by Jeremy Brown, PhD

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    00:01 So the subject of this lecture is asthma, which is one of the common forms of airways disease that affects respiratory patients. When we talk about airways disease, we mean diseases that affect the conducting airways, the trachea, the major bronchi, and the bronchioles going down as far as the terminal bronchioles. We don’t mean diseases affecting the alveoli.

    00:26 These airways diseases, in general, will present with some form of airways obstruction.

    00:31 And that will be recordable when you do lung function test as obstructive lung function changes.

    00:38 They don’t tend to show many abnormalities on a chest X-ray. That is because the bronchi are not readily detectable on X-ray, and the changes we’re talking about are relatively small changes in multiple different parts of the airways rather than a single mass lesion as if you have a cancer, for example. There are a range of potential airways diseases.

    01:02 However, this subject is dominated by two airways disease; asthma and chronic obstructive pulmonary disease. COPD, this is a subject to the next lecture as really a smoking-related lung disease. In this lecture, I will concentrate largely on asthma. In addition, I will cover post-infective bronchial hyperactivity. At third lecture, we'll discuss other airways diseases, the causes of large airway obstruction, bronchiectasis, and allergic bronchopulmonary aspergillosis. A major thing about airways disease is that the obstruction that occurs can be described as reversible or irreversible. So the prevention of effective airflow can be reversed, in reversible disease, can be improved of treatment, whereas, with irreversible disease, it can’t be. That’s the broad distinction.

    02:09 There are of course patients in between with partially reversible airways disease, where the obstruction can be partially reversed but doesn’t get as good as normal.

    02:19 Largely speaking, asthma is a reversible airways disease, whereas, COPD is an irreversible airways disease.

    02:28 Another important thing about airways disease is that expiration is always worse than inspiration with the lower airways obstruction problems. As a consequence, that means if you have significant lower airways obstruction, then you’ll end up with a degree of air trapping and accumulation of air in the lungs increasing the volume of the lungs, increasing the residual volume specifically, and making the lungs hyperexpanded. So, to talk about reversibility in a bit more detail as this is a fundamental concept for airways obstruction. What we mean by reversibility is that if there’s a 15% increase in your forced expiratory volume in one second, a measure of airflow on expiration, and that’s at least 200 ml, then there is a degree of reversibility present. Now, if that reversibility of treatment actually improves your FEV1 to the expected level for somebody of your age, sex, and height, then that will be a fully reversible situation. But if it only goes apart of the way to what you might expect to have as your FEV1, then that’s partially reversible. And that shown by this diagram on the right-hand side of this slide, the patient’s pre-treatment, pre-bronchodilator data, given FEV1 of 1.2.

    03:51 Then the patient is given some salbutamol and the FEV1 increases by 700 ml, and by over 50% to 1.9. SO that's a substantial degree of reversibility. However, because of the age, sex, and height of this patient, the FEV1 is expected to be closer to three about 2.7, 2.8. And yet, they’ve only achieved 1.9 of the bronchodilation. So that’s a partially reversed situation. Now, reversibility in asthma is often clinically very obvious. The patient may come into hospital in exacerbation, be terribly breathless, and then two weeks later, be back running their five kilometers a day. So that clearly shows somebody who has an airways disease which can be very severe, they end up in hospital. But when they’re well, it can actually allow them to function at a very high level. The treatment that we use to test for reversibility is usually just some inhaled bronchodilator, a beta2 agonist such as salbutamol, and that can be inhaled using a normal inhaler or a nebulizer. Sometimes, when we really want to test whether somebody is reversible, we increase the power of the treatment by giving them oral prednisolone, corticosteroids for three weeks potentially, and potentially giving them a nebulised salbutamol over that time. That’s the real test for full reversibility in patients where it’s not clear that their lung function can return to normal with just taking an inhaled bronchodilator. Now, as I mentioned already, asthma is largely a reversible airways disease. And COPD is largely an irreversible airways disease. But there’s such a large range of types of asthma and COPD that there is an overlap. Some patients with COPD have degree of reversibility. And some patients with asthma, especially those patients who had the disease for a very long period of time or poorly controlled disease, will develop irreversible components as well. So there is an overlap between the two.

    05:59 Another airways disease, for example, bronchiectasis, can also have reversible and irreversible and a partially reversible patients with the airways obstruction. And there are less common causes of airways obstruction, which, in general, tend to cause largely irreversible airways disease. And I’ll talk about those a little in the second lecture. So, it’s quite easy to get confused between reversible and irreversible airways disease in asthma and COPD. But the basic concept is relatively straightforward. Reversibility indicates asthma. Irreversibility suggests COPD, but there’s more to that. Patients with COPD need to have a smoking history. But there are patients who do overlap in the middle. For example, if you have an asthmatic who’s been asthmatic since childhood but has been smoking since the age of 20, at the time they get to 50, actually, they may acquire a significant degree of airways obstruction which is irreversible, and that would be COPD because of the smoking on the background of asthma. So, asthma is the commonest chronic lung disease. In fact, it’s one of the commonest chronic diseases full stopped. A significant portion of the population have asthma about 5% in the U.K. And what this reflects is chronic inflammation and what we call is hyper-reactivity of the airways.

    07:19 The airways are twitchy. They will respond by bronchoconstriction tightening up to a variety of different end results and when they bronchoconstrict, that’s when you have airways obstruction and the patient will present with symptoms. Over decades, if somebody has poorly controlled asthma with this bronchoconstriction occurring frequently, they’ll end up with a degree of irreversible disease. So the bronchoconstriction of a treatment doesn’t fully reverse to normal bronchi diameters, but there is a degree of chronic airways obstruction present as well.

    07:53 Predisposing factors for asthma, well, a family history.

    07:57 Genetics, there are certain genes that I've mentioned as polymorphisms has been associated, ADAM33, for example. A history of atopy, eczema and/or hay fever in combination of nasal parts would suggest somebody’s more chance of getting asthma. Childhood infection, specifically, respiratory syncytial virus infection bronchiolitis is closely associated with developed asthma in later life. Other associations are prematurity, low birth weight, obesity, exposure to passive smoking especially as a child, active smoking in itself would stimulate an asthmatic type situation or make asthma more likely to develop, as does, inhaling recreational drugs.

    08:39 Crack cocaine is a very good stimulant for creating asthma in patients.

    08:44 The pathogenesis of asthma is complicated. It has probably no single pathology and it causes the end result of asthma. It’s largely a cell-mediated immune response, either Th2, allergic response to inhaled antigen such as pollen, house dust mite faeces, various moulds, animal hair, cat hair, for example, or a Th17 CD4 cell-mediated immunity which is independent of allergy. That will lead to airway information. In asthma, it could be eosinophilic which tends to be a Th2 dependent or a neutrophilic which tends to be a Th17 dependent.

    09:24 And that airways information tends to stimulate smooth muscle constriction as well, and there are quite a number of key mediators of that process, IL4, IL5, IL13, leukotrienes, etc. The end result of these airways information is bronchoconstriction. Tight bronchi, smaller bronchi should be impairing airflow on expiration.

    09:48 In addition, you get mucous hypersecretion with the mucous glands producing more mucous.

    09:55 And there will be swelling of the airway, airways oedema. And eventually, over time, you get airway remodelling with some fibrosis forming around the airways leading in to the irreversible components of asthma that may develop in patients over long periods of time that I described earlier. So, who gets asthma? Well, essentially, it could be anybody, all ages; children, young adults, middle-aged adults, and even the elderly.

    10:23 New asthma in the elderly perhaps is less common. But patients, when they have asthma, it lasts potentially for their lifetime. So there are many people who’ve had asthma for 20, 30 years who are now in their 80’s. It often starts in childhood, fades in later childhood, early adulthood, and then returns later in life. But there’s a second peak of diagnosis of asthma for the first time in people aged around 60. Women tend to be more affected than men, although that’s only a mild predominance.

    10:54 The history of asthma, again, is also very variable. The key is episodic symptoms.

    11:01 So, if you have mild disease, the symptoms would be cough, maybe there’s some wheeze.

    11:05 If it’s more severe disease, it will be cough, wheeze, and breathlessness with chest tightness, and a tension that you get pretty other phlegm production. The yellow phlegm production, as well, But the point about that is this episodic- bad periods, good periods, bad periods, good periods. When you examine the patient, they’re normally not actually having the bad period, and therefore, you don’t hear much in the way of abnormalities in their chest because there’s no ongoing airways obstruction. However, if they’re poorly controlled, you might hear a polyphonic wheeze throughout both lungs.

    11:34 So, the sort of pattern of disease that patients have tends to vary a lot between different patients. So some patients have very mild disease, no symptoms in large portions of the time, and then something will kick off the asthma and they’ll have symptoms for a period of few weeks then they’ll settle down again. Some patients have symptoms the whole time, and actually does disrupt their life quite a lot. They have occasional exacerbation as well. But it’s just generally a low-level disruption of their life by symptoms most days. And then you can get acute life-threatening attacks that occur and they bring the patient into the hospital. And some patients, after long periods of asthma, can develop chronic disability through the airflow obstruction with chronic breathlessness, as well as the intermittent episodes of disability due to deteriorating asthma control as well. So there are certain triggers that characteristically worsen the symptom of asthma. These tend to vary between patients. But generally speaking, asthma has a diurnal variation. So patients who are poorly controlled will have their cough more at night and on waking first thing in the morning when the asthma is worse than they do in the evening. Exercise characteristically induces asthma attacks in some patients.

    12:58 So they’ll start to do some exercise or develop a cough, chest tightness, unable to breath and have to stop their exercise. Exposure to dust, cigarette smoke, cold air also stimulates asthma symptoms. Certain drugs, beta blockers, and also nonsteroidals such as aspirin can precipitate asthma attacks. Asthma frequently, and in fact usually, may worsen people who have a viral upper respiratory tract infection. So a very classic history is that when my wife gets a cold, it lasts--she coughs for a few days but I cough for weeks.

    13:33 What’s actually happening there is if the patient has asthma, they get the cold from their wife, they cough for a few days, but then the asthma takes over and the cough that persists for weeks is not due to the viral infection. It’s because the viral infection has kicked off the asthma inflammation and made the asthma worse.

    13:51 And people can be very allergic to very specific allergens, and they often know this. So for example, they know that when they go to a friend’s house with a cat, their asthma will get worse, or there is a thunderstorm that releases quite a lot of moulds spores into the atmosphere, and that can precipitate asthma attacks, and patients get worse during the pollen season as well because of the allergy to pollen. And then certain patients will have occupational asthma. That is asthma set off by antigens that they inhale when they’re at work. And this commonly happens in people who work as cleaners, bakers, with animals, or paint sprayers, et cetera. And the last, a very, very important component to making asthma worse is psycho-social stress. When patients are stressed, they tend to have worse asthma. And this is a major driver for many patients conditions. So, we can characterize asthma into various different subtypes as well. Chronic asthma, this is when you’ve developed an element of irreversible disease leading to chronic dyspnoea or a chronically low FEV1, and reflects poorly controlled disease over many years.

    15:00 An exacerbation, that’s an acute deterioration stimulated often by the triggers we’ve just discussed. A severe asthma is an attack of asthma that’s bad enough to require admission to hospitals. So as in exacerbation, they require somebody to come into the hospital.

    15:16 Status asthmaticus is one level above that where you have an exacerbation which is severe enough to be life-threatening and requires very close attention to treatment to ensure that the patient gets better. And there is not an instant response. It’s not with a less severe exacerbation. One dose of nebulizer is probably normal enough to restore them to reasonable health. In the status asthmaticus, it requires much more intense treatment there. Doctors often use the phrase bronchospasm, and all they mean by that is an episode of increased bronchial obstruction or an increased episode of airways obstruction, and that essentially is an exacerbation. Other subtypes of asthma include brittle asthma.

    16:02 These are patients who actually are relatively well most of the time but then can have sudden exacerbations which can be very rapidly developing. I have a patient who went down into the kitchen one day feeling perfectly well, and next time she woke up, she was in hospital intensive care. And what had happened is that somewhere in the kitchen, something had set off her asthma attack. And fortunately, the postman found her when he came to deliver a parcel that day. Otherwise she would have been dead. That’s brittle asthma, very rapid attacks, rapid falls in peak flow, very severe, and because of that, very dangerous disease. Difficult asthma is a range of problems. It’s when the asthma is poorly controlled and causing major symptoms for the patient or frequent admissions to hospital. It’s defined as difficult asthma when it’s poorly controlled despite extensive treatment and there are a variety of reasons why that might be not responding to the treatment.

    16:56 Steroid-resistant asthma is a subtype of difficult asthma which is very specific. It’s where steroids which normally work very well in asthma are not working. The type of information that patient’s asthma is due to does not respond to corticosteroid therapy for whatever reason. Cough-variant asthma is essentially very mild asthma where the only symptom the patient has is cough, and this one is quite hard to diagnose because there’s no wheeze and breathlessness and patients don’t think that the cough could be due to asthma and nor to their doctors either. Occupational asthma, we’ve already discussed, that’s asthma that’s settled by inhaled allergens that you come across during your occupation. It’s very important to identify because clearly, the patients would need to change their job circumstances, either change their job or make sure they have protective equipment when they’re doing their job to try and minimize the disease problems.

    17:50 So, how do you make a diagnosis of asthma? Essentially, we need to prove the reversible airways obstruction. Now as I mentioned, clinically, that may be obvious in some patients, and therefore, the requirements to prove that it’s present is not so important. But it can be proved in other ways. One is by response to treatment. If somebody comes to you with episodes of cough and breathlessness and wheeze and these sounds very much like they have asthma, perhaps, this diurnal variation is worse in the morning, the cough wakes them at night. Every time they get a cold, it’s made worse.

    18:24 Those sorts of patients, you probably don’t actually need to do too much besides give them the right treatment. And if they get better, then that’s asthma. If you really want to prove it’s asthma, peak flow recordings are a good way of doing that. Now, these record the airflow during expiration, and they show diurnal variation in asthmatics. So for example, in this chart you see on the right-hand side of the slide, there's a big fall in the peak flow in the morning. Now, when you start to inhale steroid, what happens is that the peak flow will gradually improve as the asthma comes under control, but not only that is at the difference between the morning and evening, the diurnal variation becomes smaller.

    19:06 So the home peak flow recordings, with and without treatment, are a very good way of identifying patients who have asthma for sure. And you can also use spirometry, the FEV1, and I showed that in a spirograph earlier with FEV1 which improves substantially after bronchodilator showing significant reversible disease, and therefore if the patient has asthma.

    19:26 Other tests, well, blood tests may show degree of blood circulation eosinophilia. And then the patient often has a raised total IgE and can be allergic to aspergillus, especially if they have allergic bronchopulmonary aspergillosis which is a complication of asthma, which are discussed in a subsequent lecture. The chest X-ray is necessary to make sure you’re not missing any other diseases, but essentially, is normal in most patients of asthma unless they have an acute attack of chronic severe disease. In which case, that will show hyperexpanded lungs. But as I said, a chest X-ray is vital during exacerbations at least to just make sure there’s no other complication such as a lobar collapse or an infection.

    20:08 We often do skin prick tests in patients with asthma, and that’s to identify specific allergic triggers for allergic asthma, house dust mites, cat fur, etc. In many ways, it’s not very practical because if a patient knows that a cat will upset his or her asthma, then they avoid cats. It’s only particularly relevant I suppose for patients where you might be considering allergic bronchopulmonary aspergillosis as a diagnosis in which case, the skin prick test will be positive to aspergillosis. Occasionally, you might come across a patient where it’s quite hard to identify they have asthma. And then we might do things like a histamine or methacholine challenge tests where the patient inhales histamine or methacholine and that causes bronchoconstriction in patients who have asthma. But it doesn’t in patients who don’t have asthma. So that’s inducible airways obstruction. It’s quite a tricky test. It needs to be done in the hospital in a fully equipped pulmonary function laboratory But it can be used to identify difficult cases of asthma to diagnose. And the sputum itself may show the evidence of airways information with the presence of eosinophilia when you send the sputum off for cytology. How do you treat asthma? Essentially, it’s via inhalers, which inhaler the patient use depends on which they get on with.

    21:31 There’s a huge variety of different types of inhalers and they all have their little pros and cons, and it depends really which the patient prefers. It’s important that the patient is compliant with treatment and is effective at using the inhaler. So one of the major things that a respiratory physician and the respiratory nurses need to be sure about and need to teach the patient about is the inhaler technique to ensure that they’re taking an adequate amount of drug and it’s reaching the lungs. With asthma, we use a stepwise treatment.

    22:03 With increasing levels of severity, we use increasingly more treatment. Mostly, that’s inhaled. But more severe chronic disease may need oral medication as well. When somebody comes to hospital with an exacerbation, the mainstay of treatment there are nebulized bronchodilators. And we’ll discuss that a little bit more detail later in the talk.

    22:27 So, what’s the aim of treatment? Well, the aim of treatment really is for the patient not to realize they have asthma anymore, to get rid of their symptom so they don’t have asthma symptoms when they’re running for a bus. They don’t wake up in the middle of the night coughing, and they can do whatever exercise they want to do without feeling that the asthma might kick off. In addition, we want to prevent acute exacerbations. We want to prevent patients having an exacerbation that means they come into hospital because that’s both life threatening, inconvenient and unpleasant for the patient and also expensive for the healthcare services. In theory, we want to minimize the need for using bronchodilator rescue treatment so that we use regular inhaler to prevent the asthma causing problems that then the patient will use ventolin salbutamol bronchodilator inhaler to improve the symptoms for. Because essentially, bronchodilators don’t treat the cause of asthma, they treat the symptoms. So, this is a description of the U.K. guidelines.

    23:34 And really, what happens here is you have a stepwise treatment, step one, step two, step three, step four, step five. And you go up these steps depending on whether the asthma is controlled by the first step, especially if the lung function shows that there’s ongoing evidence of airways obstruction with variable peak flow or an FEV1 lower than predicted or the best that the patient has ever achieved. S, for very mild disease, this is asthma which only occurs very occasionally and can be relieved easily by salbutamol inhaler, and that’s not being used very frequently. I mean, less than once a week, for example. Then you probably can just give them a short-acting bronchodilator, and that will be adequate for treatment.

    24:18 However, the majority of patients require the mainstay therapy for asthma which is inhaled corticosteroids.

    24:25 Asthma inflammation is very easily treatable in the majority of patients with corticosteroids.

    24:35 An inhaled corticosteroid means that corticosteroid is delivered directly to the lung in high enough doses to settle the lung inflammation, but in low enough doses that does not get absorbed and there are no systemic complications or it’s unlikely the patient will develop systemic complications of steroid inhaler therapy unless they take very high doses.

    24:57 An inhaled steroid will reverse the information associated with asthma and minimize the symptoms the patient has. So the step two is to start an inhaled steroid. Now, it may be that an inhaled steroid in itself is not adequate enough to control the patient’s symptoms.

    25:18 The next step, actually, will be to increase the amount of inhaled steroid the patient is taking. So you start over relatively with some low dose. And then if the patient is still not well controlled, you increase to a moderate dose.

    25:30 In addition, we do know that adding in a long-acting beta-agonist bronchodilator, such as salmeterol or formoterol is synergistic with inhaled steroids in improving control of asthma.

    25:43 So if somebody is still getting symptoms despite a medium dose with inhaled steroid, then the addition or long-acting beta-agonist is a good move and would likely make a substantial difference to their symptoms. It’s particularly useful for patients who are waking at night with cough because the long-acting beta agonist will cover the period when they’re asleep and make them less likely to wake up at night with the cough.

    26:06 Other medications that could be considered at this stage are oral theophyllines and leukotriene inhibitors. An oral theophylline is a tablet, is a bronchodilator that acts for a different mechanism to the beta-agonist and is a useful additional bronchodilator that can be used in some patients. A leukotriene inhibitor, leukotrienes are one of the main mediators of asthma, and the inhibitors can prevent information due to asthma. And in some patients, a leukotriene inhibitor has a very beneficial effect but not all.

    26:37 Now, an important point about this medication is that if the patient is well controlled on a high dose of inhaled steroid, they’ve had poor control with lots of cough, lots of breathlessness and wheeze and maybe an occasional admission to hospital, and they’re needing quite a high dose inhaled steroid to control that. Once it’s been brought under control. In fact, many patients can get away with a lower dose inhaled steroid.

    27:03 So the patient’s treatment may give up and down the stepwise model depending on the severity of the disease. Once it’s being controlled, they drop down a step or two. And then if the symptoms returned, they may need to go back up to the higher step treatment.

    27:19 Step four is when you’re actually giving patients triple therapy, essentially they have an inhaled steroid, they have a long-acting beta agonist, they may have an oral theophylline, or we may add instead a long-acting muscarinic antagonist such as tiotropium or to a leukotriene inhibitor. And then step five is really very limited number of patients reach this step.

    27:39 These has patients who have got poorly controlled disease and they may need oral corticosteroids.

    27:44 Now, we use those very frequently for exacerbations but only for five days, seven days at a time.

    27:51 For patients with long-term asthma that’s poor controlled, however, we sometimes need to use a low dose of oral corticosteroids, prednisolone 5-10 milligrams, for example, to control their disease. But they are very much the very severe under the spectrum and there should be a very limited number of people who recall oral corticosteroids because the side effects are very complicated and not good.

    28:17 So additional treatment considerations. Right, If the patient loses weight, if they stop smoking, if they avoid the allergens, then that’s all going to make the control of the asthma much better. If they’re working in a job where they are exposed in occupational trigger, clearly, it needs to be addressed as well. There are certain breathing exercises and psychological input can be beneficial as well. Of these, probably the most likely and most important here is to stop smoking. There’s something very specific about cigarette smoking that makes the ability of inhaled steroids to control asthma much worse.

    28:54 So if you smoke and have asthma, then inhaled steroids essentially are much less effective than they should be. So not only is it the smoking stimulating the airways information and kicking off the asthma, it also prevents the mainstay of therapy inhaled corticosteroids from actually controlling the disease. So smoking and asthma is a very big problem, and patients who have asthma must be strongly encouraged to stop smoking.

    29:23 So if somebody has poor control despite going through the stepwise treatment and increasing the treatment and they’re still not doing well, then there are various considerations you can think about. The first and the most obvious is, are they actually taking the inhaler? Do they fully understand that the inhaler has to be taken regularly? Because many patients will actually take the inhaler regularly. When the asthma gets a bit better, they will stop the inhaler corticosteroid, and guess what, the asthma comes back.

    29:49 Inhaled corticosteroids take about 10 to 14 days to actually improve asthma control.

    29:56 It’s actually difficult then for the patient to associate stopping inhaler with reduced control of the asthma in some ways because what will happen is that they will stop the corticosteroid and it would be a week or two before the asthma starts kicking off again. So education to make sure they’re compliant is very important. The other thing that needs to be checked is inhaler technique because it’s quite possible that the inhaler is being used in a way which means that most of the drug is not being delivered to the lung. And in that situation, it’s very easy to resolve a situation with a better inhaler technique, a different inhaler which the patient is more able to use or whatever to make sure they’re actually getting drug delivery. The third thing to think about are continuing triggers. Now, we’ve already discussed smoking. That is the most important continuing trigger.

    30:42 But psychosocial stress is often a problem and is very difficult to deal with because that’s outside the remit of the doctor. The patient may have a pet, that are setting things off, and there may be occupational asthma that’s been previously unrecognized.

    30:55 And the last thing to consider is that some patients who develop a complication of asthma called allergic bronchopulmonary aspergillosis which in itself leads to poor control of the disease, and it’s worth screening in the patients for that using the blood tests which are relevant for that and I discussed this disease in one of the later talks of this series.

    31:14 The other treatment considerations are for patients with very severe disease where they require oral prednisolone. There are some additional treatments that you may come across.

    31:23 One is an antibody treatment to deplete IgE because the IgE is the antibody that drives the allergic response, and therefore, drives the asthmatic information in some patients.

    31:35 And then there’s a a procedure called bronchial thermoplasty where the smooth muscle discoursing bronchoconstriction is damaged by applying heat within the bronchial tree. It's a slightly unusual sounding treatment. But there are reasonable data showing that it can be affected in very selected patients. Acute exacerbations of asthma. This is a common cause of medical admissions or presentation to the action to merge and then being discharged back home again and most doctors need to know how to deal with this. The patient usually knows they have asthma. The attack itself often comes on over minutes or a few hours. But it’s usually preceded by a few days where the patient has a deteriorating control of their asthma with increased breathlessness, increased cough, increased nocturnal symptoms, and increased use of their beta2 agonist rescued medication.

    32:34 So this is important because that preceding few days with correct education of the patient and a treatment plan allows you to pre-empt the potential exacerbation in many patients.

    32:46 And if that deterioration and control is treated effectively by an increased use of the inhalers, increased corticosteroids, perhaps a quart of oral prednisolone, then many exacerbations could be prevented. And the patient may not need to end up in hospital.

    33:02 There’s often actual trigger for this. The patient had a cold or flu recently. They’ve gone through particular form of stress. And occasionally, acute attacks might occur because of smoke exposure. In the old days when people used to smoking pubs, occasionally, asthma attacks would occur because an asthmatic has gone into particularly smoky pub, for example.

    33:21 And we have these situations occur occasionally during summer when there’s been a thunderstorm and the release of fungal spores actually precipitates a large number of acute exacerbations of asthma over the next few hours. The patient presents with basically exaggerated version of the normal symptoms of asthma which is breathlessness, wheeze, and cough, with breathlessness being dominant and the main reason why they’re coming to a hospital.

    33:46 And when you listen to their chest, there will be a polyphonic expiratory wheeze throughout both lungs. And importantly, their peak flow, the measure of the airways obstruction, when you repeat it in casualty, will be lower than it should be normally.

    33:59 So, it’s very important for the patient to be able to tell you what their normal peak flow is when they are well so you can compare during an exacerbation to give you a feel for how severe the exacerbation is. In normal exacerbation, they will be more breathless.

    34:16 They’ll be wheezy, and there will be a fall in peak flow. A more severe exacerbation, then the patient starts to becoming so breathless that they can’t talk in complete sentences.

    34:26 The pulse rate will be very high above 110. The respiratory rate will be greater than 25. If you measure their blood pressure, there will be a fall in systolic blood pressure and inspiration that’s called pulsus paradoxcus. And the peak flow, when you measure it, it would be less than 50% predicted or their previous best result.

    34:46 These are indicators of severe disease which is going to require quite an intense treatment.

    34:52 Now, the signs of very severe disease, in fact, when the pulse rate starts to go down or the breathing rate starts to go down, then you should really worry because the patient is close to respiratory arrest. The same with the blood pressure that starts to fall that is clearly showing severe physiological upset. And if the patient’s conscious level is fluctuating and drowsy, then again, that’s a very bad sign indeed that the patient has a very severe disease. When you listen to chest in severe asthma, you may not hear the wheeze. There’s so little air moving on inspiration that the breath sounds will be very quiet. And the peak flow unrecordable will considerably be low than normal. They are less than 30% predicted. And when the patient develops central cyanosis due to hypoxia or a CO2 that starts to increase, then you know the patient has bad disease. Normally, carbon dioxide level, actually falls in mildest attacks of acute asthma because the hyperventilation leads to a degree of respiratory alkalosis.

    36:01 As the attack becomes more severe, the carbon dioxide actually becomes normal. So a normal PaCO2 in somebody presenting an asthma attack is actually a bad sign. It suggests they have a very severe level of asthma attack. And then when it starts to rise, then that really does show that they’ve got severe hyperventilation going on and they are in danger of a respiratory arrest. The treatment for asthma exacerbations is relatively straightforward; high flow oxygen, nebulized bronchodilators, salbutamol and ipratropium, an immediate stat dose of intravenous high-dose corticosteroids. And then if there’s no immediate response to a nebulised bronchodilators with rapid improvements in peak flow in the patient’s condition, then you may want to consider intravenous bronchodilators. The commonest being used nowadays is magnesium and/or aminophylline, a theophylline based bronchodilator.

    36:57 Once you’re doing this, you need to organize a chest X-ray, and the chest X-ray is important not because it’s going to be abnormal in somebody with asthma but to make sure that when you’re examining the patient, you haven’t missed something like a pneumothorax or a lober collapse which will contribute towards why the patient is feeling so bad. And clearly, a pneumothorax can be corrected very rapidly by insertion of a chest drain. It’s a very important thing not to miss. You’ll also measure the peak flow and get the blood gases. So you have the levels available to monitor their improvements, or you have the levels available to identify the severity of the diseases that we discussed a slide or two ago. And also, so that you can monitor if the patient is improving with the medication that you’re giving.

    37:42 And you monitor using oxygen saturations, the pulse rate, the respiratory rate, and repeating the peak flow. And if the patient is not responding and it’s doing badly with very low peak flows, low conscious level, despite all that medication, then there should be no delay in intubation and mechanical ventilation of the patient to take over the work of breathing for them, because otherwise, there is a risk of cardiac respiratory arrest, and then there’s a very high chance the patient would die. And there are over a thousand deaths each year in the U.K. due to asthma, and a lot of those have been shown to be avoidable if more effective treatment was initiated, or more importantly, the exacerbation was pre-empted by effective treatment a few days before they present to the hospital. So asthma can get complicated by a variety of problems. You can get a sputum plug blocking of bronchus causing lobar collapse. You can get pneumothorax and pneumomediastinum. The drugs and cells also can cause complications. So excessive use of salbutamol will cause a tachycardia, and in fact, many patients taking beta2 agonist do complain of palpitations which reflects in that tachycardia. In fact, nebulized beta2 agonist such as salbutamol used in the hospital can drive down the potassium as well and you can get a recordable blood hypokalemia. Clearly, somebody with bad asthma can end up in respiratory failure requiring an intubation and ventilation and there is a very high risk situation which can lead to further complications. Patients with asthma for reasons which are not clear are more at risk with pneumonia and pneumococcal infection. The main problem long-term with asthma are the complications of the inhaled therapy. So the corticosteroids, even when they’re inhaled, do have significant side effects, and the main ones are oral candidiasis with sore mouth and Candida albicans visibly present in the oral pharynx. And dysphonia, and dysphonia is where the patient develops a horse or quiet voice, and in fact, they can lose their voice completely.

    39:47 And the reason for that is that the corticosteroids, as they go down into the lungs, leads to a little bit of laryngeal muscle weakness. Both of those problems are related to the dose of inhaled corticosteroids and may limit how much you can use to control the patient’s asthma. High-dose in inhaled corticosteroids also do give you a degree of risk for osteoporosis and cataracts as well. Beta2 agonist where the long-acting or short-acting as I’ve mentioned already cause hypokalaemia and tachycardia. And the muscarinic antagonists, the Atrovent and the tiotropium could have side effects of dry mouth and can sometimes precipitate glaucoma. And all inhalers seem to, in some patients, cause a paradoxical cough and bronchospasm and not that prevent the patient tolerating from using them.

    40:41 The chronic complications of asthma, well, allergic bronchopulmonary aspergillosis I’ve mentioned already. I’ve also mentioned that in patients with chronically poorly controlled disease, you may end up with irreversible airways obstruction, and that can in some very small minority patients lead to respiratory failure on a chronic basis. And then there are the complications of the therapy. Now, if you have severe enough asthma that require low-dose oral corticosteroid, step five of the treatment regimen, then the oral corticosteroids do almost invariably cause a variety of very unpleasant side effects for the patient.

    41:20 The cushingoid appearance with a fat face to the central petal deposition of fat, the thin skin, the easy bruising, and osteoporosis, osteopenia, some patients may develop diabetes, and anybody on oral corticosteroids will have an increased risk of infections where the soft tissue infections, lung infections, etc.

    41:41 So in the last part of this talk, I’m just going to talk about post-infective bronchial hyperactivity. Now, this is a syndrome of cough that occurs after somebody has had a viral infection. Now, that’s also what happens in asthma. Patients with asthma, they get a viral infection, the cough gets worse. The difference here is that these patients don’t know they have asthma. They get a respiratory tract infection and then they cough a several weeks afterwards. And this is either temporary period of asthma like inflammation that will go away eventually, or potentially, the first episode of asthma. Only time will tell.

    42:15 The nature of the cough is very similar to the asthmatic cough. It tends to be a diurnal variation that’s worse at night, is set off by cold air, smoke, and dust, and it’s relieved by beta2 agonist. And these patients with post-infective bronchi hyperactivity do very well if they’re treated with inhaled corticosteroids. That settles down that inflammation that has occurred as a consequence of the viral infection and the patient symptoms will resolve. And then they can stop the inhaled corticosteroid at a later stage. If the cough returns, then perhaps it was the first episode of asthma. If the cough doesn’t return, then there’s just one episode of post-infective bronchial hyperactivity.

    42:53 So, just to summarize the main learning points for this lecture on asthma, asthma causes intermittent reversible airways obstruction, and that causes the symptoms. Now, the clinical presentation can be very variable from mild problems of just cough alone to severe problems of cough and life threatening acute exacerbations of bronchoconstriction with breathlessness, sputum retention, etc. The diagnosis of asthma is usually relatively easy to make from the history. And the demonstration of reversible falls in the peak flow of the FEV1. The treatment is essentially dependent on inhaled corticosteroids. And these should be very effective. Poor control does result in these potentially life-threatening exacerbations that require hospital treatment. So poor control is not only a problem because it disturbs the patient’s lifestyle, but also, it makes them at risk of exacerbations that could actually end their life or at least meaning, that they have to be in the hospital for a period of time.

    44:04 So, poor control needs to be addressed. Acute deteriorations of asthma require regular nebulized bronchodilators and systemic corticosteroids if they’re severe enough to come into a hospital.

    44:16 And it’s very severe there are many intravenous bronchodilators, and potentially, intubation and ventilation. Thank you for listening today.

    About the Lecture

    The lecture Asthma by Jeremy Brown, PhD is from the course Airway Diseases. It contains the following chapters:

    • Lower airways obstruction
    • Asthma - clinical history
    • Asthma - subtypes of disease and diagnosis
    • Asthma - treatment
    • Asthma - acute exacerbations
    • Asthma - complications

    Included Quiz Questions

    1. Reduced FEV1 and FVC with a ratio of FEV1 / FVC of less than 70%
    2. Reduced FEV1 and FVC with a ratio of FEV1 / FVC of greater than 80%
    3. Reduced FEV1 with an increased FVC
    4. An increased FEV1 with a reduced FVC
    1. Haemoptysis
    2. Symptoms that get worse after an viral upper respiratory tract infection
    3. No history of childhood asthma
    4. Waking in the middle of the night due to cough
    1. A peak flow recording that increases from 200 to 350 after a salbutamol nebuliser
    2. Peripheral blood eosinophilia
    3. A chest X ray showing no obvious radiological abnormalities
    4. Oxygen saturations of 89% on air
    1. A reduced PaCO2
    2. Bradycardia
    3. Reduced conscious level
    4. Inaudible breath sounds on auscultation of the chest

    Author of lecture Asthma

     Jeremy Brown, PhD

    Jeremy Brown, PhD

    Customer reviews

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    Good talk but room for improvement
    By Hamed S. on 28. February 2017 for Asthma

    Enjoyable and informative talk. However, I think it would have been beneficial to discuss the classification and asthma in more details and features that fall into each category from intermittent, mild persistent, moderate persistent etc.. Also in the acute exacerbation section talk about risk factors and criteria for hospital admission could have been discussed.

    This is very well-explained! …
    By Peter R. on 30. April 2016 for Asthma

    This is very well-explained!