Tim Norfolk

Thank you @christoslazaridis.bsky.social for writing this 👏 . If I ever found myself on the patient side of such a scenario, I would hope to be cared for by a clinician who shared your views!

Palliative General Anesthesia at Terminal Extubation: “Go Gentle into that Good Night” - Neurocritical Care Withdrawal of life-sustaining treatments in the intensive care unit most often culminates into the discontinuation of mechanical ventilation and removal of the endotracheal tube or “terminal extubatio...

This piece eloquently articulates my own thoughts on WLST.

Current practice leads to avoidable harm, probably for many patients but definitely for their loved ones.

We can and have a duty to do better, and should be brave enough to challenge current practice

link.springer.com/article/10.1...

I was so inspired by so many amazing people, and learnt so much reading others thoughts, but also from composing my own tweetorials. I think it’s a general SoMe fatigue, but it’s all just seems a little pointless now 🤷‍♂️

This is such a cool illustration of how the Mercator map distorts the size of Greenland, which looks as big as the whole continent of Africa on that map but is actually the size of Mexico.

These may well be the best years of your life, but I’m just saying 6.30-8.30am aren’t the best hours of those best years 🫠

I’m not big on conspiracy theories but this one rings true…

#CritcalClosingCriticalSchmosing

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 🔁

Headbang Rock On GIF ALT: Headbang Rock On GIF

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)

1/2

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

a man in a suit and tie is asking if he can get an amen ? ALT: a man in a suit and tie is asking if he can get an amen ?

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 😢