Yi-Lin Hsieh, MD

Age lowers MAC about 6% per decade. Residency works faster: every 5am alarm knocks another 0.1 off my will to live.

[Josh Farkas MD 💊 @PulmCrit]

Fresh IBCC chapter: APRV guide 😁

My first APRV guide came out in 2017. I updated it during COVID in 2020. I just completely overhauled it again.

Two APRV guides were published recently (one by @TheEMNerd in 2022 and one by Nieman et al. 2026). Both guides focus on how to get patients initiated on APRV. My APRV guide is consistent with them. There is a general consensus about how to get APRV started.

Currently, the most challenging & controversial aspect is how to wean *off* APRV. Much less is written about this. I've described two possible approaches based on the best data that we have (Zhou et al. RCT) and basic vent weaning principles. But this remains murky.

Some approaches to weaning off APRV involve a gradual removal of ventilator support, without spontaneous breathing trials. This strategy isn't consistent with modern techniques of ventilator liberation (i.e., providing comfortable non-fatiguing support with intermittent spontaneous breathing trials).

APRV is a great rescue modality currently. However, for APRV to demonstrate benefit in clinical trials, proper attention is needed to rapid APRV weaning. Inadequately aggressive weaning strategies will destroy the ability of APRV to improve ventilator-free days & ICU length-of-stay.

I'd love to hear about folks' experience in terms of APRV weaning.

The role of APRV in ARDS remains controversial. It was hotly debated during COVID in a partisan fashion without any real conclusion. Hopefully further RCTs will clarify its precise use. This is tough because outcomes depend on how APRV is set (not simply the binary presence/absence of APRV).

Aside from ARDS, APRV is pretty fabulous for mucus plugging and atelectasis. Physiologically, its ability to produce biased airflow that promotes secretion clearance is simply unparalleled (slow inspiration & fast expiration clears secretions out of the airway).

So regardless of where we land with APRV for ARDS, I do think that there will always be some use for APRV in critically ill patients. So this guide will hopefully be evergreen.

(#1/2, link next)

[Cliff Reid @cliffreid]

An elevated lactate should not lead to a knee-jerk diagnosis of sepsis. Use deliberative thinking and a knowledge of very basic biochemistry to identify why the lactate is elevated.

This is non-negotiable if you are serious about striving for excellence in resuscitation.

Everything you need to know is in this video. Watch it all the way through and your practice will change for the better.

https://t.co/xb7uB7WP7J

[DAN KOE @thedankoe]

https://t.co/7l7Jef99QZ

[ICU×ID note｜Motoki Fujii @ICU_IDnote]

＜メロペネム＋バンコマイシン＋ミカファンギン投与下のショックでICUでまず考える微生物リスト＞
・ICUでこの3剤は非常に広域だが、ブレイクスルーはときどきおこる

・まずカバーできていないものを探す
・そのうえで、カバー内の菌のブレイクスルーも否定しない（特に免疫抑制が著明and/or菌量が多い=人工物感染や縫合不全等）

・非常にショックなら、耐性GNRからまず考えてみる。
・市中発症なら、非定型・抗酸菌・リケッチアも思い浮かべる
・免疫不全の種類と程度、過去の検出微生物。（ひょっとしたら隣の患者の微生物検出歴も）
・皮膚、消化管、肺の所見がないか

GNR：
・Stenotrophomonas（ST合剤 ±ミノマイシン ±キノロン。もしくはセフィデロコル単剤）
・CRE、MDR緑膿菌／アシネトバクター（感受性のある既存薬の併用。とりあえずアミノグリコシド追加？またはセフィデロコル、セフトロザン／タゾバクタムなど）

GPC：
VRE（日本では比較的稀。リネゾリド、ダプトマイシン。一部テイコプラニン：VanBには使えるがVanAには使えない）

嫌気性：
C. difficile（メトロニダゾール、経口/注腸バンコマイシン）

細胞内：
レジオネラ／マイコプラズマ（レボフロキサシン、アジスロマイシン） 、リケッチア（ミノサイクリン、ドキシサイクリン）、抗酸菌（抗酸菌薬）

真菌：
アスペルギルスの一部、ムーコル、クリプトコッカス、ミカファンギン耐性カンジダ（ボリコナゾール、イサブコナゾール、L-AMB）

ウイルス：
CMV（ガンシクロビル）、HSV/VZV（アシクロビル）

他ショックにはなりにくいが、
・Pneumocystis
・ノカルジア
はICUではときどき

非常に稀だが、輸入感染症（重症マラリア、デング等）も

[大木谷 直樹｜ER x ICU x Hospitalist @Cafe_Dogtor]

心外術後ICU管理の基礎を学びたくて探してたらめちゃくちゃ良いの見つけた。10年前だけど、二部構成でかなりわかりやすくまとまってる。初学者でもとても読みやすくてありがたい....！次は成書でも読んでみようかな。
・Part1
https://t.co/ItmOl1m5WT
・Part2
https://t.co/eSYf0fVTvi

[IMCrit @IM_Crit_]

#ICU Physiology Secrets: Is vasopressin really “pulmonary-friendly”?

I’ve heard several times that vasopressin is “lung-friendly.” That it may even dilate the pulmonary vasculature. Or that the pulmonary circulation has no vasopressin receptors. Have you heard the same?

It made me wonder how much human evidence actually supports these claims. Does vasopressin constrict the pulmonary circulation less than norepinephrine? Does it lower PVR? Does it improve RV function? Or does it simply raise systemic pressure without raising PA pressure as much? These are related questions, but they are not the same question.

So I went looking for the human evidence. With the caveat that I did not have full-text access to a few potentially relevant studies, this is what I found:

1. Start with the receptor, but don’t stop there

Liu et al. examined human arterial samples and found V1a receptor (AVPR1A) protein was abundant in pulmonary arteries: about 2.2× mesenteric, 2.2× coronary and 1.9× peripheral arteries, and similar to renal arteries. Six samples of each artery type were studied. So the pulmonary circulation clearly does not lack V1a receptors. But expression is not function, and this study didn’t show what a human pulmonary artery does when exposed to vasopressin.

2. Put human pulmonary arteries in an organ bath, and things get interesting

Currigan et al. compared isolated human pulmonary and radial arteries. Vasopressin was a potent radial-artery vasoconstrictor but produced no significant change in pulmonary arterial tone. Norepinephrine constricted both.

Hussain et al. found an even more striking contrast. Maximal contraction of human pulmonary-artery rings was 61% of the KCl response with norepinephrine (12 rings from 4 patients) versus 0.18% with vasopressin (8 rings from 2 patients). That 0.18% gets my attention, but so does the denominator: eight rings from two patients...

These experiments provide a compelling physiologic basis for vasopressin behaving differently in systemic and pulmonary arteries. Still, these are isolated vessels in a bath, not PVR measured in a hypoxemic, ventilated patient with pulmonary hypertension and a failing RV.

3. What happens in actual patients?

Mizota et al. reported a lung-transplant patient with pulmonary hypertension in whom, during pulmonary-artery clamping, a 0.5-U vasopressin bolus raised systemic systolic pressure 35.2% with minimal change in PA pressure. Norepinephrine boluses in the same patient raised systemic systolic pressure 14.8% and PA systolic pressure 6.7%. A beautiful physiologic observation but n = 1, during major surgery, with other vasoactive infusions running.

Tayama et al. studied 9 post-cardiotomy patients with vasodilatory hypotension and pulmonary hypertension. Vasopressin raised mean systemic pressure from 47.3 ± 9.5 to 76.5 ± 12.2 mmHg, while PVR did not change significantly. Cardiac index fell, although it remained in the normal range. The pulmonary/systemic pressure ratio fell from 0.66 to 0.47. Be careful with that: a ratio can fall simply because the systemic denominator rises. A falling ratio is not pulmonary vasodilation.

Adamson et al. studied 28 Fontan patients undergoing catheterization. Vasopressin raised systemic pressure and SVR while PVR fell by 0.4 ± 0.4 Wood units, with no significant change in PA pressure or cardiac index. That is human PVR data, but a small effect from a single study. And Fontan physiology has no subpulmonary ventricle, so it is not a model of the adult ICU patient whose RV is failing against a high pulmonary vascular load.

4. What does the larger comparative evidence show?

Gordon et al. analyzed 779 septic-shock patients from VASST, 241 of them managed with a PA catheter. At similar systemic pressures, vasopressin reduced norepinephrine requirements and heart rate. In the PA-catheter subset, there was no detected difference in cardiac index or stroke-volume index over the first 96 hours. Inotropes were used more often in the vasopressin group.

That is much stronger comparative evidence than an organ bath or a case report. But PVR wasn’t reported, RV function wasn’t measured directly, PA-catheter use wasn’t randomized, and these were septic-shock patients, not patients selected for RV failure.

Geube et al. studied 153 elective cardiac-surgery patients who developed intraoperative hypotension in a single-center, cluster-randomized, multiple-crossover study. They found no statistically significant difference between vasopressin and norepinephrine in the primary time-weighted mPAP/MAP ratio or in RV free-wall strain, a secondary endpoint. That doesn’t support a simple claim of pulmonary selectivity or better RV function in this setting. But a pressure ratio is not PVR and can move with the systemic denominator, and these patients weren’t selected for established RV failure.

5. PA pressure may be the wrong scorecard

Dalla et al. studied 11 septic-shock patients (a small study) in whom norepinephrine was titrated in random sequence to MAP targets of 60, 75 and 90 mmHg. At the highest versus lowest MAP, mean PA pressure rose 19%, which at first glance sounds bad for the RV. But PVRI and effective pulmonary arterial elastance did not increase, while RV function improved: free-wall strain became more negative (−19% to −25%), TAPSE rose 22% and RV stroke-work index rose 15%.

This doesn’t prove norepinephrine is better than vasopressin. It shows why PA pressure alone is a poor scorecard for what the RV is doing.

So where do I land?

Vasopressin’s “pulmonary-friendly” reputation has a legitimate physiologic basis. In small organ-bath studies, human pulmonary arteries show very little direct constriction to vasopressin. In small clinical series, systemic pressure rose without a clear rise in PA pressure. Fontan patients' data show a small fall in PVR, about 0.4 Wood units, in a circulation with no subpulmonary ventricle.

But there’s an evidentiary ladder:

Little pulmonary-artery constriction → lower PVR → better RV performance → clinical superiority over another vasopressor.

Those are four different claims, and the human evidence gets thinner with each step.

What I’d really like to see is a prospective vasopressin-vs-norepinephrine comparison in patients who actually have RV dysfunction with elevated pulmonary vascular load. It should measure systemic and PA pressures, PAOP, cardiac output, PVR, RV function, tissue perfusion and, ultimately, clinical outcomes.

Until then, I’ll still consider vasopressin an attractive pressor when the RV is in trouble. That’s a physiologically informed choice, not a proven RV-outcome advantage. “Pulmonary-friendly” is a compelling hypothesis with human support, not a guarantee that the RV benefited.

When your RV is failing, what pressor do you reach for first and what do you measure to decide whether it helped?

[positiveforward @positiveforward]

これかなり面白い

過去100年の中長距離走トレーニングの変遷にも触れながら、ノルウェー式のトレーニングモデルと、その生理学的な背景を考察したレビュー論文

しかも、なんと著者の一人に、あのマリウス・バッケン氏本人が名を連ねています

無料で読めますよ
https://t.co/5kFa1DyO31

[Cole Smith, Pharm.D, BCPS @iamcrsmith]

@DrJohnAfam Bag of spinach --> blend --> place NG tube --> administer

[Josh Farkas MD 💊 @PulmCrit]

this guideline is ridiculous

it combines every type of hypoxemic respiratory failure and makes a blanket recommendation for all of them together 🤡

we all know that different forms of hypoxemic respiratory failure respond differently (e.g., cardiogenic pulmonary edema vs pneumonia)

this will be cited a bajillion times which is great for the journal's impact factor and the authors' H-indicies, but it's still nonsense

[Mario Jiménez MD, PhD | Nefrología @DrMarioJimenez1]

Nefrología que todo internista debe saber: Mg²⁺ bajo + K⁺ bajo es una combinación que exige pensar en el riñón.

Mi algoritmo mental:

1️⃣ Confirma y revisa fármacos/pérdidas GI.
2️⃣ Si no está claro → pregunta si el riñón conserva Mg²⁺.
3️⃣ Hipomagnesemia + excreción renal inapropiadamente alta → piensa en diuréticos, tubulopatías, cisplatino, anti-EGFR, etc.
4️⃣ Corrige Mg²⁺ si la hipokalemia no responde.

El Mg²⁺ no es un “electrolito secundario”: participa en excitabilidad, arritmias, metabolismo y control tubular del K⁺.

📌 Perla para la guardia: K⁺ que no corrige → mira Mg²⁺ antes de seguir aumentando KCl.

📚 Gembillo G, et al. J Clin Med. 2026;15:7723. DOI:10.3390/jcm15197723. Revisión, no RCT.

#Electrolitos #MedicinaInterna

[なんでもないか｜当直・病棟の判断順 @naikanandemo]

『SvO2また下がってきました、強心薬で叩いたほうがいいですかね』
今朝の続き、答えです。

🫀『まず右心カテを読んでみようか』

PAPi＝(38−22)÷10＝1.6
→ 右室が送り出す力は、そこまで落ちていない

PAWP 28、CI 2.0、SvO2 58%
→ 左室の圧が高く、拍出が足りず、酸素も届いていない
＝ 左心不全による低心拍出

🫀『だから、強心薬か、インペラか、という話になるね』
👨‍⚕️『どっちにしますか』
🫀『自分ならインペラかな。治療してまだ1〜2時間で、前下行枝の病変も残ってる。強心薬は必要悪。心筋の酸素消費を増やすから、虚血が残っている心臓には使いたくない。P/Fも悪いしね』

☑PAPIで右室の力を見る：(PA収縮期−PA拡張期)÷RA。1.0を下回れば右室も弱い
☑PAWP・CI・SvO2で、左心不全の低心拍出かを判断する
☑虚血が残っているなら、強心薬を増やす前にインペラを考える
☑インペラは左室から血を抜くので、PAWPが下がり、肺水腫とP/Fの改善も見込める

インペラを入れたあと、位置・アラーム・溶血をどの順番で見るかは👇

[Philippe Rola @ThinkingCC]

Praxis is live.

If you’re looking for the H&R26 recordings (and past HRs), this is now their home.

But Praxis is becoming much more than an archive: interactive clinical cases, AI Coaches, curated newsletters, live discussions, courses and 1-on-1 or group teaching from an international faculty — built around physiology, POCUS and how we actually reason at the bedside.

For Critical Care, Internal Medicine, Emergency Medicine, Anesthesia — and essentially anyone who takes care of sick patients.

https://t.co/iVaZzVmphG

#CriticalCare #InternalMedicine #POCUS #Hemodynamics #Anesthesia

Ping @TheEMNerd @icmteaching @khaycock2 @FTeranMD @emcrit @PulmCrit @jsemccm @TrinaAugustinMD @katiewiskar @G2Disrupt @Francofoam1 @ArgaizR @NephroP @heart_lung @FH_Verbrugge @IM_Crit_ @edu_kattan @AndromedaShock @TaweevatA @SaraCrager @chatterJ5 @emireles_c @intensivaev

[Mario Jiménez MD, PhD | Nefrología @DrMarioJimenez1]

Nefrología que todo internista debe saber: fósforo bajo ≠ automáticamente “déficit nutricional”.

Ante hipofosfatemia, mi pregunta es:

¿el riñón debería estar conservando fósforo?

Si el fósforo sérico está ↓ pero la excreción urinaria sigue inapropiadamente alta → piensa en pérdida renal: hiperPTH, Fanconi, fármacos o tubulopatía.

Si el riñón lo conserva → busca redistribución o menor aporte/absorción: realimentación, insulina, alcalosis respiratoria, alcohol, malnutrición.

📌 La cifra sérica dice qué ocurrió.
La orina ayuda a explicar por qué ocurrió.

Esa distinción cambia el diagnóstico y evita limitarse a “reponer y repetir mañana”.

#MedicinaInterna #Nefrología

[Suchitha Kuntla @DocPeriop]

EPINEPHRINE FOR ANAPHYLAXIS - DRUG INTERACTIONS AND CONSIDERATIONS

A thread 🧵

Scene 1:
Epinephrine for anaphylaxis in a patient on beta blocker therapy.

-Recently, I had to manage transfusion related anaphylactic reaction in an elderly female with HFrEF, on beta blocker therapy/ T. Met XL 25mg OD.
She had:
-acute onset dyspnea with global wheeze
-HR:48/min
-BP: 76/42mm of Hg
Since IV access is in place, she was given 50mcg of Adrenaline and provided with nebulization with Salbutamol and Budecort.

-Chest condition improved quickly, with the patient being visibly less tachypneic and wheeze resolved over minutes.
-IV fluids are given cautiously, considering pt's cardiac status and Vasopressor support with Nor-adrenaline infusion initiated, which was eventually tapered off.
-HR responded well to a single dose of Atropine at 0.1mg/Kg.

That probed me to read further on managing anaphylaxis in patients on various drugs.

Interesting take-aways:

1. Cardioselectivity of the beta-blocker:

In a patient on non-cardioselective beta adrenergic blocker receiving epinephrine:
-enhanced pressor response to epi, due to beta 2 blockade in vessels, can result in reflex bradycardia and cardiac arrest.
-attenuated bronchodilating effects of epi due to beta 2 blockade at bronchial smooth muscles
-attenuated cardio-stimulatory effects of epi, due to beta 1 blockade in the heart

Thus, it is only prudent to consider using a cardioselective beta blocker in patients at higher risk for anaphylactic reactions.

GLUCAGON IN EPI-RESISTANT ANAPHYLACTIC SHOCK:

-There are 3 anecdotes of successful management of adrenaline resistant anaphylactic shock in patients on beta blockers using Glucagon, at 1-2mg IV doses.
-Glucagon directly enhances adenylate cyclase activity, bypassing the beta receptors, hence the effects.
-Theoretically, it can increase the release of vaso-dilatory mediators from mast cells too, stay watch ful.

Textbook of Trauma/ Emergency resuscitation and Perioperative anesthesia recomends, in patients on beta blockers with anaphylactic reactions, using:
-Higher dose of epinephrine boluses :50mcg-300mcg IV (caution in patients prone to infarction/ risk of intense coronary vasoconstriction)
-early use of Atropine and Glucagon (if available)

Read further:
https://t.co/VnB3R5UW4B

https://t.co/PcsClB6JPL

#Anaphylaxis
#Anesthesia

[Suchitha Kuntla @DocPeriop]

"SUCCINYLCHOLINE AND OPEN GLOBE INJURIES OF EYE"
Extraoccular muscles are a bit different from any other striated muscles in body:
1.They have multiple NMJ per cell
2.They have both mature n immature fetal type AChRs.
3.They stay contracted for longer durations on stimulation.

[CJA - Canadian Journal of Anesthesia @CJA_Journal]

An encounter of unusual pressure dynamics during thoracic epidural placement: a “breathing” syringe - Canadian Journal of Anesthesia #CJA #CJA2025 #Anesthesia #Anesthesiology https://t.co/JzLmSZ7mcX

[Donyé @donye_goodness]

Donye’s INTERNAL MEDICINE Google Drive Link.

https://t.co/mdJIvV1BEw

(will be completed before my final exams)

[GwenP00Le @Bappieidk]

So it is in 11th ed ATLS for penetrating neck

[Fumiya Yoneyama, MD, PhD | WithAScalpel @WithAScalpel]

Aortic Valve & Root Anatomy #2: Root Configuration and Surrounding Structures

👉The aortic root comprises the sinuses of Valsalva, commissures, interleaflet triangles, and sinotubular junction.
👉The root is anchored within the cardiac fibrous skeleton, with aorto-mitral continuity and proximity to the membranous septum.
👉The aortic root lies adjacent to the pulmonary root, RVOT, and septal tricuspid annulus, reflecting its central anatomical position.

[ツタンカーメン @hiiro16578023]

TEEシミュレータアプリができました。

https://t.co/WQelrqvdH0

アプリ版ではTTEとICEもシミュレータとして使えます。

web版はTEEのみですがこれまで通り使えます

https://t.co/ZiRXeb5UpC

jb potなどの参考にしてください