Below you can learn about normal breathing and the changes in breathing that happen with asthma. When most of us breathe, the muscles that are wrapped around the air tubes airways are very loose and relaxed, and the lining inside the airways is very thin. This lets the airways open up very wide so that it is easy to get air in and out of the small air sacs that make up our lungs. These small sacs are called alveoli pronounced al-vee-oh-lye.
When air moves in and out of our lungs, we call it breathing. The picture below shows what your lungs look like when everything is working normally. The muscles wrapped around the airways are very thin and loose, and the airway is wide open. Quiz questions. High-resolution CT of the lung. Pulmonary Function in Children with Idiopathic Scoliosis.
A Diagnostic Subclassification. Annals ATS. Spectrum of Pulmonary Neuroendocrine Proliferations and Neoplasms. Eur Respir J. Altered Respiratory Physiology in Obesity. Can Respir J. Promoted articles advertising. Case 1: focal air trapping in bronchial atresia Case 1: focal air trapping in bronchial atresia. Allergies and infections may cause the inflammation of the airways, and asthmatic attacks are more likely to occur with a cold or during allergy season.
Inhaled corticosteroids, which reduce airway inflammation, can reduce the frequency and severity of asthma attacks, and bronchodilators, which relax the muscles in the airways and allow them to open, can relieve asthma for most people.
Although asthma mortality rates are low, an attack can cause suffocation and death. There are about 4, asthma deaths in the U. If severe asthma is different from milder forms of the disease, and those differences can be identified, it might suggest new treatments.
On the other hand, if severe asthma is not different, only a more extreme version of the same disease, then using current treatments more aggressively might work.
He examined four aspects of lung function:. Air flow limitation. A longer period of time is required to exhale a volume of air. This is probably related to airway narrowing and is a hallmark of asthmatics, whether mild, moderate or severe. Air trapping. An inability to exhale completely. Daily salbutamol usage improved from 8. Oral corticosteroid requiring exacerbations reduced from 2. The mean baseline FEV 1 was KCO was also unaltered by BT. These changes were evident at the 6 week time period and maintained at 6 months.
Bronchial thermoplasty improves gas trapping and this effect is greatest in the most severely obstructed patients. The improvement may relate to changes in the mechanical properties of small airways that are not measured with spirometry. Peer Review reports. Bronchial thermoplasty BT offers an alternative therapeutic option for patients with severe asthma, defined by the Global Initiative for Asthma GINA as those with persistent symptoms requiring step 5 of controller treatment [ 1 ]. Performed during bronchoscopy, radiofrequency thermal impulses are delivered to airways ranging in size from 2 to 10 mm, with the intention of inducing atrophy in hypertrophied airway smooth muscle.
Histological studies in both canine and humans have demonstrated that this occurs [ 2 , 3 , 4 , 5 ]. Three randomized controlled trials have established that patients feel better after this treatment, with fewer asthma symptoms, reduced exacerbations and improved quality of life [ 6 , 7 , 8 ]. However, two of these three clinical trials showed no effect of BT on the one-second forced expiratory volume FEV 1 [ 6 , 7 ]. How is it then, that large numbers of asthmatic patients in a controlled clinical trial can experience an improvement in their symptoms and quality life, without improvement in physiological parameters such as FEV 1?
One explanation might lie in the placebo effect, known to be a powerful force in surgical treatment [ 9 ]. However, this would not explain the significantly better results observed in the active arm of a double blind, sham controlled study, namely the AIR2 trial [ 6 ]. An alternative hypothesis might be that BT leads to physiological changes which are not measured by spirometry - such as might occur in the peripheral airways. Smaller airways, less than 2 mm in diameter, have been histologically shown to be involved in asthma [ 10 ].
These smaller airways make up a large portion of the cross-sectional area of the lung, and as a result resistance in these airways is not easily detected by changes in FEV 1 [ 11 , 12 ]. A number of methods exist to evaluate physiological changes in the small airways [ 13 ]. These include i plethysmography ii impulse oscillometry iii inert gas washout and iv sophisticated imaging techniques such as hyperpolarized magnetic resonance imaging.
In this study, we report changes in plethysmographic lung volumes as measures of response to BT. This was a prospective evaluation of consecutive patients selected for BT at two Australian university teaching hospitals, between June and January Participants were referred for BT by their treating respiratory physician if they had frequent symptoms despite optimized asthma therapy including high dose inhaled corticosteroids and two long acting bronchodilators.
The baseline characteristics of the patients were collated, including age, gender, body mass index BMI , medication usage, exacerbation history, and the disease specific quality of life tool, the Asthma Control Questionnaire score ACQ The ACQ-5 was chosen as it has an established place as an evaluative tool in asthma and is known to be sensitive to change [ 15 ].
All tests were performed in the morning, and prior to the administration of any bronchodilators that day. For spirometry, at least three acceptable maneuvers were obtained, with the FEV 1 and the forced vital capacity FVC measurement values within 0. Post bronchodilator spirometry was then performed. The predicted equations used were Quanjer [ 17 ] for spirometry, and ECCS [ 18 ] for all other tests.
Testing was conducted at baseline, in the 4 weeks prior to BT being undertaken, then at 6 weeks and 6 months after the final BT procedure. Exacerbations of asthma were recorded if the patient reported a deterioration in their asthma requiring an increase in, or the commencement of, oral corticosteroids. All bronchoscopies were performed under general anesthesia. Consistent with the standard protocol, each patient was treated in three sessions, three to 4 weeks apart.
The right lower lobe was treated first, followed by the left lower lobe, and then both upper lobes during the final bronchoscopy. The right middle lobe was not treated. The number of radiofrequency actuations delivered was recorded for each patient. Prednisolone was prescribed for 3 days prior, and continued for 3 days after each BT procedure.
All patients were electively admitted to hospital for the night immediately following treatment. The primary outcomes in this study were the changes in lung function parameters measured 6 months post procedure when compared to baseline.
Secondary outcomes related to changes in ACQ-5 score, reliever and preventer medication use, and exacerbation history at 6 months. Re-evaluation at the 6 month time point was chosen so as to allow for any structural effects from BT to have been completed, yet to have avoided patients being lost to follow up or started on new medication. A paired t-test was used for paired sets of data, whilst an unpaired t-test was used to compare groups. Analysis of variance was used to compare baseline data with repeated tests over time.
For multivariate linear regression a stepwise backward model was created. Approval to collate and audit data as part of quality assurance was provided by the Human Research Ethics Committee at both participating institutions.
All participants provided informed consent for treatment and data collection. Thirty-two consecutive patients undergoing this study protocol were available for inclusion, 15 males, 17 females. No patients were lost to follow up, nor excluded. The mean age was The mean BMI was Despite this treatment, patients used a mean of 8. Seven patients had been receiving stable therapy with omalizumab, for the preceding 12 months, and no patient commenced a monoclonal antibody during study period from immediately prior to BT to the 6 month re-evaluation.
The baseline prebronchodilator FEV 1 was The mean forced expiratory ratio was The mean baseline DLCO was There were no current cigarette smokers.
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