The old DundeeChest site spawned the AskDundeeChest website, back in the day. The students found it useful, I think. So I’ll set up another one on here.
Post a comment if you have a question, and I can answer the query on the main blog.
As Ron Pickering used to say……. “Away You Go”
a heads up. A3 now has 15 people in it due to all the people resitting the year. I recon some shuffling will be required but for the time being its a huuuuge group of lovely people.
Thanks Euan. I’ll get the medical school office to look into this. We should even out the groups.
What is the relationship of intra-alveolar pressure and intrapleural pressure?
ie, During inspiration, intra-alveolar pressure falls and then rise until become equal to atmospheric pressure. However, why the intrapleural pressure keep dropping till expiration?
Does the transmural pressure gradient remains all the time?
Thanks
Jun
hi this may be a silly question and really simple but I was wandering why it is that asthma is worse at night? why is someone suffering from asthma more likely to be wheezy just before going to bed?
thanks
Thanks Jamie,
Asthmatics don’t get worse before going to bed, they get bed overnight, and early in the morning. This is felt to be most likely to be due to lower cortisol levels within the circulation throughout the night. Add into that the fact that V/Q mismatch is far worse when lying flat, and diaphragms don’t work so well lying flat, and: asthmatics get worse when lying in bed at night.
We think.
I’ll ask Dr Khogali to give you a comprehensive answer.
Actually its not related to posture becuase even when asthamitcs are upright at night -they get worse
although there is circadian cortisol with levels being at their nadir at around 7am -this is not related to nocturnal dips -if you give asthmatics with dips systemic steroid they dont always improve
There are other know factors here
1.Beta2 receptor number fall dramatically at night -which is why long acting beta stimulants help at night
2.Cholinergic tone increases at night (which is why in some cases long acting anti-muscarinics help)
3.Transbronchial biopsy studies have shown an increase in small airway inflamm cells associated with the nocturmal phenotype -but again since steroids do little to dips -thats not the sole cause.
4.Something else to always think of is acid reflux at night which is related to posture -this can be silent -so sometimes an empirical trial of PPI is indicated if all else fails.
I would say youre getting to bogged down in small print mate -this really isnt core or to be honest at all clincially relevant
Does COPD get worse at night due to the same reasons as stated above for asthma? I was talking to a patient with COPD earlier in the week, and he said he had to sleep in an upright position.
Thanks,
Caitlin.
This might be a silly question, but I was just wondering what triggers you to yawn?
Dr Khogali gave a lecture on the Control of Respiration in which he explained the neural and chemical control and I was wondering if yawning was caused by a similar mechanism?
Thanks,
Caitlin.
in copd it may well be psoture becuae of dynamic hyper-inflation of the chest the bucket handles [ie ribs] are already max expanded -so pts are very dependent on the daiphragm to increase thoraci vol -so if you are lying flat you cant use your diagrpham
Some copd pts have a sig asthmactic compoent to their condition -such pts may get nocte deterioration for the same reasons as pure asthmatics .
Re yawning -that very much depends on who is lecturing you -if you do yawn in my lecture make sure you put your hand in fornt of your mouth
Thank you.
possibly just an urban myth, but yawning to my undertsanding was caused by a fall in O2 levels and triggering a larger than normal inspiration ie. yawning to fill as much of the lungs as possible and counter this. Theres also the psychological side to it, watch someone yawn and you feel yourself wanting too, even saying yawn over and over can trigger it. not sure how this ties into tiredness though :/
Hi, can anyone explain to me ‘dynamic airway compression’ and ‘transairway pressure’ or why expiration is more difficult than inspiration in disease states like COPD or Asthma. It was mentioned towards the end of Khogali’s first lecture.
Cheers
Ritchie
Reply from Dr Khogali
“The intra-pleural pressure is always less than the intra-alveolar pressure; hence a transmural pressure gradient is always present throughout the respiratory cycle (see slide 18 in respiratory physiology lecture 1) and the lungs are stretched to some degree even during expiration.
The intra-alveolar pressure is less than atmospheric pressure during inspiration and is more than atmospheric pressure during expiration, but became equal to atmospheric pressure at the end of both inspiration and expiration as the alveoli are in direct communication with the atmosphere.
The pleural space, however, has no communication with either the atmosphere or the air in the lungs. During inspiration, the thoracic cavity expands (as a result of active contraction of inspiratory muscles) and this lowers the pressure in the pleural space (intrapleural pressure). The fall in the intrapleural pressure causes the lungs to expand passively. The expansion of the lungs, during inspiration, causes the air molecules within the alveoli to be contained within a larger volume hence the intra-alveolar pressure decreases (Boyle’s law). The air then enters the lungs from the atmosphere down its pressure gradient until the intra-alveolar pressure becomes equal to atmospheric pressure (see slide 16 in respiratory physiology lecture 1). The process is reversed during expiration, when the inspiratory muscles relax, and the intrapleural pressure and intra-alveolar pressure rise. The air then leaves the lungs down its pressure gradient until the intra-alveolar pressure becomes equal to atmospheric pressure (see slide 17 in respiratory physiology lecture 1).
I hope this helps.”
its harder to expire as the pressure pulling the airways open during inspiration is no longer present so the airways tend to be easier to collapse. to my knowledge
are there answers anywhere for the learning issues in the week 1 study guide?
Currently the answers are in our heads, and spread through the materials we delivered last week. We have provided some formative assessment for week one already on the blog and will do our best to get answers up for the learning issues, when we get a chance (and everyone is back from Barcelona……).
Hello,
Just looking over the second of Dr. Khogali’s lectures. It states: across the pulmonary capillaries, O2 moves down its pressure gradient from higher to lower partial pressures. Blood from the pulmonary arteries reaches the capillary bed at 40mmHg, becausse it is 60mmHg less than the alveolar PO2 (100mmHg), O2 diffuses from the alveoli into the blood unitl NO FURTHER GRADIENT EXISTS, in other words equilibrium has been reached. Sherwood’s then goes on to say that “as blood leaves the pulmonary capillaries, it has a PO2 equal to alveolar PO2 – at 100mmHg”. How can this be? Wouldn’t that mean that the alveolar pressure is no longer at 100mmHg and hence, not in equilirium? Equilibrium would be reached when both are at 70, is that correct?
Cheers,
Thomas
Reply from Dr Khogali
“Transairway pressure is determined by the pressure within the airway (this tends to open the airway) and the intrapleural pressure (this tends to compress the airway).
During inspiration the intrapleural pressure falls and the airways are pulled open by the expanding thorax.
Dynamic airway obstruction may become important during forced (active) expiration when the intrapleural pressure rises as this tends to compress the airways i.e. the airway resistance tends to increase during active expiration.
If there is no airway obstruction: the increased airway resistance, during active expiration, at a particular point along the airway would cause an increase in airway pressure behind that point (i.e. pressure upstream). The increase in airway pressure upstream then increases the gradient for airflow along the airway downstream. The result is that, in the absence of obstruction a rise in the pressure along the airway tends to oppose the rise in intrapleural pressure during active expiration.
If there is airway obstruction: the driving pressure gradient between the alveolus and airway is lost over the obstructed segment and the airway pressure falls downstream. Hence the airway tends to be compressed more by the unopposed rising intrapleural pressure during active expiration if there is an obstruction. Such dynamic airway compression tends to make expiration to be more difficult in patients with obstructive conditions such as asthma or COPD.
I hope this helps.”
increased intrathoracic pressure secondary to airway obstruction means the distal smaller airways tend to close at higher lung volumes than in a healthy airway
ie in a helathy subject if you do a forced exp moanouvre you wont start making a wheeze until late in expiration near to or at residual volume
in someone with severe copd or asthma you will wheeze even at tidal lung volumes -ie you dont have to breathe out much to induce a wheeze
Thomas,
You would be correct that the two oxygen levels would equilibrate at 70mmHg if the alveolus was a closed system with a finite amount of oxygen to give to the blood supply. However, as we know, the alveolus is connected to atmospheric air so as oxygen diffuses across into the blood there is a constant supply of oxygen to replenish the alveolus and maintain the partial pressure.
Hey, I was wondering if there was an SSC’s left in the respiratory side of things this year, or if I’m too late, thanks.
Dear Dr. Stretton,
Thanks for answering my question, it makes a whole lot more sense now. I have a question, referring to your lecture today on Arterial Blood Gases. Step 1 of the 5-step approach deals with assessment of oxygenation and I understand that the pO2 is taken from an arterial blood sample and should be between 10 and 13kPa (having reached equilibrium with the alveoli as aforementioned) and likewise the pCO2 should be between 4.6 and 6.0 kPa. When it comes to the A-a gradient however, I am unsure of exactly how you get a figure for the alveolar pressure (PAO2)? What calculations were done when the O2 they were supplied with was expressed as a percentage/volume? Also, what is the clinical significance of a high (or low) A-a gradient?
Cheers,
Thomas
When will the new 3rd years hear anything about RoCEs and Patient Records – I am aware from older students that we need to see a signifficant number of patients, but I am not sure if we use the same form as last year or if there is different form for this year…
Last year Dr Day gave us a lecture about RoCEs etc – when can we expect one this year/or will we not get one? Thanks. 🙂
I’ll be speaking to the 3rd years in the neurology block some time in the next couple of weeks. Don’t worry – you have a whole year to complete the RoCE patients.
Thomas,
I didn’t include this in the talk because I felt that there were enough concepts to grasp without adding more. In essence you can take the percentage of inspired oxygen and convert that number directly into kPa units the same as pO2 and pCO2. In reality it is not a direct conversion. Atmospheric pressure is 100kPa and we know that oxygen makes up 21% of air, therefore 21% of 100kPa is ……. 21 kPa. In this equation, to be completely accurate you have to take into account the partial pressure of water vapour in the air (7kPa) that makes up part of that 100kPa. The precise calculation is actually 21% of (100kPa – 7kPa) which comes out at about 20%. If you wanted to be slightly more accurate therefore you could take the % of inspired oxygen and subtract 1 and you would have the partial pressure in the alveolus. You may now start to understand why I didn’t include this in the talk. It’s a longwinded distraction that makes little difference to the end result and I instead want you to grasp the concept of the A-a gradient and not always assume that a patient with an arterial pO2 in the normal range is well. The A-a gradient (the difference between the amount of oxygen in the inspired air and the patients arterial blood) should usually be small – 1-2 kPa in the young and 2-3 kPa in the elderly. If the figure is higher it means that there is a difference in the concentration of oxygen between what the patient is breathing in and what has made it through to their arterial blood. That patient is not absorbing the oxygen for some reason, be it an acute process such as pneumonia or Pulmonary oedema or a chronic condition such as pulmonary fibrosis.
I hope this makes it a little clearer, but try to avoid getting bogged down in the minutiae of these numbers, we are more concerned that you grasp the concept more than anything else.
Was just looking over all the radiology stuff from last week (which was really good by the way) and notice that most of the ITA stuff is missing;
there was an initial lecture, some case studies and then a quiz…
but i can only find the initial lecture on dundee chest and Bb, it might be here but i can’t find it 🙁
thanks
It’s here
Hiya,
Wonder can the ITA stuff (those that were put on the board in ITA sessions) for second week be put up in DundeeChest or MyDundee?
Couldnt find it anywhere.
Thanks.
The person who has the digital copy is on holiday until Monday, so when she gets back, she’ll put it up!
I have a few questions . . .
Say you had a patient with fully compensated respiratory acidosis, from looking at their ABGs is there any way of differentiating between whether this is fully compensated respiratory acidosis or fully compensated metabolic alkalosis? Or do you need to use the history to figure it out? (e.g patient with severe vomiting would be metabolic alkalosis)
It says in Dr Stretton’s arterial blood gases lecture that uncompensated respiratory acidosis causes Acute type 2 respiratory failure. Is it also the case that uncompensated respiratory alkalosis can cause Type 1 Respiratory Failure?
Also does Shunt cause type 2 Respiratory failure and dead space cause type 1 Respiratory Failure?
Thanks
Can the updated version of ‘Maintaining Oxygenation and Respiratory Failure’ by Dr G Rodney up in Dundee Chest?
(Current one on Dundee Chest is only 20 slides, whereas the one we had on Wednesday was 60 slides)
The lecture is really useful!
Thanks.
Hi
There’s no way to tell the difference between a fully compensated metabolic alkalosis and a fully compensated respiratory acidosis, you have to go on the history, and the fact that the latter is far more common than the former. Think about it – how many diseases do you know where the patient hypo-ventilates chronically to compensate for alkalosis?
Uncompensated respiratory acidosis is the consequence of acute type 2 respiratory failure.
In type 1 respiratory failure the patient will hyperventilate to compensate for hypoxaemia, leading to hypocapnoea, and eventual respiratory alkalosis.
You have things backwards – the acid base balance scenarios are the the consequence, not the stimulus.
Shunt and dead space can both cause type 2 or type 1 failure – it’s not that simple, I’m afraid!
Dr Rodney has not given me the updates lecture, so I can’t put it up. When he does, I will.
in compensated respir acidosis the PO2 will by definition be low and the pt will have severe COPD with signs of cor pulmonle – whereas in compensated met alkalosis the PO2 will be normal
check out the slides i have out up on my bit if dundee chest which makes it easy to understand
Hello,
Just reviewing today’s lecture and trachial deviation was mentioned in passing. I understand that in collapse, the trachea deviates to the diseased side whereas in a pneumothorax, the trachea deviates away from the diseased side. I’m struggling, however, to understand the difference between atelectasis and pneumothorax, could someone explain that?
Cheers,
Thomas
atelectesis refers to subsegmental collapse -eg due to PE which is visable as line usually basal on the CXR -the degree of collape with atelectesis isnt enough to cause any deviation of the trachea to that side
Hi,
I have a couple of questions, they’re not very important, just for interest really:
1) Why does anxiety cause dyspnoea?
2) Why do antihistamines cause a prolonged QT interval on an ECG?
3) Why does COPD worsen in damp weather (or with temperature change in general)?
Cheers,
Caitlin.
1.they arent breahtless per se but just become aware of normal respiration
2.They affect myocardial repolarisation -not a problem with commonly used drugs like loratadine and ceterizine
3.Usually becuase its the viral season in the winter and because cold air causes constriction
Hello,
Looking over respiratory tract infections and in particular community acquired pneumonia. In the lecture, both amoxicillin and doxycycline are listed as treatment but according to the antibiotic man, one is the alternative for the other (should a patient be allergic to penicillin). What is the definitive treatment for CAP?
Cheers,
Thomas
Amoxicillin 1g TDS or
Doxycycline 200 mg initial dose, then 100mg OD thereafter in penicillin allergy, or those who have already received amoxicillin from their GP
Hi,
I was wondering why so many of our simulated patients and patient profiles who have asthma are on bendroflumethiazide. We learnt about this drug in the CV system- and it is commonly used as a diuretic. What is the benefit of a diuretic in asthma patients?
Thanks
Stuart
There isn’t one. It’s just a very commonly prescribed drug for hypertension. Or it was – new guidance recommends ACE inhibitor as first line.
Just saw on the last post that people had been to see some of the real MDT’s i’d really like to do that too and wondering if i could get places and times.
cheers
Why tumour that obstructing airway can cause pneumonia (before chemotherapy)?
When a tumour obstructs the bronchus it results in failure to clear secretions and any organisms distal to the obstruction -this results in distal pneumonia and if the obstruction in complete collapse of that segment or lobe
MDT times and locations? pretty please
I do write these things on the website, you just have to look for them
ah thanks, my bad