Tasty Morsels of Critical Care Andy Neill

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.