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Respiratory Disorders

by Jeremy Brown, PhD
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    00:01 So the subject of this lecture are respiratory physiology disorders. What we're going to talk about in this lecture is type I and type II respiratory failure, the differences between them and how they should be treated. A little bit about respiratory acid-based disorders, and then we are going to move on to talk about a specific cause of type I respiratory failure, the adult respiratory distressed syndrome,ARDS and also type II, causes of type II respiratory failure which affect lung ventilation but actually the lungs are normal and that's mainly obstructive sleep apnea with some discussion of obesity hypoventilation and chest wall and muscle disease. An important point is that ventilatory diseases, which cause chronic respiratory failure, are usually worse at night with worse physiological parameters overnight and first thing in the morning. Right, so type I respiratory failure, this is respiratory failure with hypoxia alone, normal PaCO2, but a PaO2, which is, less than 8 no matter what the inspired oxygen concentration is. Now this is often an acute one-off event but it can also be a complication of chronic lung diseases, largely COPD.

    01:15 What's the treatment? Well it depends on the cause, somebody comes in with pneumonia and hypoxia as a consequence of type I respiratory failure, you clearly treat that pneumonia, somebody comes has COPD, you treat the COPD. But the discussion that we are going to have today is really about oxygen, and how we use oxygen in patients with type I respiratory failure. And, essentially, the problem is how to correct the hypoxia, and we can use as much oxygen as much as it is necessary in these circumstances, and we give the oxygen normally in a controlled fashion, so we know what percentage inhaled oxygen the patient is receiving, so we use venturi masks to do that and they have different percentages, and some examples are given here 28% 35% 40%, and clearly we use the higher percent oxygen concentrations for patients with more hypoxia. If patients are very hypoxic, we may use a rebreathing bag, which allows an oxygen concentration of about 60% to be inhaled by the patient just using a mask. And what we're trying to do is we're trying to aim for saturations above 94%, correct the hypoxia completely but not only that we would like to make the patient able to breathe at a comfortable respiratory rate. Because if they're maintaining a saturation of 95%, but they're breathing at 40 per minute, that is not a good situation, that means they're struggling very hard, they will tire, and it's quite likely that they will fail to maintain their oxygenation if they have to keep persisting with a respiratory rate of 40 per minute.

    02:50 So what we do if the patient is remaining hypoxic or has a very high respiratory rate despite breathing oxygen from a mask or a rebreathing bag? Well there is a non-invasive form of ventilatory support the called the continuous positive airway pressure, CPAC.

    03:07 Now, this is a facemask that provides a small amount of additional pressure on the inhaled air, oxygen mix, 5 to 15 cm of water, and it maintains that through the whole respiration, both inspiration and expiration, and what this does is actually recruits more alveolar units that the patient can use during their respiration. It splints open and recruits more alveolar units during inspiration and that allows the inhaled oxygen concentration to maintain a better arterial oxygen level. And this is a good treatment for isolated type I respiratory failure. Somebody presenting with say for example, community acquired pneumonia or pulmonary oedema where they have type I respiratory failure, but no other major organ damage. If this is not adequate, if this starts to work, or starts to fail to work, or the patient becomes tired despite CPAP therapy, then the next step will be intubation and artificial ventilation in the intensive care department.

    04:17 So what are the common causes of type I respiratory failure? Well acutely, pneumonia, pulmonary aspiration, pulmonary oedema, exacerbations of COPD in some patients with COPD, moderately severe asthma, a large pulmonary embolus and ARDS which I'll discuss in the later slides.

    04:35 Chronically, patients can have type I respiratory failure due to interstitial lung disease, if it's severe enough, if they have had chronic pulmonary emboli leading to significant pulmonary artery damage, then they'll have type I respiratory failure, as will patients with severe pulmonary hypertension. And probably the commonest cause is COPD, but that's only in some patients.

    04:58 And the phenotype that tends to get type I respiratory failure are those of the emphysematous pink puffer type phenotype. So ARDS, now this is a disorder of an over activation of the inflammatory response and this occurs for multiple different reasons.

    05:15 It was first recognized in Vietnam, where American soldiers with gunshot wounds were developing bilateral infiltrations in their lung and hypoxia. And that was the first time that ARDS was identified, and that's trauma as a cause. But it doesn't have to be a traumatic cause, it could be in any sort of inflammatory problem where it's in the lung or distal to the lung, will cause a systemic inflammatory response. And that affects the lungs directly by through the body's own immune reaction. The cytokines they release, the activation of the neutrophils, the activation of the coagulation cascade leads to bystander damage to the respiratory endothelium and epithelium. And, as a consequence of that, you get leaked fluid into the alveoli, and that's called noncardiac pulmonary oedema, and that causes a rapid fall in the oxygenation level. You also can get proliferation of the epithelial and fibroblast cells, and that, as a complication of ARDS can result in lung fibrosis.

    06:25 So what are the causes of ARDS? As we mentioned there are multiple causes, we can divide those into lung causes, pulmonary, direct lung injury leading to ARDS causing more widespread lung injury, or extra-prolonged causes, something happening elsewhere in the body that leads to lung injury, which was otherwise not affected. So the pulmonary cause is mainly pneumonia aspiration but also occurs in environmental problems, if you had a near drowning or smoke inhalation. The extra pulmonary causes, where we mentioned severe trauma, gunshot wounds, road traffic accidents, but also extensive surgery is probably one of the commonest causes of ARDS and any sort of extensive surgery done in hospital could potentially lead to ARDS as a complication. Sepsis outside of the lungs, so septicemia due to a previous surgery or whatever could also lead to ARDS. Acute pancreatitis, drug overdose are also common causes of ARDS. The clinical presentation is basically a rapidly developing, breathlessness and hypoxemia. And the patient remains hypoxic despite receiving high flow oxygen and if you do the X ray, it will show bilateral airspace shadowing as you can see on this chest X ray. Both lungs are affected and it's quite hard to find any part of the lung, which is normal. Importantly, this is oedema of the lungs without cardiac cause. So the wedge pressure, the pressure of the pulmonary vessels is normal and there is no evidence of left ventricular failure. So how do we treat ARDS? Well, it's a severe disease and essentially the treatment is intubation and ventilation until the lungs can recover from the inflammatory insult that's occurring and this may be in a few days, but actually often can take weeks. There is, as yet no effective drug therapy for ARDS, although multiple different agents have been tried. And unfortunately, it's often goes hand-in-hand with other severe systemic upset problems such as septic shock and multiorgan failure is common with hypotension, renal failure etc. The overall mortality, perhaps 50% is a bit high, is probably lower than that now with the more effective ventilation mechanisms that we have and it can be complicated, as I've mentioned already by lung fibrosis during the recovery period. So, moving on now we're going to discuss a little bit about acid-base disorders and I'm coming to this really because of respiratory acidosis and type II respiratory failure. One of the major reasons why we do blood gases is not just to measure the PO2 and the PaCO2 but is actually to assess the acid-base balance of the patient. And if you have lung problems, there are two issues, you may have respiratory acidosis and that is a situation that occurs because when you underventilate the lung and you're not able to get rid of the carbon dioxide present in your blood, and that will lead to a low pH, a high PaCO2., and as it becomes compensated, as the body adjusts to the fact that it is unable to get rid of the carbon dioxide, then you will end up with the buffers that compensate the acidosis, increasing and we can see that in the blood gases by a high bicarbonate level and by positive base excess. The other respiratory problem that you get with acid-base balance is respiratory alkalosis, that is a problem of hyperventilation, you breathing fast, and that blows off your carbon dioxide and causes a respiratory alkalosis.

    10:00 It is not a major problem, but it is one of the reasons why you will feel fainting if you breathe fast. And in fact, actually we often create a little bit of respiratory alkalosis in our patients when we're examining them because we ask them to take deep breaths when we're listening to their lungs. If they begin to feel dizzy, that's reflecting a little bit of respiratory alkalosis. I'm not going to discuss metabolic acidosis or metabolic alkalosis, I think the important one there is in fact the metabolic acidosis and we actually do see that in lung disease but that's a consequence of the severe lung disease causing hypoxia or if you have pneumonia, septic shock, and that leading to metabolic acidosis as the oxygen delivery to the muscles and peripheral tissues is impaired.

    10:46 So, type II respiratory failure. We've mentioned type I, that's hypoxia with normal carbon dioxide, type II is respiratory failure associated with raised carbon dioxide. So it's defined as a high carbon dioxide, greater than 6, and, as I've just mentioned in the previous slide the higher the CO2, the more likely you are to have acidosis. Now that can be compensated. So for example, you may get somebody with an acute asthma attack, who is normally has got a normal PCO2, comes in to a hospital with a severe asthma attack, the CO2 is rising because they've almost got status ashtmaticus and may need ventilation. So they have a CO2 of 6.57, they will be quite acidotic because it's an acute event and compensation has not had time to occur. Now, in contrast, patients with COPD who may have a degree of type II respiratory failure chronically, they come into hospital, they can have a CO2 of 10, 12 even higher than that, and that pH may still be considerably higher than the patient presenting with acute asthma and a CO2 of only 7 and that's because of compensation.

    12:01 And in that situation the COPD patients with a bicarbonate of 35, approaching 40 perhaps.

    12:10 The big problem with type II respiratory failure is that oxygen can be dangerous and we see this repeatedly in patients presenting with COPD with an acute exacerbation, who have been given a high flow oxygen on the way into hospital. And that high flow oxygen unfortunately leads to an increase in the respiratory acidosis. The mechanism of that is that if you have type II respiratory failure, your ventilatory drive is actually taken over by the low oxygen level in your blood, so having a low oxygen keeps the ventilator drive going when you have type II respiratory failure. And if you give the patient too much oxygen and it comes up too high, you lose that ventilatory drive. The hypoxic drive for breathing is lost, and as a consequence you actually create a situation with a hypoventilation, the underventilation of the lungs, becomes more of a problem. As a consequence of that, the PCO2 will, PaCO2 will rise, and the pH will fall, and the respiratory acidosis will worsen.

    13:18 So the underlying principle for the treatment of type II respiratory failure is to give them controlled oxygen supplementation, but aiming for a lower saturation than you would normally in somebody with type I respiratory failure. You need to aim for a saturation, which is about 92 to 94%, a sort of safe PO2 of around 8 kPa where the risk of hypoxia causing a cardiac respiratory arrest is much lower than it would be, but still the POa2 is not in the normal range. And you do that by giving the patient a controlled oxygen therapy by a venturi mask of 24 to 28%. You can give a similar level of oxygen concentration with nasal specula, prongs that go into the nose, although in fact, you cannot be precisely sure what percentage oxygen the patient is receiving with nasal specula compared to a venturi mask. Importantly if patients are receiving oxygen and they have type II respiratory failure, you need to monitor what's happening to the carbon dioxide level in the blood.

    14:20 And to do that you have to repeat the blood gases and that will tell you whether the oxygen therapy is causing a rise in the CO2 and a fall in the pH and therefore it needs to be titrated downwards to a lower concentration of oxygen. If you're giving somebody some oxygen for type II respiratory failure and it's worsening the type II respiratory failure, and they're developing a respiratory acidosis, then you might need to consider nasal ventilation, or noninvasive ventilation. Now this is given via nasal or full face mask; what it does, is that unlike CPAP which gives a constant pressure during inspiration and expiration, this is a bi-level form of noninvasive ventilation, where on inspiration, it pushes the air in at a higher pressure than it does when the patient breathes out. That allows a better ventilation of the lung, it counteracts the hypoventilation that the disease is causing and will allow the CO2 to be removed and correction of the respiratory acidosis. And it's known that if you use nasal ventilation or noninvasive ventilation in patients presenting with type II respiratory failure due to COPD for example, then that reduces the need for intubation and mechanical ventilation. But there are some issues with this. The patient has to be able to take the mask on the face and coordinate with the breathing and feel comfortable with it. They have to be cooperative if not too agitated. And also you need to decide whether the patient, if they cannot cope with the nasal ventilation, the noninvasive ventilation, whether they would be suitable for intubation and ventilation and I'll discuss that in a little bit more detail later. Type II respiratory failure then, what are the common causes, well, the acute and chronic causes are pretty much the same, it's largely airways disease, COPD and severe asthma. Sometimes with patient with severe bronchiectasis, although in fact the diseases that cause type I respiratory failure such as interstitial lung disease, when they are end-stage, the CO2 will start to rise as well. So the common presentation in hospital type II respiratory failure would be an exacerbation of COPD. However, there are a range of diseases, which don't affect the lungs directly, but affect the chest wall and the ventilation of the lungs. So for example, obstructive sleep apnea, which we will discuss later in this lecture. That causes obstruction of the upper airways and that leads to type II respiratory failure in some patients. If you give somebody sedative drugs then they are going to breathe at a lower level and that will cause type II respiratory failure.

    17:16 This is important because if you give people who have other reasons for type II respiratory failure such as COPD or chest wall disease or obstructive sleep apnea, if you give them opiates and sedatives, you are likely to make the type II respiratory failure worse and that is often something that can be altered in those patients to improve the respiratory failure that they are presenting with. Obesity hypoventilation is a very specific cause of type II respiratory failure, which we will discuss later in this lecture.

    17:43 And then if you have problems affecting the chest wall and the muscles and the nerves that control the chest movements during ventilation, and we're talking about Guillam-Barre syndrome, motor neuron disease, various nerve palsies or the kyphoscoliosis that you can get in some patients affecting the ability of the chest movement during ventilation. They will all lead to type II respiratory failure and need to be considered in some patients.

    18:09 So moving on to obstructive sleep apnea, this is one of the commonest respiratory diseases, it's up there with asthma and COPD, not quite as common as those conditions but it is very common. Now, what happens in this is that you have some degree of upper airways obstruction when asleep and the reason for that is that the fat that accumulates, as you get older in life is deposited, in men specifically, around the neck, and that compresses the pharynx and makes it narrowed during sleep. Especially this is important during sleep because as you sleep your muscles relax and that allows the effects of this obstruction to be more obvious and the narrowed pharynx occurs as you sleep. And that generates the noise, one cause of snoring, but in addition, it generates obstruction to get in the air from the atmosphere down into the lungs and that leads to cyclical desaturations in your blood levels of oxygen.

    19:13 It's a hypoventilation disorder that occurs repeatedly throughout the night. This leads to poor sleep quality not surprisingly, and as a consequence of that, patients tend to be very sleepy during the day and could fall asleep very easily during everyday tasks such as reading, watching television etc. driving a car in fact. And the physiological disturbance at night has bad consequences for the cardiovascular system, leading to hypertension precipitating ischemic heart disease and if it is very severe you might develop type II respiratory failure and pulmonary hypertension or cor pulmonale type situation.

    19:52 Now this can affect about 1% of men in the Western world, it's much commoner in men than it is in women and the reason for that is not entirely clear but it seems to be about fat distribution. Most patients will be over 40 years of age and they'll be obese, they'll have a significant BMI and with that, their neck circumference will be large, over 43 cm. As I mentioned earlier, sedative drugs may cause a type II respiratory failure and hypoventilation worse, so drinking alcohol before you go to bed would make patients of OSA have more severe symptoms. Occasionally they may have an existing pathology of the upper airways which might make them more likely to get obstruction, a deviated septum, and the position of the jaw micrognathia, a small jaw or a jaw that projects backwards or forwards would make you more likely to get OSA and acromegaly disease, a growth hormone production very rarely is a predisposing factor for OSA. So the thing about obstructive sleep apnea is that actually it remains undiagnosed in lots of people. Many people snore, many of those will be snoring actually will be having a degree of OSA as well. The patient actually might complaint about daytime sleepiness and feeling un-refreshed after a night's sleep.

    21:10 They might have to get up at night to pass water and they may have a poor concentration and memory due to this recurrent hypoxia occurring at night. The patient's spouse might say “I get scared because he stops breathing in the middle of the night, and then gives a big snort and starts breathing again”, that's a fairly common and that's an apneic episode where the problem with ventilation, actually the obstruction completely stops the breathing for a few seconds. There aren't really many signs in OSA, you can look at the back of the throat and there is a is a score that you can use to see whether the obstruction is quite likely to present, depending on what's visible at the back of the throat, but we don't need to know that in detail. What are the problems of OSA? Well, the serious consequences are car traffic accidents; a classic example would be, a heavy goods vehicle driver, 45-year-old man, drinks a bit before he goes to bed, might be weighing 20 stone, obstructive sleep apnea, chance of him having an accident is much higher than if he doesn't have OSA and that can have very serious consequences clearly. The OSA itself in severe cases can lead to pulmonary hypertension, cor pulmonale, and type II respiratory failure and there are these consequences on the cardiovascular system with hypertension, ischemic heart disease, dysrhythmias and there is a relationship between OSA and diabetes as well.

    22:40 The biggest differential diagnosis is just simple snoring, snoring without obstructive sleep apnea. You can investigate these patients to identify whether it's just snoring or OSA, and the way to do that is by the sleep study, and I'll discuss that in a little bit more detail in a while. Other tests we may want to do, chest X ray, spirometry, blood tests, and these are all to look for associated diseases, for example co-existing COPD is quite common, hyperthyroidism is a cause of OSA etc. There's something called the Epworth sleepiness score, which is a method of marking how sleepy somebody is during the day and therefore whether they potentially have OSA, or not. Personally, I don't think it's particularly helpful, but it does identify patients who have significant sleep disturbance and therefore may need to have a sleep study. Now the sleep study, the simplest one is where you just record the overnight oxygen saturations when the patient is asleep and if you have obstructive sleep apnea, they fall repeatedly throughout the night. There are more complex sleep studies that can be done that measure chest wall movement, a sleep state using EEG, muscle movement using EMG, carbon dioxide levels etc. etc., but they're not usually required for very standard cases of obstructive sleep apnea.

    24:03 This is a sleep study with moderately severe OSA and you can see the saw tooth pattern of recurrent hypo apneic episodes where the desaturation is occurring several times a minute, several times an hour out during the night. And you can define how severe OSA is by how may desaturations occurring throughout the night, with over 30 an hour meaning severe disease. How do we treat? Well very simply, if the patient can lose a lot of weight that will make a substantial difference, they need to stop drinking alcohol while having sedatives at night. You treat the hypothyroidism the acromegaly. If people have mild OSA, then there is a mandibular advancement device that pushes their mandible forward a little and that actually improves the obstruction at the back of the throat, and has substantial benefits in patients with milder disease.

    24:55 Chronic disease needs treatment with continuous positive airways suppression. This is a small amount of airways pressure given as the patient breathes in, and that splints open the back of the pharynx, and is a very effective treatment for severe and moderate OSA. Surgery is not really effective unless there is a very specific problem of the upper airways that can be corrected by the surgical intervention. A very important point is that because of this risk of road traffic accidents, driving should be forbidden with patients with severe disease unless they have been effectively treated.

    25:30 Right, moving on to another sleep related disorder, called obesity hyperventilation syndrome.

    25:36 This is an increasingly common problem. The pathogenesis of this disease is not terribly clear, essentially the obesity results in reduced chest wall movements and restrictive lung function, and this seems to have a knock on effect on the central control of ventilations, so that as a consequence of the problems of actually moving the lungs during respiration.

    26:01 The brain decides to hyperventilate, it doesn't seem entirely logical why this may happen, but this is exactly what happens. The brain signals for ventilation are turned down and the consequences of that is that you end up with hypoventilation, hypercapnia, type II respiratory failure, and this is a vicious circle. Because one of the problems of a high PaCO2, raised carbon dioxide levels is that CO2 in itself is a narcotic, and will, if it is high enough, turn down ventilation because of its central effects on the brain.

    26:36 And these patients present with acute or chronic type II respiratory failure, pulmonary hypertension and cor pulmonale, the sort of problems that we've discussed already.

    26:44 It's actually obesity hyperventilation syndrome is frequently misdiagnosed as either COPD or OSA, other potential causes of type II respiratory failure, the prevalence is not really known but is very much related to obesity, so it’s a very high body mass index and it seems to be more specifically a problem of women than necessarily men. Solicited drugs exaggerate the problem and similar to obstructive sleep apnea, it will present with daytime hypersomnolence, but more marked problems, the patient will be confused, cor pulmonale is common, and is probably, in fact the second commonest cause of admissions to hospitals with acute hypercapnia, the first commonest being COPD.

    27:27 Sleep studies are used to show the overnight hypoventilation that is occurring; you need the blood gases to identify their respiratory failure. The lung function tests show restrictive changes due to the obesity and in the chest X ray actually the lungs will look normal and you may want to echo and ECG to look for cor pulmonale.

    27:46 Treatment is very difficult, essentially weight loss, weight loss and weight loss, but that's obviously very hard to achieve, Bariatric surgery can be very helpful in those circumstances.

    27:56 And the patient may need some form of ventilatory support long-term, oxygen and often actually, they need noninvasive ventilation as a long-term treatment. The treatment for acute presentations, this is type II respiratory failures, so it's controlled oxygen, nasal ventilation, treatment of the cor pulmonale, getting rid of the distal oedema with diuretics etc.

    28:24 Just moving on, chest wall and muscle diseases, now we've discussed these briefly already, these are a mixed bag of diseases where you underventilate the lungs because the mechanical, the muscle or the nerve input to ventilation has been impaired, so acutely this might happen if somebody has had a road traffic accident, they get a flail chest that's where the ribs are broken on both sides and that means that you don't get movement of that portion of the chest during respiration and that hyperventilates. Guillam-Barre syndrome is an acute polyneuropathy, which can ascend to affect the nerves that control the respiration, and these patients need to have their FEV1 monitored, because if it falls then they're likely to develop respiratory failure. And again a high cervical cord lesion during a road traffic accident or something like that would cause diaphragmatic weakness. The chronic causes muscular dystrophies, motor neuron disease, severe kyphoscoliosis, and obesity as we've discussed already and again the high cervical cord lesion would persistently cause underventilation of the lungs. And these patients present similarly to the presentation of anybody with chronic type II respiratory failure, morning headaches due to the high CO2, general deterioration in their overall condition, feeling tired and sleepy. Their spirometry is very important because with these disorders you cannot develop type II respiratory failure unless you have significant restrictive lung function.

    30:01 The oxygen saturations may be a little low but the important test is blood gases because that will identify whether there is type II respiratory failure present or not.

    30:09 The treatment is long-term ventilation, if you give patients long-term noninvasive ventilation overnight, then if you have a nonprogressive cause, such as kyphoscoliosis, then their prognosis is very good. Unfortunately, with progressive causes, it is only a temporary treatment, so patients with motor neuron disease for example, they will usually die because of type II respiratory failure despite noninvasive ventilation as the disease progresses.

    30:35 Two various types of underventilation of the lung is obstructive sleep apnea and obesity hyperventilation syndrome. Obstructive sleep apnea is a very common condition, mainly affecting men in which the pharynx is recurrently obstructed at nights during sleep leading to recurrent dips in the arterial oxygen concentration. And this is diagnosed using a sleep study and treatment is essentially weight loss, and if necessary, you can use CPAP therapy overnight, which for the patients with more severe disease and that can be very effective. Obesity hypoventilation is related to central underventilation and that is caused by obesity, it tends to be in women rather than men, although it’s both sexes and that's an increasingly common cause of acute and chronic type II respiratory failure which can often be very difficult to treat because the underlying problem, obesity is not quick to be resolved. Thank you for listening


    About the Lecture

    The lecture Respiratory Disorders by Jeremy Brown, PhD is from the course Other Respiratory Disorders. It contains the following chapters:

    • Disorders of respiratory physiology
    • Adult respiratory distress disorders
    • Patterns of acid-base disorders
    • Type 2 respiratory failure - treatment
    • Obstructive sleep apnoea
    • Obesity hypoventilation syndrome
    • Chest wall and muscle disease

    Included Quiz Questions

    1. PaO2 7.5 PaCO2 5.3
    2. PaO2 7.5 PaCO2 6.3
    3. PaO2 8.5 PaCO2 5.3
    4. PaO2 8.5 PaCO2 6.3
    1. Raised pulmonary venous pressure
    2. Bilateral shadowing on the chest X ray
    3. Marked hypoxia
    4. An obvious potential preceding cause
    1. Pneumonia
    2. Respiratory muscle diosrders
    3. Overdose of opiate
    4. Obesity hypoventilation
    1. PaO2 7.5 PaCO2 8.4 pH 7.15 HCO3- 25 BE +1
    2. PaO2 12.5 PaCO2 3.4 pH 7.15 HCO3- 15 BE -5
    3. PaO2 7.5 PaCO2 8.4 pH 7.28 HCO3- 35 BE +7
    4. PaO2 12.5 PaCO2 3.3 pH 7.49 HCO3- 15 BE +1
    1. More common in men
    2. Associated with obesity
    3. Can cause type 2 respiratory failure
    4. Physiological disturbance is worse at night

    Author of lecture Respiratory Disorders

     Jeremy Brown, PhD

    Jeremy Brown, PhD


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    Hungry for more knowledge
    By Hamed S. on 02. March 2017 for Respiratory Disorders

    Well explained lecture. However, more time should have been extended on discussion of interpreting ABG, anion gap A-a gradient. Moreover, no mention of Central vs obstructive apnoea