). "Relationship between the humidity and temperature of inspired gas and the function of the airway mucosa". Critical Care Medicine. 24 (11): 1920–9. doi:10.1097/00003246-199611000-00025. PMID 8917046.
  3. ↑ "Wasted Ventilation". Ccmtutorials.com. Retrieved 2013-11-27.
  4. 1 2 3 4 Fowler W.S. (1948). "Lung Function studies. II. The respiratory dead space". Am. J. Physiol. 154 (3): 405–416. doi:10.1152/ajplegacy.1948.154.3.405. PMID 18101134.
  5. ↑ Heller H, Könen-Bergmann M, Schuster K (1999). "An algebraic solution to dead space determination according to Fowler's graphical method". Comput Biomed Res. 32 (2): 161–7. doi:10.1006/cbmr.1998.1504. PMID 10337497.
  6. ↑ Burke, TV; Küng, M; Burki, NK (1989). "Pulmonary gas exchange during histamine-induced bronchoconstriction in asthmatic subjects". Chest. 96 (4): 752–6. doi:10.1378/chest.96.4.752. PMID 2791669.
  7. ↑ West, JB (2009). "Comparative physiology of the pulmonary blood-gas barrier: the unique avian solution". American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 297 (6): R1625-34. doi:10.1152/ajpregu.00459.2009. PMC 2803621. PMID 19793953.
  8. 1 2 Bohr, C. (1891). Über die Lungenathmung. Skand. Arch. Physiol. 2: 236-268.
  9. ↑ Klocke R (2006). "Dead space: simplicity to complexity". J Appl Physiol. 100 (1): 1–2. doi:10.1152/classicessays.00037.2005. PMID 16357075. article
  10. ↑ Severinghaus, JW; Stupfel, MA; Bradley, AF (May 1957). "Alveolar dead space and arterial to end-tidal carbon dioxide differences during hypothermia in dog and man". J Appl Physiol. 10 (3): 349–55. doi:10.1152/jappl.1957.10.3.349. PMID 13438782.
  11. ↑ Gravenstein, J.S. (ed.), Jaffe, M.B. (ed.), Gravenstein, N. (ed.), Paulus, D.A. (ed) (2010). Capnography (2nd ed.). Cambridge: Cambridge University Press. ISBN 978-0521514781. {{cite book}}: |first= has generic name (help)

Further reading

  • Arend Bouhuys. 1964. "Respiratory dead space." in Handbook of Physiology. Section 3: Respiration. Vol 1. Wallace O. Fenn and Hermann Rahn (eds). Washington: American Physiological Society.
  • John B. West. 2011. Respiratory Physiology: The Essentials. Lippincott Williams & Wilkins; Ninth edition. ISBN 978-1609136406.
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