PHYSIOLOGIC ADAPTATIONS

Although information specific to the equine patient is limited, physiologic adaptations with changes in elevation are well documented in humans. Readers may have faced the consequences of a rapid ascent to high altitude, which in the initial stages manifests as tachypnea, tachycardia, headache, altered mentation, decreased appetite, nausea, vomiting, and insomnia. High-altitude pulmonary and cerebral edema can be severe and life-threatening complications. These changes are largely the result of hypoxia and associated hypoxic ventilatory drive, respiratory alkalemia, metabolic acidemia, and changes in the pulmonary and cerebral vascular tone. Veterinarians may also be aware of pulmonary hypertension and subsequent right-sided heart failure (so-called brisket disease) in cattle living at high altitude.

A change in elevation from sea level to 5000 feet (1523 m) above sea level, the approximate altitude at Denver, Colorado, results in a barometric pressure change from 760 mm Hg (101 kilopascals [kPa]) to 639 mm Hg (85 kPa). At 9000 feet above sea level, this decreases to 554 mmHg (73 kPa). Consequently the arterial partial pressure of oxygen (PaO₂) in a normally ventilating healthy equine patient breathing ambient air decreases from 80 to 105 mm Hg at sea level to 65 to 80 mm Hg in Denver. The alveolar gas equation (Box 7-1) may be used to calculate the change in the alveolar partial pressure of oxygen (PAO₂) for a given altitude and barometric pressure. This formula may also be used to determine the impact of a change in ventilatory status (PaCO₂) and percent inspired oxygen (FiO₂). The PaO₂ differs from this by less than 10% at lower FiO₂ values and up to 25% at high FiO₂ in a patient with normal lungs.

On the basis of the formula in text Box 7-1, the predicted PAO₂

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