some says #POCUS answers (to the basic #FICE#CUSIC#FAMUS questions) are binary: yes/no.
but imo there must be 3:
- yes
- no
- i don’t know
3rd is not cool, but absolutely valid and most importantly: safe
Rapid sequence induction
There is insufficient evidence for many of the elements of RSI to determine whether they reduce patient harm or to state confidently that they do not.
@doctimcook@altgm#AnSky#MedX#MedTwitter
https://t.co/KWapu6ge9z
I just updated the IBCC chapter on pulmonary vasodilators, here are new pearls I learned 🤯
🫁 The dosing of inhaled pulmonary vasodilators is a little different for ARDS versus for treatment of RV failure. In ARDS, you're shooting for selective vasodilation of the best-ventilated alveoli to maximize V-Q matching, so you want a mid-range dose (too high and you start vasodilating the worse-ventilated alveoli). In RV failure you're trying to vasodilate every alveoli as much as possible to bring down the pulmonary vascular resistance, so go high.
🫁 Nebulized milrinone causes selective pulmonary vasodilation for ~20-30 minutes, then gets systemically absorbed. One dose of nebulized milrinone in the OR is great, but scheduling milrinone nebs q4hr doesn't make pharmacological sense (it doesn't achieve consistent pulmonary vasodilation and there are risks of systemic accumulation in renal failure). IMHO milrinone nebs don't have much role in ICU. If you want to give milrinone just give it IV.
🫁 There's a gradually escalating amount of evidence supporting combined simultaneous use of inhaled epoprostenol and inhaled NO to treat RV failure. See the article by Andre Denault below. This may be a good option for RV failure before escalating to an Impella RP Flex. It's pretty easy to trial a patient on inhaled pulmonary vasodilators - if they work great, if they don't work you haven't lost much.
#1/2, link in next post.
Voting for @ICS_updates council members is now open. My very good friend Jennie Stephens is running. I’ve worked with her in various ICS capacities for many years now and I can’t think of anyone who would be a better council member. She will be brilliant if elected. Please consider voting for her if you are an ICS member.
The signal to noise ratio describes the strength of a desired information signal against the level of unwanted background signal. How easy is it for the audience to clearly determine the message of a presentation.
Please read, comment and RT https://t.co/IASRWNbFhr
All the hot topics in septic shock resuscitation with the ANDROMEDA-SHOCK- NETWORK at full throttle; First World Summit! 53 faculties. Our next research projects discussed at length. Registration open, full programme (QR). Bidirectional translation. Videos available 6months
Pleased to see this published
NARRATIVE REVIEW OF RSI
Loads of information & we hope a good overview
The topic is very controversial, sadly sometimes driven by not being up to dare with the existing evidence.
Feel free to read, discuss & dispute!
https://t.co/i0aWjaMkeR
🧠 ❤️ Is a normal blood pressure enough to guarantee cerebral perfusion? The emerging role of transcranial Doppler
In acute brain injury, we frequently target mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) using predefined thresholds.
However, CPP = MAP -ICP does not tell us whether cerebral blood flow is adequate.
Cerebral perfusion also depends on vascular resistance, autoregulation, cardiac output and arterial CO₂.
This article by Melo and Robba explores how transcranial Doppler (TCD) could help individualize blood pressure targets at the bedside.
The key is understanding the Doppler waveform.
Diastolic flow velocity (FVd) reflects forward flow during diastole and is sensitive to downstream perfusion conditions.
The pulsatility index (PI) reflects the interaction between pulsatile inflow and distal cerebrovascular resistance.
A low FVd with elevated PI may suggest increased downstream resistance or reduced perfusion pressure.
However, PI is not a direct measurement of ICP, and TCD velocity is not equivalent to volumetric cerebral blood flow.
What happens when we increase MAP?
Consider a patient with traumatic brain injury, MAP 67 mmHg, FVd 14 cm/s and PI 1.5.
After norepinephrine titration:
At MAP 77 mmHg, FVd increases to 19 cm/s and PI decreases to 1.2.
At MAP 83 mmHg, FVd reaches 23 cm/s and PI falls to 1.0.
Further MAP augmentation produces little additional improvement.
This illustrative case demonstrates a physiological principle: the optimal pressure may be the range where cerebral flow dynamics become more favorable, not simply the highest achievable MAP.
Yet interpretation requires caution.
Increasing FVd during MAP augmentation may indicate pressure-dependent circulation with impaired autoregulation. Minimal changes may indicate preserved autoregulation or already adequate perfusion.
The systemic circulation cannot be ignored.
A low FVd does not automatically justify more vasopressors.
If cardiac output is reduced, fluid responsiveness is present, or severe hypovolemia exists, the underlying hemodynamic mechanism must be addressed.
Conversely, additional fluids in an unresponsive, congested patient may worsen cerebral edema or pulmonary dysfunction without improving cerebral perfusion.
TCD should therefore complement echocardiography, cardiac output assessment, ICP, brain oxygenation and neurological evaluation.
The important limitation: Doppler-guided pressure targeting remains physiologically promising but lacks robust trials demonstrating improved clinical outcomes.
Reference 📚
Melo RH, Robba C. 2026. Critical Care. https://t.co/6oWhuEEeKN
#NeurocriticalCare #TranscranialDoppler #CerebralPerfusion #Hemodynamics #CriticalCare
🛑 ¡No pinches este derrame!
Parece fácil: grande, varios espacios intercostales… pero hay una fina capa de pulmón atelectásico adherida a toda la pared. Una punción convencional atravesaría parénquima.
¿Lo habrías visto? 👇
#InternistaIntervencionista
Early bird extended! 🧙♂️
Resuscitation Wizardry, 7–8 Dec in London: two days of case-based resus, from airway, shock and neuroprotection through to how to make things happen when the system is working against you.
£330 early bird now runs until 7 Nov (then £385).
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£330 until 31 October
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Being "intravascularly dry" is often suspected when:
1. Furosemide monotherapy for diuresis is used, which produces metabolic alkalosis and hypernatremia irrespective of someone's true volume status.
2. Low MSFP shock due to vasoplegia in conditions like sepsis. The issue isn't about volume, but rather the pressure driving venous return.
3. Oliguria in the ICU. Many cases are 1) not AKI 2) not fluid responsive and 3) congestive
4. The patient has intracavitary gradients or dynamic LVOTo. These patients behave "super dry" . Preload helps temporarily, but afterload, beta blockade etc. accomplishes same goal in more durable fashion.
5. Pancreatitis patients. These patients have third spacing, sure, but actually are often more distributive. They require some fluids, but routine use of 100+ml/hr IV fluids in the absence of objective markers of low stroke volume and fluid responsiveness leads to many of the iatrogenic complications of pancreatitis we see!
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