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Depending on the severity of baseline COPD, further derangements can manifest, inclusive of hypoxemia, deteriorating hypercapnia with deteriorating lower extremity oedema, or altered mental status. The core goal in treating acute exacerbations of COPD centres on restoring the patient's previous stable baseline and safeguarding against the possibility of recurrence (Roberts et al., 2002).
b) Mechanisms by which Oxygen Therapy can lead to Hypercapnia
Oxygen is considered a critical drug necessary for the management of hypoxemia and other states associated with hypoxic conditions. As such oxygen is utilized for a significant number of pulmonary and non-pulmonary diseases owing to its definitive, supplementary, or palliative role. Patients with COPD frequently manifest chronic hypoxemia with or without CO2 retention. An acute exacerbation of airway obstruction occurs after a respiratory tract infections yields to worsening of hypoxia. High concentrations of oxygen blunt the hypoxic ventilation drive that may hasten hypoventilation and CO2 retention (Hurst et al., 2010). Ventilation failure details a rise in PaO2 (hypercapnia) that manifests when the respiratory load can no longer be sustained by the strength or activity of the system. The role of oxygen therapy centres on correcting the hypoxemia that mainly accompanies AECOPD. The result centres on sustaining oxygen at approximately 60-65mm Hg, thereby guaranteeing near-maximal haemoglobin saturation, while, at the same time, minimizing the potential for deleterious hypercapnia. Hypercapnia, which complicates the supplemental oxygen usually emanates from a ventilation-perfusion mismatch. Hypercapnia and Acidosis Hypercapnia and acidosis manifest in patients with acute exacerbations of chronic airways obstruction. An understanding of its pathogenesis is critical if successfully strategies to limit the rise in arterial carbon dioxide tension (PaO2). The acute rise in PaO2 amid oxygen therapy is first ascribed to reduced hypoxic drive owing to rise in PaO2, an acquired insensitivity to CO2, and consequent hypoventilation. During this time, the alveolar ventilation either fall or fails to increase sufficiently in response to enhanced CO2 production (Costello, Deegan, Fitzpatrick & McNicholas, 1997). Minute ventilation drops when there is an imbalance between the load on the respiratory system and neuromuscular competence for a successful inspiratory effort. The balance between load (elastic, resistive, and minute ventilation) and neuromuscular competence (manifested by transmission drive, and muscle strength) shapes the capability to maintain alveolar ventilation. Hypercapnia minimizes arterial pH (respiratory acidosis) and severe academia pH
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(“Acute Exacerbation of COPD. Acute respiratory distress syndrome (ARDS) Essay”, n.d.)
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