Welcome back to the tasty morsels of critical care podcast.
Today we look at the other diabetes. We are of course all familiar with the sweet urine of diabetes mellitus but this time we will look at the tasteless or insipid urine of diabetes insipidus. This will as always be a critical care type primer on the topic designed to help you survive a critical care fellowship exam. I would certainly not claim endocrine as my strong suit.
There are 2 forms we’re likely to encounter in the ICU. The first is a deficiency or absence of antidiuretic hormone.The second is an resistance to ADH. You’ll notice this is just like diabetes mellitues where type I is an absence of insulin and type II a resistance to insulin. However because endocrinology has to be the most obtuse and complex specialty they refrain from calling it type I and type II and instead refer to them as cranial DI (deficiency of ADH) and nephrogenic DI (resistance to ADH).
Just to note ADH also goes by the moniker of  arginine vasopressin (AVP) or even argipressin. For the sake of simplicity I’ll just refer to it as ADH.
Given the number of TBI and ICH we see in the ICU we obviously see a lot more of the cranial DI than the nephrogenic DI.
We’ll come back to the 2 types of DI later, but a brief section on the function of ADH is unfortunately warranted. As the name suggests ADH reduces urine output. It does this by promoting free water reabsorption in the kidneys. It does this by stimulating V2 receptors in the kidney increasing the number of aquaporin channels in the tubules. Hence more ADH, more water reabsorption, less urine. ADH is released primarily in response to a rise in osmolality. For example in hot weather you get dehydrated, your osmolality rises, your pituitary releases ADH, you reabsorb more water slowing the rise in osmolality.
In diabetes insipidus either absence of ADH or resistance to ADH will lead to reduced water reabsoprtion in response to increased tonicity. Ongoing free water loss will result in rising tonicity driven by a rising sodium concentration.
So that’s the basics of the pathophysiology, lets’s go back to our 2 types, cranial DI and nephrogenic DI.
Cranial DI happens when the pituitary is so injured that we lose production of ADH. This could be something rare like infarction or an auto immune issue of the pituitary or much more likely in our context some devastating intracranial event leading to a massive rise in ICP. The urine starts pouring out at 300-400 ml/hr and then the Na starts rising. The patient may or may or may not continue to progress towards brainstem herniation.
The context makes the diagnosis here usually fairly obvious but it’s worth sending a urinary Na and osmolality and in this case we’re expecting to see a very dilute urine (eg an osm <200 ) with a low Na which is inappropriate when the serum Na is high.
Treatment is relatively straightforward in the acute stage. We should give some ADH replacement typically in the form of DDAVP but you could of course vasopressin or argipressin because they’re the same thing really. Replacing the ADH will allow water reabsorption and correction of the tonicity. We will usually have to replace some of the free water and 5% dextrose is a reasonable way to do this, just be sure to control the urine output with the DDAVP first. Chasing a 600 ml/hr urine output with 1000ml/hr of 5% dextrose will lead to a dextrose driven diuresis making things even worse.
Of note there are different phases to this type of DI and if the patient survives the first few days then you may well see some lessening of the polyuria for a period. Management of cranial DI beyond the first week is certainty beyond the scope of this podcast.
Nephrogenic DI is more often going to be a label that comes with a patient to the ICU...

Welcome back to the tasty morsels of critical care podcast.
Following on from the recent post on Heparin, today we’re going to talk about one of its more significant complications – Heparin Induced Thromboyctopaenia or HIT for short. In my notes I had it down as HITTS for hepain induced thrombotic thrombocytopaenia syndrome which I kind of liked as it included the important presence of thrombosis in the context of low platelets. But HIT is definitely snappier
There are incidentally 2 forms of HIT. Type 1 is an entirely benign phenomenon where the platelets transiently drop in the first few days of heparin exposure and spontaneously recover even with ongoing heparin use. There is no thrombosis associated and no doubt it happens all the time and we miss it.
From our perspective we’re only interested in type 2 HIT which is a serious immune phenomenon where the major concern is not bleeding but clotting despite the low platelet count.
Unsurprisingly a necessity for this condition is an exposure to heparin. This can be UFH or LMWH. It is an immune phenomenon so you don’t typically get it on the first exposure but it’s the ongoing or repeat exposure can cause the immune reaction. As part of normal heparin function it, at various points binds to something on platelets called PF4 – platelet factor 4. For reasons beyond the comprehension of this narrator, the body can produce IgG against this heparin-PF4 complex. The IgG has now labelled these platelets for destruction by macrophages hence the thrombocytopaenia. Again, for reasons beyond this narrator’s comprehension there is also activation of other platelets resulting in both arterial and venous thrombosis.
Incidence is estimated about 1-5% of those on UFH and <1% on those on LMWH. Interestingly the antibody reaction is quite common but even when present only ~10% of those with the antibody develop HIT properly.
The classic presentation is a fall in platelets somewhere 5-10 days following first heparin exposure. Counts usually are between 40 and 80 but 10% can be under 20. The 4T score has been developed as a means of establishing a pre-test probability for HIT.
I’ll outline the 4 categories briefly

* severity of the thrombocytopaenia. ie platelets of 10  or 120 make it unlikely while platelets of 50 are in the zone
* timing of the fall – 5-10 days being the sweet spot. The catastrophic fall in the first 48hrs of overwhelming sepsis for example would not be consistent with HIT
* presence of thrombosis. This can a bit equivocal as it can be difficult to find all the clot and a clotted CRRT filter maybe shouldn’t carry as much weight as a clotted femoral artery
* is presence of another reason for thromboyctopaenia likely – this is of course like the wells score very open to interpretation

A high 4T score usually prompts formal testing and usually a switch to an alternate anticoagulation regime pending the results. This is frequently misunderstood as it seems most are happy to stop heparin pending the test but disregard the fact that clotting is actually the problem so alternate anticoagulation is really needed.
Testing usually comes in 2 stages. The first is a more rapid easily available screening test which i believe is a PF4 immunoassay. This can be followed up by a fancier (checks notes) Heparin Induced Platelet Activation functional assay. I can attest that we have two tests available in our place but I wouldn’t swear they are the ones described above.
The main dilemma we’re left with, is when we suspect HIT but have not got a definitive test to confirm it. We need to make a probability and risk based decision on whether to commit to the diagnosis or not.
Let’s say we’ve decided it’s HIT and we need to anticoagu...

Welcome back to the tasty morsels of critical care podcast.
Following on from our initial post in this entirely accidental series on “things you don’t want to find in the chest drain” we turn our eyes (if not our noses) to empyema.
Many penumonias will develope a parapneumonic effusion. This is largely reactive and inflammatory but by no means does it mean there is infection. On the other hand parapneumonic effusions can become the seed for an empyema proper, something seen relatively commonly with something like strep pneumo.
The commonest bugs described in empyema are strep pneumo and staph aureus, both of which occur as complications of pneumonia with said bugs. If on the other hand you have perforated your oesophagus into your pleural space then expect to find a different selection of microbiological beasties.
While perhaps obvious, the clinical features we’ll be looking for are fever and pleural effusion either on CXR, CT or US. Fever despite appropriate antibiotics always should make us think about source control so if the CXR looks funny then put the probe on or run them through the CT scanner. You can see pleural enhancement on CT scans which in my somewhat limited experience seems quite specific but not especially sensitive. Similarly loculations can be very easily seen with ultrasound, better than CT it seems but again don’t necessarily correlate that well with empyema.
As such the best thing to do it seems is to get a sample. It is my contention that if you’re going so far as to get a sample then why not leave a little teeny weeny drain in there while you’re at it. The advent of US guidance and pig tails and a substantial literature base all suggest that small. bore drainage is actually often quite effective and the old days of just assuming everyone needs a 28fr drain are probably past. My own practice is to use an 8Fr pigtail and see what happens.
I have in my notes a list of fluid criteria that apparently define an empyema. I am unclear of the provenance of this list but it seems to have been drawn loosely from the 2017 thoracic surgery guidelines and some the intereventional trials we’ll talk about later.
So definitionally if we have pus it’s an empyema, if we have a positive gram stain it’s an empyema, if we have growth it’s an empyema. Other features suggestive on pleural fluid analysis include

* pH<7.2
* LDH>1000
* Sugar <2.2
* high lactate

So now let’s assume you’ve got your sample and you’ve tried small bore drainage and you still have a big collection there. What are your options?
Well, adding extra or bigger drains is all very reasonable and it would seem wise to involve a thoracic surgeon at some point. Unresolved these empyemas develop into what is known as the “rind” causing a trapped lung and many will need the rather brutal procedure of decortication to strip it away. However in the early days we’re likely to more interested in simply getting source control and sometimes it’s the loulcations that are our enemy.
There are a number of trials and indeed published guidelines suggesting the use of injected pleural therapies to aid drainage. This consists of 2 agents
1) DNAase
2) our old friend tPA
The intervention involves placing a small drain then injecting DNAase and tPA into the drain every 12 hrs. This has been moderately well studied with MIST-2 2011 and the Picollo trial (2014) being  commonly quoted trials suggesting benefit. There is a cochrane review looking at tPA on its own that also suggests less need for surgery
The major downside, understandably is pleural bleeding, that occurs in about 2-5% in the studied cohorts. This can be clinically significant though very rarely does it seem to b...

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.
Reading
Deranged Physiology is excellently referenced, detailed and humorous in equal proportion
LITFL

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 

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,

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.

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 in...

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.

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.

Welcome back to the tasty morsels of critical care podcast.
Today we’ll talk about one of the niche and shall I say “advanced” in inverted commas therapies in intensive care practice. ECMO. And to be precise we’ll be talking about 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 t...

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

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

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

Welcome back to the tasty morsels of critical care podcast.
Today we tackle a somewhat nebulous syndrome. Something we throw around with a few hand wavy explanations but often light on detail. Hopefully in a few minutes you’ll at least have a few morsels more of information to stave off all the trainees who are undoubtedly much smarter than you on the ward round. But perhaps I’m getting too autobiographical already.
This does not appear with any great frequency in Oh’s manual but there is a nice scientific statement from the AHA that is referenced below. Though when you call it a statement you imagine some nervous spokesman in front of a camera trying to explain why is boss has done something naughty. Instead this is a 39 page epic review of the topic.
To start with there are apparently 5 types of cardiorenal syndrome. I’ll let that sink in. You all thought there was one didn’t you?
Type 1 is the acute deterioration in kidney function seen in cardiogenic shock from ACS. Type 2 is the slow and chronic deterioration of kidney function in the chronically failing heart.
They get sneaky with type 3 calling it renocardiac syndrome. You see what they did there they just reversed cardiorenal syndrome and called it renocardiac syndrome. In this scenario the kidney has acutely been injured and the consequences such as fluid overload cause heart failure. Type 4 is again renocardiac with the kidneys causing the heart failure but on a chronic basis. With me so far?
Type 5 is the big bucket where they put all the left over disease that cause both kidney and heart failure eg things like amyloid, or sepsis or cirrhosis.
Certainly when i use the term in daily practice i was only ever thinking of types 1 and 2 and that’s what we’re going to focus on in this  tasty morsel.
Why does this happen. I’ll paraphrase the opening part of the pathophys section from the scientific statement. Conventionally we focus on poor forward flow from the heart causing poor renal perfusion, poor GFR and activation of the RAAS. But in the style of a telemarketing TV advert “wait there’s more”. Poor forward flow is by no means the only pathology and in fact high pressures on the venous side likely contribute to the phenomenon of cardiorenal syndrome. for example we know that a MAP of 65mmHg is a generic target for perfusion pressure for most organ beds. However the actual calculation of perfusion pressure is probably better represented as MAP-CVP. Therefore in those with CVPs chronically sitting in the 10-15 range, you are going to struggle to effectively perfuse their kidneys. You’ll even here this called congestive renal failure on occasion.
Along the same lines it’s worth thinking about the impact of intrabdominal pressure on renal perfusion, those with tense ascites from heart failure are also going to struggle. There are of course much more complex neurohumoral, inflammatory type cytokiney thingies going on but as you can tell they are well over my head so I’ve skipped them for now.
You might think that diagnosis of cardiorenal syndrome might be straightforward. We just check a creatinine and if it’s high it’s a problem. But there are a fairly bewildering array of tests available for assessing renal function beyond the very blunt stick of creatinine. Things that rejoice in names like NGAL or cystatin C or looking at albuminuria; all may have a role in teasing out CRS from other issues. Valuable as it is for filling the 39 pages of the scientific statement i can’t see any great relevance to the jobbing intensivist. Of note in the paper, and perhaps obscured by the detail of the available biomarkers is the note that fluctuations in creatinine are often poor representations of actual kidney injury.

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,

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

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

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

* time (in the case of mandatory ventilation, in fairness this is not really a trigger as the patient has no input)
* pressure trigger. The patient must produce enough negative pressure in the circuit to trigger the vent
* 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 deflecti...

Welcome back to the tasty morsels of critical care podcast.
Today we are going to do our best to charm the yellow snake of the intensive care unit and cover the pulmonary artery floatation catheter. Like a lot, indeed practically all of these topics, I do not in any way consider myself to have great expertise in the topic but I have had to upskill as much as I possibly can in lieu of the typical mis spent youth doing cardiac anaesthesia that most of my colleagues have had.
As such the source list for this post is quite varied in terms of its references.
The focus here will be on the basis, the nuts and bolts of how to put in and what type of numbers you might obtain from a PAC.
The insertion carries a lot of similar complications to any typical central vascular access procedure. But the big ones come from the fact that you’re trying to place the catheter through the heart rather than in close proximity to it. Perforation is of course a real possibility but perhaps more likely are nasty arrhythmias precipitated by the catheter irritating the myocardium. Expect to see this more in the cold, shocked post bypass patient or in someone who’s already having a lot of arrhythmias.
The PAC is also famous for the knots it can manage to tie itself into that can make extraction more than a little challenging.
There are lots of good materials online on insertion so I’ll only mention a few basics in passing. The tiny little balloon at the tip catches the flow of the venous return and pulls the catheter along with the flow.
In the absence of flurosocopy it can be tricky to know quite where the tip of the catheter is at any given time so we use the changes in waveforms to tell us what chamber or vessel the tip is at any given time. The pattern we expect to see should be CVP waveform, RV waveform then PA waveform and finally a wedged waveform. If all plays ball the you should those patterns at roughly 20cm, 30cm, 40cm and 50 cm respectively. The challenge is usually transitioning from the RV to the PA and the key change in waveform to look for is the “step up” in the diastolic pressure from the RV waveform which has a diastolic in the low single digits to a PA diastolic which is in the low double digits.
Once the procedure bit is done we typically take a CXR looking for the tip. Typically the natural curve of the catheter leads it to ending up in the right PA most commonly though this is by no means guaranteed. It can be tricky to tell from a simple CXR but ideally we want the tip in a West zone 3 part of the lung, typically in the inferior portions. West zones may be a distant memory from medical school but for our purposes the estimate of the left atrial pressure produced by our pulmonary capillary wedge pressure is only valid when the alveolar pressure is less than the pulmonary venous pressure, a situation that exists only in West zone 3. If you’re in zone 3 you should be able to see a and v waves (analagous to the a and v waves of the CVP waveform)
In some of the linked papers at the end there are some excellent images of troubleshooting various waveforms. One of the more useful ones was dealing with the failing RV (the very scenario where a PAC is likely to be needed) In this scenario, the RV diastolic pressures can approach the PA diastolic pressures with a loss of the “step up” as you move into the PA. The key difference to note in this scenario is that when the PAC is in the RV the diastolic run off (the period before the next ejection) is upsloping and the disatolic run off is downsloping when the PAC is in the PA.
There are lots of measurements we can take from the PAC. Directly measured PA pressures are of course useful but the typical catheters used these days also hav...