Kids Living at Altitude are Built Different: How Phenotypic Variations in Pediatric Patients Born at Altitude Help Them Compensate for Their Hypoxic Environment

One of the phenomena I experienced while caring for pediatric patients in Summit County was the image of a [1] child with an oxygen saturation of 83% who wasn’t in any respiratory distress. This got me thinking: do adaptations in children exposed to chronic hypoxia at altitude prepare them to encounter an episode of acute hypoxia?

It turns out this phenomenon has been studied previously. Children permanently residing at high altitudes exhibit phenotypic variations to help them adapt to their chronically hypoxic environment. According to de Meer, K., et al., for those children living at altitudes greater than 3000m above sea level since gametogenesis, the opportunities for phenotypic plasticity are particularly excellent.

These changes in phenotypic expression have led to both theorized and proven physiologic differences in oxygen uptake, transport, systemic circulation, and consumption, allowing them to overcome the effects of chronic high-altitude hypoxia.

The lower partial pressure of oxygen causes high-altitude hypoxia to those who are visiting from lower altitudes. With less oxygen in the air, increased respiratory effort would be required to maintain the same oxygen levels as those children living at sea level. However, children living at altitude have physiologic increases in ventilation, lung compliance, and pulmonary diffusion, which help negate the need for augmented respiratory effort.

To conserve respiratory rate, increases in lung compliance and tidal volume have been observed in children living at altitude. In one study by Mortola, J. P., et al., lung compliance and tidal volume remained increased even while participants were on 100% supplemental oxygen.      This suggests that this is a permanent physiological adaptation in kids living at altitude.2

Additionally, children living at altitude are more efficient at delivering oxygen to their tissues. An increase in pulmonary diffusion capacity facilitates this improved efficiency. Pulmonary diffusion capacity is determined by the surface area available for diffusion. Assuming all other anatomic variables are the same in highlanders and lowlanders[2] , this increased capacity can only be explained by an increase in the number and size of alveoli.1 To study this possibility, researchers compared the lung volumes and chest dimensions of children exposed to chronic hypoxia at altitude since birth to those of children living at sea level and found that lung volumes and chest dimensions of children residing at altitude indeed were greater.

Despite this opportunity for increased oxygen uptake by the lungs of children living at altitude, the partial pressure of oxygen in their blood is still substantially lower. This decrease in arterial blood oxygen concentration that is associated with hypoxia encourages the kidneys to release erythropoietin, which subsequently stimulates the production of erythrocytes contributing to an increased erythrocyte and hemoglobin concentration in children living at altitude. Elevated hemoglobin concentration leads to a relative increase in arterial oxygen saturation, which compensates for the lower availability of oxygen at altitude.1

Despite the witnessed phenomenon of the ability of children living at altitude to adapt to acute hypoxia, it is still debated whether chronic hypoxemia in this population results in decreased oxygen consumption. New research has concluded that previously observed decreases in oxygen metabolism in newborns at altitude are reactions to acute stress and hypoxia and should not be considered an effect of chronic exposure to hypoxia.1 In other words, the ability of children living at altitude to decrease ventilation during an episode of acute hypoxia is due to a decrease in tissue metabolism only during that event of respiratory stress.

Like most things in life, these advantages do not come without consequences. Humans exposed to chronic hypoxia are prone to pulmonary hypertension; in fact, phenotypic, physiological changes in tidal volume and lung diffusion that improve oxygen uptake contribute to pulmonary hypertension. However, unlike children who develop pulmonary hypertension unrelated to altitude, highland children often present with a less severe clinical picture and fewer irreversible complications.1

Children born and residing at altitude offer a window into a world of medical phenomena that are little understood. The more we know about the physiological differences in this population, the better we can serve them as clinicians.

References

  1. de Meer, K., et al. “Physical Adaptation of Children to Life at High Altitude.” European Journal of Pediatrics, vol. 154, no. 4, Apr. 1995, pp. 263–72. Springer Link, https://doi.org/10.1007/BF01957359.
  2. Mortola, J. P., et al. “Compliance of the Respiratory System in Infants Born at High Altitude.” The American Review of Respiratory Disease, vol. 142, no. 1, July 1990, pp. 43–48. PubMed, https://doi.org/10.1164/ajrccm/142.1.43.

Lauren Thompson is a second-year Physician Assistant Student at Drexel University in Philadelphia. She is here all the way from sunny sea level, Florida, where she got her degree in Psychology with a minor in Biology from Florida State University. She is currently completing her clinical rotation, which has taken her all over the country with her feline and canine companions, Duke and Remi. Before PA school, Lauren worked as a Certified Nursing Assistant at a local hospital and a Medical Assistant at a pediatric specialty clinic. Outside of medicine, Lauren enjoys traveling, spending time with her animals, singing karaoke, playing disc golf, and taking in all of what mother nature has to offer, whether it’s hiking, skiing, diving, or enjoying the beach.