Tim Norfolk

Congratulations! 🥳

The New England Journal of Medicine Potassium in Patients at High Risk for Ventricular Arrhythmias A Research Summary based on Jøns C et al. | 10.1056/NEJMoa2509542 | Published on August 29, 2025 Visual representations of the patients in the trial and the treatments they were assigned. Read the full Research Summary at NEJM.org.

In patients with cardiovascular disease and an implantable cardioverter–defibrillator, increasing potassium levels to the high-normal range reduced the risk of arrhythmia events, hospitalizations, and death. Full POTCAST trial results and Research Summary: nej.md/4oQtHTN

#MedSky

I often wonder when you see patients whose hypoxaemia appears disproportionate to their parenchymal pathology, if impaired pulmonary vasoconstriction due to antihypertensives plays a role. You see some CTs where the consolidated/atelectaric lung looks just so well vascularised 🧐

Curious to hear why you’d reach for the washing machine if there’s cerebral oedema? I’d worry it could drag your osmolality down further 🤔

No right or wrong answer, but my Monday morning QB response… I think pH is lowest priority. I’d aim for pCO2 4-4.5, bolus 1-2ml/kg 8.4% HCO3 as hyperosmolar therapy, half insulin/dextrose & get a CT to look for features of cerebral oedema

a woman in a red dress is saying we go hard bravo ALT: a woman in a red dress is saying we go hard bravo

The doses of bicarb used were aggressive

Interquartile range for total cumulative dose was 500-1000 ml of 4.2% bicarbonate

That's equivalent to 5-10 amps (50 ml vials) of 8.4% in the USA

You can use a LOT of bicarb if you have to (titrated to effect; also look at Na levels & avoid hyperNa)

#4/4

If you increase your RR from 14 -18 CO2 elimination increases. If production remains constant PaCO2 doesn’t continue to fall indefinitely, a new equilibrium is reached.

This is because there’s negative feedback in the loop. Lower blood CO2 levels also mean less CO2 is delivered to alveoli 🔁

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Only a real rockstar wouldn’t care about losing rockstar levels of engagement 🤟

It is, but you seem to imply that a sustained increase in EtCO2 isn’t possible.

If you increase your RR and MV, CO2 elimination increases, PaCO2 falls and this is sustained.

If CO increases, EtCO2 rises, CO2 elimination increases, PaCO2 falls and this is also sustained.

EtCO2 is essentially determined by what % of alveoli emptying at end expiration are perfused x PcalillaryCO2.

The rise in EtCO2 from better alveolar ventilation will diminish a little as enhanced CO2 clearance leads to a lower PcapCO2 but an equilibrium will be established with sustained ⬆️ EtCO2

I’m not sure that’s correct, this assumes there is some fixed baseline EtCO2 value linked to VCO2. In a cardiac arrest EtCO2 falls super low, with ROSC it increases but doesn’t then gradually fall back to the level during the arrest. The rise is sustained, with the sustained CO/alveolar ventilation

I really can’t tell if the answer is you, Zoey (I have a 5-yr old daughter so am WELL versed with the characters) or both

CO2 production is independent of ventilation, altering alveolar ventilation just affects where the generated CO2 goes. With our simplistic model it can either be blown off, or remain in the body/blood

If an ⬆️ in CO, increases EtCO2 then PaCO2 ⬇️ as more CO2 is blown off. PvCO2 will also ⬇️ because of the lower initial PaCO2 & the PvaCO2 gap will fall with the ⬆️ in tissue capillary blood flow.

If the exhaled CO2 increases, and VCO2 is constant then CO2 bound to blood will fall in proportion

Exactly what you’re imagining

Simplify things. Imagine all CO2 produced is either blown off or dissolved in blood then:

VCO2 = Exhaled CO2 + CaCO2

CO increases ➡️ alveolar ventilation increases ➡️ EtCO2 increases ➡️ CO2 elimination increases ➡️ PaCO2 decreases 🔁 to equilibrium

More CO2 is blown off but less is stored in blood

If CO2 production/ventilation is constant and dead space reduces with increasing CO then yes, you will eliminate more CO2 so PaCO2 will also fall, as EtCO2 rises and they’ll get close to meeting in the middle, as a new equilibrium is established.

2/2

EtCO2 increases with CO because of a reduction in dead space. Better perfusion to ventilated alveolar units, means more CO2 diffusing to be exhaled.

There is a ceiling effect as CO increases and V/Q matching is optimal. EtCO2 will never exceed PaCO2 (although can in funny situations)

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That looks excellent!

In honor of spooky month, share a 4 word horror story only someone in your profession would understand

“Remember that patient you…”

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normal mentation *doesn't* indicate adequate systemic perfusion

especially in cardiogenic shock, people can mentate well despite terrible CO & systemic perfusion

poor mentation is sometimes an early sign of *septic* shock, but often a very late indicator of other shock states #EMIMCC

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One memorable patient for me, transitioned to palliative care for decompensated advanced heart failure. They had a CVP ≈25 and a MAP in the 40s & were mentating just fine for quite some time. There was very little perfusion pressure/CO but the brain clung on til the last possible moment 😢

My argument is that experiencing pain is patient focused, even when there is no recall. For example: when people reduce fractures using morphine/midazolam & pts scream in agony, before minutes later asking if anyones pulled their ankle yet. They HAVE suffered, & we should strive to do better.

You can do this without lying, which is virtually always the preferable option

If our scientific understanding evolves to suggest our current practice is leading to a degree of awareness that causes suffering, even if not recalled by patients, we have a moral imperative to change our practice, and not accept the current standard of care (or by extension, option 1)

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So Pete forgive my ignorance around the IFT literature, but have people tried doing it and instead of asking squeeze my hand, saying squeeze my hand if you’re suffering (or something akin to this)? Then we could delineate if the experience at that time was one we should strive to avoid

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I don’t think you can genuinely be a number 1 can you, if using any normal/non-IFT definition of awareness. Would you agree to undergo an operation with awareness but the guarantee of being given a perfect amnesiac at the end so you forgot the whole tortuous experience?

This is likely why we may be talking at cross purposes then. My gold standard of awareness definitely mandates conscious experience, isolated forearm technique be damned 🤣