![]() In COPD, patients optimise their gas exchange by hypoxic vasoconstriction leading to altered alveolar ventilation-perfusion (Va/Q) ratios.increased V/Q mismatch (most important).Patients suffering from COPD exacerbation, regardless of whether they have CO2 retention, generally have supra-normal respiratory drive (unless there is impending hypercapnic coma).the traditional theory is that oxygen administration to CO2 retainers causes loss of hypoxic drive, resulting in hypoventilation and type 2 respiratory failure.The same phenomenon has also been described in severe asthma, community-acquired pneumonia and obesity hypoventilation syndrome and any patient with chronic respiratory failure may be at risk.COPD patients with more severe hypoxemia are at higher risk of CO2 retention from uncontrolled O2 administration.Excessive oxygen administration can lead to hypercapnic respiratory failure in some COPD patients.Neck extension and jaw protrusion (can increase it twofold).General anesthesia – multifactorial, including loss of skeletal muscle tone and bronchoconstrictor tone.The ratio of physiologic dead space to tidal volume is usually about 1/3. Alveolar dead space is the volume of gas within unperfused alveoli (and thus not participating in gas exchange either) it is usually negligible in the healthy, awake patient. Anatomic dead space is the volume of gas within the conducting zone (as opposed to the transitional and respiratory zones) and includes the trachea, bronchus, bronchioles, and terminal bronchioles it is approximately 2 mL/kg in the upright position. Physiologic or total dead space is the sum of anatomic dead space and alveolar dead space. Dead space is the volume of a breath that does not participate in gas exchange.
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