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Question:

An 80-year-old man has been participating in a longitudinal study of aging.  He has no major medical conditions.  Arterial blood gas samples are obtained every decade, on room air at sea level, to monitor long-term changes in pulmonary gas exchange.  Compared to 30 years ago, which of the following results is most consistent with normal aging?

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Explanation:

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The human respiratory system undergoes significant changes during normal aging.  Pulmonary gas exchange becomes subtly impaired due to a sequence of gradual changes:

  • Lung elastin degrades over time, leading to alveolar simplification (loss of surface area due to airspace enlargement).  Loss of elastic fiber support causes dynamic airflow obstruction resembling emphysema, leading to hyperinflation.  Therefore, inspired tidal volume has less opportunity to participate in gas exchange.  In other words, physiologic dead space is increased.
  • The muscles of respiration (chiefly the diaphragm) undergo remodeling over time, with atrophy of fast-twitch muscle fibers.  This leads to lower peak force production for maneuvers such as deep inspiration or coughing.  In combination with chest wall stiffening, this allows a small degree of microatelectasis to develop at the lung bases.  This results in intrapulmonary shunting (perfusion of blood through atelectatic [nonventilated] alveoli).
  • This combination of increased dead space and increased shunt effect leads to greater ventilation-perfusion mismatch.  This ultimately causes the alveolar-arterial (A-a) oxygen gradient to progressively widen over decades.  When evaluating an elevated A-a gradient, patient age must be accounted for to determine whether it is within the expected limits of normal aging (expected A-a gradient = age/3 mm Hg).
  • Because of the higher A-a gradient, arterial partial pressure of oxygen (PaO2) falls during aging (from 90 to 70 mm Hg by age 80).  Since PaO2 still remains on the plateau portion of the oxyhemoglobin desaturation curve, no change in SaO2 would be detected by simple pulse oximetry.

In contrast to decreased PaO2, the partial pressure of carbon dioxide in arterial blood (PaCO2) (reflecting total alveolar ventilation) is not significantly changed.  Although dead space increases and peak diaphragm strength is reduced, these changes are not enough to cause alveolar hypoventilation by themselves; resting hypoventilation (elevated PaCO2) at any age is always pathologic.  Instead, elderly persons are less able to compensate for high minute ventilation loads (eg, sepsis, thyrotoxicosis), making them prone to hypercapnia when acutely ill.

Educational objective:
Normal aging is characterized by a gradual increase in ventilation-perfusion mismatch (due to basilar microatelectasis causing shunt effect) and increased dead space (loss of alveolar surface area).  This manifests as a wider alveolar-arterial oxygen gradient (ie, decline in PaO2) without hypoventilation (normal PaCO2).