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Oxygenation: AECOPD - Coggle Diagram
Oxygenation: AECOPD
S&S
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change in mental status: lethargy, somnolence
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Treatment
Pharm: carefully titrated O2, bronchodilators, systemic corticosteroids, anticholinergics/ beta2 agonists, antibiotics if appropriate
Removal of causative agent: smoking cessation, infection treatments, removal of environmental factors
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diagnostics
EKG: tall P waves indicate right sided hypertrophy of atrium, tall QRS indicates ventricular hypertrophy, depressed ST segment indicates cardiac ischemia
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Labs: ABG, CBC, CRP, metabolic, sputum culture, BUN/creatinine
Acute exacerbation comes about from a triggering event such as pulmonary infections or increased exposure to irritants (smoking pollution etc.) As a result inflammation of lung tissues increases resulting in edema of the bronchial tissues resulting in bronchoconstriction ultimately increasing the work of breathing and decreasing ventilation. Further, mucus production increases leading to more airway obstructions, which worsen gas exchange and increase hyperinflation of the lungs. As a result lung tissue is damaged and scarring/ loss of elasticity occurs further impairing ventilation and decreasing gas exchange. This ultimately results in hypercapnia and hypoxemia which causes vasoconstriction of pulmonary vessels increasing the workload of the right side of the heart. This can then lead to cor pulmonade (right sided heart failure). All told acute exacerbations can lead to permanent worsening of COPD and produce increased imbalances between ventilation and perfusion.