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Chronic mountain sickness: the reaction of physical disorders to chronic hypoxia

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Chronic mountain sickness (CMS) is a condition in which hematocrit is increased above the normal level in residents at high altitude. In this article we take issue with the ‘Consensus Statement On Chronic And Subacute High Altitude Diseases” of 2005 on two essential points: using a questionnaire to evaluate the symptoms of CMS to use the term “loss of adaptation” as opposed to “adaptation to disease in the hypoxic environment”. We opine that CMS is rather an adaptive reaction to an underlying malfunction of some organs and no specific symptoms could be quantified. To substantiate our line of reasoning we reviewed 240 CMS cases seen at the High Altitude Pathology Institute in La Paz. Patients who had a high hematocrit (>58%) underwent pulmonary function studies in search for the cause of hypoxia: hypoventilation, diffusion alteration, shunts, and uneven ventilation-perfusion. The tests included arterial blood gas tests, chest x-rays, spirometry, hyperoxic tests, flow-volume curves, ventilation studies at rest and during exercise, ECG, exercise testing and doppler color echocardiography to assess heart structure and function. When correlated with clinical history these results revealed that CMS is practically always secondary to some type of anomaly in cardio-respiratory or renal function. Therefore, a questionnaire that tries to catalog symptoms common to many types of diseases that lead to hypoxia is flawed because it leads to incomplete diagnosis and inappropriate treatment. CMS, once again, was shown to be an adaptation of the blood transport system to a deficient organs’ function due to diverse disease processes; the adaptation aimed at sustaining normoxia at the cellular level in the hypoxic environment at high altitude.
Pulse oximetry during breath-holding (BH) in normal residents at high altitude (3510 m) shows a typical graph pattern. Following a deep inspiration to total lung capacity (TLC) and subsequent breath-holding, a fall in oxyhemoglobin saturation (SaO2) is observed after 16 s. The down-pointed peak in SaO2 corresponds to the blood circulation time from the alveoli to the finger where the pulse oximeter probe is placed. This simple maneuver corroborates the measurement of circulation time by other methods. This phenomenon is even observed when the subject breathes 88% oxygen (PIO2 = 403 mmHg for a barometric pressure of 495 mmHg). BH time is, as expected, prolonged under these circumstances. Thus the time delay of blood circulation from pulmonary alveoli to a finger is measured non-invasively. In the present study we used this method to compare the circulation time in 20 healthy male high altitude residents (Group N with a mean hematocrit of 50%) and 17 chronic mountain sickness patients (Group CMS with a mean hematocrit of 69%). In the two study groups, the mean circulation time amounted to 15.94 ±2.57 s (SD) and to 15.66 ±2.74 s, respectively. The minimal difference was not significant. We conclude that the CMS patients adapted their oxygen transport rate to the rise in hematocrit and blood viscosity.
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