Tasty Morsels of Critical Care

Welcome back to the tasty morsels of critical care podcast. Today we’re going to look at the red stuff – blood, and when to give it. This will cover some of Oh’s Manual chapter 97 covering blood transfusion. But we’ll have a focus on transfusion targets. There’s a nice narrative of evidence here over the past 20 years that has given us a relatively robust evidence base for practice in this area, something quite novel in critical care. Blood is expensive and unlike fossil fuels currently remains a renewable resource in the healthy population, it is obviously quite limited and nations frequently experience shortage of various blood groups and products that can have significant impacts on health care delivery. The red cells we give undergo a number of changes in the donation process with “storage lesions” becoming more prevalent over the duration of storage. A list of potential problems with stored red cells might run as follows: red cells change in shape biconvave to spherocytes (echinocytes) losing flexibility change in red cell membrane leading to sticking to the endothelium (esp in activated states like sepsis) 2,3 DPG depletion (which means Hb holds onto Oxy) reduced NO progressive increase in K+ acidosis The ABO reactions of transfusion should be dealt with by good governance of your transfusion service but fevers and other reactions are still an issue. The wonderfully named TRALI and TACO are also well described and space precludes a detailed discussion of these in this post. Now that we know giving red cells is not an entirely benign intervention we are left with the question that all competitive limbo dancers are faced with on a daily basis – how low can you go. What would be an appropriate Hb target for a critically ill patient. So let me tell you a little story… back in the late 90s when i was binging on OK Computer some Canadians led by Paul Hebert produced a large observational cohort of ICU patients called the TRICC trial suggesting that those with lower Hb did poorly and those who got more transfusions did better. But they were good empiricists and acknowledged that this could all be confounded by unmeasured factors. The only way to deal with that is randomisation and so 2 years later, Paul Hebert was at it again producing the TRICC 2 trial. This time an 800 pt multicentre randomised trial looking at Hb of 7 v 10. The headline result here was that the restrictive group did at least as well and probably better than the liberal transfusion group. This was a major trial and I’m pretty sure triggered a major change in practice. The caveats to this were as expected – those with ischaemic heart disease should probably have a higher target. Things went quiet for a few years but in 2010 we saw the TRACS trial from Brazil looking at one of the sacred cows of transfusion targets – cardiac surgery. Can we lower the Hb target in those with dodgy coronaries? They looked at Hb 9 vs 10.5 and found no difference. Villaneueva in 2013 took on upper GI bleeds. They smartly excluded the unstable active bleeders but in 500 patients randomised to 7 v 9, the lower target won out. The trials started to come thick and fast now with TRISS trial in 2014 taking on sepsis. The problem in sepsis is oxygen delivery so surely more Hb is good. But yet again, in 1000 pts with sepsis there was no benefit in targeting 9 vs 7 2015 brought the TRIGGER trial (hopefully you’re starting to see the unofficial naming convention here…) looking again at UGIB and again finding no benefit to the higher target 2017 brought the TRICS 3 trial, looking at 5000 patients undergoing cardiac surgery. Again randomised, this time 7.5 v 9.5, again no advantage to the higher target in 2021 they took on ACS patients in the REALITY trial, the most obviously ischaemic group and randomised 8 v 11 and no benefit to the higher target Most recently in 2025 the TOP RCT looked at vasculopaths having vascular surgery and in 3000 pts there was no benefit to the higher target. Phew… that’s a lot of trials but I think you’re starting to get the point that in general the answer to the question “what is your Hb target” is going to be 7-8 There are of course caveats to throw in at this stage. Firstly, it’s important to note that none of these trials looked at the exsanguinating patient where you should be targeting physiology like HR and BP and perfusion rather than Hb. Restrictive Hb targets are in general questions for the daily ward round rather than the massive transfusion protocol. Finally, in the past couple of years we’ve seen 2 RCTs looking at critically ill patients with sick brains. One looking at TBI and the other looking at SAH. Both suggest that if you have a sick brain you probably should be targeting a higher Hb of 9 or so. When you look at their outcomes the differences do not reach statistical difference in either trial but the trends are clearly to my eye towards more blood leading to better outcomes. Reading: LITFL has a lovely written summary of all the major trials I have included the two neuro trials here as they’re not noted in the LITFL summary Turgeon, A. F. et al. Liberal or Restrictive Transfusion Strategy in Patients with Traumatic Brain Injury. N. Engl. J. Med. (2024) doi:10.1056/nejmoa2404360. English, S. W. et al. Liberal or Restrictive Transfusion Strategy in Aneurysmal Subarachnoid Hemorrhage. N. Engl. J. Med. 392, 1079–1088 (2025).

Welcome back to the tasty morsels of critical care podcast. Today we look at something we do fairly frequently in ICU, especially in the post COVID era: prone positioning or to use its preferred technical term: adult tummy time. This has been around for a long time but was uncommonly done in the pre COVID days and was always a talking point when it did happen. But then 2020 came and you’d spend significant portions of the day proning and supinating patients in the unit. Fair to say it’s something we should have a keen understanding of. Firstly we’ll talk about the physiology and potential mechanism of benefit behind proning. This comes from the proning chapter in Tobin’s mechanical ventilation textbook. Written by none other than the late, great Gattanoni. He argues that there are 3 mechanisms by which proning affects ventilation and oxygenation changes in inflation redistribution of ventilation redistribution of perfusion A lot of this comes from Gattanoni’s early work where they managed to do a whole bunch of CT scans on critically people with ARDS in both the supine and the prone position. Yes you heard that right they did the CT scan prone. The typical CT scan for many ARDS patients is a basal dorsal distribution of disease. One would think that flipping the patient might redistribute this atelectasis to the ventral surface. But what seems to happen is more of a homogenisation of the lung with an overall improved inflation of the lung tissue. No longer are you just hyperinflating the baby lung and doing nothing for the atelectatic lung. This should lead to better recruitment, better perfusion/ventilation matching, better oxygenation and in turn better clinical outcomes. There are some suggestions it may also aid secretion clearance which in a paralysed supine patient is obviously a problem. Proning (as we shall we see) does seem to improve outcomes but the precise mechanism is unclear. Improved oxygenation seems plausible but it may also be a reduction in VILI by having a more homogenous lung that is less prone to injury of the baby lung. Guerin (lead PROSEVA author) wrote a nice review article in 2020 highlighting that proning can make chest wall compliance worse. The anterior ventral wall is normally more mobile than the dorsal chest wall. When prone the ventral bit is now wedged and immobile against the bed hence the fall in chest wall compliance. However lung compliance is probably improved and now that the chest wall is moving less it’s probably increased diaphragmatic movement that recruits the bases. Overall compliance should improve. We turn now to the evidence base for proning our patients. This, like many critical care interventions, this  has a little bit of a narrative to it with some early trials lacking benefit followed by the paradigmatic trial that shapes practice. What follows is a brief summary of some of the important studies and is neither intended nor considered to be comprehensive. Back in the early noughties there were a flurry of RCTs looking at prone positioning in ARDS. The late and great Gattanoi was of course involved in some. The “dose” of proning was variable with sometimes only short periods like 6 hours being used. Results were variable and a 2011 meta analysis of 7 RCTs did not show a definitive mortality benefit but did suggest that those with the sicker lungs had a benefit Enter PROSEVA. A name, that if you’re going into an ICU viva, is probably something that you should keep in your head. This was 26 centres in France who were already experienced with proning. They took people with severe ARDS and randomised them to 16 hrs a day of proning vs no proning. They used mortality at 28 days as a primary outcome and they were looking for a 15% absolute reduction in mortality (which is pretty huge). It was, for obvious reasons, an open label trial. They enrolled 450 patients and found a 32% vs a 16% mortality favoring proning. It’s possible this trial found a benefit due to the dose – they proned for much longer than many of the other trials. It’s worth having some problems related to proning in your back pocket to pull out. The list of potential contraindications was initially quite long pre-COVID but it turns out that when your back is up against the wall we all became a little bolder with our proning. While you can prone the vast majority of patients it’s not going to be possible in those with unstable spinal injuries. One would think that abdominal surgery or advanced pregnancy might be a problem but you can usually work round this with some discussion with your surgeons. The main downsides (beyond the hassle factor) are related to safety. The facial oedema and skin injuries are not insignificant and no matter how careful you are some people just aren’t a great shape for proning. There is a chance that the ET tube can kink or dislodge either on the proning or on the head turns so you need to have a good plan in your head how to confirm this and get someone flipped back if they need it. Reading Tobin Chapter 49 Deranged Physiology  Prone Position and Mechanical Ventilation Guerin, C. et al. Prone Positioning in Severe Acute Respiratory Distress Syndrome. New England Journal of Medicine 368, 2159–2168 (2013). Guérin, C. et al. Prone position in ARDS patients: why, when, how and for whom. Intens Care Med 46, 2385–2396 (2020).

Welcome back to the tasty morsels of critical care podcast. Today we’re going to have a quick overview of the oesophageal balloon. If you’re directed to a patient in your long case who has an oesophageal balloon in, then you’re probably having a bad day. It would seem very unfair to have too many questions on this but an awareness of their existence and some cliff notes on their basic use might come in handy especially if you’re doing well and you’re in the medal type territory of the exam. Exams aside they’re a useful gateway drug into some important respiratory mechanics that are relevant to all of us. At their most basic these are fancy NG tubes with an inflatable balloon that should end up in the lower third of the oesophagus. Inflating the balloon with a small amount of air allows you to transduce the pressure at the area the balloon lies. While that sounds straightforward there are large sections of review papers dedicated to troubleshooting placement and means of assuring the number you generate is actually accurate. I refer you to the below references for further reading. The pressure measured is called the oesophageal pressure, often abbreviated to Pes because it seems the Americans won the spelling war on that one. Oesophageal pressure is a reasonable surrogate (with assumptions of course) for pressure within the pleural space. Once we have an estimate of pleural pressure we can subtract that from the plateau pressure displayed on the vent and we end up with a fancy number called the transpulmonary pressure. The transpulmonary pressure or Ptp is the distending pressure applied to the lung either from the muscles of spontaneous ventilation or from positive pressure ventilation from the ventilator. Whoopdy do says the examiner – you now have another number you don’t really know what to do with. What should we use this data for, the examiner is asking? Well a short list of useful aspects you can look at with the oesophageal balloon include compensating for the effect of the chest wall on respiratory mechanics appropriate titration of PEEP assessing the contribution of respiratory muscle use to potential lung injury assessing triggering and synchrony issues At this stage you’d be hoping the examiner is satiated and you can move on to something else but in the unlikely and terrifying event that they ask for more detail you might want to mention some of the following. Our typical approach to safe ventilation in the passively ventilated patient is to look at driving pressures and tidal volumes. But this takes no account for the contribution of the chest wall. In the very obese patient there is a lot of flesh pressing down on the chest wall, this leads to an increasingly positive pleural pressure. It would make sense that we would need more pressure to distend the lungs in this scenario. The balloon in this scenario will allow you to set your PEEP appropriately. The Ptp at end expiration needs to sit somewhere in the 0-10cmH20 range to avoid derecruitment and in end inspiration it needs to be less than 25cmH20. This may need a lot more PEEP or less driving pressure than you’re used to giving and the balloon can help you feel safe about doing that. In the patient weaning from the ventilator in a spontaneous mode the oesohpageal balloon can be used to make an estimate of the contribution of the patients muscular effort to the transpulmonary pressure. Your patient may be on 10/5 on a pressure support mode and you may well be lulled into a false sense of security that because the pressure numbers on the vent are modest then the pressures being exerted across the lung are also modest. What we are not measuring in this scenario is the distending pressure being applied to the lungs by the respiratory muscles, the Pmus. The balloon in this scenario can give an estimate of this as it reflects the negative pleural pressure generated by the patients inspiratory efforts allowing us to come up with a Ptp number that takes Pmus into consideration. Sometimes this might encourage you to increase the support from the vent, sometimes this might encourage you to increase the sedation depending on the context. So given all the wonderful things the balloon can do for us why are we not doing it on everyone? A list of reasons not to use oesophagaeal balloons might include cost – these fancy NG tubes are pricier than you would think compatible software on the ventilators. These frequently don’t come as standard appropriate placement. These are tricky to get right and knowing that the number generated is valid is not entirely straightforward. Lots of assumptions are made the Pes number reflects pleural pressure only at a single location and does not take account of heterogeneity. the evidence base is unclear if this adds anything over doing something like simply following the high PEEP table from ARDSnet. Interestingly several research groups (thinking the folk from Toronto or Luigi Camporata in london)  have used balloons to identify surrogate ways of measuring recruitment or estimating Pmus that we can easily measure on a standard ventilator set up. This may well be a way of bringing the important concepts of transpulmonary pressure to the bedside. Reading: The Toronto Mechanical Vent Course was an excellent intro for resp mechanics for me. They offer a virtual version Mauri, T. et al. Esophageal and transpulmonary pressure in the clinical setting: meaning, usefulness and perspectives. Intens Care Med 42, 1360–1373 (2016). Yoshida, T., Grieco, D. L. & Brochard, L. Guiding ventilation with transpulmonary pressure. Intensive Care Med 45, 535–538 (2019). Mireles-Cabodevila, E., Fischer, M., Wiles, S. & Chatburn, R. L. Esophageal Pressure Measurement: A Primer. Respir. Care respcare.11157 (2023) doi:10.4187/respcare.11157. Jonkman, A. H., Telias, I., Spinelli, E., Akoumianaki, E. & Piquilloud, L. The oesophageal balloon for respiratory monitoring in ventilated patients: updated clinical review and practical aspects. Eur. Respir. Rev. 32, 220186 (2023). Deragned Physiology LITFL

Welcome back to the tasty morsels of critical care podcast. This is the second of 2 parts on PE in critical care. The first focused on risk stratification and this one will focus on management. There is a link to a transcript of a more comprehensive talk with references on emergencymedicineireland.com for those keen enough to dive a little deeper. As noted in the last podcast this one leans very heavily on “in the my experience” level of the evidence pyramid and should be weighted as such. For this discussion I’m going to assume your patient is in the ESC High risk category, ie hypotensive with a PE on imaging and you’re satisfied that the PE is causing the hypotension. I do believe there is a tiny cohort of the PE population who warrant aggressive reperfusion even with a normal appearing BP but at this stage I cannot say I have any evidence or guidance to really identify who they are and back that up. For the original talk I gave on this to an EM audience, I split the interventions into helpful , distractions, and not helpful. It was probably a little bit of a provocative division if I’m honest. The slide is on the site for reference and viewing it will likely make what follows more edifying. For the resus room patient in the first 30-60 mins I feel comfortable to standby my assertion that a short list of “helpful interventions” should includes lysis, anticoagulation, noradrenaline, oxygen and some CPR. In the ICU however we’re often present both at the first 30-60 mins but over next hours and many of the items on the “distraction” list become a little more relevant with time. Number 1 on my list of helpful interventions is thrombolysis. As mentioned, if you have found PE and you have satisfied yourself that the sickness and hypotension you’re seeing is caused by that PE then you need to have a good reason not give thrombolysis. The evidence base is not high level RCTs but it is a class 1 recommendation on the ESC guidelines and the list of class 1 interventions is really quite short. In the 25 year old in resus with a massive PE day 3 after an arthroscopy the decision here seems pretty straightforward. However in the post trauma patient in the ICU with massive PE with a small traumatic SAH and an improving SDH and a recent laparotomy then the decision is orders of magnitude more complex and you may well find a very good reason why lysis is not an option. There is not a straightforward answer to lysis because it will vary from patient to patient but I would emphasis that it is a question worth dedicating a decent chunk of your cognitive bandwidth to. Dosing in an unstable patient is often 10mg of alteplase followed by 90mg over 2 hrs. Dosing in a cardiac arrest situation is typically a 50mg bolus. Anticoagulation is one of the other class 1 recommendations on the ESC list. Opinions vary on agent of choice. With my ICU hat on I will almost always advocate for UFH as I feel confident that if i stop it, the heparin effect will be gone in a couple of hours when the inevitable bleeding starts. Opinions vary and I know smart people who advocate for LMWH in this scenario with one of the arguments being you probably get more reliable and quicker anti Xa effect. Both the guidelines and your esteemed narrator recommend against volume resuscitation. Dumping a litre of crystalloid into the venous circulation will shift the IVS further towards the left impairing cardiac filling and doing the opposite of what you intended. A much better resuscitation fluid would be noradrenaline. This is remarkably effective in improving BP and perfusion and I have often used it when I am 90% sure the patient has a PE but haven’t quite got the CT scan to prove it. The noradrenaline can also buy you a little time to make a better decision about the lysis and reperfusion, converting what would have been an immediate decision into something that you maybe have more like 30 mins to make. Certainly if the noradrenaline dosage is rising and the right heart is struggling then adrenaline would be my add on inotrope of choice. Of course we know in the ICU we have a plethora of other agents available to us with lots of theoretical advantage on pulmonary vascular resistance etc. They would rarely be my first line, certainly not in the ED population but I would often reach for them a little further down the line once i have a better handle on the physiology and what they might tolerate. Enough to say that staring someone on 0.5mcg/kg/min milrinone as a single agent with a starting BP of 60/40 is not likely to end well in this context Oxygenation is strongly endorsed given its proclivity for reduction in PVR, however intubating someone in this context to facilitate oxygenation is likely to result in a catastrophic haemodynamic collapse. The adage “resuscitate before you intubate” or even “reperfuse before you intubate” has some relevance here. I find CPR to be helpful in the context of massive PE, not simply for the usual reasons of preserving some degree of forward flow but I suspect there is a mechanical effect of breaking up or moving clot more distally. I have frequently seen stuttering intermittent ROSC in this context. I would suggest caution with the mechanical CPR devices as the presence of a liver lac in the context of tPA is unlikely to be well tolerated. While not available or that relevant to the emergency medicine population I do think the addition of nitric in the ventilated ICU patient who develops nasty PE seems like a low risk intervention with potentially massive gains. There is a small RCT of nitric in the spontaneous breathing PE population that did not however show benefit. I put mechanical devices in the “distraction” category in my original talk as I don’t think they have much relevance in the early stage of resuscitation. However if you have kept them alive long enough or if you have a true contraindication to lysis or a failed lysis then they may well have a role. I have found the evidence base so far here decidedly underwhelming and for catheter directed lysis in particular i struggle to see how a mg/hr tpa via a pulmonary catheter is any different than a mg/hr of tpa via a peripheral IV line given that the entire venous return ends up in the pulmonary circulation either way. The thrombectomy devices are certainly more compelling from a physiological perspective and the obvious and dramatic changes in physiology on removal of clot are quite compelling. But they are a tremendous faff requiring a catheter akin to an ECMO catheter to be threaded into the pulmonary circulation. The recent PEERLESS trial gave an average 90 min procedure time emphasizing the need to keep the patient alive long enough to receive the intervention. I do feel this has a role in our management quiver I am just unsure what that role is, but more evidence in the coming years will likely clarify VA ECMO is undoubtedly a fantastic physiological support for a dying PE patient but bear in mind it is almost definitely not available to you in the vast majority of hospitals in the Ireland and the UK. PERT teams are groups of relevant physicians willing to weigh in on difficult PE cases to advise on management. I put PERT teams in the distraction category. And I feel bad about that because they're usually filled with knowledgeable and enthusiastic people . But there are 2 errors I've seen on this that we should be aware of. One is on us as primary clinicians where we outsource the decision to lyse in someone who has a clear indication. This is not necessarily the fault of the PERT team but there is risk to the patient in delaying as it is a tremendous faff trying to get hold of the relevant people and then get them to agree. The second distraction that can happen is the recommendation for interventions in a patient that they have not seen and are not present to. A couple of times I have had to talk people out of IR interventions that frankly were not needed because the patient was getting better with conventional treatment. Do not underestimate the importance of being at the bedside and seeing the patient and evaluating response to treatment. Surgery, in terms of pulmonary embolectomy is the third and final class 1 recommendation in the ESC guidelines for high risk PE. All be it with a very low evidence rating. It gets talked about in papers and guidelines but you're talking about taking someone who is already mostly dead into theatre, lined, anaesthetised, chest opened and onto bypass. There probably is a role for it somewhere and in certain institutions and it's often raised in the context of contraindications to lysis but those same contraindications to lysis usually apply to the 30000 units of heparin you need to get them on bypass. It seems to suffer from the old goldilocks flaw of “not sick enough” for theatre or “too sick” for theatre I have clearly done way beyond my usual brevity in this scenario but honestly didn’t think anyone could tolerate a 3rd part on PE. Full refunds are available on request For further reading it is probably best to visit the original lecture post where the relevant papers are all listed with a little smattering of critical appraisal thrown in for good measure.

Welcome back to the tasty morsels of critical care podcast. I haven't managed to cover PE on the podcast yet. I have been involved in lots of small PE projects over the years and have developed something of an interest ... Read More »

Welcome back to the tasty morsels of critical care podcast. Hypertriglyceridaemua induced pancreatitis came up at a recent trainee presentation and I thought despite it being pretty niche and rare, it's still common enough that it might be fair game ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we're going to try and cover the not insubstantial topic of acute liver failure from Oh's Manual chapter 44. As you can imagine this will be a superficial skim ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we look at the other diabetes. We are of course all familiar with the sweet urine of diabetes mellitus but this time we will look at the tasteless or ... Read More »

Welcome back to the tasty morsels of critical care podcast. Following on from the recent post on Heparin, today we're going to talk about one of its more significant complications – Heparin Induced Thromboyctopaenia or HIT for short. In my ... Read More »

Welcome back to the tasty morsels of critical care podcast. Following on from our initial post in this entirely accidental series on “things you don't want to find in the chest drain” we turn our eyes (if not our noses) ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we look at quite a niche topic, that of chylothorax. We are used to many things in the pleural space, like simple fluid or blood or air but the ... Read More »

Welcome back to the tasty morsels of critical care podcast. We're going to cover a bit of an environmental/tox topic today and look at carbon monoxide poisoning from Oh's manual chapter 83 on burns. I have previously covered this on ... Read More »

Welcome back to the tasty morsels of critical care podcast. We've been talking about pulmonary hypertension, last time we had a pretty broad overview with a focus on group 1 or pulmonary arterial hypertension. This time we're going to go ... Read More »

Welcome back to the tasty morsels of critical care podcast. This time we're looking at pulmonary hypertension. Mainly cause I recently had to give a talk on it so it's fresh in my rapidly diminishing brain cells and thought I ... Read More »

Welcome back to the tasty morsels of critical care podcast. Last time i was butchering my way through a diagnostic approach to hyponatraemia, particularly the forms likely to end up in the critical care end of the hospital. This time ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we cover an incredibly common inpatient issue – hypnatraemia. We'll often find 1 or 2 of these in our high dependency unit at any given time, mainly due to ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we'll cover some key exam content, all be it not something you're likely to run into in the ICU too often. The thyroid is a deceptive little organ, tucked ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we'll talk about one of the niche and shall I say “advanced” in inverted commas therapies in intensive care practice. ECMO. And to be precise we'll be talking about ... Read More »

Welcome back to the tasty morsels of critical care podcast. Way back in the way back in tasty morsel number 43 we discussed inotropes and vasopressors but there was a noticeable AHD analogue shaped hole in that post that i ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we're going to verge into challenging territory for an audio podcast in that we're going to the discuss the very visual topic of dynamic LV outflow tract obstruction. This ... Read More »

Welcome back to the tasty morsels of critical care podcast. Following hot on the heels of tasty morsel number 72 on cardio renal syndrome is its partner in nephron injury: hepatorenal syndrome. This gets covered in a sub section of ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we tackle a somewhat nebulous syndrome. Something we throw around with a few hand wavy explanations but often light on detail. Hopefully in a few minutes you'll at least ... Read More »

Welcome back to the tasty morsels of critical care podcast. Oh Chapter 37 is dedicated to NIV in the ICU and is probably worth some time given that this is a common respiratory support both in the ICU and throughout ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we're covering the ambitious topic of CRRT in the ICU. Something that occupies a central part of the daily job, but also occupies Oh Chapter 48, Irwin and Rippe ... Read More »

Welcome back to the tasty morsels of critical care podcast. Nestled towards the end of Oh Chapter 51 we have a section dedicated to SAH. Given that a lot of ICU bed days are given over to managing SAH, I ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we are going to talk about triggering on the ventilator. Now given the ubiquity of the word “triggering” in contemporary discourse I must confess that i do find it ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we are going to do our best to charm the yellow snake of the intensive care unit and cover the pulmonary artery floatation catheter. Like a lot, indeed practically ... Read More »

Welcome back to the tasty morsels of critical care podcast. This time we look at Oh Chapter 52, focused on cerebral protection. There is, I must admit some repetition and cross over here, particularly with tasty morsels 20 and 39 ... Read More »

Welcome back to the tasty morsels of critical care podcast. The subject of solid tumours in the ICU gets a whole chapter in Oh's hallowed pages, number 46. I suppose the term solid is in place to distinguish it from ... Read More »

Welcome back to the tasty morsels of critical care podcast. In yet another departure from the stone tablets of Oh's manual, today we'll talk a little about one of favourite gram +ve cocci: staphylococcus aureus. Diagnosis and management of infections ... Read More »

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 ... Read More »

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 ... Read More »

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 ... Read More »

Welcome back to the tasty morsels of critical care podcast. Oh chapter 26 devotes a whole chapter to this and for those of us in cardiac units the arrival of several post cardiac surgery patients a day in your unit ... Read More »

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 ... Read More »

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 ... Read More »

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 ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we look at everyone's favorite mould – aspergillus. We see a number of fungal infections in the ICU, most commonly it'll be the yeasts – forms of candida. Yeasts ... Read More »

Welcome back to the tasty morsels of critical care podcast. This time round we'll look at an oldie but a goodie: salicylate poisoning. I have not seen one of these in quite some time but it is a classic tox ... Read More »

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 ... Read More »

Welcome back to the tasty morsels of critical care podcast. Usually the topics here follow the well trodden path of Oh's manual, but we're looking at something primarily because it is  an ideal question for a fellowship exam. In this ... Read More »

Welcome back to the tasty morsels of critical care podcast. There's not a huge amount of notes on procedural stuff that I accumulated for the exams but I did collect some interesting bits on bronchoscopy, particularly because it was so ... Read More »

Welcome back to the tasty morsels of critical care podcast. Sometimes the tasty morsels are exam sized snippets of my knowledge on a given topic. More frequently they are literally all I know on the subject. Today's topic of parenteral ... Read More »

Welcome back to the tasty morsels of critical care podcast. This is number 50, so for all 7 of you out there, well done for making it this far especially when you can't even get CPD points for it. Today ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we'll look at everyone's favourite yeast – Candida. Firstly, remember the distinction between yeasts and moulds. Yeasts, like Candida species are single celled critters whereas moulds like aspergillus are ... Read More »

Welcome back to the tasty morsels of critical care podcast. Today we look at anaphylaxis. Oh's Manual 67 forms the basis for most of this. In many ways this is fairly straightforward. You give adrenaline and they get better. However ... Read More »

Welcome back to the tasty morsels of critical care podcast. This week we'll make a fly by at part of Oh Chapter 100 looking at haemostatic failure. The understanding of the haemostatic system seems a little like the universe at ... Read More »

Welcome back to the tasty morsels of critical care podcast. This week we're looking at the other ACS, the surgical ACS, the old abdominal compartment syndrome. This is common, especially in the surgical population and does not always immediately jump ... Read More »

Welcome back to the tasty morsels of critical care podcast. Oh dedicates an entire chapter, number 88 to CBRN issues. While not commonly seen you can rest assured that critical care will be expected to turn up and manage these ... Read More »

Welcome back to the tasty morsels of critical care podcast. It is with trepidation that I approach any topic that involves the negative feedback loops of endocrine control as I really struggle to keep it all straight in my head, ... Read More »

Welcome back to the tasty morsels of critical care podcast. Condensing all of “inotropes and vasopressors” into a single 5 minute podcast is of course doomed to fail but that's never stopped me before. The main reference for this is ... Read More »