Ten cognitive check points (general rules or heuristics to help guide my practice) I use in the ICU to help make sure I don't get too far off track. A thread🧵👇
1/10: Shock with a narrow pulse pressure (<30mmHg) needs an urgent #POCUS (or echo) to identify occult RV/LV failure, obstructive shock, or severe hypovolemia.
2/10: When you see a pt. who is "persistently hypovolemic" that transiently responds to fluid loading. First, ensure not bleeding.🩸 Second, instead of assuming they are just really dry, think about dynamic LVOTo, intracavitary gradients, or diastolic dysfunction. Giving them 15L of fluid to treat persistent fluid responsiveness is likely not the right move.
3/10: If a nurse (or anyone!) asks you the same question twice (e.g. should we consider getting a CT scan) don't take it that your judgement is being question - this is often a great indicator they have a different mental model about your pt. Explore the why and challenge your own assumptions.
4/10: The diagnosis of "septic shock" does mean the patient has distributive shock. 🫀❌ Even if it is pure septic shock, patients may have any phenotype of shock depending on their chronic comorbidities, acute cardiomyopathy, or secondary processes (core pulmonale, pericardial effusions etc.)
5/10: A persistently elevated lactate in a septic pt does NOT mean they are under-resuscitated or "dry" Step 1) do you have source control Step 2) Are you treating the right phenotype of shock? Step 3) Can we optimize real-time markers of perfusion (e.g. cap refill time) through volume, inotropes, MAP challenge, inodilators etc.
6/10: Be wary of admitting a patient to the ICU with a diagnosis of sepsis NYD (not yet diagnosed)- in the ICU, we should be able to figure out the D (diagnosis). Repeat the primary history, re-examine, consider pan-CT, echo, focused TEE etc. Think about where infection can hide! (valves, belly, heart etc.)
7/10: There is no such thing as a 'stable' post cardiac arrest patient. They just died. They are by definition the patient closest to death in your department/hospital. The disease that caused them to die is still at play, time matters! 🫀⌛️Prioritize diagnosis, ensuring adequate access (Art + venous), and definitive treatment.
8/10: Post cardiac arrest pts. are simultaneously a 1) cardiac patient (their heart stopped) 2) neuro patient (we care about their brain) 3) and trauma patient (someone just crushed their chest for like 30 min).
If you are CT scanning post arrest, low threshold to PAN scan (head, chest, abdo)
Also, if you are going to order a CT chest, consider a PE protocol so you never have to discuss on rounds whether the patient could have an occult PE as the etiology arrest!!! 🫀🧠🦴
9/10: If you are using POCUS to justify giving more fluids, you are probably doing it wrong.
10/10: If a pt or family says they want everything done - clarify this!!!
When you dive into it, it often means not giving up on them. They want you to try to diagnosis them, correct treatable causes, and if they are dying, provide them a comfortable and dignified death.
Rarely is it life at all cost or indefinite prolongation of dying with life support.
These are just a few observations from a very early career intensivist! Would love to hear everyone else's heuristics they use in their practice. @emily_fri @nickmmark @emcrit @PulmCrit @iceman_ex @IM_Crit_ @ThinkingCC @AndromedaShock @ChrisCarrollMD @precordialthump @Wilkinsonjonny @jon_silversides @Bram_Rochwerg @KimLewisMD
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Here are the top 5 myths about volume status in medicine.
Thinking about asking @netflix to turn this into a mini-series (or maybe )@MythBusters
Episode outline below, share to get the producers ready.
Episode 1: Myth: Volume Status is a single clinical entity.
In practice it means should I give Lasix, Fluids, or nothing.
That encompasses so many things into 1 concept: 1) Fluid Tolerance 2) Fluid Responsiveness 3) Stroke Volume 4) Microcirculation 5) Organ Dysfunction 6) Etiology of AKI 7) Congestion (right and left)
Instead, be specific about the patients physiology.
Episode 2: Myth: Volume Status is assessed from the JVP
JVP (or VeXUS, IVC POCUS etc.) are single measurements of right sided congestion.
If you are going to be assessing right sided congestion:
VeXUS > IVC > JVP (horrible interrater reliability) but still is only 1 piece of the puzzle.
(1/x) Normotensive shock is common yet often missed because there are actually multiple phenotypes to consider👇
(2/x) Shock is inadequate tissue perfusion (think end organs).
Blood pressure is not the same as flow.
Forward flow does not equal tissue perfusion.
Tissue perfusion is a complex interplay between:
Blood Pressure - minimum pressure is required
Forward Flow (cardiac output)
Back Pressure/Flow (congestion)
Tissue Level Hemodynamics (e.g. macrohemodynamics being translated into tissue level perfusion).
Any one of these alone is not sufficient for adequate organ perfusion.
(3/x) Normotensive shock can happen for a number of reasons:
1. MAP preserved but only at the expense of high vascular resistance. This is seen commonly in hemorrhagic and cardiogenic shock (including PE) where high SVR maintains MAP despite low CO.
MAP = CO x SVR
Clues: 1. Normotensive but low pulse pressure 2. Normotensive but tachycardic (compensatory) 3. Normotensive but poor perfusion (cap refill, mottling, lactate).
Easiest way to figure out --> echo/POCUS with a VTI as a surrogate of SV
2. MAP and CO preserved but significant congestion causing organ failure.
This happens commonly in heart failure patients, but also in up to 20% of patients with septic shock on ICU admission!
Forward flow AND MAP are okay, but severe congestion impairs tissue organ deliver.
Easiest way to figure out is to perform Doppler of organs like the liver, kidney. High CVP can be a cluse.
3. Normal MAP, CO, and congestion but severe microcirculatory dysfunction.
Some patients are hemodynamically incoherent, where normal systemic hemodynamics (or interventions that improve those hemodynamics) are not translated to the microcirculation.
How to assess? Ongoing poor cap refill, lactate, mottling despite optimized hemodynamic parameters.
Consider: augmenting MAP (improving capillary function) and PREVENTING. Volume overload/congestion can contribute to hemodynamic incoherence.
(1/x) When you trying to decongest patients in the ICU, there are lots of drugs available... not just lasix
Here are some tips for diuresing patients🧵
Furosemide - backbone of diuresis. Start at a higher than you think and back off if diuresis achieved.
Metolazone (or other thiazides). Use when Na on the higher side as helps prevent distal Na resorption. You get more naturesis.
Acetazolamide. Use to prevent metabolic alkalosis. Aids in decongestion.
Spironolactone. Use to prevent K+ wasting and to achieve more natriuresis.
3% saline. Consider in diuretic resistant heart failure with hypochloremia.
(2/x) Tip: Goal of diuresis is not just to produce lots of urine... its to produce lots of salty (high Na) urine.
This is because natriuresis (salt) > aquaresis (water) for decongesting patients.
Ways to achieve more natriuresis: 1. Multi-modal diuresis 2. Check urine Na during diuresis (ideally random urine Na > 100).. add more multi-modal diuresis if not achieving.
(3/x) If you have a patient with venous congestion (e.g. objective congestion on ultrasound) expect an increase in Cr with diuresis... ride that out and treat the patients venous congestion / overload.. it will come down once the patients high venous pressures improve.
The intervention used Cap Refill Time as a surrogate of end-organ perfusion, and if abnormal, did physiology informed maneuvers (fluids, vasopressors, inotropes) to improve perfusion.
They found "there were 131 131 wins (48.9%) in the CRT-PHR group vs 112 787 (42.1%) in the usual care group for the hierarchical composite primary outcome, with a win ratio of 1.16 (95% CI, 1.02-1.33; P = .04)."
Most of this was driven by lower organ support in the phenotyped (intervention) arm.
Patients in the intervention arm received 1) less fluids 2) more inotropes 3) had improved SOFA/lactates 4) and less organ support (vasopressors primarily).
So is this patient important?
(3/x) It is important to contextualize this in the broader sepsis research landscape.
EGDT in 2001 --> 46.5 vs. 30.5% mortality
ARISE in 2014 --> ~19%
PROCESS in 2014 --> ~21%
PROMISE in 2015 --> ~29%
ANDROMEDA-SHOCK in 2019 ~43% vs 35% (intervention)
Why a higher mortality for Andromeda-Shock than the older ARISE/PROCESS/PROMISE?
It may be related to patient demographics, particularly recruiting patients from more low-middle income countries where sepsis mortalities are higher.
In Andromeda-Shock 2, mortality was only 26%, 10-15% lower than the previous study (and lower than expected) likely reflecting improved sepsis care globally.
The truth is, for any septic shock study, an outcome like mortality is only modifiable for a subset of patients.
Some are too sick and will die regardless of resuscitation.
Some are well enough that they will live despite what we do.
There is a window of patients in the middle whose mortality is modifiable... but as baseline mortality decreases and overall sepsis care improves, this mortality modifiable group becomes smaller.
(1/9) Here’s how to become the best doctor you can in 2025…
Some advice (e.g. learn from your pts) is timeless but some thing are different than when Osler trained.
🧵
(2/9) Learn from your patients
Learning ~= cases seen × learning extracted per case
Maximizing both is key.
Volume exposes you to varied presentations, and reflection deepens your understanding.
There’s no substitute for either. Perhaps in the coming years AI simulated presentations may assist in pattern recognition (e.g. high exposure to simulated pathology) but not quite there yet.
(3/9) Develop skills beyond knowledge
Knowledge matters, but communication, listening, problem-solving, studying, and teamwork matter more in practice.
When trainees struggle, it’s often these skills, not medical knowledge, that hold them back.