Tasty Morsels of Critical Care

Welcome back to the tasty morsels of critical care podcast. Today we’re not so much looking at a chapter of Oh’s manual but at the physiologic concept of respiratory compliance. I approach this with a degree of trepidation as the probability of screwing this up is infinitely higher than simply translating Oh’s manual into podcast form. Compliance is relatively simply defined as change in volume per change in pressure. Put another way, for every 1 cmH20 pressure i apply with the ventilator I get 100mls of volume. The compliance in this scenario would be 100, ie 100 divided by 1 = 100. 100ml/cmH20 also happens to be normal compliance of the human lung.  You’ll sometimes see compliance written as delta volume divided by delta pressure. There are a few different types of compliance described for the respiratory system. static compliance = compliance in the absence of flow. This consists of the compliance of the lung tissue and the chest wall and is the number we look at generally dynamic compliance = compliance in the presence of flow. This consists of chest wall and lung tissue compliance AND airway resistance (and will always be lower than static compliance) specific compliance = compliance normalised for lung volume (kind of like an indexed value so adults and kids can be compared) Compliance will vary depending on distension of the lung with ideal compliance usually just above the FRC. When overdistended and about to pop, you can imagine that increases in pressure will only produce small changes in volume. The same is true when the lung is at very low, atelectactic volumes where the lung tissue is squished solid and large changes in pressure are needed to produce a change in volume. This is nicely represented in the graph from deranged physiology in the show notes that shows a nice sigmoid curve of lung volume plotted against airway pressure. The steep part of the curve represents the ideal compliance as you get the most “bang for your buck” in that small increases in pressure will result in substantial increases in volume. We are very interested in lung compliance in the intensive care unit. We talk a lot about stiff lungs and spend a lot of our time and energies trying to optimise ventilation of those with poor compliance. So how do we measure or assess compliance? This becomes a sort of reflex over time where you simply walk in the room and look at the vent and the driving pressure and the tidal volume produced and a synapse somewhere ignites and tells you  that 25cmH20 pressure to produce 250 mls of tidal volume is not good. If you do the basic calculation of delta volume divided by delta pressure, of 250/25 you get 10 which is indeed a very low compliance and of great concern. This is most of what you need to know for day to day practice. However for examinations of brownie points you might wish to know more and understand many of the circumstances where that kind of heuristic might be wrong. The gold standard is apparently something called the super syringe method which involves inflating the lung in 100ml increments with a 2-3 sec pause at each inflation. This measures static compliance and i mention it mainly cause it has a cool name. In real life we measure compliance by fiddling with the inspiratory and expiratory hold buttons and looking at what the ventilator spits out. This is technically the compliance of the respiratory system rather than true static compliance but I remain somewhat in the dark as to the subtleties of the difference. What you do with the number is a whole different question. Stiff lungs do worse. That’s hardly a surprise. Given that compliance is typically best just above the FRC we can titrate PEEP to idealised compliance. This is best explained on a critical care now post by Matt Siuba, linked in the show notes. The basics of this involve a passive patient in a volume control mode and the PEEP is dialled up and down with a fixed volume to see at which PEEP you get the best driving pressure (ie the lowest amount of pressure to produce the set volume).  This should place you on the steep part of that curve and just above the FRC. There are actual a number of methods trying to attain the same thing and I don’t mean to imply that this is proven best but I have put a few links in the show notes for those looking more and will hopefully do a whole post on setting PEEP and recruitment at some point. Reading Deranged Physiology Critical Care Now Sahetya, S. K., Hager, D. N., Stephens, R. S., Needham, D. M. & Brower, R. G. PEEP Titration to Minimize Driving Pressure in Subjects With ARDS: A Prospective Physiological Study. Respiratory care 65, 583–589 (2020).    

Welcome back to the tasty morsels of critical care podcast. Today we’re going to talk about some of the basics of some of our favorite drugs intensive care – the diuretics. As always this is planned to be a brief overview of the essentials rather than the deep dive. Click for source As a starter pretty much all diuresis is conducted by convincing the kidney to lose more Na. Lose the Na and the water will follow. First on the list of course is furosemide. This is one of the commonest drugs we use in intensive care and we really should just be mixing it in with the NG feed or the propofol given how commonly we use it. Furosemide is one of several loop diuretics. By loop we mean its site of action is at the loop of henle, site of the much loved countercurrent mulitplication system. In particular furosemide acts by blocking the NaK2Cl pump in the thick ascending loop of henle. This sounds all very technical and impressive but how does blocking said channel cause an increase in the wee wee in the bag? Ultimately you end up with a lot more sodium arriving at the collecting duct. The presence of extra sodium in the collecting duct decreases the osmotic gradient between the medulla and the tubule and as a result less water is reabsorbed and more comes out in the urine. Furosemide is normally highly protein bound. As a result it can’t get into the nephron through the glomerulus, which in the healthy state won’t let large things like albumin through. Therefore to get to its site of action in the loop of Henle it gets secreted into the proximal tubule and washed along with the ultrafiltrate towards the loop. This feature of secretion in the proximal tubules is one of the things we see with the furosemide stress test, typically used to predict need for RRT in AKI. A lack of response to a healthy (ie  at least 1mg/kg) dose of furosemide tells us the proximal tubules are in big trouble and there will be a likely need for RRT. In terms of side effects the ones that are perhaps clinically most apparent are the electrolyte losses (primarily potassium and magnesium) and hypernatraemia (as the water loss is in excess of the Na loss). There is a corresponding “contraction alkalosis” that is nicely explained at the deranged physiology post or in audio form over at the curious clinicians. Longer term the one worth knowing about is the ototoxicity commonly seen with high doses of furosemide especially in conjunction with our other favourite ototoxic drugs – the aminoglycosides. Though to be honest, only our most chronically critically ill patients stay long enough with us for us to pick up the ototoxicity. Next on the list are our thiazides. Typically for our local practice that means metolazone. Thiazides work just a little further down the windy nephron river from the loop of Henle at the distal convoluted tubule. Once there it inhibits the NaCl transporter system again meaning increased delivery of Na to the distal tubule where most of the water reabsorption occurs. Thiazides aren’t especially powerful as a diuretic strategy but they are additive from a Na wasting (and hence water losing) perspective as you’re targeting a different part of the nephron. I find the metolazone often gets added when you still want to diurese but you’re a bit worried about the rising Na. The idea is that you get the Na content of the urine to the sweet spot where you lose equal amounts of salt and water and the serum concentration stays the same. Like most things in ICU this is likely physiological wishful thinking rather than good science and it keeps us amused while the disease process resolves on its own. Continuing our journey through the nephron we have the aldosterone receptor antagonists. A class largely occupied by spironolactone. Spiro (to its friends) works by blocking the very important ENaC (or epithelial sodium channel), especially in the collecting duct. When these are blocked Na no longer is reabsorbed in the collecting duct and hey presto water follows the Na out of the nephron into the ureters. The main side effect of the increased concentration of Na in the collecting duct will be a reluctance to secrete K into the duct thus preventing K wastage and ultimately increasing the serum K. It is not an especially effective diuretic in terms of producing volumes of urine but more importantly it does have a significant long term mortality benefit in patients with heart failure unlike crowd favourite furosemide. It is of course difficult to extrapolate findings from massive cardiology heart failure trials to the ventilated patient with a dodgy ticker with multi organ failure in the ICU but there you go. The final drug we’ll mention today is acetazolamide. It has its site of action way back in the early nephron at the proximal convoluted tubule. It is a carbonic anhydrase inhibtor, unsurprisingly inhibiting the action of carbonic anhydrase. From the name “carbonic anydrase” we can hopefully deduce that it inhibits the process of removing water from carbonic acid. Ultimately this impairs HCO3 reabsorption at the proximal tubule creating a scenario somewhat similar to renal tubular acidosis. The drug clearly causes a diuresis and does indeed increase the Na wasted in the urine though the precise mechanism is not entirely clear. My anecdotal experience when taking the stuff climbing Kilimanjaro nearly 20 years ago suggests indeed it does make you want to pee a lot more. There are a a few small trials looking at its use in ICU none of which are hugely compelling for benefit but I find myself reaching for it when the fursoemide driven alkalosis is causing issues or you’re playing a game of “diuresis jedi” and want to complete all the steps of the “nephron bomb” Reading: Deranged Physiology Overview of diuretics Curious Clinicians Mullens, W., Verbrugge, F. H., Nijst, P. & Tang, W. H. W. Renal sodium avidity in heart failure: from pathophysiology to treatment strategies. Eur Heart J 38, 1872–1882 (2017). Bell, R. & Mandalia, R. Diuretics and the kidney. Bja Educ 22, 216–223 (2022).

Welcome back to the tasty morsels of critical care podcast. Today we’re looking at asthma. In reality I find this is much more commonly discussed than seen in real life. No doubt this is due in part, to an improvement in asthma care chronically which is of course a good thing. I think it gets discussed and comes up on exam papers so much partly because it is such a nice illustration of physiology and ventilation. I am guilty of over teaching this myself having delivered not one, but 2 talks on the subject, and even a prior tasty morsel of EM on the subject. Oh’s manual devotes a whole chapter, number 35 to the subject. We definitely see much less of this than we used to. I suspect that’s largely due to better access and provision of primary care but there remains a cohort of fairly brittle folk out there who will occasional crop up in resus or the ICU. To begin with, let’s cover some aetiology and pathophysiology, asthma has well described allergic and atopic associations as we all learn in medical school but also some important environmental triggers such as the infamous “thunderstorm asthma” that occurred in Australia some years back with 1000s of patients affected. There are several major consequences of severe asthma that Oh describes: increased work of breathing – dynamic hyperinflation a big part of this V/Q mismatch and shunting CV instability from intrathoracic pressure Status asthmaticus is a term commonly found in textbooks but I don’t think it has anywhere near the utility of it’s Latin equivalent status epilepticus. Oh applies the term to those not responding to nebulised bronchodilators which could be fairly broad. For management of asthma like this, the mainstay of treatment is inhaled beta agonists with a chaser of ipratropium and some steroid. There is plenty of evidence suggesting simple inhaled beta agonist with an MDI can be as effective as neublisation but for ICU level asthma (which this post is aimed at) you will be reaching for an oxygen driven nebuliser aiming to get particle sizes somewhere in the 1-3um range. however it is well known that <10% of the drug gets delivered to target and it is likely that in the most severe asthmatics where very little gas is moving that the drug delivery is even worse. Hence the existence of the IV therapies. All of these are controversial on some level and I am not here to advocate for one or the other but more to provide a pithy line or two on each that one could reasonably throw into an SAQ or a viva answer and look somewhat smart. IV salbutamol is commonly used in the UK and Ireland but like pretty much all of these therapies could not be said to have a robust evidence base. Concerns have been expressed that it adds a significant metabolic load to the work of breathing with the inevitable rise in lactate and fall in BE leading to an increased minute volume and an increase burden of respiration. IV magnesium is likely more benign and given out extremely commonly in these cases but once again the evidence base is hardly stellar. IV adrenaline is a common go to and has some physiolgoic rationale beyond flogging the already overstimulated beta agonists. It’s alpha agonist effect may have beneficial effects on secretion burden and plugging. Aminophylline continues to be used though anecdotally I’ve not seen it to be that helpful Heliox often crops up in the text books as it allows for the goldilocks phenomenon of laminar flow. However given the limtations on FiO2 at ~30% (generally 30:70 seems to be the mix) it’s not a great option in a population where hypoxia is a real concern. No post would be complete without mention of crowd favourite ketamine and its potential bronchodilating properties. It is likely overstated but as an induction drug would seem reasonable. Inhalational anaesthetics are somewhat similar but importantly likely to be inaccessible when you need them. Let’s say you’ve failed all these therapies and a tube has gone in. How would one ventilate such a patient. The answer should be “with great difficulty”. If it turns out they’re completely easy to ventilate with normal pressures and no gas trapping then you have just intubated someone with vocal cord dysfunction, sometimes known as paradoxical vocal cord motion. Worth another post perhaps but can be a common mimic of life threatening asthma. More likely you’ll find yourself faced with a ventilator complaining loudly that all the pressures are too high. If lucky you’ll sort things before the inevitable CV collapse from intrathoracic pressures or tension pneumo. The emergent response if you’re faced with high pressures and hypotension is disconnect the patient from the vent. If high intrathoracic pressures are the problem then decompressing the thorax through the ETT may be  sufficient to temporarily fix the problem. If they have a PTX they’ll need a decompression of the pleural space of some kind. Disconnecting the vent is of course not a long term solution so how should we appropriately ventilate these patients. The simple answer is probably “very slowly”. The best thing I’ve seen on this is Dave Tuxen’s paper from the late 1980s and the more recent podcast he recorded with the Intensive Podcast. A fairly simple summary is keep the minute volume low ie 6-7L/min at most. If you try harder you’ll cause harm. You can get this with a resp rate of around 10-12/minute with a Vt of ~500-600mls. Without even touching the I:E ratio you’ll end up with an expiratory time around 4 seconds. Tuxen argues that there’s little to be gained by prolonging expiration beyond this or lowering your minute volume below this. The 1980s paper provides some data to back this up. You will undoubtedly get high peak pressures on the vent that reflect airway resistance rather than the pressure being felt at the alveoli. Plateau pressures here are important here to ensure safe pressures and an aspirational goal of <25 cmH20 seems reasonably. Volume vs pressure control is a great debate it seems but my own preference would probably be volume control for what it is worth. Finally my preference would be to have these people deeply sedated and even paralysed but there is an association between paralysis and a necrotic myositis that can be an issue in weaning and rehab and this is distinct from the usual ICU acquired weakness and myopathy. References: IBCC Deranged Physiology My talk at EuSEM 2021 David Tuxen on intensive podcast Tuxen, D. V. & Lane, S. The Effects of Ventilatory Pattern on Hyperinflation, Airway Pressures, and Circulation in Mechanical Ventilation of Patients with Severe Air-Flow Obstruction. Am Rev Respir Dis 136, 872–879 (1987).

This podcast explores the significance of post-cardiac surgery in the ICU and the management of these patients. It discusses key information gathering during handover process, monitoring drains, assessing abnormalities, fluid resuscitation, surgical bleeding, tamponade, imaging for diagnosis, management of atrial fibrillation, and leaving the pericardium open to reduce post-op fibrillation.

Welcome back to the tasty morsels of critical care podcast. Today we’re talking about dead space. While it may sound like something from The Expanse, we’re actually talking about the physiological concept of dead space here. This is pretty core physiology that crops up in clinical practice all the time so I think it’s worth thinking about. As usual this represents a sort of idiot’s guide to the topic with just enough information to scrape by in an exam and in clinical practice but likely with large gaps, simplifications and occasional frank errors in description. Definition is “the fraction of tidal volume which does not participate in gas exchange.” But let’s be clear the word participation here refers more to an inability rather than a surly choice by the dead space fraction not to participate as it didn’t get picked for football till last. The dead space fraction never has the option of participating in gas exchange as it never reaches any functional gas exchange surface. At its most basic (and that’s the only form I’m interested in) it can be split into: Apparatus dead space – the amount of gas in the circuit and associated dongles like ETT, an NIV face mask or an HME. Physiological dead space – this is split further into: anatomic- gas in the conducting airways and alveolar – gas in non perfused alveoli Phsyiological dead space usually takes up ~20-30% of the Vt. As mentioned above it splits into two components, anatomic and alveolar. As you can imagine the anatomic is pretty fixed but the alveolar dead space can vary markedly depending on V/Q matching. Anatomic dead space is ~2ml/kg (about 150mls) but this includes the oropharynx that will be bypassed with the placement of an ETT or even better a tracheostomy with both of these interventions reducing anatomic dead space. I think the most important clinical take away about anatomical dead space is that it is fairly fixed. Assuming a 2ml/kg anatomic dead space, if you’re ventilating someone at 8ml/kg PBW and want to reduce to 6ml/kg PBW the fraction of anatomic dead space in each breath goes from 20% to 33%. In other words, while you’ve only reduced the Vt by 20% you’ve reduced the portion of gas participating in gas exchange by a third. There is of course good empiric evidence that a lower Vt is better but in terms of clearing CO2 dropping the Vt disproportionately reduces the fraction of gas available at the alveolus and may cause big issues with your CO2. Indeed at some point a rate reduction rather than Vt reduction may be the more favorable factor to reduce overall mechanical power delivered to the lung. That all seees very persuasive and logical but is countered by the simple fact that it doesn’t seem to be true when tested. It seems that at very low Vt gas exchange continues to be more effective than one might expect likely due to 2 mechanisms beyond simple mass gas movement. laminar flow occurs allowing a central column of gas to move in and out there is expiratory gas mixing – basically diffusive gas mixing that ensures the right molecules are in the right place at the right time Moving onto alveolar dead space, there are a number of things that might increase it: reduced cardiac output: eventually lung units stop receiving perfusion parenchymal disease: air space cavities no longer with effective perfusion due to thickening of interstitium high airway pressures: ensures aerated alveoli but may limit blood inflow to the lung unit pulmonary vascular occlusion: eg PE (one of probably several mechanisms of hypoxia) Posture – this will affect the west zone of particular lung units The main consequence of increased dead space will be primarily seen in your CO2 with either hypercapnia or a requirement for a huge minute volume. As noted in the alveolar gas equation it will affect oxygenation much less but eventually it will impair oxygenation. Reading Deranged Physiology The unfortunately short lived and much missed basic science clinic podcasts from Steve Morgan and Sophie Connolly.

Welcome back to the tasty morsels of critical care podcast. Of the many things I poorly understand, I suspect that haematology holds a special place. Knowing the intricacies of the haematological malignancies was not exactly core knowledge for emergency medicine and to be fair an exhaustive knowledge is hardly key to ICM either. However in ICM there is a need to have a broad understanding of what some of the haematological acronyms might mean given that a fair number of these patients end up in the ICU. Most of this post will be navigating the basics of the diseases rather than super specific ICU management. Oh dedicates a whole chapter, number 101 to the haematoloigical malignancies implying that it is certainly worth our attention. As a broad definition haematological malignancies involve the bone marrow or the lymphoid tissue, they occupy a different niche in the oncology world with the haematologists running the show rather than the general oncologists. They are also distinct in histology and outcomes from the solid organ malignancies. We’ll start with the leukaemias and these can be split neatly into myeloid and lymphoid leukaemia. The cells gone bad in AML are the myeloid precursor cells, the cells gone bad in ALL are the lymphoid precursor cells. This type of statement is however only useful if you have any concept of how a myeloid precursor cell is different from any other type of cell in the bone marrow. The attached image on the show notes, comes from the leading source of all medical knowledge, wikipedia. It’s a nice overview of the different types of cells stemming (see what i did there…) from myeloid and lymphoid precursors. It clearly works really well as an educational aid in audio form… Myeloid cells differentiate into, well, most of blood cells that appear on your FBC, things like red cells, platelets, neutrophils, basophils. On the other hand, lymphoid cells have a much smaller and narrower family tree differentiating into different types of lymphocytes and plasma cells. For AML there are a variety of causes from various genetically triggered issues, to transformation from a myelodysplastic syndrome or related to prior chemo or radiotherapy. It also includes the very ICU relevant disease of acute promyelocytic leukaemia. As a result, expect to see more AML in the older adult population. ALL is much more common in younger people with a much heavier CNS component, hence the prevalence of intra thecal treatment. Each of the acute leukaemias has it’s own chronic version. With CLL being a form low grade lymphoma. CML begins as a chronic, somewhat indolent process that accelerates towards a blast crisis towards the end of the disease and for most people is more of a comorbidity than a malignancy. Lymphomas, understandably come from lymphoid cells, these could be b cells or t cells for example. Classically lymphomas get lumped into two big categories of hodgkins and non-hodgkins with the former generally having the better outcomes. Finally on the list of common haematological malignancies is multiple myeloma. This is a cancer of plasma cells which are the grown up and left home versions of B lymphocytes. In general plasma cells have developed to produce large amounts of proteinaceous antibodies and are triggered as part of an immune response. In myeloma they are inappropriately making large amounts of their specific protein or globulin reflected in the high total protein count and hyponatraemia associated with this disease. So that’s a very broad, sub medical student overview of the different malignancies but why would they end up in your ICU? Sepsis is probably number 1 on the list. People have no immune system due to marrow infiltration or their marrow being wiped out with treatment, and they tend to struggle with the old bugs. They get all the usual bugs that we see, but also we need to worry about candida and aspergillus, plus all their vascular access devices and a wide range of other opportunistic infections. Treat early and broadly and involve your micro or ID folk to be sure you’re getting the right cover for the known and unknowns. There are a number of rather intense treatments used for haematological malignancy that often precipitate an ICU admission. We’ve already mentioned infection which is a common sequelae of chemotherapy but we’ve covered a lot of the issues in tasty morsel number 34 on chemo agents. Overall chemotherapy treatment can be viewed in 3 stages: induction: achieving remission by making the level of leukaemic cells undetectable consolidation: eliminates residual undetectable disease – this is when you might tentatively start using the word “cure” maintenance: used sometimes in ALL and AML to maintain remission (stage 1) Predicting outcomes in these patients is tricky and historically there has been a degree of skepticsm in admitting them to intensive care as things end badly with a high degree of frequency. Oh quotes a large case series that currently puts mortality at 60% for this cohort of ICU patients. This is of course high but when you compare it to things like OOHCA it’s certainly not awful. Finally haematopoetic stem cell transplant is an increasingly used potentially curative treatment for all kinds of hematological malignancies. This has a whole variety of specific indications and complications and rightly deserves its own note in due course. Reading Oh Chpater 101    

Welcome back to the tasty morsels of critical care podcast. Today we’re looking at a small section of Oh Chapter 58 covering myasthenia gravis. I don’t think I’ve ever looked after a true myasthenic crisis in the ICU. Likely because they’re well managed by their neurologists on an OPD basis or well managed from an anaesthetic perspetive when they need an operation done. I have made the diagnosis twice de novo in the ED (or at least admitted them with that as the leadning diagosis) so it is out there. It does make excellent exam level material as there is some interesting physiology and compare and contrast type tables to be made comapring with other neuromuscular diseases. To give a flavour of what might you see in the ED (and these patients will rarely need ICU) it’s typically some kind of cranial nerve issue, typically ptosis and diplopia complaints, sometimes with some speech and swallowing issues. The cardinal features of the neuro dysfunction is flucutating weakness. Typically this is described as fatigueability. For example the ptosis isn’t too bad in the morning but by afternoon it’s much worse. Involvement of bulbar muscles (BTW, bulbar being an archaic name for the medulla and the cranial nerves that stem off it) should be recongised as a bit of a concern given that swallowing and airway protection fall under the remit of cranial nerves 9-12. The edrophonium test that you may have heard about in medical school can be safely forgotten about as it is no longer recommended. On the other hand the ice test can be used as a cool demonstration of the physiology. In its essence, the ptosis that improves after having some ice on the eyelids would suggest myasthenia. The pathophysiology of the illness is likely one of the more testable aspects here. Myasthenia is an auto immune disease where antibodies are made against acetylcholine receptors in the post synaptic neuromuscular junction. As a result Ach cannot bind to these receptors and therefore cannot complete the transmission of neurologic impulse to the muscle. The ice test works because NM transmission is apparently more efficient at lower temperatures. Once the diagnosis is made you can look super smart by thinking about their thymus as thymomas are found in ~15% of people with antibody +ve myasthenia. Many more are found to have some kind of abnormality in the normally negleted and unloved thymus. As an outpatient these people will typically be established on pyridostigmine, a nifty medication that potentiates the remaining ACh at the NM junction. They are usually immunosupopressed on some kind of steroid or maybe some azathioprine. Some may have had their unsuspecting thymus removed in the interim. In the ICU we’re likely to see someone in myasthenic crisis. This is commonly seen when tapering immunosuppressives or when faced with some sort of actue stress like spending time under anaesthesia while a surgeon ectomises some part of your body. There are also a large list of drugs that we can misprescribe that can mess people up. The fundamental feature of a myasthenic crisis will be respiratory insufficiency, this is defined as need for NIV or intubation. Remember it is unusual for myasthenia to affect respiratory muscles so if it is you’re looking at big trouble. Expect this to be a quiet, undramatic sort of respiratory failure. FVC and cough will quietly disappear without any of the usual increased work of breathing we usually use to quantify respiratory failure. Hence they look fine until they’re really not. There are a variety of vital capacity cut offs described as reasons to intubate. But as discussed in the GBS post these are somewhat arbitary. For exams a VC of 15ml/kg is certainly a good red flag to keep in mind. Conveniently the same number can be spouted for a question on GBS. Without getting into the weeds on NMBA in myasthenia, for a non depolarising agent like roc you can expect the effect to last much longer so people have suggested a smaller dose. Given that if they’re being intuabted in ICU the prolonged effect is much less of a concern as long as you’re runnning the sedation which of course you are. Once they’re in ICU and ick enough to be tubed we need chart ourselves and the patient a way out of this mess. The key treatments for both real life and for examinations are going to be plasma exchange or IVIG. Plasma exchange removes all the nasty antibodies. IVIG on the other hand does something akin to witchacraft and probably binds the antibodies. There is no clear data favouring one over the other with the only RCT being neutral but the trend it seems is towards PLEX. As is typical for these immune binding/removal type therapies they need an immunosuppressive “chaser” to stop production of more autoantibodies. Typcially this will be steroids and typically you’ll not be making the decision anyhow. The more interesting question for us is time to resolution. A common quoted median is 2 weeks of invasive ventilation. This is much shorter than might be expected for a GBS case where it is not uncommon to intubate and tracheostomise in the same day given the expected course. For myasthenia it might be reasonable to give them some time to assess response to treatment before commiting to the tracheostomy. In terms of meds to be cautious with, the list is long but the commonly implicated bad actors include NMBA, aminoglycosides, the fluroquinonlones and crowd favourite magnesium is more likely to cause NM weakness than usual. Finally it’s worth knowing that there is such a thing as a “cholinergic crisis” desrcibed in myasthenia that is due to excessive cholinergic effects from too much pyridostigmine. It is vanishingly rare at this stage. It’s interest is that it forms another cause of respiratory failure in the myasthenia patient that you might mistake for a myasthenic crisis but if you’re a betting man or woman (and in medicine we all are) then if your myasthenia patient has respiratory failure it’s goint to be the myasthenia almost every time References UTD Oh’s manual 58  

Today's episode of Tasty Morsels of Critical Care delves into the topic of aspergillosis, discussing its different types, challenges in diagnosis and treatment, and risk factors associated with the disease. They also highlight the difficulty in distinguishing colonization from invasive disease and emphasize the need for expert advice in treatment decisions for chronically comorbid patients infected with COVID-19.

Exploring salicylate poisoning in this episode, covering symptoms, metabolic effects, diagnostic cues, and complications like CNS penetration and acidosis. Delving into management complexities, blood pH role, absorption, and treatment strategies. Discussing hemodialysis criteria, pH maintenance, intubation challenges, and the link between INR and salicylate poisoning.

Welcome back to the tasty morsels of critical care podcast. This time round we’re going to have a look at some chest wall injuries you should know about. The main reference here is Oh’s manual chapter 79. The vast majority of what we see here is going to be simple pneumothoraces and the elderly patient with some rib fractures and contusions or a developing pneumonia. That kind of thing is our bread and butter. This post will focus on some of the more esoteric injuries which of course occur with disproportionate frequency in fellowship examinations. There are a fairly small number of immediately life threatening injuries we need to recognise and the list could include: tension PTX open/sucking PTX massive haemothorax pericardial tamponade Massive haemothorax is typically defined as >1500mls immediately or more than 200ml/hr is certainly a concern that should prompt a surgeon to have a look inside. While not mentioned in Oh, the main concern with these is a sort of “damned if you do, damned if you don’t” scenario. When presented with a massive haemothorax and hypotension, it is not always immediately clear what the primary physiology causing the hypotension is. For example a large haemothorax with tension physiology will kink the SVC and obstruct the IVC leading to hypotension due to low preload to the heart. They may also be hypotensive form frank hypovolaemia because all the blood is in the pleural cavity instead of the blood vessels. The bit you can’t account for is how much this tension phenomenon is actually providing some kind of tamponade effect and keeping the remaining intravascular volume in the vasculature. The concern here is that when you decompress the haemothorax the patient is no less hypovolaemic than they were before. The blood is now in the chest drain rather than the pleural space. This hasn’t really fixed the hypovolaemia but has relieved the tension phenomenon obstructing the preload to the heart. Unfortunately it may have also unleashed the remaining circulating volume to enter the pleural cavity and swiftly out through the plastic conduit you’ve placed and into the chest drain. All this is a very long and convoluted way to say that it’s complicated. I think we will always end up draining that massive haemothorax but it would be wise to have someone capable of dealing with major bleeding inside the chest, immediately on hand. Speaking of thoracotomies, what follows is a list of interventions that might be potentially useful to do once the chest is open. drain pericardial tamponade, this is 1st, 2nd and 3rd for me in terms of importance and utility. control intrathoracic bleeding – which is a nice coverall term for all the various bits blood could be squirting out of control of massive broncho venous embolism. In this scenario a pulmonary vein is lacerated and air is being entrained into the left side of the heart. This is bad form as one might imagine so it would be wise to clamp it control of massive bronchopleural fistula. Maybe a lung has been avulsed proximally and you can see the ET tube through the bronchus. All the Vt is disappearing into the pleural space and you should something to stop it temporary blocking of the aorta. Commonly done in an attempt to preserve the circulating volume to the heart and brain. You might better achieve this without opening the chest with a REBOA or a SAAP catheter but that’s a whole different kettle of fish internal cardiac massage. In terms of aortic injuries these are often fatal pre-hospital but if you do find one they’ll typically be at the junction of the fixed and tethered aorta and the slightly more mobile arch. This junction occurs at the isthmus  just distal to the take off of the left subclavian. Your cardiac surgeons will likely decide but this may be an open repair or some kind of TEVAR type stenting if they survive long enough. As mentioned briefly above, tracheobronchial injuries can be a real challenge. The classic region of injury in blunt trauma is at the take off point of the right main possibly because of the steep angle from the trachea. Expect to see a PTX and some mediastinal emphysema. In itself, that might not be a big issue but the real clincher to the diagnosis is the massive PTX and emphysema that occurs when they get intubated and transition to positive pressure ventilation. The flexible bronch is your friend here and allows you to confirm diagnosis as a quick look down the tube will let you see mediastinum and pleura through the bronchus. Systemic air embolism is more typical in penetrating than blunt injuries and again the problems really begin when you move to positive pressure ventilation. In this instance we’re talking about pulm vein or maybe SVC injury. In negative pressure ventilation the pressure in the pleural space is lower than in the vasculature so blood will flow into the pleural space which is a problem in itself, however this pressure gradient will ensure air is not entering the circulation. Once intubated and in positive pressure ventilation then the gradient reverses and air can enter the vasculature with disastrous haemodynamic and even neurologic consequences if it enters the left sided circulation. A few rescue moves might be to selectively intubate the good lung, get them spontaneously breathing by reversing the rocuronium and get them on 100% O2 in the hope of switching out the non absorbable nitrogen for oxygen.  Thoracotomy is likely the next step but again a decision for the surgeons. There are of course other chest injuries out there but I suspect that’s plenty of exam worthy minutiae for today. Reading Oh’s Manual Chapter 79