34

34 CASE 34


A 62-year-old man comes to the ski resort clinic on a mountain peak (14,000 ft) complaining of dyspnea, headache, dizziness, and inability to sleep. He was short of breath while climbing the stairs at the lodge and noticed that he was breathing rapidly even when sitting down.


The patient arrived at the resort yesterday from a sea-level town and reports no current health issues or medications. He plans to remain at the resort for a week.



PHYSICAL EXAMINATION



VS: T 37°C, P 80/min, R 42/min, BP 110/80 mm Hg, BMI 26

PE: Patient has a rapid, shallow breathing pattern. Pulse is slightly elevated. Fingernails show slight cyanosis.


LABORATORY STUDIES



End-tidal gases: PO2 60 mm Hg, PCO2 30 mm Hg

Pulse oximetry: 70% saturated


DIAGNOSIS


Acute mountain sickness



COURSE


Severe cases of acute mountain sickness can lead to high-altitude pulmonary edema (HAPE), characterized by crackles in the lungs and further impaired oxygen uptake. In addition, high-altitude cerebral edema (HACE) can develop and become life threatening.



PATHOPHYSIOLOGY OF KEY SYMPTOMS


The initiating event is the arterial hypoxia caused by the decline in inspired O2 due to the drop in barometric pressure. At 14,000 ft, inspired air has a PO2 of approximately 93 mm Hg and alveolar air has a PO2 of around 55 mm Hg (Table 34-1).



TABLE 34–1 Effects of Acute Exposure to Low Atmospheric Pressures on Alveolar Gas Concentrations and Arterial Oxygen Saturation∗

image

Ventilation is controlled by respiratory centers in the pons and the medulla. The intrinsic activity of the respiratory centers is altered by both descending input from the higher brain areas and negative feedback control from peripheral and central chemoreceptors. The central chemoreceptors respond only to CO2/pH, and the peripheral chemoreceptors respond both to CO2/pH and to O2. At rest, negative feedback control of ventilation is tied to CO2 levels. Hypoxia only becomes a significant ventilatory stimulus when PO2 levels drop below 60 mm Hg.


An end-tidal gas measurement indicates that the alveolar PO2 in this patient is 60 mm Hg. Arterial blood gas values will be even lower because of venous admixture. This level of hypoxia is sufficient to stimulate the arterial chemoreceptors and cause an increase in ventilation. Hyperventilation leads to a drop in CO2 levels, and the patient will have a mild respiratory alkalosis. The hypocapnia removes some of the normal respiratory drive from CO2, and the increase in ventilation is attenuated but remains elevated compared with sea level (Fig. 34-1).


image

FIGURE 34–1 Partial pressures of oxygen and carbon dioxide in the various portions of normal expired air.

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Jul 4, 2016 | Posted by in PHYSIOLOGY | Comments Off on 34

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