[Case Report] 47yo with rapidly progressive respiratory failure requiring ECMO

[Case Report] 47yo with rapidly progressive respiratory failure requiring ECMO
Date:
20 November 2024
Category:

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In 2019 a man was referred to Royal Adelaide Hospital with worsening breathlessness and a productive cough. He was a 47 year old electrician with a history of tobacco smoking who’d been well before the onset of symptoms. Over a couple of admissions the patient’s condition progressed to type 2 respiratory failure. While the ultimate explanation for this presentation was a bit of a unicorn, the dramatic escalation of examinations and interventions runs through some textbook respiratory medicine; ECMO, infectious diseases, bronchoscopy, CT, interpretation of blood gases and the alveolar gas equation, stenting and ultimately transplantation. This is discussed in the careful manner expected of a long-case presentation in the physician training exams.

Credits

Guest
Dr Thomas Crowhurst FRACP (Northern Adelaide Local Health Network)

Hosts
Associate Professor Stephen Bacchi (Lyell McEwin Hospital; University of Adelaide)
Dr Brandon Stretton (Central Adelaide Local Health Network)

Production
Produced by Stephen Bacchi and Mic Cavazzini. Music licenced from Epidemic Sound includes ‘Rockin’ for Decades’ by Blue Texas and ‘Brighton Breakdown’ by BDBs. Image created and copyrighted by RACP. Editorial feedback kindly provided by RACP physicians Aidan Tan and Fionnuala Fagan.

Key Reference (Spoiler Alert)

Case report of severe bronchial web-like stenoses after 'surviving the unsurvivable' [BMC Pulm Med. 2019]

See also
The interpretation of arterial blood gases [Australian Prescriber]
Oxygen tension - based indices of oxygenation [Deranged Physiology]
A-a gradient [Life in the Fast Lane]

Extracorporeal Membrane Oxygenation in Adults [StatPearls]
Venoarterial ECMO Hemodynamics - StatPearls [StatPearls]
Incidence of death or disability at 6 months after extracorporeal membrane oxygenation in Australia: a prospective, multicentre, registry-embedded cohort study [Lancet Respir Med. 2022]

The International Society for Heart and Lung Transplantation guidelines

 

Transcript

PLEASE NOTE: While an effort has been made to correct errors in this AI-generated transcript, some mistakes may have been missed by the non-clinician moderator. This transcript should be taken merely as supporting material to the podcast discussion and neither is as an authoritative last word on the subject matter.

MIC CAVAZZINI: Welcome to Pomegranate Case Reports, developed by Trainees of the Royal Australasian College of Physicians. Today’s story comes from a presentation to the Royal Adelaide Hospital Department of Thoracic Medicine in 2019. The patient was a 47 year old man who had over several days been coughing up mucus and blood and experiencing worsening breathlessness. He had a history of tobacco smoking but had been otherwise well before the onset of symptoms. Over a couple of admissions the patient’s condition deteriorated to type 2 respiratory failure. While the ultimate cause of this proved to be a bit of a unicorn, the workup and interventions demonstrate some textbook respiratory medicine. You can find some of the chest imaging in the case report published in BMC Pulmonary Medicine which is linked in the show notes. But I suggest you let yourself be guided, spoiler-free, by series host, Associate Professor Stephen Bacchi.

STEPHEN BACCHI:            Hi, I'm Stephen. I'm a neurology Fellow at the Massachusetts General Hospital, and today with me, I have Dr Tom Crowhurst, who's a consultant respiratory and sleep physician at the Northern Adelaide Local Health Network. He conducted a fellowship in lung transplantation at the Alfred in 2021. And we also have Dr Brandon Stretton, who's a basic physician trainee in the Central Adelaide Local Health Network, who has an interest in all things evidence-based medicine. Thank you for joining us.

THOMAS CROWHURST:                 Good to be with you.

BRANDON STRETTON:   Likewise.

STEPHEN BACCHI:            So as previously, we'll be discussing a published case report in a step-by-step manner, with a focus on content that's relevant for trainees and a generalist audience. So, in this case, we have a 47-year-old male who's from rural Australia, and he has presented with five days of shortness of breath. He also had a productive cough and occasional haemoptysis. He's had a course of antibiotics and steroids, but without benefit. His only past medical history is depression and being an active smoker. So, he is admitted to hospital, and it was a good thing too, because he had a rapidly progressive course. Over one day he developed a complete white out of both lungs on chest X-ray, which was clear on the day of presentation, and developed severe type 1 respiratory failure. This is a striking and fulminant presentation and he was commenced on veno-venous extra corporeal membrane oxygenation, or ECMO. Clearly, there's a long way to go in this case, but Dr Crowhurst, could you please briefly review for us the types of ECMO and their indications.

THOMAS CROWHURST: Certainly. So, ECMO is really the preserve of intensivists, but there have been major improvements in this therapy over the past few years, so it's important for the physician community to develop familiarity with this form of advanced life support. ECMO itself falls under a broader term of extracorporeal life support or ECLS. And essentially, these therapies provide oxygenation and carbon dioxide removal and, in some forms, also circulatory support. But it doesn't include cardiopulmonary bypass surgery, which has obviously been in existence for much longer.

Broadly speaking, ECMO can be venovenous, so VV-ECMO or venoarterial, VA-ECMO. The former is used for otherwise unsupportable respiratory failure, while the latter is used for circulatory failure. And essentially, the treatment involves removing blood from a central vein or cardiac chamber, pumping it through a membrane lung to achieve gas exchange, and then returning it either to a central vein or artery or appropriate cardiac chamber, depending on the form of ECMO that you're providing. VV-ECMO relies on native cardiac function to pump blood through the circuit, and this can be done to and from anatomically distinct sites or back and forth to the same location through a single, large double-lumen cannula. VA-ECMO provides circulatory support so there is a pump separate to the heart. So, blood is removed from a central vein and usually reinfused into the femoral artery or to two separate arterial sites.

Common indications, as you can imagine, for VV-ECMO, include pneumonia and other acute respiratory insults where there's adequate cardiac function. While common indications of VA-ECMO include heart failure, massive PE or refractory shock. It's very important to keep front of mind that these treatments are bridges, they're not destination therapies. And it's vital that careful thought is exercised to use these invasive and resource intensive bridges in scenarios where there's likely to be firm land on the other side. So ECMO can be a bridge to recovery where the illness is reversible. It can be a bridge to another life-saving intervention that will treat the primary illness, such as a valve replacement, or it can be a bridge to transplantation. But this final bridge is the most fraught of all and, generally speaking, ECMO as a bridge to transplant would only be considered where the patient has already been worked up and wait listed. The bridge-to-nowhere scenario is a bad outcome for everyone; for the patient, for their family and for the institution.

As you can imagine, ECMO is, or can be, fraught with danger. Complications include haemorrhage, thrombosis, infection, haemolysis within the circuit, thrombocytopenia, including HIT [Heparin-Induced Thrombocytopenia] and obviously, perforation from the from the cannula, or dislodgement of the cannula. This is a potentially life-saving treatment, but as you can imagine, the patients are critically unwell and the outcomes are sobering. So, there's a there's an Australian audit by Carol Hodgson and colleagues that was published in The Lancet Respiratory Medicine Journal in 2022 and they looked at about 450 ECMO survivors, and at six months post-ECMO, two thirds were either dead or had moderate to severe disabilities. So, the outcomes are sobering.

BRANDON STRETTON:   Well, the black magic of ECMO is starting to make a bit of sense, thankyou for that. Moving on, bronchoscopy showed diffuse, severe, purulent and ulcerative airway inflammation. Biopsy from the bronchoscopy demonstrated a necrotising inflammatory process, and workup revealed only rhinovirus on PCR. After treatment with broad spectrum antimicrobials, he was discharged 27 days later with no symptoms at rest. He represented six days later with worsening shortness of breath and cough. A CT at this stage demonstrated bronchial wall thickening of the large and medium airways. Repeat bronchoscopy showed patchy airway mucus, although markedly better than his first presentation. An ABG at this point demonstrated a partially compensated type 2 respiratory failure with a normal Aa gradient. And so, for the physician trainees preparing for their exams, Dr Crowhurst, could you please remind us of what an Aa gradient is and the significance in relation to this case?

THOMAS CROWHURST: Yep, the Aa gradient is a is a very important piece of physiology. So, as a respiratory physician, I’m very glad you've picked on this for me to talk about. Essentially, the Aa gradient describes the gradient of partial pressure of oxygen between the alveolar space, denoted by the capital A, and the arterial space, which is the lower case a. and it's a very useful tool in assessing the extent to which pulmonary parenchymal disease, and therefore inefficiency of gas exchange, is contributing to respiratory failure. If a patient has respiratory failure but has a normal Aa gradient, this indicates that gas exchange is occurring with normal efficiency in the ventilated alveoli, and therefore the cause of the respiratory failure is exclusively hypoventilation. The arterial pressure of oxygen is measured in millimetres of mercury via ABG, and the alveolar partial pressure of oxygen is calculated by the alveolar gas equation. And the gradient is just the difference between these two numbers.

So, the alveolar gas equation should hopefully be familiar to listeners, but essentially it incorporates the fraction of inspired oxygen; the atmospheric pressure; the assumed partial pressure of water vapor in the alveolus; the partial pressure of carbon dioxide, which is measured by the same ABG; and the respiratory quotient, which is the ratio of carbon dioxide emitted for oxygen consumed in metabolic processes within the organism as a whole, and that's usually 0.8 for the typical Western diet. So, assuming you know the atmospheric pressure at your institution, so that’s 760 millimetres of mercury at sea level, you can fairly easily complete the alveolar gas equation to find the alveolar partial pressure of oxygen by doing an ABG and noting the FiO2 that the patient's receiving at the time the ABG is done. The normal Aa gradient does increase with age, and a rough rule of thumb for the upper limit of normal, is age in years divided by four plus four millimetres of mercury ( ).

There's a rough and ready tool to apply if you're assessing a patient on oxygen therapy, which can sometimes mask the severity of underlying respiratory failure, which is the P to F ratio, or PF ratio, and this is the ratio of the measured arterial partial pressure of oxygen against the FiO2. So, in normal health, the PF ratio is above 400 given that a normal partial pressure of oxygen via ABG, is greater than 80 millimetres of mercury and as you know, the normal FiO2 is 0.21.

STEPHEN BACCHI:            Brilliant, so, that's really helpful. In this case, he's got a normal Aa gradient. So, you know, if we were thinking about parenchymal lung disease, less likely, and, I guess, the imaging doesn't necessarily support it. So, repeat CT shows persistent bronchial wall thickening and significant gas trapping. The patient then deteriorated despite non-invasive ventilation and required intubation and ventilation. Bronchoscopy was undertaken and demonstrate multiple stenoses in lobar and segmental bronchi bilaterally. These multiple bilateral stenoses were concentric and fibrous, giving them a web like appearance. Okay, so now we're getting into some pretty specialized territory. I must admit that I haven't encountered bronchial stenosis particularly often, especially at multiple sites bilaterally. Could you please talk us through when you would normally encounter bronchial stenoses, and what's so unusual about this patient's case?

THOMAS CROWHURST: Yeah, this is a highly unusual scenario. Bronchial stenosis as a singular issue are themselves relatively uncommon problems in respiratory medicine, and the vast majority of them are due to bronchogenic malignancy, although there are other causes; congenital lesions; infection, especially from tuberculosis; autoimmune disorders like granulomatosis and polyangiitis, sarcoidosis; inflammatory bowel disease-related airway disease and relapsing polychondratis, although that's rare. You can also have treatment related stenosis following radiotherapy. Tracheal stenoses are probably, except for malignant singular bronchial stenosis, tracheal stenosis are actually probably a bit more common, and these typically occur in the subglottic region and often don't have an identifiable cause, classically occurring in middle-aged women with otherwise unexplained dyspnoea. But these are, these are a separate disorder from what we've just discussed.

Multiple bronchial stenoses are very rare, and this is one of the reasons that we wrote up this this case. There's only a handful of cases reported in the literature, and most seem to be secondary to infection, for example, from influenza A; inhalational injury, which you can see would make sense; or a systemic autoimmune disease. They can be very difficult to identify on imaging, particularly if they're limited in length. So, if you're thinking of a stenosis, you need to flag this specifically with the radiologist. But really, bronchoscopy is the optimal method of identifying and analysing these lesions.

If the underlying cause is identifiable, then this is treated. Stenosis of a single, smaller bronchus is not necessarily of any great functional significance, depending on its location and its severity. and lung function testing might be normal, but these lesions can still pose issues with recurrent post obstructive infection and may require treatment simply for this reason. There are a range of things you can do for stenoses. So, you can use stents, and these days, stents are typically reserved for the palliation of large central airway tumours. They were used with more enthusiasm in the past, but with advances in oncological therapies and more awareness of stent complications like migration and stenosis and infection, they've to some extent fallen out of favour, but they do have a role in select cases. Other options for intervening on stenosis include using argon plasma coagulation or APC, laser and cryoreduction, as well as balloon dilatation. And the choice of the technique would depend on the experience of the procedure list as well as the location and type of the stenosis.

STEPHEN BACCHI:            Alright, so in this case, the patient had balloon dilatation of multiple stenoses, and stenting was not undertaken. He was also treated with pulsed methyl prednisolone, and he improved to the point of discharge. Unfortunately, he was readmitted again. Again, six days after discharge, he was readmitted with dyspnoea and type one respiratory failure. So now repeat bronchoscopy has demonstrated recurrence of the stenosis with complete occlusion of segmental bronchi. The trachea was largely spared.

And the diagnosis at this stage was considered to be a fulminant inflammatory response secondary to a previous unknown inhaled toxin exposure and lung transplant workup was considered and rapidly undertaken. But before we talk about lung transplant, just could you explain again just for me, sorry, why was stenting not undertaken in this case?

THOMAS CROWHURST: So, stents are most useful for stenosis in the central proximal airway. So, trachea, main bronchus. These stenoses were in the more peripheral airways, so in segmental bronchi, and stents in that location are and not really manufactured for that size. And would be very liable to become plugged with mucus rapidly because the lumen there is quite narrow. There were also there were also lots and lots and lots of these stenoses. Essentially, almost every airway was stenosed at one point or another. So it even if it would have been a durable option and it would have been impractical because of the large number.

Watching the procedure was quite amazing. So, these stenosis, even though the patient had only been unwell for a few weeks, these stenoses were so tough that they had to be punctured with a needle to create a hole so that the balloon could be forced through the hole and then inflated to dilate the stenosis. So, the airways looked horrendous and the initial treatment was successful in improving his respiratory failure. But as more webs developed, the response to treatment was less convincing, and overall, his pulmonary reserve was starting to look considerably, fraught.

BRANDON STRETTON:   Excellent. Thank you for that. So looping back to the case, acknowledging that the diagnosis in this setting is exceptionally rare, the topic of lung transplant candidacy and work up is a fairly common thing for BPTs to encounter, particularly in their long cases. So Dr Crowhurst, could you please talk us through in general, your approach first to considering the indications for lung transplant and lung transplant candidacy.

THOMAS CROWHURST: Yes, it's definitely worth having a good working knowledge of the problems that lung transplantation can fix and what it can't fix. So, it's a highly complex treatment. It's a treatment that can offer transformative morbidity benefit and often mortality benefit, as well, in carefully selected cases. I think the first general point to make is that it's always worth asking the question and asking the question early, because the lead time for assessment and transplantation can be significant, and it's important that the patient receive accurate information on his or her prospects or lack thereof with respect to transplantation.

Each state is linked with a lung transplantation centre, and usually, contact would be made with the local respiratory unit, who would then refer on to the transplantation centre when considered appropriate. I think the first question to ask yourself with respect to lung transplantation is, “will lung transplantation fix this patient's problem?” It will fix the lungs, and in the setting of pulmonary hypertension, it can enable quite amazing readjustment of the right heart. And sometimes in those patients, it will also lead to a degree of improvement in renal function where there's been chronic renal underperfusion.

But lung transplantation will not fix any other problems, so it's essentially a therapy for single organ failure. It won't fix respiratory failure secondary to chest wall deformity or neuromuscular disease. And it won't fix frailty, sarcopenia or left heart failure, or so on. The I think the second question is, or the second thought is, to screen for any contraindications beyond significant non pulmonary end organ dysfunction, as we've just discussed. Examples include smoking, alcohol, be on the most modest levels. Any illicit drug use, not adherence with medical therapy, and importantly, lack of the psychosocial and cognitive capabilities to succeed with a very complex therapy like lung transplantation. Age over 70 years is generally considered to be an absolute contraindication, except in very compelling cases. Not because the system is ageist, but because the outcomes really do fall away substantially beyond the late 60s.

And I think another interesting piece of data that helps highlight the importance of the psychosocial and cognitive element in candidacy are the outcomes for younger patients. So, lung transplant in a child is also is always a very emotionally distressing scenario, but children often have quite good short and medium term outcomes, but those outcomes deteriorate significantly in adolescence and early adulthood. It doesn't take much non-adherence with immunosuppression to enable allograft rejection to arise, especially in young people who have otherwise brisk immune systems. So, selecting a patient who can cope with the complexity and the commitment is very important.

The final question not that there's any particular order in which you need to consider these questions, but the third piece of the puzzle is, “is this going is this patient going to survive to transplantation, in a state that will enable them to successfully recuperate and receive a mortality benefit?” So, the concept is the transplant window, you need to be sick enough so that you can achieve a mortality benefit, but not so sick that you are too unwell and too frail to then climb out of the hole that you wake up in after a transplant.

So, in summary, you're looking for a non smoking, adherent patient under 70 who has severe lung disease, meaning they have an estimated 50% or greater chance of dying from their lung disease within the next few years. And an absence of other significant end organ disease, and someone who has the psychosocial and cognitive capabilities to deal with a complex therapy. The International Society for Heart and Lung Transplantation publishes guidelines around lung transplant assessment, and they have disease-specific guides on when it's appropriate to refer and when it's appropriate to waitlist. So, there's various things you can look at there for specific diseases.

I think for the examination as a BBT, there are two key things you need to know. One is that one is to use the concept of the Bode index for assessing severity of COPD. That's a little old-fashioned now. And into that, I would add the frequencies of exacerbations, and any type two respiratory failure, as well as obviously any cor pulmonale. And then the other is if someone has a diagnosis of RPF that that is a malignant disorder, the average survival pre anti fibrotic was three to four years. So, if someone has a diagnosis of RPF, even if it's relatively early, they should be carefully assessed. And the international guidelines recommend referral at diagnosis for appropriate patients

STEPHEN BACCHI:            So in Australia, there's only a select number of centres that can perform the operations necessary for lung transplant. Could you please talk to us about some of the logistics around lung transplant in an Australian context?

THOMAS CROWHURST: It's definitely worth having a general understanding of how the process works. But also to highlight that if you do have a patient who you think needs to be considered for lung transplantation, and involving the local respiratory service is the first step, and they should really take it from there in consultation with the transplant centre. So, every state has a transplant centre. Tasmania tends to be served very well by the Alfred in Melbourne and the Northern Territory has sort of links to various states, including Queensland, New South Wales and Victoria depending on the specific patient. And often where their social networks are determines where they end up going.

The logistics in terms of the process involved in work up, it is exhaustive. Generally speaking, for an outpatient, it involves a referral and an initial consultation with the lung transplant physician who will go through the history with a fine tooth comb and form an overall view about whether it's appropriate to proceed with work up; or whether the patient might benefit from transplantation in the future but it's too early to begin work up, in which case monitoring would be undertaken; or whether it's obvious that the patient will never be suitable for transplantation, and they're discharged back to the referring team.

The work up, I conceptualize it as having three phases. So, the first phase is a screening set of bloods to look for obvious problems, like renal dysfunction or liver dysfunction. If they're satisfactory and the patient is looking like an appropriate candidate who needs to progress through their work up, then the second phase is a host of radiology investigations and multi-D assessments. The multi-D assessments are absolutely crucial, and there's a huge team involved; physiotherapy, psychology, pharmacy are involved dietetics, occupational therapy, and depending on the needs of the patient, you may also have input from psychiatry, other medical specialties and the list goes on. Obviously, they also see the surgeon and the intensivists and anaesthetists.

At the end of that, the information is packaged up and presented to a very big MDM panel. And that panel, at least in my simplistic brain, provides a traffic light type response. So, if the patient is an appropriate candidate, they get a green light, and usually after that they unless they are young, with no risk factors, they would typically go on to have a coronary angiogram. That's saved until after the green light is given because of the procedural risks. And if that's satisfactory, then usually they are consented, which is a process in itself, and then they're listed.

Sometimes there might be a renal lesion, or they might not quite be sick enough, or there might be some other complicating factor, but they're still considered likely to get over the line. And that's an orange light scenario where the transplant physician continues to work things up and represents them at a later time. And obviously, unfortunately, for some patients, it's just not a suitable treatment, and the answer has to be no.

The management of the wait list is also quite interesting. A lot of patients think that it is literally a list, so, you get listed, you start at the bottom of list, and you slowly work your way to the top. But that's not at all how it works. When a set of donor lungs become available, they need to be matched to blood group and to size, and that often narrows down the list quite substantially. After that, they also need to be assessed in terms of the severity of illness and who would benefit most from those lungs within the subgroup for which the lungs would be appropriate. And also, there's a process, which is now virtual, for cross matching to ensure that the recipient doesn't have antibodies against HLA, that is likely to be problematic. And that's a highly complex area that the lung transplant physician on call manages during the donor assessment and matching process.

BRANDON STRETTON:   Excellent. We often talk about the patient being appropriate for a transplant, but it's interesting to think about the lungs being appropriate for the patient in the context of size. It's not something I'd actually considered before. And so, finishing up now, in this case, the patient underwent bilateral, sequential lung transplant at a quaternary centre. Even with the implanted specimen, no specific diagnosis could be reached beyond that which had been previously posited. Twelve months following the transplant, there was no recurrence, and the patient is doing well, and now I know that the actual diagnosis in this case is phenomenally rare and not really the key learning point for trainees and the rest of our generalist listeners. So to wrap up the case, could you please outline a couple of key learning points or take home messages that trainees could take away from this case?

THOMAS CROWHURST: Sam, yes, but first, I have a very exciting update about this case that I heard about just recently. So, Sam Brooks, one of the advanced trainees at the Royal Adelaide Hospital, is writing up a sequel to this case report, so listeners can keep their eye out for that. But this patient has developed a recurrence of their native lung disease in the allograft. And he's been very thoroughly assessed. One of the differentials for his original presentation was inflammatory bowel disease related airway disease, but it wasn't considered that seriously prior to transplantation. The explant was probably a bit more compelling in that regard, but nothing was really ever done about it, because he never had any evidence of inflammatory bowel disease, and that remains the case. He's been very thoroughly assessed so there's no evidence of inflammatory bowel disease, but the repeat biopsies of his in very inflamed stenosed allograft airways look again like Crohn's, and so in the absence of any evidence, he's been treated phenotypically within infliximab and has responded magnificently, and his airways have essentially normalized. So quite an amazing story for this case,

BRANDON STRETTON:   That’s wild. What a case.

BRANDON STRETTON:   Yeah, that’s awesome.

THOMAS CROWHURST: Yeah it’s funny. I think it wasn’t that long after you’d reached out and I heard about this recurrence. And I couldn’t believe it and I got sent the draft and the pictures are quite incredible. But it's unlikely anyone will ever see something similar again. So, in terms of the general take home messages for learning, I think firstly, it's worth understanding the different forms of ECMO, and most importantly, remembering that ECMO is a bridge, a bridge to recovery, a bridge to another life-saving therapy, or in appropriate patients, a bridge to transplantation. The second key take home message is to appreciate the profound beauty of respiratory physiology and the light it shines on so many common clinical presentations, and to ensure that you read West's textbook of respiratory physiology. The third is, don't worry too much about bronchial stenosis. And the fourth is to think about lung transplantation as an option for patients with severe lung disease, and to always pick up the phone if you think it needs to be considered.

STEPHEN BACCHI:            Well, thank you. Dr Crowhurst, that was a fantastic case. I feel like I'm ready to go and sit a respiratory long case again now. So, if readers would like the full details of the first part of the case. It was titled Case report of severe bronchial web like stenosis after surviving the unsurvivable and it was published in BMC pulmonary medicine in 2019, the first author, Dr Tom Crowhurst and senior author, Prof Holmes Liew, and we will anxiously await the follow up. Thanks again, Dr Crowhurst, really appreciate it.

THOMAS CROWHURST: My pleasure. Thank you for inviting me.


MIC CAVAZZINI: Many thanks also to Stephen Bacchi and Brandon Stretton for putting together this resource for other trainees and generalists. Please remember that this is a passion project they’ve developed in their spare time. The podcast and transcript should be taken as a prompt for further reading, not the authoritative last word on the subject.

There are some great explainers for the alveolar gas equation or the P to F ratio from websites like Life in the Fast Lane, StatPearls (alveolar gas equation), Deranged Physiology (alveolar gas equation) and Australian Prescriber. And, of course, you can find online plug and play versions of the algorithm on sites like MD Calc.

If you want some more support that’s been vetted by the College educational committees, go to the College Learning Series at elearning.racp.edu.au. There are at least 20 lectures on respiratory and sleep medicine, including some on respiratory failure and lung transplantation. There are another 12 dedicated paediatric respiratory medicine.

If you have any suggestions or feedback for future episodes of Pomegranate Health do send them in to podcast@racp.edu.au. And please spread the word by telling your colleagues to subscribe via Apple Podcasts, Spotify, Castbox or any other app. For late adopters there’s also an email alerts list that they can sign up to at our landing page, racp.edu.au/podcast.

This show was produced on the lands of the Gadigal clans of the Yura nation. I pay respect to their wisdom and teaching over tens of thousands of years. I’m Mic Cavazzini. Thanks for listening.


 

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09 Feb 2025
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