Physiological dead space is calculated as follows:Īlveolar dead space is calculated as follows: Slowly the expirate is switched to Douglas bag once the respiration became steady. The rate of respiration and minute volume are recorded. The expirate is passed through the dry gas meter and into the atmosphere via two-way tap. The latter is firmly supported in the mouth by the standard mouth piece. A nose clip is applied and the subject is asked to breathe in and out through Ruben non-return valve. The examination is carried out by subject lying on the bed supported by pillow. Treatment includes management of the patient’s asthma and chronic rhinosinusitis, avoiding NSAIDs and desensitization if NSAID use is required.The anatomic dead space is measured by Fowler’s method. Instead, arachidonic acid is diverted to the production of leukotrienes via the 5-lipoxygenase pathway. The breakdown of arachidonic acid to prostaglandins is mediated by COX1 and COX2 and is inhibited by aspirin. AERD symptoms are similar to flares of the underlying asthmatic or allergic condition and patients may not relate the symptoms to medication use, especially if they have been accustomed to taking the medication without difficulty.ĪERD pathogenesis involved increased production of pro-inflammatory leukotrienes and decreased production of anti-inflammatory prostaglandins. About 10-20% of patients with asthma may develop AERD.ĪERD usually presents with asthmatic symptoms (cough, wheezing, chest tightness), nasal and ocular symptoms (nasal congestion, rhinorrhea, or periorbital edema), and facial flushing within 30 minutes to 3 hours after NSAID ingestion. They are NOT Ig-E mediated but usually occur in patients with comorbid asthma, chronic rhinosinusitis with nasal polyposis, or chronic urticaria. It is a pseudoallergic reaction to NSAIDs.
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