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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 presence of the myseterious substance chyle is a much more unusual and note worthy event.

As a reminder of the basics which I of course knew implicitly and definitely did not have to resort to wikipedia to check…

Chyle is largely formed in the small intestine as the gut transports free fatty acids from the intestinal lumen. This combined with lymphatic flow is transported via the thoracic duct to the vasculature where it enters the circulation proper. The lipids in the chyle are transported in the form of wonderfully named chylomicrons.

The cisterna chyli is akin to the gall bladder of the lymphatic system, situated in the upper abdomen it drains a lot of the lymphatics from the gut before sending it on it’s jolly way through the diaphragm into the thoracic duct. Once in the thorax the thoracic duct has to run the gauntlet of the posterior mediastinum where it is frequently hunted and subjected to extreme violence by cardiothoracic or upper GI surgeons who are purportedly there for completely unrelated reasons. If the thoracic duct survives this odyssee then it drains into the sub clavian vein on the left.

As suggested, the commonest time we find chyle in the pleural space is when we notice the milky stuff in the drains that were left in place after said surgery. The other common context is apparently lymphoma or a number of other malignancies.

Chyle in the chest drain can be a yellowy milky thing or blood tinged. As a Deranged Physiology post quotes one group “to our surprise a quantity of fluid which resembled pale tomato soup was withdrawn”

To be definitive about the fluid you can measure triglycerides or even use electrophoresis to identify the above named chylomicrons.

Assuming we’re comfortable with the diagnosis, let’s turn to management. The duct is a fragile little beast, apparently too fragile for the surgeons to spot when they’re doing their original surgery and certainly not amenable to surgical repair. So like a lot of things in medicine it’s best to let the body sort it out itself and the body is best able to do this if we can reduce the flow through the duct.

Perhaps number one is the low fat diet, or at least providing fats in the form of medium chain fatty acids that can be absorbed through the portal vein bypassing the thoracic duct altogether. PN is naturally an option here. Our universal secretion dryer upper octreotide has also been used frequently and to effect.

This strategy appears effective in a certain somewhat undefined proportion cases. If it is not settling and still causing issues then our beloved friends in IR now have techniques allowing them to embolise the duct and our surgical colleagues, while not able to repair the duct can at least tie it off.

ReadingDeranged Physiology is excellently referenced, detailed and humorous in equal proportion

LITFL

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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 the old tasty morsels of EM series back when i was doing my EM fellowship exams.

As you no doubt remember from school chemistry classes, carbon monoxide is a colourless, odourless, tasteless gas produced when combustion occurs with insufficient oxygen.

We’re likely to see this in a couple of contexts.

1) the house fire victim, pulled from the fire unconscious and sick

2) the sub acute or chronic poisoning in a patient presenting with headaches and flu symptoms that seem to get better when they leave the problem environment. The classic EM example is the whole family who present with flu symptoms and no fever and even the dog is sick. We’re much less likely to see this cohort in the critical care side of things.

How does it make people sick? Haemoglobin is a fickle little protein, while evolved to carry oxygen to needy tissue beds it actually has a distinct preference not for our beloved oxygen but for carbon monoxide. Introduce some carbon monoxide at the alveolus and the haemoglobin molecule will bind to CO with an affinity 240 times that than for oxygen. I take that number of 240 somewhat at face value but I presume someone got a PhD from working that out. In visual form my preferred means of explanation for this would be the distracted boyfriend meme where the haemoglobin boyfriend looks longingly over his shoulder at the carobon monoxide while his oxygen girlfriend looks on in horror. Hopefully you get the idea.

So instead of having lots of circulating oxyhaemoglobin we’re instead left with lots of not especially useful carboxyhaemoglobin. Let’s imagine 50% of our Hb is now carboxyHb and 50% is OxyHb we’re left with a sort of severe fucntional anaemia where half of our Hb is out of action. One might be inclined to think that this is the major cause of morbidity and mortality in CO poisoning but in fact this is only a small portion of the problem. CoHb actually has a direct cytotoxic effect on things cytochrome oxidase and myoglobin function. As such it interrupts the whole process of oxidative metabolism and life as we know it.

We can measure the level of CO fairly easily, any blood gas machine worth its salt should be able to give you a break down of the types of Hb present in the sample. This is co-oximetry and typically it’ll show you oxy, deoxy, carboxy and met haemoglobins. All these different forms of Hb absorb different wavelengths of light. The lowly pulse oximeter does not have the subtlety to distinguish the different wavelengths as it only functions at wavelengths of 940 and 660nm. Indeed the pulse ox often demonstrates a non diagnostic number somewhere in the 80s rather than a true reflection of the CarboxyHb or OxyHb present.

Severe CO poisoning resulting in obtundation is going to have high level of COHb on our cooximeter. >10% is quoted but it’s more often over 30%. Patients are going to be pretty sick often from multiple pathologies but COHb on its own is enough to produce severe neurological injury, shock and even cardiac injury is also quite prevalent. Expect a high lactate given the disruption of oxidative metabolism. Resuscitate and investigate as you would any sick patient.

Treatment is nice and simple in that we just give loads of oxygen. Oxygen reduces the half life of CO in the blood quite dramatically, commonly quoted numbers are

• the haf-life of COHb in an FiO2 of 0.21 is 300 minutes
• the half-life of COHb in an FiO2 of 1.0 is 60-90 minutes

There is a substantial rationale and literature on the use of hyperbaric oxygen as a means of accelerated clearance of COHb. But the RCTs that have been done don’t seem (to me at least) to give a clear benefit. The Lindell Weaver NEJM RCT in 2002 did suggest a neuro benefit but only 8% of the patients in this trial were intubated. A follow up trial in 2011 by ICU steroid guru Djilalli Annane did not find a benefit . So if anyone should get this it might be the non intubated isolated COHb poisoining. This is not really our cohort. Our cohort is likely to be tubed, shocked, with multiple injuruies and not someone you want to transport cross county to put in a single person hyperbaric chamber for hours at a time.

ReadingOh Manual Chapter 83

Weaver, L. K. et al. Hyperbaric oxygen for acute carbon monoxide poisoning. The New England journal of medicine 347, 1057–1067 (2002).Annane, D. et al. Hyperbaric oxygen therapy for acute domestic carbon monoxide poisoning: two randomized controlled trials. Intensive Care Medicine 37, 486–492 (2011).

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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 through some management strategies that might keep you between the hedges on a night on call or a fellowship exam viva.

We briefly mentioned the PH specific drugs that someone might be on. The evidence base for these is almost exclusively in group 1 PH. But what should we do with these meds in someone with group 1 PH who has just arrived back from theater after a laparotomy and a hartmans and they’re on a bit of noradrenaline? The simple answer is continue them. The more complicated answer is you should usually continue them. For example there will be the very rare patient whose pulmonary vascular resistance is kept low in the community with a PICC line and an epoprostenol pump. They are critically dependent on this drug with a very short half life and it should be continued at all costs. Think about it like an adrenaline infusion running at 10mcg/min, not something you can tolerate a break in.

A recurring message from the review papers on critically ill patients with PH is to focus on treating PVR not PA pressures. This is a somewhat philosophical approach that reminds us that the PA pressures themselves don’t prognosticate especially well but a failure of flow from right to left will result in cardiogenic shock and death.

We have a lot of vasoactives to choose from in helping with this, most of which have varying impacts on the PVR. Vasopressin has some animal data suggesting it causes less rise in PVR than our beloved noradrenaline but take that with an appropriately loosely defined portion of salt given that animal data is not ICU patients. Milrinone seems like a great idea as an inotrope that is easy on the PVR but the often dramatic drop in SVR is often a disaster. Dobutamine has the benefit of at least having substantial clinical experience in PH patients even if the tachycardia and even worse the a fib is less than desirable.

The ventilator is a bit of a poisoned chalice. Not only do you have to tolerate a significant risk of peri-intubation cardiac arrest even once you get them on the vent you have to deal with the adverse effects of positive pressure on the RV. The only upside of the vent is that it might make them easier to oxygenate but only if the cause of the hypoxia was a big shunt physiology like a pnuemonia. Oxygen is a great tool for reducing PVR so if we can leverage that then that’s great. However, a lot of hypoxia in end stage PH is reduced mixed venous oxygenation due to low cardiac output and the vent does nothing good for this.

Once on the vent we want a goldilocks’s zone of lung unit recruitment. Too little PEEP we have atelectasis and shunt and hypoxia and vasoconstriction. Too much PEEP and we have overdistension which itself can raise PVR by squeezing the pulmonary vasculature. Finding that sweet spot for the PEEP is a whole post or 10 on its own.

While on the vent it’s a good opportunity to deliver some inhaled therapies. The original gangster here is of course nitric oxide which is one of our target molecules in PH. In a crisis and a failing RV, this might get you out of a tricky spot. But given its expense and not being widely available its worth considering other inhaled options, particularly intermittent nebs of iloprost or a continuously nebulised eporprostenol solution both of which i have seen implemented to good effect.

In terms of monitoring should we be reaching for a PAC? Well, take a step back to start with. We probably need the CVP more. The RV is the first downstream organ that suffers under the burden of worsening PH and if the RV is failing then the CVP will be rising. Like any monitoring tool, a PAC in itself is going to do nothing but provide you with scary looking numbers, particularly the PA pressures which, remember, you should largely ignore. But picking up a severely raised wedge for example might push you to be much more aggressive with your diuresis and left heart management. A continuous cardiac output monitor will allow you to titrate your vasoactives with a great deal more confidence and accuracy

The other monitor I would reach for would be echo. I am a self confessed echo phile so take that into consideration but one of my targets of treatment is going to be how the heart looks. Is the IVS becoming less flattened, is the RV less distended, is the TAPSE improving etc… Echo early, echo often in my book.

Atrial fibrillation is something of a right of passage in the ICU. Have you really been critically ill if you haven’t even had an episode of fast AF? When it comes to PH it’s often poorly tolerated and the approach to rhythm and rate control probably needs to be a bit more aggressive than usual. Our usual choice of vitamin A, amiodarone is a good start but you may need other agents like dig or even DCC to get control. A consistent message from the reviews is to avoid beta blockers. The negative inotropic effect on an RV that is already functioning at peak capacity is not going to be good.

Our first reaction when faced with hypotension is often to load with fluid, this makes sense when we think of the frank starling mechanism, we want to be sure our LV is appropriately pre loaded. But in PH the issue is a failure to deliver volume or flow from the right heart to the left. We can dump a litre into the venous side of the circulation but the PVR just stops it getting efficiently through to the LV. If your patient is hypotensive then the RV is already failing in its basic function of delivering volume and flow to the LV while keeping the CVP low. More fluid is almost never going to fix this.

Indeed diuresing the hypotensive patient may well be the way to go. If you can decongest the right side and reduce the bowing of the septum you’ll get both the RV and the LV working more efficiently

This is only a taster of things you might want to try in a critically ill patient with severe PH. It is important to emphasis that they are not evidence based overall. Most of it is interpretation of clinical physiology at the bedside and applying the available manipulations. Which is of course what makes it so much fun.2

ReadingMy own rambling review of pulmonary hypertension on JFICMI website.

2022 ESC Guidance

McLaughlin, V. V., Shah, S. J., Souza, R. & Humbert, M. Management of Pulmonary Arterial Hypertension. J. Am. Coll. Cardiol. 65, 1976–1997 (2015).Jentzer, J. C. & Mathier, M. A. Pulmonary Hypertension in the Intensive Care Unit. J. Intensiv. Care Med. 31, 369–385 (2015).Johnson, S. et al. Pulmonary Hypertension: A Contemporary Review. Am. J. Respir. Crit. Care Med. 208, 528–548 (2023).Barnett, C. F., O’Brien, C. & Marco, T. D. Critical care management of the patient with pulmonary hypertension. Eur. Hear. J. Acute Cardiovasc. Care 11, 77–83 (2022).

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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 should get it all written down before I forget it. We’re going to try it as a 2 parter. Part 1 will cover a broad overview of pulmonary hypertension and part 2 will focus on management strategies for a PH patient in the ICU.

Saying a patient has PH does not really tell you very much. All we mean is that pressures in pulmonary circulation are higher than they should be. Saying someone has PH and not quantifying it is a little like saying someone has cancer but not saying which organ or how advanced it is. We need to go a bit further than just say they have PH and quantify the cause or rather which group of PH they’re in. We also need some way of quantifying the severity of it.

The definition of PH since the 2022 ESC guidelines is a mean PAP of 20mmHg on a right heart catheter. Echo can be used to screen for “probability” of PH but the right heart cath is needed to make the diagnosis. Once you’ve defined that the pressure is high the real doctory work begins as you have to figure out the likely cause. The language the guidelines use is “group”. You should be able to put your patient into 1 of 5 groups.

To give an example you are handed over someone who has known PH. You dig a little deeper and see they have an mPAP of 27 on a recent right heart cath. Their echo shows a poorly functioning LV and severe MR. The PH here is going to be group 2, PH secondary to left heart disease. This is by far the commonest.

Or another example, you are told someone has PH. You dig a little deeper and see an echo report that says the left heart works well but the right side is dilated. You dig a little deeper and see the clinic letters describing severe end stage emphysema. This is likely to be group 3 PH, PH secondary to lung disease.

In both those examples the PH is a problem but it is a downstream effect of other disease. And unless you can fix the heart or lung disease then the patient is in trouble, indeed if the patient dies in the coming weeks to months it’s likely going to be the left heart disease or the lung disease that kills them.

Let’s spend a few minutes talking about group 1 PH, sometimes called PAH. This is rare but often very severe and progressive and comes with some unique medications so it’s worth discussing. These people should have normal lung parenchyma and normal left hearts. There are a variety of specific causes in group 1 but a lot of it is described as “idiopathic”. It is a progressive pulmonary vasculopathy where the tiny arterioles suffer intimal proliferation and eventual fibrosis due to a variety of vasoactive molecules. This transforms the pulmonary circulation from a very compliant, low resistant circuit into a narrow and stiff group of pipes. The right heart is evolved and very comfortable with assisting large volumes of blood through a low resistance circuit. In hroup 1 PH, the change in pulmonary vascular resistance is more than the right heart can cope with and the right heart over time starts to fail in its primary purpose of maintaining a low CVP while delivering preload to the LV.

Over the past decades a number of classes of drugs have been developed that target the vasoactive molecules that cause the vascular changes. These can be split into 3 classes

1) endothelin receptor angtagonists which do exactly what the name says: reducing endothelin. Drugs like macitentan fall in that category

2) PDE5 inhibitors. These inhibit the enzyme you expect from the name but the key outcome is that there is an increase in nitric oxide something that causes pulmonary vasodialtion. Sildenafil or tadalafil are two common drugs in this group

3) prostacyclins. These vasodilate and reduce proliferation in the vascular bed and typically IV epoprostenol is the drug of choice here.

These drugs have proven disease modifying benefit but only in group 1 PH. We have not been able to prove any benefit for those with PH from left heart disease or lung disease. The more severe their disease the more drugs they might be on. Some patients are even on IV epoprostenol in the community to keep their PVR compatible with life.

These 3 classes of drugs have had a significant impact on both length and quality of life in PH. But the prognosis in group 1 PH is still one of progressive irreversible disease in the longer run. There are lots of features that are well validated on an outpatient basis to determine prognosis however that is rarely the question we’re faced with. For example we know ICU admission is a poor prognostic sign in severe PH but this is generally the very point we get involved at. As usual i suspect decisions about prognosis in the ICU setting are typically decisions about limitation or withdrawal of life sustaining therapy and they all depend on reversibility. If someone with severe PH has a pneunonia then we can probably turn that around then that’s something to consider. However if the right heart and liver are failing due to worsening congestion from progressive PH then that’s a different question.

That’s enough for today and to give you an overview of PH, next time we’ll focus on some management strategies.

ReadingMy own rambling review of pulmonary hypertension on JFICMI website.

2022 ESC Guidance

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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 we’ll take a punt at how you might approach management. In an ideal world of course you would have all of the diagnostic tests back and you’ve been able to make a very solid diagnosis of the cause of hyponatraemia and you would institute a bespoke treatment course for the underlying disease and the resultant hyponatraemia. But as we all know in critical care we often work with less than ideal information and have to begin treatment while the diagnostic process is ongoing. Hopefully what follows will provide enough broad brush strokes to get you through a night on call or even worse a viva.

We’ll start with truly emergent situations. Older person presents to the ED after being unwell for several weeks. They have a seizure on arrival and a Na comes back at 105. This is a fairly solid indication to give hypertonic saline. In this scenario they are seizing because of the low Na and rapid increase of the Na is needed to stop the seizure. The European Hyponatraemia Guidelines would suggest 150mls of 3% saline over 20 mins aiming for a rise in the Na of 5mmol/L. This bit is usually pretty straightforward. The sodium rises, the patient stops seizing everyone relaxes but then the Na continues to rise, well above the 5mmol we wanted and a panic ensues.

The guidelines suggest a max rise of 10mmol in the first 24 hrs and 8 mmol/day after that. It is hard to overemphasise how easy it is to blow past that target unless you are paying attention. So how do you control the rise in the Na? If it’s rising too quick it’s often because the patient is losing lots of water through the kidneys which concentrates the plasma raising the Na in the blood. You can replace that water loss by giving a decent bolus of free water in the form of something like 5% dextrose. An alternative method involves using the wonderfully named DDAVP clamp. In this scenario you’re using the DDAVP to tell the kidneys to excrete less water therefore limiting the rise of the Na. I have not seen particularly strong data on one method vs the other for limiting the rise and indeed I have seen clinicians use either or indeed both to good effect.

The European guidelines do use the phrase “severe symptoms” as an indication for a bolus of hypertonic. Unfortunately it’s a little less clear what constitutes severe symptoms. A seizure seems fairly easy to define but “coma” is a little bit more vague. The guidelines are clear that you have to be able to put the symptoms down to the hyponatraemia and not some other cause. But as we all know patients often have multiple reasons to be obtunded including sepsis or intoxication or multiple other causes. As such the decision to give hypertonic can be a little subjective and fudgeable.

For many patients the best thing you can do is very little. A former consultant I worked for had somewhat facetious plans to start a hyponatraemia clinic that involved locking the patient in a room and denying them access to water and letting the body sort it out over several days. There is an element of truth to that as for many of the hyponatraemics simple fluid restriction and time will correct things.

Lastly, our hypertonic of choice is typically 3% saline with an osmolality somewhere in the range of 1000 or so. Typically we’re a bit reticent to give such concentrated solutions through a peripheral IV but there are a few papers suggesting that this is fine at least on a limited basis. I will say that once the hypertonic is in and you’re reaching for a 2nd or a 3rd you should probably be thinking about a CVC as the access for administration and indeed regular sampling is really helpful.

ReadingEuropean Hyponatraemia Guidelines

Oh Chapter 95

Khasiyev, F., Hakoun, A., Christopher, K., Braun, J. & Wang, F. Safety and Effect on Intracranial Pressure of 3% Hypertonic Saline Bolus Via Peripheral Intravenous Catheter for Neurological Emergencies. Neurocritical Care 1–6 (2024) doi:10.1007/s12028-024-01941-3.

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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 the requirement for frequent testing of Na levels that seems beyond the remit of normal ward level care. The approach I describe here is neither comprehensive or especially robust but it is how I approach it. Caveat emptor and all that.

The over bearing demyelinating elephant in the room in hyponatraemia is the risk of osmotic demyelinating syndrome (the pathology formerly known as central pontine myelinolysis). If we correct the Na too fast will our patients end up with a severe brain injury? This is rare but is a very real phenomenon.The brain is actually quite good at adapting to sodium levels that have lowered over a few days or weeks. Hence why the slow developing sodium of 120 often causes minimal or no symptoms. However once the patient is in this adapted state (as mentioned this probably is after a few days at a minimum) then a rapid return to baseline sodium can cause ODS. By contrast a rapid drop in sodium, eg over a few hours drinking litres of unnecessary water during a marathon, is poorly tolerated but the plus side is it can be corrected fairly rapidly without harm.

Most of the hyponatraemia we see admitted through the ED will be hypoosmotic hyponatraemia. The bucket here will include heart failure, cirrhosis, SIADH, tea and toast and beer potomania. I’m going to put these common ones to one side for a minute and look at some of the niche exam ones.

For example, i said hypoosmotic hyponnatraemia there, so presumably there could be an isotonic and a hypertonic verison. There is indeed. The isotonic hyponatraemias are usually from spurious results. For example, when you have high lipids (super high, like high enough to cause pancreatitis high) or high proteins (eg high paraproteins like myleoma) the measurement method can underestimate the sodium. You can work this out by always sending a serum osmolality. If this is normal but the Na is 125 and your calculated osmolality is low, then you have an isoosmotic hyponatraemia. You should then check the lipids and the protein. Hypertonic hyponatraemia is another strange beast. This time the tonicity is high from something else such as high glucose or mannitol drawing water from cells into plasma. Again a mix of clinical context and a serum osm will help you out here.

Let’s go back to the bread and butter (or should i say the “tea and toast”) hyponatraemia, the hypotonic or hypoosmotic hyponatraemia. Context as always will give you lots of clues, if the patient has consumed nothing but beer for weeks then the likely causes is beer potomania. If the patient has a new cancer then SIADH is high up your list.

I confess I lean heavily on the approach you can see on Deranged Physiology and have Alex Yartsev’s flow diagram saved on my phone and i look at it almost every time i’m trying to work this out. The first test (assuming you’ve confirmed this is hypotonic hyponatraemia) in this algorithm is urinary osm, the question you are asking here is whether the kidneys are doing what they’re meant to be doing in the face of a low sodium. A normal sane and functioning kidney will try and lose water to conentrate the plasma in order to bring the sodium back up to normal, in other words the kidney should be producing a dilute urine with a low osm. Next step is to check the concentration of sodium in this dilute urine. If the kidney is doing what it should be doing it should be holding onto to all the sodium it can and urine sodium should be low. The problem here is too much water, not enough solute. Think, beer potomania, tea and toast, and polydipsia. If the urine is dilute but the sodium is high then you know something has gone wonky in the kidney itself, typically AKI or resolving ATN.

On the other side of the algorithm we have a concentrated urine, in other words, a high urine osm. The kidney is holding onto water and concentrating the urine. This may be a very sane and sensible response by the kidney if you are frankly hypovolaemic from eg gastroenteritis. The kidney also gets tricked by a few conditions into thinking its hypovolaemic, things like CHF or cirrhosis where the kidney itself just mightn’t be being perfused very well. In this scenario you should have a concentrated urine with a high osm and a low urinary Na as the kidney holds onto Na for all its worth in an effort to maintain effective circulating volume. On the other hand you might find a concentrated urine with a high osm but a high sodium also. This tells us that the kidney is handling water reabsorption OK but has lost the run of itself when it comes to regulating sodium. Something may be strong arming the kidney into losing more sodium than it should, like thiazides or an external actor like ADH, in this case it would be inappropriate ADH, hence the syndrome of inappropriate ADH. In addition a lack of steroid (and in particular the mineralocorticoid part) or a dodgy thyroid may cause the kidney to lose sodium when you shouldn’t. Or of course this scenario could be due to intrinsic renal disease.

So that’s 8 or 900 hundred words running through the deranged physiology algorithm and you can imagine that simply looking at the algorithm would probably be a better use of your time so go do that.

Next time we’ll have a look at how we might manage hyponatraemia

ReadingDeranged Physiology – Wonderfully titled ” A Lazy Man’s Classification”

Oh Chapter 95

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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 in the neck, quietly secreting hormones and interfering in negative feedback loops. It usually restricts its mischief to outpatient clinics by running hot or cold on a chronic basis, occasionally hypertrophying and interfering with its more important neighbour the airway. But every now and then in a pique it decides it’s fed up of this low level mischief and uses its deeply embedded relationship with the rest of the body to wreak havoc.

We’ll split this into 2 parts, one when the thyroid goes on strike and is under active and the other when it goes bananas and secretes far too much hormone

Some basic physiology. Thyroid hormones are essential for all organ systems. The active forms are T3 and T4. T3 is generally the more active one. They are synthesised by incorporating iodine into tyrosine residues in thyroglobulin in the thyroid gland. Hence how iodine deficiency can cause a deficit in thyroid hromone. Their release into the circulation is stimulated by TSH. TSH causes endocytosis of this thyroglobulin into the follicular cells where they undergo hydrolysis into T3 and T4 which is released into the circulation. Both are highly protein bound to thyroid binding globulin.

Our first relevant condition is the wonderfully named thyroid storm. Most commonly you might see this as part of untreated Grave’s disease. It can be precipitated by the usual physiological stressors such as surgery or sepsis etc…

Expect to see (at least in an exam scenario)

• fever
• tachycardia or fast AF
• jaundice
• delirium
• heart failure
• eye signs or a goitre consistent with thyroid disease

For awareness there is a clinical prediction tool that rejoices in the name Burch-Wartofsky Point Scale. This includes most of the features listed above. It’s clear that the features listed above are fairly non specific and like always it’s likely just sepsis. But if something in the spidey sense tingles then finding undetectable TSH and high T3 or T4 should really get you going. In reality this is an incredibly rare diagnosis, one which in its fulminant form i have yet to see. Or perhaps more accurately one that i have failed to diagnose as yet. This is of course hardly surprising as it is hopefully clear by now on this podcast that I am not especially good at what i do and continue to put my appointment to my current job down as some kind of administrative error that is yet to be detected.

Once you’ve decided you’ve made the diagnosis then you’ll need a few basic principles of treatment. Firstly do a bit of resuscitation. There may well be some co existing sepsis so give some antibiotics. If they’re hypoxic give some oxygen. They may need some fluid or indeed they may be in congestive heart failure. The key is to do an assessment, this likely includes having a sneaky peak at the heart and the lungs with ultrasound. A commonly recommended treatment is propanolol to help with the tachycardia. Many patients will be hyperdynamic and tachycardic and giving a beta blocker may well be a good idea but giving a negative inotrope to someone who’s heart is a bit clapped out is generally considered bad form. The key message is to assess comprehensively and then decide.

For specific therapies, your list should include some steroids, this reduces the release of thyroid hormone from the gland. There is occasionally some coexisting adrenal insufficiency so you’ll treat that as well. You’ll need to use something like PTU (propylthiouracil) or carbimazole in order to block new production of thyroid hormone. Good luck finding PTU at 3am. Having performed one miracle in locating PTU you are now expected to perform a further miracle and find something that sounds more like a tonic you’d buy from a wild west apothecary. This is of course “Lugol’s Solution”. Only give this once thyroid production has been blocked (recommendations suggest an hour afterward). It contains typically a bunch of iodine and will block the release of any T3/4 left in the gland.

Your next patient in your exam viva comes from the opposite end of the spectrum. Myxoedema coma. As an aside, myxoedema coma is a terrible name, the patient may not have oedema or be in a coma. Again, Farkas on the IBCC uses the term “decompensated hypothyroidism” which i think is much more descriptive and accurate. This is hypothyroidism but not as you’ve seen it before. Typical features or as Josh Farkas calls them “cognitive triggers” to consider myxoedema coma include

• neuromusclular features like reduced consciousness, delirium, slow reflexes and weakness
• hyothermia. the classic is someone found unresponsive with a much lower temp than expected for the environmental conditions
• endocrine issues like low sugars and low sodiums
• cardiovascular features such as bradycardia, hypotension and pericardial effusion
• respiratory features like alkalosis and pleural effusions
• GI issues like ileus and weight gain

Again lots of these are non specific so keep the differential broad before anchoring too early. As expected TFTs will be helpful and in general expect to find a high TSH and low T3/4

Management will involve your usual assessment and resuscitation but the specific therapy here is IV thyroid hormone. It does exist but is also hard to track down at 3am. Your ICU probably has it and you’ve typically only seen it as part of management of a potential organ donor in brain death. T4 is the one typically recommended (which will converted intracellularly to the more active T3). But in Ireland the most commonly available will be T3.

These people also need steroid, typically some hydrocortisone for the ubiquitous adrenal insufficiency. Indeed giving thyroid hormone without steroid may cause an adrenal crisis.

Reading:Oh Chapter 61

Tasty Morsels of EM 130

The IBCC

Deranged Physiology

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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 VV ECMO. Indeed saying that you are “putting someone on ECMO” is a woefully incomplete sentence as the support and physiological difference between venovenous ECMO and venoarterial ECMO is really rather profound.

The post will be an intentionally broad description of the therapy and perhaps less on the nuances of managing a patient on VV ECMO, as at fellowship exam level I suspect you’d only be expected to have an overview of what it it is, what it can (and can’t do) and when to ask for it. I acknowledge the glaring gaps in the post and the likely criminal omission of the oxygen carrying capacity calculation. It would be fair to call this an idiot’s guide. And given that these posts are generated from my own notes then we all know who the idiot in that title it refers to is.

We’ll start at its simplest level, which is how i try to describe to friends and non medical people about how ECMO works. Blood is removed from the veins in one pipe and put through an artificial lung type device where CO2 is removed and Oxygen added, then blood is returned to the veins via a second pipe. If you’re lungs don’t work so well then the device can replace a lot of their function in the short term. Lay person explanation ends.

The degree to which we can replace lung function, primarily the degree to which we can oxygenate, is determined by the amount of the venous return coming back to the heart we can divert through the machine. Let’s say the cardiac output is a healthy 5L/min. That means that 5L/min is being ejected from the left ventricle and 5L/min is returning to the right ventricle. If the lungs aren’t working well then we need to capture at least 60% or so of this venous return and stick it through the oxygenator in order to maintain tolerable saturation of haemoglobin with oxygen. So in our example we’ll have to be siphoning off at least 3L/min from the venous return, putting it through the oxygenator and returning it back to the right side of the heart. With me so far?

It is at this stage that we immediately run into one of the physics challenges of VV ECMO. Pulling off 3L/min of blood requires pipes of substantial diameter. Typically these are in the 23 to 27Fr range. (ie 8-9mm internal diameter). You want to place this drainage pipe somewhere where there is a high flow of blood in a large vessel capable of accommodating it. Typically this will be in the SVC or the IVC, typically reached by an insertion point in the IJ or femoral vein respectively. It becomes really quite tricky to drain more than 3L/min of blood (or 60% of the venous return) with a single pipe as you can really only drain either the SVC (venous return from the upper body) or the IVC (venous return from the lower body) and as should be obvious the venous return from the body is split between these. In addition to the limitations of the physical size of the pipes you have to remember that the vessels within which these pipes are placed are not rigid fixed stented things, they dilate and contract in response to intravascular volume and intravascular tone. If you try to suck blood out of them with too much negative pressure the vessels will collapse around the pipe blocking all the holes and stopping all drainage.

All this to say that oxygenation is determined by the proportion of venous return we can divert through the ECMO machine. And capturing that venous return should be the priority when it comes to deciding on drainage pipe size and placement. once the blood is out of the body and through the oxygenator it turns out that it’s quite east to get it back into the budy. Pushing blood back into the body is much easier and can be done with a much smaller pipe. Pulling is harder than pushing in this context.

The key factor in returning blood back to the body in VV ECMO is 1) it has to return to a vein, hence the second V in VV ECMO and 2) it needs to return to the venous circulation at a healthy distance from the drainage pipe. It would be bad form to return 3L/min of beautifully oxygenated blood directly into the inlet holes of the drainage pipe and through the circuit for a second entirely pointless run. We call this re circulation and we get around it by placing the tip of our return pipe somewhat remote to the access pipe. For example we could drain blood from the SVC and return it to the IVC or if both of our pipes were in the IVC we could ensure that the return of blood happens much closer to the heart in the IVC or even in the RA but importantly a healthy distance away from where the drainage pipe is in the IVC.

Why would one want to initiate such a therapy? There are a number of indications, or should i say circumstances where VV ECMO might have a role. A reasonable list for examination purposes might run as follows.

• Refractory hypoxaemia is a good coverall term but better teased out into some specifics below;
  • ARDS where you can’t maintain safe settings on a ventilator or safe numbers in terms of oxygenation and CO2 clearance
    • of note you can squeeze in almost every pathologic lung condition under the ARDS umbrella so think pneumonia, pulm vasculitis etc…
    • this is the vast majority of VV ECMO runs.
  • primary graft dysfunction post lung transplant
  • refractory asthma
  • a bronchopleural fistula where continuing to ventilate with pressure is probably not the best thing for healing the hole in the lung.
• refractory hypercapnoea where the hypercapnoea is causing life threatening problems despite a thorough effort to fix it
• the occasional slightly bonkers airway surgery where you may have no means to oxygenate or ventilate for a substantial period of time

There is lots of debate and indeed variations in practice on when you might initiate VV ECMO. There are a number of published criteria for when ECMO is indicated but you have to remember that a single PaO2 of 6.5kPa on 100% does not actually tell you how sick a patient is or if you’ve truly exhausted your conventional management. Either way at the end of a viva question on management strategies for severe ARDS, once you’ve been through high PEEPs, permissive hypercapnoea, diuresis, proning, and a nuanced discussion on steroids and nitric you should probably mention VV ECMO.

It’s worth noting some reasons when doing VV ECMO is not a great idea. As with almost all intensive care organ supports there’s not much point in adding it if you don’t have a way to fix the underlying organ. For example, if you have ARDS from pneumonia we can probably fix that, however if you have end stage COPD we can’t fix that. Adding the device will not change things. There are some programs who will use VV ECMO as a bridge to transplant but this is beyond the scope of this post. But it is commonly used in the immediate post lung tx phase when the new lungs are a bit heavy, wet and not working too well.

If your circulation is falling apart and you’re on 2mcg/kg/min of noradrenaline and the LV is clapped out from septic cardiomyopathy then it’s hard to see how fixing the hypoxic part of the multiorgan failure is going to turn things around. That being said if you’re hypoxic with a struggling RV then adding VV ECMO might be enough to correct the circulatory issues simply by fixing the hypoxia and hypercarbia.

If you wanted to end your SAQ with a flourish and add some complications then a convenient top 5 might run as follows

• bleeding
• bleeding
• bleeding
• clotting
• bleeding

I am of course being a little bit facetious here but i’m not that far off the mark. Anticoagulation is typically used to keep the VV ECMO circuit running but even on those without anticoagulation they still bleed. And the bleeding is often spontaneously into non compressible sites like the pleura, GI tract or retroperitoneum.

References:Oh chapter 41

The ELSO red book

Alfred ECMO Site

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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 promised to discuss at a future stage. Well, that time has come and it’s time to run through vasopressin.

You probably first encourntered vasopressin when you heard about ADH in medical school. Anti diruetic hormone, named for what it stops Its discussion in medical school involved delving into the world of endocrinology and negative feedback loops. Something we will be studiously avoiding here. Vasopressin is an ADH analogue, very simillar in structure with very similar effects. As such vasopresin exhibits the same ADH effects but this maxes out at very low doses, much lower than what we use in sepsis. At the very high doses we use, much higher than the pituitary can secrete, it acts as a pure pressor without the inotropic effect we’re use to when using more familiar agents like noradrenaline or adrenaline.

How does it work? Well this is where the fun beings. We’re used to messing around with the adrenergic receptors but vasopressin opens up a whole new bunch of confusing letters that have a whole myriad of effects. Some of these receptors are even shared with other molecules like oxytocin. The main we’re interested in is the V1 receptor, this is found throughout vascular smooth muscle. Stimulating it causes calcium release from the sarcoplasmic reticulum leading to increased vascular tone. Note noradrenaline has the same mechanism (ca release) just through a different receptor. This vasoconstriction affects pretty much all the vasculature including things like the coronaries (not so good) but does seem to spare the pulmonary arteries meaning it may be good in those with pulmonary hypertension.

What other receptors is it worth knowing about? both for exams and the all important one-upmanship on the ward round. V2 receptors are mainly in the renal collecting ducts, this is where we get the ADH effect primarily be increasing the number and effect of something called aquaporin 2 channels. The V3 receptor causes increased ACTH, increasing cortisol secretion, and then there are the OTR and P2 receptors which my notes make no elaboration upon and i will make the dangerous assumption that they have no relevance to what we do in ICM.

Why pull out the vaso when we can get the same vasopressor effect from our beloved noradrenaline. In theory the vasopressin receptors should remain fully funcitonal in the depths of horrific metabolic acidosis that has led your patient into intensive care, the same acidosis in theory should be causing issues with the effectiveness of your catecholamines. It should cause less pulmonary arterial constriction than a catecholamine and should even have less tachyphylaxis. the above list of advantages seems to come straight from the manufacturers advert, so why doesn’t it come pre attached to every patient?

The issue gets a bit clouded due to the somewhat clouded evidence base. I’m going to run through a few of the bigger name trials that one may trot out in a viva type setting, and with all good controversial issues in ICM you could easily go the track of “on the one hand this and the other hand that” and come up with an answer with both buttocks firmly on the fence of the issue.

First up is the VASST trial, (Russel et al 2008 NEJM). Done in North America and Oz, they enrolled septic patients and randomised them to vasopressin vs a blinded infusion of 15mcg/min of norad. Once maxed out on the study drug, then open label additional norad could then be titrated to keep the MAP at target. Enrolled 800 fairly typical ICU patients, and found a 35% vs 39% mortality benefit favouring the vaso but of course this was below the somewhat arbitrary statistical significance. A somewhat underwhelming start

Second is the VANISH trial by Gordon et al, JAMA 2016. This was closer to home in the UK, with 18 ICUs. Septic patients randomised similar to the VASST trial, vaso vs blinded norad, this time at 12mcg/min. Primary outcome here was kidney based rather than mortality. 400 pts here, no clear benefit for vaso. Again, hardly compelling

Enter the meta analysis. Nagendran 2019 in CCM. This was of a decent standard being not just a mix of numbers from the trials but an individual patient meta analysis that takes individual patient data points rather than the trial aggregate. This included all the trials but unsurprisingly VASST and VANISH make up most of the numbers. No mortality benefit found but there was less need for CRRT and less arrhythmias. There was some more digital ischaemia but no clear sign of increased mesenteric ischaemia.

Hence the “on the one hand this, on the other hand that” and widely varying opinions on use of vaso. It would be perfectly reasonable to say this drug adds nothing to usual practice and i’ll stick with my catecholamines. And lots of other reasonable people look at the data and say, well this is a catecholamine sparing agent and is a balanced approach to receptor manipulation and just might spare a few filters. As you can imagine (though please don’t actually imagine this) my buttocks remain firmly on the fence getting splinters.

ReadingDeranged Physiology

LITFL

Russell, J. A. et al. Vasopressin versus norepinephrine infusion in patients with septic shock. New Engl J Medicine 358, 877–87 (2008).

Gordon, A. C. et al. Effect of Early Vasopressin vs Norepinephrine on Kidney Failure in Patients With Septic Shock: The VANISH Randomized Clinical Trial. Jama 316, 509–518 (2016).Nagendran, M. et al. Vasopressin in septic shock: an individual patient data meta-analysis of randomised controlled trials. Intens Care Med 45, 844–855 (2019).

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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 is something fairly dependent on echocardiography for diagnosis which as you can imagine translates poorly to audio format. This also means you’ll be denied my interpretative dance as i simulate the mitral valve leaflets being pulled over towards the septum via the Venturi effect. But alas i digress.

In essence dynamic LVOTO occurs when the closure point and tips of mitral valve tips are pulled into the left ventricular outflow tract during systole forming an anatomic obstruction to LV outflow thus reducing SV, CO, perfusion etc… This is reflected in poor blood pressure to which we respond by giving more catecholamines which makes this whole thing worse in a horrible cycle of nastiness.

Perhaps it’s best to start by identifying contexts where we should be on the look out for this. We’ll start with sepsis. Sepsis is a state of low systemic vascular resistance leading to reduced preload and afterload in the heart. The LV receives less than usual volume to stretch it and the low afterload makes it incredibly easy for the LV to empty itself of this load. This results in a small cavity LV where the LVOT and the mitral valve find themselves in much closer proximity than they are normally used to. If it gets out of hand bits of the mitral valve find themselves in the LVOT itself causing all kinds of bother.

The incidence of dynamic LVOTO in those with septic shock is remarkably high and is reported to be 20% in one study from ICU echo guru Michel Slama. Even if it’s not that common it’s yet another reason why the super shocked patient should get a timely echo.

So let’s say we’re worried about our septic patient: within that cohort who is at risk? Classically it would be the older person with LVH or a thickened septal bulge, sometimes called a sigmoid septum. Going with that is a stiff ventricle that fills poorly and has diastolic dysfunction.

As noted at the beginning it’s clear that echo is a key part of the diagnosis here and if you do one you may see some of the baseline features just mentioned but with the addition of SAM or systolic anterior motion of the mitral valve. Most dynamic LVOTO has SAM but not all SAM has LVOTO. SAM can be quite a common out patient echo finding and so in addition to SAM you might want to look for flow acceleration. Just as a river approaching a narrow point accelerates and becomes turbulent so does blood flow in the LVOT approaching an unwelcome and intrusive mitral apparatus. This flow acceleration can be easily measured with doppler and produces characteristic patterns that get echo nerds like me all hot under the collar and is largely beyond the scope of the podcast.

Before we get onto management I want to mention another at risk cohort. These are usually easy to spot as they return from theatre with a big sternotomy following an AV replacement or mitral valve repair. To take the example of the aortic valve. Aortic stenosis leads to severe LVH as the LV has to generate an enormous pressure to get the crusty calcified stenotic valve to open. The heart slowly adapts and learns to live with this very high afterload. Then one day someone opens their chest and pops in a nice shiny new valve that opens like a dream. The LV is not used to this and continues to eject blood like pompeii on a bad day. This hyperdynamic contraction in an LV not used to it has a tendency to drag the mitral apparatus into the LVOT forming an obstruction. Patients following MV repair are also at risk as the change in shape of the annulus and final position of the coaptation point at end repair can also lead to the MV getting pulled into the LVOT. If you’ve ever done the TOE board examinations you will curse yourself learning the 8 echocardiographic risk factors for SAM post MV repair…

So we’ve talked about what it is, and a few at risk populations (sepsis and cardiac surgery). The clinical appearance is typically rapidly worsening shock and rising pressors, hypotension and rising lactate. Let’s say you’ve even managed to diagnose it using echo. How should you manage the thing?

Increasing the preload can help, typically best done with volume expansion. Part of the mechanism here is an empty LV so filling it up can help. You can of course increase preload with noradrenaline but it comes with the unfortunate side effect of inotropy which is how we got into this mess in the first place. As such you find yourself having to do something quite uncomfortable and reduce or stop your catecholamines even when you think they might be keeping the patient alive. If that’s not bad enough, you probably want to swap them out for…. eughhh, and i struggle to say this… phenylephrine… Much derided and neglected it may well have a role here and it does hold the title of “pure alpha” and as such gives pressor effect without inotropy. Vasopressin is of course a reasonable option but as you know it is not the most titratable drug.

The next step might make you even more uncomfortable. Understandably these patients are often very tachycardic. This tachycardia leaves less time for diastole, less time for cardiac filling, again worsening the LVOTO. As such beta blockers become a very attractive option. Even though beta blocking a very sick patient seems like a slightly insane idea. But of course you’ll only be doing this after a high quality, well interpreted echo that shows a hyperdynamic LV so that should give you a little reassurance. Esmolol is probably the agent of choice here given it’s titratability. The dosing can be tricksy as it’s in the mcg/kg/min range and is not a daily use drug for most of us. I tend to skip the loading dose. In other words look it up.

Usually with filling and removal of inotropy and chronotropy you can ride it out and you should see some improvement in your haemodynamics. A failure to respond to treatment should make you question your diagnosis, that high lactate may well be due to dead gut rather than low output due to LVOTO.

References Chapter 13, Oxford Textbook of Advanced Critical Care Echocardiography covers this nicely. * Chauvet, J.-L. et al. Early dynamic left intraventricular obstruction is associated with hypovolemia and high mortality in septic shock patients. Critical Care 19, 1–8 (2015). * Slama, M., Tribouilloy, C. & Maizel, J. Left ventricular outflow tract obstruction in ICU patients. Current Opinion in Critical Care 22, 260–266 (2016). * Pollick, C., Shmueli, H., Maalouf, N. & Zadikany, R. H. Left ventricular cavity obliteration: Mechanism of the intracavitary gradient and differentiation from hypertrophic obstructive cardiomyopathy. Echocardiogr Mt Kisco N Y 37*, 822–831 (2020). * Deranged Physiology. (Also contains mention of the wonderfully named Brockenbrough–Braunwald-Morrow phenomenon, which seems ripe for morning ward round pontification)

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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 Oh’s manual chapter 44 on liver issues but there are a variety of other sources mentioned at the end that are worth a read.

It can be a little tricky to pin down this diagnosis. A lot of that comes because it is a “syndrome”, ie a collection of clinical findings that someone has put into a big bucket and mixed around without paying too much attention to hard core diagnostic information like histology or a true pathological diagnosis.

To start with we need context. We should have an AKI in the setting of advanced chronic liver disease and portal hypertension ie cirrhosis. But of course there are multiple reasons for AKI in this context so we have to work through them a little before the label of hepatorenal gets attached. Our friends in the international club of ascites (yes that’s a thing, i didn’t make it up) suggest that you need an AKI with a failure to respond to simple things like withdrawal of nephrotoxic agents, treatment of infection and, importantly a decent trial of albumin. You also have to exclude intrinsic renal diseases that lose protein and blood but this is usually fairly straightforward to exclude. However you can quickly see that a lot of this is pretty nebulous and it can be hard to really draw a line under. As such it’s fair to say that your patient may have several causes for their AKI in cirrhosis and hepatorenal may only be part of the problem.

To take hepatorenal per se, what’s the purported pathogenesis? Well we think that increasing portal venous pressures and cirrhosis leads to splanchnic vascular vasodilation. The vessels in our gut lose tone and we develop this chronic high output, low SVR state. This state of reduced pressure leads to activation of the RAAS causing increased resistance in the renal arteries (in distinction to the very low resistance state of the splanchnic vasculature). As such, perfusing pressure to the glomerulus falls and GFR falls. This is reflected in oliguria and the usual renal response to a crisis of hanging onto Na for all its worth with a urine Na typically <10 if you do go looking for it. In the background you’ve got all this chronic ascites that is adding to the compartment pressure in the abdomen making things worse. That’s the basic bedtime story version of the pathophys that i received, I understand there’s a competing theory where the chronic bacterial translocation of a leaky liver leads to a chronic inflammatory process buggering the kidneys but i digress.

At this stage, it’s worth noting that just like our cardiorenal syndrome we can split hepatorenal into a couple of types. This is all about timing of onset. The in-patient with a rapidly rising creatinine in the hospital setting is more likely to have type I or acute HRS while the stable out patient cirrhotic with a gradually rising creatinine is going to have the type II or chronic HRS.

HRS itself can be precipitated by the usual chronic liver disease decompensations – ie , bleeding, infection, SBP and also large volume paracentesces without appropriate albumin replacement.

How should we treat. First off an important reminder that cirrhosis is not a reversible pathology and if you’re decompensating then the only real treatment to turn the whole thing around is a transplant. All the rest of it is a little bit like rearranging the deck chairs on the Titanic. I don’t mean to imply that the deck chairs should not be rearranged; rearranging the deck chairs may well lead to some meaningful short term outcomes and quality of life improvement but the hole in the hull from the iceberg isn’t going to get any better without the transplant.

As mentioned in the diagnostic bit, they probably should’ve got some albumin. I don’t deny that albumin has a limited role in the ICU, gone are the days where we could make bold assertions about colloid osmotic pressures and how albumin was better than crystalloid. We studied it and it turns out it doesn’t seem to be any better than salty water. But i still think that in the livers it still has an important role and HRS is probably one of those scenarios. The data for its use in HRS is not exactly stellar, and no where near as good as it is say for albumin in ascites drainage in SBP where it has a mortality benefit.

I confess i have done the sneaky move “push the MAP up to 75 mmHg” for a few days to see if that makes a difference but i can’t say I’m standing on solid ground doing that but it does get a mention in the relevant UpToDate article. Of course given that we have access to terlipressin in Ireland and the UK, these types of haemodynamic manipulations could even be done on the ward before rushing to commit yourself to CRRT and an ICU admission.

TIPS has been described to be helpful in improving renal function in HRS but only on a very limited basis so probably worth a discussion with your local liver experts but not something you can use evidence to make a compelling argument for.

If the HRS fails to respond to such therapies then the option of CRRT is usually raised. This will indeed replace the failing kidney but like many things in intensive care, there’s not much point in starting it if there’s no chance of reversibility. Some HRS may be in the context of something like acute alcoholic hepatitis where the chance of recovery of some hepatic function is reasonable and hence a trial of the CRRT while the liver settles is reasonable. In addition if the patient is already on the transplant list then keeping them going with CRRT pending the transplant would also be reasonable. However the more common scenario is the burnt out cirrhotic who is having increasing frequency of decompensations. The prognosis here is dismal and adding more machines at the end of life is probably not going to help. The tricky bit for us is teasing out so much of what we’ve discussed above, eg is this one of the many other eminently reversible causes of AKI in the context of cirrhosis or is this all driven by the chronic progressive liver failure. This as you’ve probably discovered by now is a core part of ICM and best learnt in the unit and on the wards rather than on the podcast.

ReadingICA Guidelines

Deranged Physiology

LITFL CCC

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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 »

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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.
  1. 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
  2. improving oxygenation by recruiting alveoli
  3. reducing work of breathing by giving a little boost as the chest wall tries to expand those wet and heavy lungs
  4. 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

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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 chapter 201 and a few other review papers thrown in for good measure. We’re only going to get so far as the modes today so let’s not get too carried away.

The obvious initial distinction in RRT modes is between IHD and CRRT with IHD being intermittent as the name suggests and CRRT being continuous. These are obvious temporal discriminators to do with how long the machine is attached to the patient but under the hood there are more fundamental differences between how the two modes work.

In broad terms we can compare dialysis (the movement of small molecules across a membrane along an osmotic gradient) with ultrafiltration (the squeezing of plasma through a big sieve that retains the big bits of the plasma and lets the other bits leak out). The best analogy I’ve seen for this comes from one of my colleagues in his yearly introduction talk to RRT. Dialysis is the tea bag as ultrafiltration is to the espresso machine.

Alas such simply categorisations fall by the way side when we encounter the actual workings of one of the big green machines in the unit as it often presents several modes to us. We can run a continuous heamofiltration, a continuous haemodialysis or a combo mode of continuous haemodialfiltration. These rejoice in the acronyms CVVH, CVVHD and CVVHDF respectively.

Lets start with CVVH, continous venoveno heamofiltration. In this set up blood is drained from the venous side and entered a circuit initially under negative pressure then post pump becomes positive pressure. This positive pressure is used to force blood through a haemofilter containing many hollow fibre microtubules making up around a metre squared squeezed into that tiny plastic cylinder. Hydrostatic pressure drives the water into the filter compartment from the blood compartment with “solute drag” bringing along small and middle molecules with it. The principle here is convection with both the transmembrane pressure and the semipermeable barrier characteristics both contributing to how much filtrate is generated. The filtrate produced looks just like urine and collects in a big bag at the bottom of the machine. The yellow stuff contains things we want out of the body like potassium and urea. It is very easy to remove water from the body in this manner and in general if left to filter without replacement fluid then your patient will become very negative very quickly, hence the large 5L bags of replacement crystalloid fluid that run simultaneously as the yellow stuff is being produced. At its simplest the yellow ultrafiltrate has all the same concentrations in it as the plasma minus the large molecules like albumin.

In pure CVVHD (continuous venovenous haemodialysis) the patient’s blood is on one side of a membrane with a dialysate fluid running in the opposite direction on the other side of the membrane. In this scenario solutes (such as Na and K and urea) leave the blood compartment to the dialysate compartment down a concentration gradient. In this scenario the water follows the solute which is in distinction to haemofiltration. When running CVVHD the dialysate flow rates are usually very modest at maybe 30ml/min in distinction to IHD dialysate flow rates of 500-800ml/min

CVVHDF is a combination of the two with a little bit from column A and little bit from column B so to speak, with plasma being squeezed through the haemofilter and a modest counter current dialysate flow happening at the same time. The yellow stuff produced in this mode is a combination of ultrafiltrate and the spent dialysate that has passed through the filter.

One would think that we’ve already covered enough acronyms for one day but unfortunately there are several other important ones still to cover, thankfully they use most of the physiological principles already covered.

Let’s start with SCUF, slow continuous ultrafiltration. Simply put this is CVVHaemofiltration without fluid replacement. Blood enters a haemofilter and through the interaction of hydrostatic pressure and membrane characteristics ultrafiltrate is produced and the remaining blood is returned to the body minus some electrolytes and water. Because the electrolyte concentration in the ultrafiltrate is the same concentration as that in the blood there’s no major drops in Na or K to worry about as long as you don’t remove too much fluid. Solute clearance overall is very poor as effluent rates are more like 100-200/hr (~2ml/kg/hr) vs the usual 2000ml/hr (25ml/kg/hr) produced in CRRT. But this is not an issue as this is a mode that you use in someone who has reasonably working kidneys but has about 10 or 15 kg of water to remove. Removing 100-200ml of ultrafiltrate an hour will rapidly dry out your patient as you might imagine.

The final ICU specific mode of RRT is probably SLED. Slow, Low efficiency Dialysis. It must be said that they’re really not selling it with a name like that and perhaps the inventors need to up their branding game a little. Unlike all the other modes so far this needs a standard IHD machine and the plumbing that goes with it. The idea here is to run the blood and dialysate flows at a much lower rate over a longer period of time. Given that it’s a diffusion mode it is much more effective at solute removal than CRRT. The idea is that your ICU patient can have a busy day with trips to CT, line changes, rehab activities and then get plugged in for the night shift to SLED to give the blood a nice wash ready for another day of clinical progress the next day. I have zero experience with this but people who do have it feel it’s the best thing since loaves came pre-cut up and ready for the toaster.

CRRT is clearly ubiquitous in every day ICU practice and one might think this is due to an overwhelming collection of evidence suggesting its superiority over IHD but perhaps unsurprisingly such an evidence base supporting a mortality benefit does not exist and the stability and availability of CRRT has led to its current market leading position. There does seem to be a suggestion of better renal recovery with CRRT over IHD which might be related to less kidney hypoperfusing episodes of hyoptension when CRRT is used.

Reading:Oh Chapter 40

Iriwin and Rippe 201

Deranged Physiology

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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 felt it might have warranted its own chapter. Indeed, looking at its prevalence in fellowship examinations it does seem that a fair deal of attention should be given to SAH. It stands apart from the usual intracranial bleeding where the typical treatment and discussions are all focussed on supportive care and the the nuance only comes in when you get to BP management. Whereas in SAH you have a whole bunch of interesting and well proven interventions that can improve outcome for the lucky patients who haven’t already prognosticated themselves by presenting with a GCS of 3.

As a starter for 10: in which meningeal space in the brain do you find an SAH? The clue, thankfully is in the name. The space between the brain adhering pia matter and the filmy arachnoid matter is where you’ll find an SAH. This is the space that CSF flows in from it’s genesis in the choroid plexi of the ventricles on its journey to reabsorption in the arachnoid granulations. Also in this space lies the cerebral vasculature that has a tendency to become aneurysmal and rupture arterial blood into this space.

Blood in the sub arachnoid space is easily seen on a simple dry CT scan, particularly in the first few hours. It has now become a test so good that people would suggest that if you have a negative CT in the first 6 hrs then you probably can skip the de rigeur LP that has been all the rage for the past century. Though i’ll admit that that question is delving much more into the realm of EM than hard core crit care.

In a critical care exam type stem you might be faced with someone in their 60s with a history of poorly controlled hypertension, who smokes, takes cocaine and has polycstic kidneys. All of these are identified as risk factors for SAH, though such a combination, i imagine only exists on exams. In the stem they’re likely to have a reduced GCS in the 13-14 range with a BP of somewhere north of 170mmHg. You’ll be given a CT scan showing some diffuse SAH but you’re waiting on an angio etc… Imagine a question like: what are your immediate priorities in management.

Given that 85% of SAH is aneurysmal, and they need definitive treatment likely not available in your hospital then getting that angio done is certainly a priority. But probably more acutely will be the basics of assessments of ABCs with particular attention to getting that BP under control. The biggest risk to life in the first few hours is going to be a rebleed which happens in maybe 20% of patients. Getting the BP down to somewhere south of 160 is likely a good idea with the ubiquitous labetalol probably being the most accessible and available option. Avoid the GTN and the foil wrapped madness of nitroprusside as both can cause a little cerebral vasodilation that you want to avoid. Bonus points for a decent analgesic (which will help the pain) and an antiemetic as vomiting does indeed tend to make the BP spike a little.

The stem continues and the plot thickens. While waiting for the CT angio the patient becomes obtunded gets intubated (where great attention was paid to the heamodynamics). Now the CT shows more blood, some hydrocephalus and a big posterior communicating aneurysm. What now genius?

Hydrocephalus is a relatively common event in SAH and the theory is that blood in the CSF space blocks up the arachnoid granulations preventing reabsorption and with ongoing production and failure to reabsorb you get hydrocephalus. There may be other reasons including a clot in one of the intricate drainage canals in the brain but either way you get more CSF than you want with a concomitant rise in ICP that quickly becomes life threatening if not drained with an EVD. Now if you’re a neurosurgeon and someone gives you the story of GCS 13-14 with SAH and an aneurysm your interest is definitely piqued but this is likely to be a transfer within 24 hrs to get some coiling done but is unlikely to require any surgery per se by the neurosurgeon at 3am. However if you give them that same story but now add some hydro and a falling GCS you have the type of thing that will buy your patient an emergency blue light transfer over to the OT in the neurosurgical centre.

So what’s going to happen with the aneurysm? Assuming we keep the BP under control and correct any coagulopathy then it needs secured. If possible this should be done by a neurointerventionalist with a coiling procedure, and not by craniotomy and clipping of aneurysm. This is now well defined and supported by randomised controlled level evidence. Given the complexity of these procedures the timescales provided for which it has to be secured is generally in the 24-48hr range and this allows them to be done as day time procedures most of the time.

The scene fades and the time jumps and the question stem now is in the ICU on day 5. On your daily sedation break it is noted the patient is not moving the left side. What pray tell is this new calamity? Has the poor soul now had a big embolic stroke in addition to his SAH? While this is definitely cerebral ischaemia it is not stroke and instead rejoices in the name of “Delayed cerebral ischaemia” or DCI to its friends or “vasospasm” to the people it knew in high school but haven’t bothered to stay in touch. DCI is a clearly recognized phenomenon in SAH patients and is typically found to co exist with the radiological phenomenon of vasospasm where the artery spasms and has reduced flow. Vasospasm itself is very common in up to 70% of SAH patients but only about 30% of vasospasm is DCI. DCI requires a focal deficit or drop in GCS in addition to imaging findings of ischaemia.

The typical response in days of yore would have been “triple H therapy” consisting of hypervolaemia, hypertension and high haemoglobin. Over the passage of years the only remaining tenet of the grlorious trio is induced hypertension which does seem to have some kind of effect on improving those ischaemic symptoms. Don’t be surprised to find your neurosurgeons requesting MAP targets like 90 or 100mmHg in these scenarios. The single best treatment for DCI we have is actually a prophylactic treatment in the form of the calcium channel blocker nimodipine. 60mg given 4 hrly is the standard recommended from day of rupture given for 3 weeks or so. It’s not entirely clear how this works but it’s fairly clear that it does. lastly it’s worth noting that DCI is not a day 1 concern for your SAH patient with incidence peaking in the 4-10 day range.

Reading:

As a broad overview Oh Chapter 51 covers all the bases.

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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 quite “triggering” to walk up to a vent and see the pressure support set at 11 or some other horror show like a PEEP of 7… I mean, who would do such a thing. But let me clear we are talking about a very different type of triggering.

If i was on a ventilator and somewhat engaged in the process of respiration at least at a brainstem level, I would feel a much more content if the ventilator cycled to inspiration whenever I requested it to. Indeed I would also find myself greatly contented if said ventilator did not randomly produce new inspirations any time it detected the slightest change in airway pressure. All of this is dependant on ventilator triggering.

Let’s start with the basics, the ventilator can be triggered to cycle to inspiration in a number of ways:

1. time (in the case of mandatory ventilation, in fairness this is not really a trigger as the patient has no input)
2. pressure trigger. The patient must produce enough negative pressure in the circuit to trigger the vent
3. flow. The patient must produce a certain amount of inspiratory flow in the circuit to trigger the vent

My experience has been overwhelmingly with the ubiquitous servo ventilators found in many ICUs in Ireland. On the servo-i when you scroll through the menus you’ll see a dial for trigger. This dial is defaulted to flow trigger with a dimensionless number from 1-10 based on a proprietary software from Maquet. The more clockwise you turn the knob the lower the flow in the circuit the patient has to generate and therefore the easier it is to trigger inspiration. Swing it all the way right for the poor GBS patient who struggles to trigger. As the dial is turned left (or anticlockwise) then the trigger will magically switch to a pressure trigger with actual numbers in cm H20. These define the negative pressure in the circuit that has to be generated before the vent will trigger a breath. Thus flow triggers are easier for the patient and pressure triggers harder.

But when would you ever want to make the trigger harder for the patient? Typically it’s not actually that you want to make it harder for the patient, it’s more that you want to avoid autotriggering. A good example of auto triggering is commonly seen in the patient who has become dead by neurological criteria. The story at handover will typically be a devastating brain injury with some haemodynamic instability and loss of pupilary and cough reflexes but the trainee notes that brain death cannot have occurred because they are still triggering the vent. In this scenario it is quite common for the ventilatory to be auto triggering due to the minor fluctuations of flow within the circuit caused by the substantial cardiac oscillations of the hyperdynamic circulation of the person undergoing brain death. Simply switching from a flow trigger to a pressure trigger typically eliminates these auto triggers. Alternate sources of auto triggering can be the big air leaks of a bronchopleural fistula or a water logged circuit with a meniscus of rained out water oscillating back and forth in the tubing.

Failure of triggering is very common. In this scenario there has been a neurological trigger that may have even initiated some diaphragmatic contraction but it was missed by the ventilator. An oesophageal balloon is probably the gold standard here and you can use it to see if a negative deflection on the balloon is matched by a breath.

In the absence of a balloon (and aren’t we all?) we have to use some surrogates. It’s hard to detect but in some patients you can see a -ve deflection in the pressure waverform that is not matched by a breath. This may be the patient trying to trigger but failing. The flow waveform is similar but this time we’re looking for a +ve deflection of the expiratory slope. There are some nice pictures in the multiple references at the end of the post.

While it may seem inconceivable to many there is always the option of actually examining the patient. A hand on the sternocleidomastoid or tummy might make patient generated effort easier to recognise.

Intrinsic PEEP or gas trapping is one of the commonest causes of a failed trigger. Let’s say a COPD patient is emerging from propofol and fentanyl induced haze of 3 or 4 days on the vent for pneumonia. They are transitioning to a spontaneous mode as their respiratory drive increases. Unfortunately their obstructive lung disease is still an issue and the expiratory flow has not returned to zero before they try and take their next breath. Air is still exiting their body at a certain flow and pressure so they need to generate enough flow and pressure to reverse this gas in the circuit in order for gas flow to move from expiratory to inspiratory limb to allow the vent to recognize a trigger. You can often see this as artefact in the flow waveform.

There is an interesting technology called NAVA or Neurally Adjusted Ventilatory Assist . This involves a fancy NG tube that is placed in the distal oesophagus and picks up electrical signals from the diaphragm. This is then connected to the vent and allows the vent to know with a high degree of precision when the diaphragm is contracting and match the beginning of the breath to this. So even if the diaphragm is weak and ineffective the NAVA can pick up on the neural signal to breathe. Like most such things it’s been tricky to bring to widespread practice and trials showing signficant benefit are sparse.

Moving on from failed triggers there are 2 more concepts to discuss. 1) double triggering 2) reverse triggering. These can look quite similar at times and are often mistaken from each other but are quite distinct. Double triggering can be seen when neural inspiration is longer than mechanical inspiration; in other words the patient wants to take a really long drawn out breath in but the vent for any number of reasons has cycled to expiration before the patient was finished. This will be particularly common in partially controlled mode of vent where you’ve tried to set a small and “safe” tidal volume but the patients brainstem is having none of it.

The second one, reverse triggering is much more recently described and can be really quite subtle. It is usually seen in deeply sedated patients undergoing a control mode of ventilation. In this scenario the vent triggers the breath itself based on the set program. During the mandatory breath the diaphragm is activated and so as soon as the mandatory breath is over the vent senses the diagphrgm induced flow change and cycles into inspiration again. If you have something like NAVA or an oesophageal balloon you can see the diaphragmatic activation on the trace. Without one of these it can look almost like a hiccup. In addition look for a mandatory breath followed by a triggered breath during the expiratory phase.

As always this is by no means a comprehensive review of triggering but hopefully a little intro to some potential very examinable topics.

Reading:
– Georgopoulos, D. & Roussos, C. Control of breathing in mechanically ventilated patients. Eur Respir J 9, 2151–2160 (1996).
– Good lecture on triggering from Brochard at the Toronto course
– Dres, M., Rittayamai, N. & Brochard, L. Monitoring patient–ventilator asynchrony. Curr Opin Crit Care 22, 246–253 (2016).
– Artigas, R. M. et al. Reverse Triggering Dyssynchrony 24 h after Initiation of Mechanical Ventilation. Anesthesiology 134, 760–769 (2021).
– Oto, B., Annesi, J. & Foley, R. J. Patient–ventilator dyssynchrony in the intensive care unit: A practical approach to diagnosis and management. Anaesth Intens Care 49, 86–97 (2021). [images above]

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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

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Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. If you were tuning in to try and pick up some core exam level content then this is probably not it. ... Read More »

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Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. Today we’re looking at Oh Chapter 64 covering some of the absolute basics of pre eclampsia. ICU level pre eclampsia is ... Read More »

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Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. Today’s podcast is mostly taken from Oh’s manual Chapter 96 covering critical care nutrition. Something we all know and love deeply ... Read More »

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Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. GBS management can be nicely split into disease specific management and ICU supportive care. In terms of specific treatment this is ... Read More »

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Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. GBS is a clinically important diagnosis for both the emergency department and the ICU. Its rareish but common enough that you ... Read More »

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Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. We see C. Diff in the ICU in a couple of contexts. Firstly the poor unfortunate soul who starts with a ... Read More »

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Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. HIV in the ICU is becoming a bit of a rare beast as the ID docs seem to have it so ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Plasmapheresis (or PLEX) is one of the machines we tend not to have responsibility for in the ICU. Unlike CRRT we tend to defer to another specialty to do this. ... Read More »

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Welcome back to the tasty morsels of critical care podcast. SBS is not a common thing to find in the ICU and the most likely context here is going to be receiving someone from the operating theatre who has had ... Read More »

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Welcome back to the tasty morsels of critical care podcast. The commonest time we think of adrenocortical insufficiency in the ICU is probably in sepsis. This post will definititely not cover the beast that is steroid use in the intensive ... Read More »

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Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care exam preparation. The aminoglycosides see themselves as a bit special. Not content with producing deafness and killing kidneys they’ve also demanded awkward dosing schedules, ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Cardiac pacing comes in a variety of flavours in critical care but a reasonable list of class I indications for permanent pacing might include: 2nd/3rd block with symptoms and bradycardia, ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Continuing along a theme of words with with too many i’s in them, (see TM 007 for more) today we look at necrotising fasciitis or “nec fasc” to its friends. ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Ventilators remain one of the dark arts and hidden mysteries of critical care. Intensive care is a fairly generalist specialty overall and we share our core knowledge with a lot ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Like most spaces within the body, the contents within the cranium are under a certain degree of pressure. The skull being a rigid box can accommodate pressure much less than ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Welcome back to what I hope will be the final little segment (boom boom) on liver transplant. Part 1 lives here. Though at this stage I certainly can’t rule out ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Today we’re covering Oh’s Manual Chapter 103 looking at liver transplant. There are two types of liver disease that might put you in line for a transplant acute liver failure ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Today we have one of the jewels of critical care exam preparation. Not only does this involve niche clinical contexts, the gamma glutamate cycle but also everyone’s favourite acid base ... Read More »

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Welcome back to the tasty morsels of critical care podcast. So, from the ultra broad topic of AKI in the last podcast to the super specific question of when we should pursue an open lung biopsy in an ICU patient. ... Read More »

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Welcome back to the tasty morsels of critical care podcast. This is a somewhat basic and general episode, even for this podcast which indulges in frequent generalisation and summaries of pre existing summaries. It covers Oh’s Manual Chapter 47 looking ... Read More »

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Welcome back to the tasty morsels of critical care podcast. In a break from the not quite established tradition on this show, I’ve split this into two parts. Number 13 covers the process of putting them in. This one focusses ... Read More »

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Welcome back to the tasty morsels of critical care podcast. In a breaking from what could only loosely be described as tradition at this point, this podcast is going to be in 2 parts. Intensivists have embraced the tracheostomy as ... Read More »

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Welcome back to the tasty morsels of critical care podcast. This is a mammoth topic that listening to 5 mins of me rambling will in no way seriously prepare you to either practice clinically or write a semi coherent exam ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Thanks to the wonders of preemptive rasburicase (which i have a tendency to associate with Rasputin at this point) I don’t think this as common as it used to be. ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Critical illness in pregnancy is remarkably rare given the somewhat bonkers system for reproduction that we seem to have evolved over the past million or years. Improved care of complex ... Read More »

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Welcome back to the tasty morsels of critical care podcast. As an EM trainee doing intensive care I will confess that I struggle to work up the enthusiasm to cover a nutrition guideline. With my deepest apologies to all the ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Just to be clear up front we’re going to be talking about taking the lid off for stroke, NOT taking the lid off for TBI. I will get to TBI ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Pneumocystis Jriovecii Pneumonia, the infection formerly known as Pneumocystis Carinii Pneumonia The official change in name from Carinii to Jirovecii was in the late 1990s to emphasise the distinct organism ... Read More »

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Welcome back to the tasty morsels of critical care podcast. Today we’re talking about chylothorax, not something I’ve not had the joy of managing as yet. Chyle is produced through digestion and absorption of emulsified fats from the small intestine. ... Read More »

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Welcome back to the tasty morsels of critical care podcast. One would think that the term drowning should be relatively straightforward, however there have been a plethora of descriptions including wet drowning, dry drowning and near drowning. These have all ... Read More »

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Welcome back to the tasty morsels of critical care podcast. All of these posts are simplifications of much more complex topics but when it comes to the immunosuppressants used in solid organ transplant I’m wading out of my depth even ... Read More »

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Welcome back to the tasty morsels of critical care podcast. DKA is bread and butter for critical care providers. In fact the combination of bread and butter in the absence of insulin is a core part of the pathophysiology of ... Read More »

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Welcome back to the tasty morsels of critical care podcast. In the main we get excited about systolic dysfunction. We obsess over the ejection fraction with numbers like EF of 12% being reproduced recurrently in handover sheets. But this is ... Read More »

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Welcome back to the tasty morsels of critical care podcast. TTP is a lovely ICU diagnosis. Not so much for the patient but it’s one of those ones that is niche enough to not have been picked up via the ... Read More »

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At this stage (Oct 2020), PGY17 and still in training I have done a fair number of exams and I feel that now, pushing 40 and vowing never to do another exam, I may have finally perfected my examination technique. ... Read More »