The best treatment is avoidance of conditions predisposing to attacks, when possible. In athletes who wish to continue their sport or do so in adverse conditions, preventive measures include altered training techniques and medications.

Some take advantage of the refractory period by precipitating an attack by "warming up," and then timing competition such that it occurs during the refractory period. Step-wise training works in a similar fashion. Warm up occurs in stages of increasing intensity, using the refractory period generated by each stage to reach a full workload.

The treatment of EIB has been extensively studied in asthmatic subjects over the last 30 years, but not so in EIB. Thus, it is not known whether athletes with EIB or ‘sports asthma’ respond similarly to subjects with classical allergic or nonallergic asthma. However, there is no evidence supporting different treatment for EIB in asthmatic athletes and nonathletes.

The most common medication used is a beta agonist taken about 20 minutes before exercise. Some physicians prescribe inhaled anti-inflammatory mists such as corticosteroids or leukotriene antagonists, and mast cell stabilizers have also proven effective. A randomized crossover study compared oral montelukast with inhaled salmeterol, both given two hours before exercise. Both drugs had similar benefit but montelukast lasted 24 hours.

Three randomized double-blind cross-over trials have examined the effect of vitamin C on EIB. Pooling the results of the three vitamin C trials indicates an average 48% reduction in the FEV1 decline caused by exericise (Figure). The systematic review concluded that "given the safety and low cost of vitamin C, and the positive findings for vitamin C administration in the three EIB studies, it seems reasonable for physically active people to test vitamin C when they have respiratory symptoms such as cough associated with exercise." It should be acknowledged that the total number of subjects involved in all three trials was only 40.

Figure: This forest plot shows the effect of vitamin C (0.5–2 g/day) on post-exercise decline in FEV1 in three studies with asthmatic participants. Constructed from data in Fig. 4 of Hemilä (2013).

The three horizontal lines indicate the three studies, and the diamond shape at the bottom indicates the pooled effect of vitamin C: decrease in the post-exercise decline in FEV1 by 48% (95%CI: 33 to 64%).

In May 2013, the American Thoracic Society issued the first treatment guidelines for EIB.

Interventions include intravenous (IV) medications (e.g. magnesium sulfate), aerosolized medications to dilate the airways (bronchodilation) (e.g., albuterol or ipratropium bromide/salbutamol), and positive-pressure therapy, including mechanical ventilation. Multiple therapies may be used simultaneously to rapidly reverse the effects of status asthmaticus and reduce permanent damage of the airways. Intravenous corticosteroids and methylxanthines are often given. If the person with a severe asthma exacerbation is on a mechanical ventilator, certain sedating medications such as ketamine or propofol, have bronchodilating properties. According to a new randomized control trial ketamine and aminophylline are also effective in children with acute asthma who responds poorly to standard therapy.

Short-acting beta-agonists like salbutamol or terbutaline or long-acting beta-agonists like salmeterol and formoterol dilate airways which relieve the symptoms thus reducing the severity of the reaction. Some patients also use it just before work to avoid a drop in the FEV.

Anti-inflammatory agents like corticosteroids, LKTRA or mast cell stabilizers can also be used depending on the severity of the case.

Underlying disease must be controlled to prevent exacerbation and worsening of ABPA, and in most patients this consists of managing their asthma or CF. Any other co-morbidities, such as sinusitis or rhinitis, should also be addressed.

Hypersensitivity mechanisms, as described above, contribute to progression of the disease over time and, when left untreated, result in extensive fibrosis of lung tissue. In order to reduce this, corticosteroid therapy is the mainstay of treatment (for example with prednisone); however, studies involving corticosteroids in ABPA are limited by small cohorts and are often not double-blinded. Despite this, there is evidence that acute-onset ABPA is improved by corticosteroid treatment as it reduces episodes of consolidation. There are challenges involved in long-term therapy with corticosteroids—which can induce severe immune dysfunction when used chronically, as well as metabolic disorders—and approaches have been developed to manage ABPA alongside potential adverse effects from corticosteroids.

The most commonly described technique, known as sparing, involves using an antifungal agent to clear spores from airways adjacent to corticosteroid therapy. The antifungal aspect aims to reduce fungal causes of bronchial inflammation, whilst also minimising the dose of corticosteroid required to reduce the immune system’s input to disease progression. The strongest evidence (double-blinded, randomized, placebo-controlled trials) is for itraconazole twice daily for four months, which resulted in significant clinical improvement compared to placebo, and was mirrored in CF patients. Using itraconazole appears to outweigh the risk from long-term and high-dose prednisone. Newer triazole drugs—such as posaconazole or voriconazole—have not yet been studied in-depth through clinical trials in this context.

Whilst the benefits of using corticosteroids in the short term are notable, and improve quality of life scores, there are cases of ABPA converting to invasive aspergillosis whilst undergoing corticosteroid treatment. Furthermore, in concurrent use with itraconazole, there is potential for drug interaction and the induction of Cushing syndrome in rare instances. Metabolic disorders, such as diabetes mellitus and osteoporosis, can also be induced.

In order to mitigate these risks, corticosteroid doses are decreased biweekly assuming no further progression of disease after each reduction. When no exacerbations from the disease are seen within three months after discontinuing corticosteroids, the patient is considered to be in complete remission. The exception to this rule is patients who are diagnosed with advanced ABPA; in this case removing corticosteroids almost always results in exacerbation and these patients are continued on low-dose corticosteroids (preferably on an alternate-day schedule).

Serum IgE can be used to guide treatment, and levels are checked every 6–8 week after steroid treatment commences, followed by every 8 weeks for one year. This allows for determination of baseline IgE levels, though it’s important to note that most patients do not entirely reduce IgE levels to baseline. Chest X-ray or CT scans are performed after 1–2 months of treatment to ensure infiltrates are resolving.

When asthma is unresponsive to usual medications, other options are available for both emergency management and prevention of flareups. For emergency management other options include:

- Oxygen to alleviate hypoxia if saturations fall below 92%.

- Corticosteroid by mouth are recommended with five days of prednisone being the same 2 days of dexamethasone. One review recommended a seven-day course of steroids.

- Magnesium sulfate intravenous treatment increases bronchodilation when used in addition to other treatment in moderate severe acute asthma attacks. In adults it results in a reduction of hospital admissions.

- Heliox, a mixture of helium and oxygen, may also be considered in severe unresponsive cases.

- Intravenous salbutamol is not supported by available evidence and is thus used only in extreme cases.

- Methylxanthines (such as theophylline) were once widely used, but do not add significantly to the effects of inhaled beta-agonists. Their use in acute exacerbations is controversial.

- The dissociative anesthetic ketamine is theoretically useful if intubation and mechanical ventilation is needed in people who are approaching respiratory arrest; however, there is no evidence from clinical trials to support this.

- For those with severe persistent asthma not controlled by inhaled corticosteroids and LABAs, bronchial thermoplasty may be an option. It involves the delivery of controlled thermal energy to the airway wall during a series of bronchoscopies. While it may increase exacerbation frequency in the first few months it appears to decrease the subsequent rate. Effects beyond one year are unknown.

- Evidence suggests that sublingual immunotherapy in those with both allergic rhinitis and asthma improve outcomes.

- Omalizumab may also be useful in those with poorly controlled allergic asthma.

- It is unclear if non-invasive positive pressure ventilation in children is of use as it has not been sufficiently studied.

Although feline asthma is incurable, ongoing treatments allow many domestic cats to live normal lives. Feline asthma is commonly managed through use of bronchodilators for mild cases, or glucocorticosteroids with bronchodilators for moderate to severe cases.

Previously, standard veterinary practice recommended injected and oral medications for control of the disease. These drugs may have systemic side effects including diabetes and pancreatitis. In 2000, Dr. Philip Padrid pioneered inhaled medications using a pediatric chamber and mask using Flovent(r) (fluticasone) and salbutamol. Inhaled treatments reduce or eliminate systemic effects. In 2003 a chamber called the AeroKat Feline Aerosol Chamber was designed specifically for cats, significantly improving efficiency and reducing cost for the caregiver. Medicine can also be administered using a human baby spacer device. Inhaled steroid usually takes 10-14 days to reach an effective dose.

Long-term use of inhaled corticosteroids at conventional doses carries a minor risk of adverse effects. Risks include thrush, the development of cataracts, and a slightly slowed rate of growth. Higher doses of inhaled steroids may result in lower bone mineral density.

Inhaled bronchodilators are the primary medications used, and result in a small overall benefit. The two major types are β agonists and anticholinergics; both exist in long-acting and short-acting forms. They reduce shortness of breath, wheeze, and exercise limitation, resulting in an improved quality of life. It is unclear if they change the progression of the underlying disease.

In those with mild disease, short-acting agents are recommended on an as needed basis. In those with more severe disease, long-acting agents are recommended. Long-acting agents partly work by improving hyperinflation. If long-acting bronchodilators are insufficient, then inhaled corticosteroids are typically added. With respect to long-acting agents, if tiotropium (a long-acting anticholinergic) or long-acting beta agonists (LABAs) are better is unclear, and trying each and continuing the one that worked best may be advisable. Both types of agent appear to reduce the risk of acute exacerbations by 15–25%. While both may be used at the same time, any benefit is of questionable significance.

Several short-acting β agonists are available, including salbutamol (albuterol) and terbutaline. They provide some relief of symptoms for four to six hours. Long-acting β agonists such as salmeterol, formoterol, and indacaterol are often used as maintenance therapy. Some feel the evidence of benefits is limited while others view the evidence of benefit as established. Long-term use appears safe in COPD with adverse effects include shakiness and heart palpitations. When used with inhaled steroids they increase the risk of pneumonia. While steroids and LABAs may work better together, it is unclear if this slight benefit outweighs the increased risks. Indacaterol requires an inhaled dose once a day, and is as effective as the other long-acting β agonist drugs that require twice-daily dosing for people with stable COPD.

Two main anticholinergics are used in COPD, ipratropium and tiotropium. Ipratropium is a short-acting agent, while tiotropium is long-acting. Tiotropium is associated with a decrease in exacerbations and improved quality of life, and tiotropium provides those benefits better than ipratropium. It does not appear to affect mortality or the overall hospitalization rate. Anticholinergics can cause dry mouth and urinary tract symptoms. They are also associated with increased risk of heart disease and stroke. Aclidinium, another long acting agent, reduces hospitalizations associated with COPD and improves quality of life. Aclinidinium has been used as an alternative to tiotropium, but which drug is more effective is not known.

Corticosteroids are usually used in inhaled form, but may also be used as tablets to treat and prevent acute exacerbations. While inhaled corticosteroids (ICSs) have not shown benefit for people with mild COPD, they decrease acute exacerbations in those with either moderate or severe disease. By themselves, they have no effect on overall one-year mortality. Whether they affect the progression of the disease is unknown. When used in combination with a LABA, they may decrease mortality compared to either ICSs or LABA alone. Inhaled steroids are associated with increased rates of pneumonia. Long-term treatment with steroid tablets is associated with significant side effects.

Recovery is directly dependent on the duration and level of exposure to the causative agent. Depending on the severity of the case, the condition of the patient can improve dramatically during the first year after removal from exposure.

Three basic types of procedures are used for treating the affected workers: reducing a worker's exposure, removing a worker from the environment with the asthma-causing agent, and treatment with asthma medications. Completely stopping exposure is more effective treatment than reducing exposure. By reducing exposure, the probability of suffering another reaction is lowered. Methods of reducing exposure include transferring an affected worker to a position without the relevant asthmagen, use of respiratory protection, and engineering controls. In 1984 innovator David Cornell discovered and invented effective control equipment in the UK for the removal of many harmful workplace fumes. 'BOFA' extraction products are now found in over 100 countries worldwide.

People affected by occupational asthma that occurred after a latency period, whether a few months or years, should be immediately removed from exposure to the causative agent. However, this can entail severe socio-economic consequences for the worker as well as the employer due to loss of job, unemployment, compensation issues, quasi-permanent medical expenditures, and hiring and re-training of new personnel. This can be mitigated by transferring the worker within a company.

In addition to any issues of treatment compliance, and maximised corticosteroids (inhaled or oral) and beta agonist, brittle asthma treatment also involves for type 1 additional subcutaneous injections of beta2 agonist and inhalation of long acting beta-adrenoceptor agonist, whilst type 2 needs allergen avoidance and self-management approaches. Since catastrophic attacks are unpredictable in type 2, patients may display identification of the issue, such as a MedicAlert bracelet, and carry an epinephrine autoinjector.

The preferred treatment for many patients is desensitization to aspirin, undertaken at a clinic or hospital specializing in such treatment. In the United States, the Scripps Clinic in San Diego, CA, the Massachusetts General Hospital in Boston, MA, the Brigham and Women's Hospital in Boston, MA, National Jewish Hospital in Denver and Stanford University Adult ENT Clinic have allergists who routinely perform aspirin desensitization procedures for patients with aspirin-induced asthma. Patients who are desensitized then take a maintenance dose of aspirin daily and while on daily aspirin they often have reduced need for supporting medications, fewer asthma and sinusitis symptoms than previously, and many have an improved sense of smell. Desensitization to aspirin reduces the chance of nasal polyp recurrence, and can slow the regrowth of nasal polyps. Even patients desensitized to aspirin may continue to need other medications including nasal steroids, inhaled steroids, and leukotriene antagonists.

Leukotriene antagonists and inhibitors (montelukast, zafirlukast, and zileuton) are often helpful in treating the symptoms of aspirin-induced asthma. Some patients require oral steroids to alleviate asthma and congestion, and most patients will have recurring or chronic sinusitis due to the nasal inflammation.

The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage. Corticosteroids such as prednisolone may help to control symptoms but may produce side-effects.

Often surgery is required to remove nasal polyps, although they typically recur, particularly if aspirin desensitization is not undertaken. 90% of patients have been shown to have recurrence of nasal polyps within 5 years after surgery, with 47% requiring revision surgery in the same time period.

The administration of oxygen as a medical intervention is common in diving medicine, both for first aid and for longer term treatment.

Treatment of diving disorders depends on the specific disorder or combination of disorders, but two treatments are commonly associated with first aid and definitive treatment where diving is involved. These are first aid oxygen administration at high concentration, which is seldom contraindicated, and generally recommended as a default option in diving accidents where there is any significant probability of hypoxia, and hyperbaric oxygen therapy (HBO), which is the definitive treatment for most incidences of decompression illness. Hyperbaric treatment on other breathing gases is also used for treatment of decompression sickness if HBO is inadequate.

Feline asthma and other respiratory diseases may be prevented by cat owners by eliminating as many allergens as possible. Allergens that can be found in a cat’s habitual environment include: pollen, molds, dust from cat litter, perfumes, room fresheners, carpet deodorizers, hairspray, aerosol cleaners, cigarette smoke, and some foods. Avoid using cat litters that create lots of dust, scented cat litters or litter additives. Of course eliminating all of these can be very difficult and unnecessary, especially since a cat is only affected by one or two. It can be very challenging to find the allergen that is creating asthmatic symptoms in a particular cat and requires a lot of work on both the owner’s and the veterinarian's part. But just like any disease, the severity of an asthma attack can be propelled by more than just the allergens, common factors include: obesity, stress, parasites and pre-existing heart conditions. Dry air encourages asthma attacks so keep a good humidifier going especially during winter months.

Avoidance of ethanol is the safest, surest, and cheapest treatment. Indeed, surveys find a positive correlation between high incidences of glu487lys ALDH2 allele-related alcohol-induced respiratory reactions as well as other causes of these reactions and low levels of alcohol consumption, alcoholism, and alcohol-related diseases. Evidently, people suffering these reaction self-impose avoidance behavior. There is a proviso here: ethanol, at surprisingly high concentrations, is used as a solvent to dissolve many types of medicines and other ingredients. This pertains particularly to liquid cold medicines and mouthwashes. Ethanol avoidance includes avoiding the ingestion of and, depending on an individual's history, mouth washing with, such agents.

Type H1 antagonists in the histamine antagonist family of drugs were tested in Japanese volunteers with alcohol-induced asthma (who presumably have glu487lys ALDH2 allele-associated asthma) and found to be completely effective in blocking bronchoconstriction responses to alcoholic beverages; these blockers, it is suggested, may be taken 1–2 hours before consumption of alcohol beverages as a preventative of alcohol-induced respiratory reactions. In the absence of specific studies on the prevention of classical alcohol induced rhinitis and asthma due to allergens in alcoholic beverages, see asthma section on Prevention and rhinitis section on Prevention of allergen-induced reactions.

In the absence of specific studies on the treatment of acute alcohol-induced bronchoconstriction and rhinitis, treatment guidelines should probably follow those of their comparable allergen-induced classical allergic reactions (see asthma section on Treatment and rhinitis section on Treatment) but possibly favoring the testing of H1 antagonist anti-histamines as part of the initial protocol.

When laryngospasm is coincident with a cold or flu, it may be helpful for some sufferers to take acid reflux medication to limit the irritants in the area. If a cough is present, then treat a wet cough; but limit coughing whenever possible, as it is only likely to trigger a spasm. Drink water or tea to keep the area from drying up. Saline drops also help to keep the area moist. Pseudoephederine may also help to clear any mucus that may cause coughing and thereby triggering more spasms.

Medical often works in conjunction with behavioral approaches. A pulmonary or ENT (otolaryngologist) specialist will screen for and address any potential underlying pathology that may be associated with VCD. Managing GERD has also been found to relieve laryngospasm, a spasm of the vocal cords that makes breathing and speaking difficult.

Non-invasive positive pressure ventilation can be used if a patient's vocal cords adduct (close) during exhalation. Mild sedatives have also been employed to reduce anxiety as well as reduce acute symptoms of VCD. Benzodiazepines are an example of one such treatment, though they have been linked to a risk of suppression of the respiratory drive. While Ketamine, a dissociative anesthetic, does not suppress respiratory drive, it has been thought to be associated with laryngospasms.

For more severe VCD cases, physicians may inject botulinum toxin into the vocal (thyroarytenoid) muscles to weaken or decrease muscle tension. Nebulized Lignocaine can also been used in acute cases and helium-oxygen inhalation given by face mask has been used in cases of respiratory distress.

Minor laryngospasm will generally resolve spontaneously in the majority of cases.

Laryngospasm in the operating room is treated by hyperextending the patient's neck and administering assisted ventilation with 100% oxygen. In more severe cases it may require the administration of an intravenous muscle relaxant, such as Succinylcholine, and reintubation.

When Gastroesophageal Reflux Disease (GERD) is the trigger, treatment of GERD can help manage laryngospasm. Proton pump inhibitors such as Dexlansoprazole (Dexilant), Esomeprazole (Nexium), and Lansoprazole (Prevacid) reduce the production of stomach acids, making reflux fluids less irritant. Prokinetic agents reduce the amount of acid available by stimulating movement in the digestive tract.

Spontaneous laryngospasm can be treated by staying calm and breathing slowly, instead of gasping for air. Drinking (tiny sips) of ice water to wash away any irritants that may be the cause of the spasm can also help greatly.

Patients who are prone to laryngospasm during illness can take measures to prevent irritation such as antacids to avoid acid reflux, and constantly drinking water or tea keep the area clear of irritants.

Additionally, laryngospasms can result from hypocalcemia, causing muscle spasms and/or tetany. Na+ channels remain open even if there is very little increase in the membrane potential. This affects the small muscles of the vocal folds.

Speech-language pathologists provide behavioral treatment of VCD. Speech therapy usually involves educating the client on the nature of the problem, what happens when symptoms are present, and then comparing this to what happens during normal breathing and phonation. Intervention goals target teaching a client breathing and relaxation exercises so that they can control their throat muscles and keep the airway open, allowing air to flow in and out.

Breathing techniques can be taught to reduce tension in the throat, neck, and upper body and bring attention to the flow of air during respiration. Diaphragm support during breathing decreases muscle tension in the larynx. These techniques are meant to move awareness away from the act of breathing in and focus on the auditory feedback provided by the air moving in and out.

Other techniques can involve breathing through a straw and panting, which widens the opening of the throat by activating the Posterior cricoarytenoid (PCA) muscle. Endoscopic feedback can also be used to show a patient what is happening when they are doing simple tasks such as taking a deep breath or speaking on an inspiration. This provides the client with visual information so that they can actually see what behaviours help to open the throat and what behaviors constrict the throat. Respiratory muscle strength training, a form of increased resistance training using a hand-held breathing device has also been reported to alleviate symptoms.

Speech therapy has been found to eliminate up to 90% of ER visits in patients suffering from VCD.

The tissues in the mediastinum will slowly resorb the air in the cavity so most pneumomediastinums are treated conservatively. Breathing high flow oxygen will increase the absorption of the air.

If the air is under pressure and compressing the heart, a needle may be inserted into the cavity, releasing the air.

Surgery may be needed to repair the hole in the trachea, esophagus or bowel.

If there is lung collapse, it is imperative the affected individual lies on the side of the collapse, although painful, this allows full inflation of the unaffected lung.

Sirolimus is an mTOR inhibitor that stabilizes lung function and improves some measures of life in LAM patients. It is approved by the FDA for use in LAM, based on the results of the Multicenter International LAM Efficacy and Safety of Sirolimus (MILES) Trial. MILES data supports the use of sirolimus in patients who have abnormal lung function (i.e. FEV1<70% predicted). Whether the benefits of treatment outweigh the risks for asymptomatic LAM patients with normal lung function is not clear, but some physicians consider treatment for declining patients who are approaching the abnormal range for FEV1. Sirolimus also appears to be effective for the treatment chylous effusions and lymphangioleiomyomatosis. The benefits of sirolimus only persist while treatment continues. The safety of long term therapy has not been studied.

Potential side effects from mTOR inhibitors include swelling in the ankles, acne, oral ulcers, dyspepsia, diarrhea, elevation of cholesterol and triglycerides, hypertension and headache. Sirolimus pneumonitis and latent malignancy are more serious concerns, but occur infrequently. Sirolimus inhibits wound healing. It is important to stop therapy with the drug for 1–2 weeks before and after elective procedures that require optimal wound healing. Precautions must be taken to avoid prolonged sun exposure due to increased skin cancer risk.

Treatment with another mTOR inhibitor, everolimus, was reported in a small, open-label trial to be associated with improvement in FEV1 and six-minute walk distance. Serum levels of VEGF-D and collagen IV were reduced by treatment. Adverse events were generally consistent with those known to be associated with mTOR inhibitors, although some were serious and included peripheral edema, pneumonia, cardiac failure and "Pneumocystis jirovecii" infection. Escalating doses of everolimus were used, up to 10 mg per day; higher than what is typically used clinically for LAM.

Serum VEGF-D concentration is useful, predictive and prognostic biomarker. Higher baseline VEGF-D levels predicts more rapid disease progression and a more robust treatment response.

Hormonal approaches to treatment have never been tested in proper trials. In the absence of proven benefit, therapy with progesterone, GnRh agonists (e.g., Lupron, goserelin) and tamoxifen are not routinely recommended. Doxycycline had no effect on the rate of lung function decline in a double blind trial.

Sirolimus is often effective as first-line management for chylothorax. If chylous leakage or accumulations persist despite treatment, imaging with heavy T2 weighted MRI, MRI lymphangiography or thoracic duct lymphangiography can be considered. Pleural fusion procedures can be considered in refractory cases.