Use of Oxygen Therapy in COPDAcute exacerbations of chronic obstructive pulmonary disease (COPD[/code]Acute exacerbations of chronic obstructive pulmonary disease (COPD) are treated with oxygen (in hypoxemic patients), inhaled beta2 agonists, inhaled anticholinergics, antibiotics and systemic corticosteroids. Methylxanthine therapy may be considered in patients who do not respond to other bronchodilators. Antibiotic therapy is directed at the most common pathogens, including Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. Mild to moderate exacerbations of COPD are usually treated with older broad-spectrum antibiotics such as doxycycline, trimethoprim-sulfamethoxazole and amoxicillin-clavulanate potassium. Treatment with augmented penicillins, fluoroquinolones, third-generation cephalosporins or aminoglycosides may be considered in patients with more severe exacerbations. The management of chronic stable COPD always includes smoking cessation and oxygen therapy. Inhaled beta2 agonists, inhaled anticholinergics and systemic corticosteroids provide short-term benefits in patients with chronic stable disease. Inhaled corticosteroids decrease airway reactivity and reduce the use of health care services for management of respiratory symptoms. Preventing acute exacerbations helps to reduce long-term complications. Long-term oxygen therapy, regular monitoring of pulmonary function and referral for pulmonary rehabilitation are often indicated. Influenza and pneumococcal vaccines should be given. Patients who do not respond to standard therapies may benefit from surgery.
http://www.aafp.org/afp/2001/0815/p603.htmlGeneral points about oxygen therapy in chronic obstructive pulmonary disease
•The respiratory drive is normally largely initiated by PaCO2 but in chronic obstructive pulmonary disease (COPD) hypoxia can be a strong driving force and so if the hypoxia is corrected then the respiratory drive will be reduced. There will also be a loss of physiological hypoxic vasoconstriction which is partly protecting the patient from the effects of areas of gross alveolar hypoventilation.[1]
•Therefore, oxygen therapy in COPD must be used with care in the acute setting but it can have distinct benefits in the long-term. Chronic hypoxaemia causes slowly progressive pulmonary hypertension with the development of right ventricular hypertrophy and possible cor pulmonale with secondary polycythaemia. Secondary polycythaemia increases blood viscosity and hence resistance to flow. There is also sludging and a tendency to thrombosis.
•A Cochrane review of randomised controlled trials (RCTs) of long-term oxygen therapy for COPD had the main outcome measure of survival on home oxygen therapy.[2] The conclusions from the 5 trials were:
•Long-term oxygen therapy (LTOT) improved survival in COPD patients with severe hypoxaemia but few comorbidities.
•LTOT did not improve survival in patients with moderate hypoxaemia or in those with mild-to-moderate hypoxaemia and arterial desaturation at night.
•Those with desaturation at night were probably getting benefit from nocturnal oxygen and did not need it for a full 15 hours a day.
•LTOT reduces mortality from secondary vascular complications but does not affect the progression of the airways disease.
•Clinical Knowledge Summaries recommend that, if the patient will not stop smoking, oxygen therapy should be withheld.[3] There is a real risk of fire and burns to the face and any benefit relating to polycythaemia is counteracted by smoking.
Oxygen therapy in the acute setting (in hospital)
•For most COPD patients, you should be aiming for an SaO2 of 88-92%,[4] (compared with 94-98% for most acutely ill patients NOT at risk of hypercapnic respiratory failure). Mark the target saturation clearly on the drug chart.
•The aim of (controlled) oxygen therapy is to raise the PaO2 without worsening the acidosis. Therefore give oxygen at no more than 28% (via venturi mask, 4l/min) or no more than 2 L/minute (via nasal prongs) in patients with a history of COPD until arterial blood gases (ABGs) have been checked.[5] Treat patients aged over 50 with possible COPD in the same way (eg long-term smokers with a history of chronic breathlessness) and get ABGs urgently.
It is particularly important to check ABGs promptly if the patient has been brought in as emergency by an ambulance: ambulance crews have to give high flow oxygen if a patient is hypoxic, regardless of previous history.
•Measure ABGs within 60 minutes of starting supplemental oxygen or changing its concentration. If PaO2 improves with an associated drop in PaCO2 and the pH is relatively unaffected (pH >7.26) then the concentration of the supplemental oxygen may be increased to maintain PaO2 >7.5 kPa.
•Oxygen therapy will have to be complemented with bronchodilators (eg salbutamol 5 mg or terbutaline 10 mg, made up to 5 mL with normal saline) and high-dose oral steroids (eg prednisolone 30 mg daily).[1] In the presence of purulent sputum, antibiotics will also be required (see your local hospital policy for choice of antibiotic).
•If acidosis develops (falling pH) with a rising PaCO2, other therapeutic interventions need to be discussed with the acute medical team; the intensive treatment unit (ITU) may need to be involved and decisions regarding ceiling of care have to take place at this point. Noninvasive positive pressure ventilation (NIPPV), intermittent positive pressure ventilation (IPPV) and doxapram are all options.
•Check ABGs on air before discharge in those who presented with a low pO2 and/or hyper[/hide]capnia to guide later formal assessment for LTOT.
•4 to 6 weeks' follow-up should include consideration of LTOT assessment - not before, as the patient needs to be clinically stable
The correct answer is A
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