Page 149 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003
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Effects of High Altitude on Respiration  prevail. Stimulation of O 2 chemosensors at
                                       high altitudes also leads to an increase in the
       At sea level, the average barometric pressure  heart rate and a corresponding increase in car-
       (PB) ! 101 kPa (760 mmHg), the O 2 fraction in  diac output, thereby increasing the O 2 supply
       ambient air (FI O 2 ) is 0.209, and the inspiratory  to the tissues.
       partial pressure of O 2 (PI O 2 ) ! 21 kPa (! p. 106).  High altitude also stimulates erythropoiesis
       However, PB decreases with increasing altitude  (! p. 88ff.). Prolonged exposure to high alti-
       (h, in km):                     tudes increases the hematocrit levels, al-
       PB (at h) = PB (at sea level) ! e -0.127 ! h  [5.9]  though this is limited by the corresponding
       This results in a drop in PI O 2 (! A, column 1),  rise in blood viscosity (! pp. 92, 188).
       alveolar P O 2 (PA O 2 ) and arterial P O 2 (Pa O 2 ). The  Breathing oxygen from pressurized O 2 cyl-
       PA O 2 at sea level is about 13 kPa (! A, column  inders is necessary for survival at altitudes
       2). PA O 2 is an important measure of oxygen  above 7000 m, where PI O 2 is almost as high as
       supply. If the PA O 2 falls below a critical level (ca.  the barometric pressure PB (! A, column 3).
       4.7 kPa = 35 mmHg), hypoxia (! p. 130) and  The critical PA O 2 level now occurs at an altitude
       impairment of cerebral function will occur.  of about 12 km with normal ventilation, and at
       The critical PA O 2 would be reached at heights of  about 14 km with increased ventilation. Mod-
                                       ern long-distance planes fly slightly below this
       about 4000 m above sea level during normal
    Respiration  However, the low Pa O 2 triggers chemosensors  altitude to ensure that the passengers can sur-
       ventilation (! A, dotted line in column 2).
                                       vive with an oxygen mask in case the cabin
                                       pressure drops unexpectedly.
       (! p. 132) that stimulate an increase in total
               .
                                        Survival at altitudes above 14 km is not
    5  ventilation (V E); this is called O 2 deficiency  possible without pressurized chambers or
       ventilation (! A, column 4). As a result, larger
       volumes of CO 2 are exhaled, and the PA CO 2 and  pressurized suits like those used in space
       Pa CO 2 decrease (see below). As described by the  travel. Otherwise, the body fluids would begin
       alveolar gas equation,          to boil at altitudes of 20 km or so (! A), where
                                       PB is lower than water vapor pressure at body
         PA O 2 ! PI O 2 "      [5.10]
                 PA CO 2
                  RQ                   temperature (37 #C).
       where  RQ  is  the  respiratory  quotient
       (! pp. 120 and 228), any fall in PA CO 2 will lead  Oxygen Toxicity
       to a rise in the PA O 2 . O 2 deficiency ventilation
       stops the PA O 2 from becoming critical up to alti-  Hyperoxia occurs when PI O 2 is above normal
       tudes of about 7000 m (altitude gain, ! A).  ($ 22 kPa or 165 mmHg) due to an increased
         The maximal increase in ventilation (! 3 "  O 2 fraction (oxygen therapy) or to an overall
       resting rate) during acute O 2 deficiency is rela-  pressure increase with a normal O 2 fraction
       tively small compared to the increase (! 10  (e.g. in diving, ! p. 134). The degree of O 2 tox-
       times the resting rate) during strenuous physi-  icity depends on the PI O 2 level (critical: ca.
       cal exercise at normal altitudes (! p. 74, C3)  40 kPa or 300 mmHg) and duration of hyper-
       because increased ventilation at high altitudes  oxia. Lung dysfunction (! p. 118, surfactant
       reduces the Pa CO 2 (= hyperventilation, ! p.  deficiency) occurs when a PI O 2 of about 70 kPa
       108), resulting in the development of respira-  (525 mmHg) persists for several days or
       tory alkalosis (! p. 144). Central chemosen-  200 kPa (1500 mmHg) for 3–6 hours. Lung dys-
       sors (! p. 132) then emit signals to lower the  function initially manifests as coughing and
       respiratory drive, thereby counteracting the  painful breathing. Seizures and unconscious-
       signals from O 2 chemosensors to increase the  ness occur at PI O 2 levels above 220 kPa
       respiratory drive. As the mountain climber  (1650 mmHg), e.g., when diving at a depth of
       adapts, respiratory alkalosis is compensated  about 100 m using pressurized air.
                                   –
       for by increased renal excretion of HCO 3  Newborns will go blind if exposed to PIO 2
       (! p. 144). This helps return the pH of the  levels much greater than 40 kPa (300 mmHg)
       blood toward normal, and the O 2 deficiency-  for long periods of time (e.g., in an incubator),
  136  related increase in respiratory drive can now  because the vitreous body then opacifies.
       Despopoulos, Color Atlas of Physiology © 2003 Thieme
       All rights reserved. Usage subject to terms and conditions of license.
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