Tasty Morsels of Critical Care

The podcast discusses hepatorenal syndrome, a kidney dysfunction in advanced chronic liver disease. It delves into the diagnosis, pathogenesis, types, precipitating factors, and treatment options for HRS. The importance of proper diagnosis and reversibility before initiating continuous renal replacement therapy is mentioned.

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 have a few morsels more of information to stave off all the trainees who are undoubtedly much smarter than you on the ward round. But perhaps I’m getting too autobiographical already. This does not appear with any great frequency in Oh’s manual but there is a nice scientific statement from the AHA that is referenced below. Though when you call it a statement you imagine some nervous spokesman in front of a camera trying to explain why is boss has done something naughty. Instead this is a 39 page epic review of the topic. To start with there are apparently 5 types of cardiorenal syndrome. I’ll let that sink in. You all thought there was one didn’t you? Type 1 is the acute deterioration in kidney function seen in cardiogenic shock from ACS. Type 2 is the slow and chronic deterioration of kidney function in the chronically failing heart. They get sneaky with type 3 calling it renocardiac syndrome. You see what they did there they just reversed cardiorenal syndrome and called it renocardiac syndrome. In this scenario the kidney has acutely been injured and the consequences such as fluid overload cause heart failure. Type 4 is again renocardiac with the kidneys causing the heart failure but on a chronic basis. With me so far? Type 5 is the big bucket where they put all the left over disease that cause both kidney and heart failure eg things like amyloid, or sepsis or cirrhosis. Certainly when i use the term in daily practice i was only ever thinking of types 1 and 2 and that’s what we’re going to focus on in this  tasty morsel. Why does this happen. I’ll paraphrase the opening part of the pathophys section from the scientific statement. Conventionally we focus on poor forward flow from the heart causing poor renal perfusion, poor GFR and activation of the RAAS. But in the style of a telemarketing TV advert “wait there’s more”. Poor forward flow is by no means the only pathology and in fact high pressures on the venous side likely contribute to the phenomenon of cardiorenal syndrome. for example we know that a MAP of 65mmHg is a generic target for perfusion pressure for most organ beds. However the actual calculation of perfusion pressure is probably better represented as MAP-CVP. Therefore in those with CVPs chronically sitting in the 10-15 range, you are going to struggle to effectively perfuse their kidneys. You’ll even here this called congestive renal failure on occasion. Along the same lines it’s worth thinking about the impact of intrabdominal pressure on renal perfusion, those with tense ascites from heart failure are also going to struggle. There are of course much more complex neurohumoral, inflammatory type cytokiney thingies going on but as you can tell they are well over my head so I’ve skipped them for now. You might think that diagnosis of cardiorenal syndrome might be straightforward. We just check a creatinine and if it’s high it’s a problem. But there are a fairly bewildering array of tests available for assessing renal function beyond the very blunt stick of creatinine. Things that rejoice in names like NGAL or cystatin C or looking at albuminuria; all may have a role in teasing out CRS from other issues. Valuable as it is for filling the 39 pages of the scientific statement i can’t see any great relevance to the jobbing intensivist. Of note in the paper, and perhaps obscured by the detail of the available biomarkers is the note that fluctuations in creatinine are often poor representations of actual kidney injury. I took home from this discussion that as long as they are still diuresing effectively we shouldn’t be in a rush to hold the diuretics purely because the creatinine bumped. Of note as part of the diagnostic work up the statement does give a shout out to the much maligned and greatly missed PAC. This might allow us to effectively assess congestion while avoiding the terrors of hypoperfusion from volume removal. Moving swiftly on to management strategies I think it’s clear that diuretics have a clear role in congested heart failure patients. However there does seem to be a reluctance to give diuretics once the creatinine bumps up anywhere above the normal range. There is a pervasive (and unfounded) belief that loop diuretics are directly nephrotoxic and as such should not be given. But if we’ve been paying attention so far we’ll realise that congestion itself may be causing the kidney injury and decongestion may well fix things. Now of course we need to be a doctor about this and have a think about other causes of AKI beyond simple congestion but for the sake of the podcast we will assume that we have the correct diagnosis. Let’s say we have done the right thing and given a decent dose of loop diuretic despite the bump in the creatinine, we often encounter something called the “braking phenomenon”. This refers to the idea that we get less and less response to each successive dose of diuretic, and this can develop over hours. The pathophys of this is beyond the scope of this podcast but involves the nephron doing what it does best in a crisis and tries to hold on to more sodium. You can get around this by making a flanking attack on the nephron by bringing in something like a thiazide in addition. Indeed the concept of the Nephron Bomb covered in tasty morsel 68 (first made popular to me by Joel Topf known as kidneyboy on twitter) is a clinically compelling and somewhat entertaining way to approach pharmacology of diuresis. Of note there comes a certain point where no matter the diuretic stratgey the volume of wee wee produced is insufficient. And this indeed portends a poor prognosis. Ultrafiltration with whatever mode of RRT you choose seems a compelling option but has performed poorly in most trials to date. Either because it simply doesn’t work or possibly because those sick enough to qualify for an ultrafiltration trial have already found themselves in a category of patients likely to do poorly no matter what. This segues relatively nicely into a section of the document on palliative care. It is important to realise that a referral to ICU for refractory cardiorenal syndrome may simply be a sign that the patient is reaching end of life. Adding an extra machine to a patient at end of life is not good form and it is incumbent upon us to do the work to figure out if we have some degree of reversibility (eg from acute congestion) or if this is just progression of an underlying irreversible disease process Reading: – Rangaswami, J. et al. Cardiorenal Syndrome: Classification, Pathophysiology, Diagnosis, and Treatment Strategies: A Scientific Statement From the American Heart Association. Circulation 139, e840–e878 (2019). – 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). – Mullens, W. et al. Evaluation of kidney function throughout the heart failure trajectory – a position statement from the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail 22, 584–603 (2020).  

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.