Tasty Morsels of Critical Care

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 the hospital. Many of the benefits of NIV are similar to those seen with ventilation with the blue plastic tube through the vocal cords.For example you still get: positive airway pressure which recruits alveoli and improves oxygenation improved alveolar ventilation which improves minute volume and lowers CO2 reduction in work of breathing as the machine is doing some of the work stabilisation of the chest wall eg in rib fractures reduction in transmural LV pressures acting as a sort of poor man’s IABP (more on that later) The big advantage of course is that you get all the positives but avoid the blue plastic tube through the cords and all the hassle and complications that come with that. But it’s not all unicorns and rose petals, the mask itself has a tendency to macerate the face over time and patients who are already feeling breathless and suffocating often don’t take kindly to having a plastic mask shoved over their face. Even if they do tolerate the mask it is frequently difficult to make a decent seal and maintain that lovely positive mean airway pressure that you’re looking for. And while i did wax lyrical about the potential positives of positive pressure ventilation at the beginning of the post, it seems only fair to point out the negatives of positive pressure ventilation. It is clear that positive pressure ventilation is non physiological and is known to cause its own form of lung injury when applied through a plastic tube through the cords. The alveoli only see the pressure and care not which device it’s being delivered through, so there’s no good reason why NIV wouldn’t cause similar problems. This of course brings up the unanswered and quite entertaining controversy over P-SILI or patient self induced lung injury that hit its zenith during the worst days of the COVID-19 pandemic. There were back and forth letters in the journals between some of the heaviest hitters in the ventilation world bouncing back and forth whether they actually believed self induced lung injury was a thing. Now this is not the post to explore it, but perhaps suffice to say that someone sitting with a resp rate of 30 for a week on 80% O2 and a PEEP of 10 on NIV may well be undergoing some of the same lung stress that any typical ventilated ARDS patient may be undergoing. NIV is not necessarily a free pass. When it comes to modes, the names are, as ever, confusing and baffling. Overall they split into some kind of CPAP mode where airway pressure is constant throughout the respiratory cycle and a mode with pressure support set above the PEEP where the pressure increases above the baseline CPAP when the patient inspires. To make matters worse there’s no clear consensus in how the numbers are described. For example, our portable, single limb circuit, ward based NIV machines use the terminology EPAP and IPAP to describe the pressures with both numbers starting from zero. for example 10/5 would be a CPAP of 5 with an additional 5cmH2O pressure support whenever the patient expires. On an ICU vent this would be described as 5/5. When would you reach for NIV over say one of the aforementioned blue plastic tubes through the cords? Well there are a number of now well established indications where it is entirely appropriate to try and temporise with NIV rather than just putting the tube in. I’ll give a brief summary of a few of them below: Pulmonary oedema. the heart is poor, the lungs are wet and heavy and the sats are low. The patient is crying out for some CPAP. How might it help, let me count the ways. by increasing intrathoracic pressure you are decreasing the gradient of pressure between the low pressure at end disastole in the LV and the high pressure at end diastole in the aorta. As a result the LV has to do less work to pop open the AV and get blood moving forward to the aorta. This mechanism is somewhat akin (though probably not nearly as effective)  to the afterload reduction with an IABP. hence the description of CPAP as the poor man’s balloon pump improving oxygenation by recruiting alveoli reducing work of breathing by giving a little boost as the chest wall tries to expand those wet and heavy lungs applying a little +ve hydrostatic pressure to the alveoli to get the fluid back into the vasculature where the furosemide can do its glorious work of diuresis. there is a clearly proven benefit for reducing intubations and improving oxygenation though the signal for mortality improvement is not as clear. Exacerbations of COPD in this scenario the lungs are scarred and the airways constricted and obstructed. A minor sniffles can be enough to push them over the edge of respiratory failure and the CO2 is rising and the pH is falling and they do not have the respiratory reserve to up their work of breathing NIV, and in particular a mode with increased support during inspiration can improve the minute volume and clear the CO2 and wake them from their CO2 narcosis. This is a very well supported intervention with 14 or so RCTs showing benefit and an NNT to avoid intubation and death of 4 and 10 respectively . Asthma now we have rapidly strayed into the evidence lite zone. It seems somewhat counterintuitive that a disease where the main issue is difficulty breathing out would be helped by adding positive pressure down the airway but it may be that the extrinsic PEEP is helping them overcome the intrinsic PEEP, or it could be that its reducing the work of breathing or it could be any number of  potential arguable benefits. Still to be proven but commonly tried. ARDS For a long time this was firmly in the controversial box and many would have argued that ARDS needs low volume low pressure ventilation, all of which we can not control in NIV. Meaningful trials were lacking. Then COVID came along and we all went mad with the old CPAP handing out CPAP masks with the coffee and dexamethasone on the morning ward round. Allowing that the bilateral infiltrates of COVID meet the definition of ARDS by any standard then it seems that NIV had found a role in the world of ARDS. That role and how far you might push CPAP before biting the bullet and tubing them remains to be defined. Yes I can keep this person going for 2 weeks on 90% FiO2 and a PEEP of 10 but is that really the best thing to do? There’s no sarcasm here, i really don’t know the answer to that… Post extubation support so you’ve taken the tube out and they’re struggling, should you stick an NIV mask on or just put the tube back in? Again, data not exactly clear on that but it seems that if they’re failing extubation due to either pulmonary oedema or bronchospasm/COPD then it’s probably worth a go. hardly surprising seeing as they’re the two most solid indications we have already. If its’ not either of those then probably best just to put the tube back in.   Reading: Oh’s Manual of intensive Care chapter 37  

Delving into CRRT modes in critical care, the podcast distinguishes between IHD and CRRT, discussing CVVH, CVVHD, and CVVHDF. It explores scuff and sled as modes of renal replacement therapy, highlighting ultrafiltration processes and solute clearance rates.

Exploring the challenges of treating Subarachnoid hemorrhage, managing intracranial pressure, securing aneurysms, controlling blood pressure, and discussing delayed cerebral ischemia and vasospasm in patients.

The podcast discusses the concept of triggering on the ventilator, including the three types of triggers: time, pressure, and flow. It explores the importance of adjusting trigger settings on the servo eye ventilator to prevent auto-triggering. The failure of ventilator triggering is also explored, along with the role of intrinsic PEEP. The chapter concludes by discussing the differentiation between double and reverse triggering, and the significance of NAVA technology in precise breath timing.

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 all of these topics, I do not in any way consider myself to have great expertise in the topic but I have had to upskill as much as I possibly can in lieu of the typical mis spent youth doing cardiac anaesthesia that most of my colleagues have had. As such the source list for this post is quite varied in terms of its references. The focus here will be on the basis, the nuts and bolts of how to put in and what type of numbers you might obtain from a PAC. The insertion carries a lot of similar complications to any typical central vascular access procedure. But the big ones come from the fact that you’re trying to place the catheter through the heart rather than in close proximity to it. Perforation is of course a real possibility but perhaps more likely are nasty arrhythmias precipitated by the catheter irritating the myocardium. Expect to see this more in the cold, shocked post bypass patient or in someone who’s already having a lot of arrhythmias. The PAC is also famous for the knots it can manage to tie itself into that can make extraction more than a little challenging. There are lots of good materials online on insertion so I’ll only mention a few basics in passing. The tiny little balloon at the tip catches the flow of the venous return and pulls the catheter along with the flow. In the absence of flurosocopy it can be tricky to know quite where the tip of the catheter is at any given time so we use the changes in waveforms to tell us what chamber or vessel the tip is at any given time. The pattern we expect to see should be CVP waveform, RV waveform then PA waveform and finally a wedged waveform. If all plays ball the you should those patterns at roughly 20cm, 30cm, 40cm and 50 cm respectively. The challenge is usually transitioning from the RV to the PA and the key change in waveform to look for is the “step up” in the diastolic pressure from the RV waveform which has a diastolic in the low single digits to a PA diastolic which is in the low double digits. Once the procedure bit is done we typically take a CXR looking for the tip. Typically the natural curve of the catheter leads it to ending up in the right PA most commonly though this is by no means guaranteed. It can be tricky to tell from a simple CXR but ideally we want the tip in a West zone 3 part of the lung, typically in the inferior portions. West zones may be a distant memory from medical school but for our purposes the estimate of the left atrial pressure produced by our pulmonary capillary wedge pressure is only valid when the alveolar pressure is less than the pulmonary venous pressure, a situation that exists only in West zone 3. If you’re in zone 3 you should be able to see a and v waves (analagous to the a and v waves of the CVP waveform) In some of the linked papers at the end there are some excellent images of troubleshooting various waveforms. One of the more useful ones was dealing with the failing RV (the very scenario where a PAC is likely to be needed) In this scenario, the RV diastolic pressures can approach the PA diastolic pressures with a loss of the “step up” as you move into the PA. The key difference to note in this scenario is that when the PAC is in the RV the diastolic run off (the period before the next ejection) is upsloping and the disatolic run off is downsloping when the PAC is in the PA. There are lots of measurements we can take from the PAC. Directly measured PA pressures are of course useful but the typical catheters used these days also have a thermodilution filament built in so that we can measure continuous cardiac output (on the principle that the RV cardiac output is equivalent to the LV cardiac output). The contemporary catheters use semi random pulses of heat (up to 44 degrees) in order to calculate a thermodilution cardiac output. In general it needs at least a 15% difference in CO to be detectable and it averages things over 5-10 minutes rather than from beat to beat. There is often a “stat CO” measure that averages it over a more like 60 seconds. In another success of marketing over function there is typically a continuous oxygenation sensor at the tip of the catheter. This gives a continuous reading of the true mixed venous oxygenation but is probably worth calibrating with an actual co-oximetry reading from a blood gas taken from the tip of the catheter. With a PAC in place we have the potential for measuring the pulmonary capillary wedge pressure which given a long number of assumptions can allow us to infer things like a left atrial pressure or left ventricular end diastolic pressure, key variables for assessing the filling status of the left heart. The principle involves the tip being in a west zone 3 branch vessel, the balloon is then blown up creating a theoretical continuous column of blood between the tip of the catheter and the left atrium. Once wedged the displayed number will typically be a mean, however the PAOP should be obtained at end expiration and in end diastole which often means reviewing a screenshot with your monitor and using a cursor to identify the pressure, timed at the onset of the QRS. There of course are lots of subtleties and caveats to the number obtained and even more about how to respond to it. Finally if you want to be really hard core there is a way of compensating for the effect of high levels of PEEP (>10) on the PAOP. The transmission index (TI) gives you a “corrected” PAOP taking this into account. The TI is calculated by looking at the PAOP  in inspiration and expiration. The difference between these two numbers is then divided by the driving pressure on the ventilator, this is your TI. The corrected PAOP is then the measured PAOP minus the total PEEP multiplied by the TI. This type of maths does not translate well to audio format and indeed there are actually several of these calculations available just to make it even more confusing. There is a substantial literature behind the utility, or lack thereof of the PAC that has led to a massive decline in its use preceding the mid noughties when i started practicing. However they remain a key tool in the intensivists arsenal and if you deal with sick hearts on a regular basis it’s vital you have a decent grasp on charming the yellow snake. Reading: Irwin & Rippe Chapter 19 (an excellent source of a textbook if you want detail on any topic not particularly well served by Oh) Deranged physiology has as expected an even higher level of excruciating details for those interests, presented of course in an excellent fashion. LITFL – Bootsma, I. T., Boerma, E. C., Scheeren, T. W. L. & Lange, F. de. The contemporary pulmonary artery catheter. Part 2: measurements, limitations, and clinical applications. J Clin Monitor Comp 1–15 (2021) doi:10.1007/s10877-021-00673-5. – Bootsma, I. T., Boerma, E. C., Lange, F. de & Scheeren, T. W. L. The contemporary pulmonary artery catheter. Part 1: placement and waveform analysis. J Clin Monitor Comp 1–11 (2021) doi:10.1007/s10877-021-00662-8. – Teboul JL, Pinsky MR, Mercat A, Anguel N, Bernardin G, Achard JM, Boulain T, Richard C. Estimating cardiac filling pressure in mechanically ventilated patients with hyperinflation. Crit Care Med. 2000 Nov;28(11):3631-6. doi: 10.1097/00003246-200011000-00014. PMID: 11098965

This podcast discusses the changing perspective on admitting patients with metastatic diseases to the ICU, potential complications of chemotherapeutic agents, the importance of pre-treatment echocardiograms for oncologists when dealing with cardiotoxic agents, and the caution against using gentamicin in certain cases.

Explore the critical importance of maintaining proper glucose and oxygen supply for optimal brain function, the complexities of cerebral protection and blood flow regulation, and essential techniques for traumatic brain injury management in this entertaining podcast.

In this episode, they discuss the common types of Staph aureus infections in the ICU, including skin infections, sepsis, pneumonia, and bloodstream infections. They highlight the seriousness of Staph aureus bacteremia and the potential need for surgical intervention. They also explore the use of PET CT scan for diagnosing and managing infections, and provide guidelines for antibiotic duration.

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).