(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.

(1/x) In fellowship, I managed a peri-arrest patient in the middle of the night who changed my understanding and appreciation for hemodynamics, ultrasound, and TEE.

I've seen similar cases dozens of times now, yet this commonly gets missed, even at top institutions worldwide.

A 🧵 (2/x) When I met this pt. they had a HR of 170 and a blood pressure on arterial line of 50/30. They were mottled head to toe, ashen, and looked like they were seconds away from arresting.

They had a recent NSTEMI and my first thought was cardiogenic shock or a mechanical complication of their MI --> VSD, tamponade, free wall rupture etc.

No transthoracic views on echo.

(0/x) How do I approach the first 2 minutes of meeting a new critically ill pt?

My approach has been forged from my learnings as a paramedic.

Here's my approach as an ICU doc 🧵 (1/x) I start with a scene survey.

I want to understand who's in the room and what are their roles. Is someone currently leading the resuscitation? What monitors are on the patient? What drugs are hooked up to the patient?

In EMS, one of the first things we are taught is to not rush to the patient.

This is for your own safety in case there's a hazard, but also because you can learn so much about what's going on by observing your environment as you approach the patient.

This gets missed in the hospitals.

Take some time and even by understanding what pumps they're on, you can often learn a lot about what might be going on in this very moment. You can also learn what help you might have if 💩🪭

(0/x) For the past 2 years I have worked in our chronic ICU helping wean difficult to wean patients with neurological weakness.

Here are some of the things I’ve learned from my vastly expert multi-disciplinary team 🧵

Really these are just great practices for weaning ALL ICU pts. off ventilators... (1/x) Deeming a patient impossible to wean should only be done by groups of clinicians with extensive experience in this.

In fact, evidence suggests that physicians are often poor at predicting weaning failure.

We've had patients with neuromuscular weakness who have been ventilated for close to a year or longer who have successfully weaned entirely from mechanical ventilation with thoughtful, deliberate weaning strategies.

(1/9) Its July and medical trainees are starting their medical school residency or fellowship.

Here is my advice for any ICU fellows starting out to avoid making some of the same mistakes that I've made in the past.

A 🧵 Tip 1: Just go see the patient.

When somebody is calling the intensive care unit in the hospital, they are calling for help. We are the 911 for hospitalized patients.

Even if there may not be a clear ICU indication based on your initial phone call with the referring physician or nurse, just go see the patient.

Often I find that we can still improve patient care for those patients even if they don't need vasopressors, ventilator, or inotropes. Often they are quite sick, and our expertise managing sick patients can be very useful.

In 2025, we need to move away from the restricted notion that the intensive care unit expertise only pertains to ventilators, vasopressors, and inotropes.

We are experts in managing acutely unwell patients even before they require ICU, so we should lend our expertise to help patients anywhere in the hospital.

(0/x) Do you want to be the Obi-Wan of diuresis? (or Darth Vader if you tilt to darkness)

Are you still starting diuresis with 40mg of 80mg of IV lasix?

Below are the lessons I learned from @ArgaizR and @FH_Verbrugge on our most recent HCProunds as they show us how to wield the ‘force’ to make sodium disappear from the body 👇 (1/x) If you missed the webinar, check it out here 👇- it is one of our best.

Recording: hcprounds.com/episodes/diure…

Here are some take homes though:

First, we need to separate a patient's volume status from their electrolytes.

Contraction alkalosis is a misnomer because, yes, when you diuresis patients with Lasix monotherapy, they become alkalotic and their volume status contracts, but this is not a cause-and-effect relationship.

The contraction of the volume status is not what's driving the alkalosis.

If you use multi-modal diuresis, e.g., integrating acetazolamide early on, you will find that your patient's bicarb will not increase, and then you can assess your volume status clinically based on physical exam and potentially ultrasound to assess for congestion on the right or left side.

(1/x) Septic shock is the leading cause of death in most ICUs worldwide.

Unfortunately, the hemodynamics of sepsis are still often taught incorrectly in medical school.

A 🧵 (2/x) In medical school, septic shock is described as a distributive shock where patients have hyperdynamic circulation with bounding pulses and warm extremities.

This is true in some patients, but not the majority. The problem here is that the cause of the shock is being equated to the phenotype of shock.

In a pulmonary embolism, for example, high RV afterload causes RV failure which causes shock. The cause and the phenotype are congruent.

In septic shock, these can differ. Septic shock can have any phenotype of shock. The phenotype depends on a number of clinical factors we will explore.

(0/5) Here are five of the commonest cognitive traps in medicine (and forcing strategies to avoid each)👇 (1/5) Cognitive Trap: Search Satisficing Bias.

As humans, when we find one abnormal finding. We often give ourselves permission to stop looking. Remember, for patients, there can be multiple abnormalities happening at once.

How to avoid this?

Force yourself to use a systematic approach to different presentations even when an 'obvious' answer has already presented itself.

For patients with sepsis, for example, even after I find a viable source of sepsis, I force myself to go through anatomically and think about any other sources I might be missing.

(1/x) Alright, given the amount of 'passionate' disagreement people have had with this post, let me give my more nuanced approach👇

https://twitter.com/ross_prager/status/1935671737485504561

(2/x) Of course, fluids may be beneficial in sepsis for some patients! However, this requires a few things to be true.

First, the patient must have microcirculatory dysfunction that will respond to augmenting cardiac output through IV fluids. Even if a patient is fluid responsive, if their microcirculation is dysfunctional and they are "hemodynamically incoherent" changes to their systemic hemodynamics may not improve tissue perfusion which is our goal.

This is something we are actively studying and considering with both @AndromedaShock 2 RCT and Andromeda-VEXUS.

(1/x) Here's what not to do when leading a code 👇

(based on first hand observations...) (2/x) Don't yell 'everyone who doesn't need to be here leave'.

This is a sure sign you have lost control of the room.

If needed, get people's attention with a "hey, the volume in the room is too high to allow for excellent communication. Let's all bring our volumes down."

As you are saying this you can bring your own voice down, others will follow.

Anecdotally, I notice that loud codes are typically a sign that the leader is nervous / not being listened to.

Be calm yourself and this will project to the entire room.

(1/x) We need to stop 'feeling for a pulse' while CPR is ongoing in cardiac arrest.

Here's why 🧵 (2/x) The reason why clinicians feel for the pulse makes sense - we want our CPR to be generating enough stroke volume to create a palpable pulse.

The problem with this, however, is that in many cases the pulse felt is VENOUS from retrograde flow.

Need proof? Place a linear probe on the groin next arrest. The vein is pulsating and where you feel the pulse is more medial than the artery!

(0/5) Shock is the nextdoor neighbor to death. Here are 5 tips for managing shock that you can use right now👇

🧵

(repost if you want me to turn this movie cover into a short film) (1/5) Start by assessing the microcirculation (and its surrogates) to determine how severely end organs are impacted. This should help guide how aggressive you are at its management.

Hypotensive but normal microcirculation --> figure out why and gentle treat

Hypotensive with profound microcirculatory dysfunction = death in a few hours (or less)

Microcriculatory Surrogates you can use at bedside
Cap Refil (normal 2s or less) is my fav
Lactate (caused by multiple things so only 1 piece)
Pulse Ox Pleth
Mottling
Urine output

We discuss this more on HCProunds with @AndromedaShock and @ArgaizR here: youtu.be/5Xyo5wbQBzE?si…

Here are 10 lessons they don't teach in medical school (but should) that I've learned the hard way over the years.

🧵

(0/10) (1/10) Patients don't care how much you know, but rather, how you make them feel.

Tips:
1) Sit down with your patients (standing seems impatient)
2) Identify and acknowledge emotions. Being sick is scary. "I imagine this must be stressful"
3) Don't forget it is OK to be human. We error. Relax and lean into that. Patients appreciate connecting with a real person, not some idolized version of a doctor.

(1/x) Authors have sued the six largest academic publishers for running an illegal cartel that violates US antitrust law.

Here are the key points from the biggest lawsuit in academia 🧵

Please retweet to help promote FAIR publication. (2/x) Who’s being sued?

Elsevier, Wiley, Springer Nature, Wolters Kluwer, Sage, and Taylor & Francis.

Together, they control 53% of all academic journals. The suit calls them the “Publisher Defendants.”

(1/x) Non-invasive ventilation (BIPAP/CPAP) is one of the few interventions that consistently demonstrates improvement in patient important outcomes... but only if done correctly.

A 🧵on avoiding the 6 biggest NIV mistakes (2/x) To start, if a non-invasive ventilation (NIV) mask has a good seal, there are really only two key differences between invasive and non-invasive ventilation

1) Access into the trachea for pulmonary toilet
2) Sedation (and thus passive ventilation)

The mistakes made for NIV initiation and maintenance relate primarily to these concepts.

The only diuretic that has demonstrated to reduce mortality is... 3% saline?

A 🧵

TLDR: it's not about sodium (for once). (2/x) A systematic review with meta-analysis of RCTs by Liu et al. 2021 in Critical Care Medicine demonstrated ....

3% saline in addition to Furosemide resulted in a robust mortality reduction compared with furosemide alone ☠️

If you haven't already, check out this paper! pubmed.ncbi.nlm.nih.gov/34166286/

(1/x) Differential Hypoxia on VA-ECMO – A 🧵

Let’s talk about Harlequin Syndrome and what to do about it. 👇 (2/x)💡 What is Differential Hypoxia?

Differential hypoxia occurs on peripheral veno-arterial (VA)-ECMO when native cardiac function recovers enough to eject blood through the heart, but the lungs are diseased (e.g. pulmonary edema, ARDS, pneumonia etc.) and not sufficiently oxygenating the blood still flowing through the heart.

This means that blood leaving the heart is poorly oxygenated, and blood coming retrograde up the aorta from the ECMO circuit is oxygenated.

The location of where the oxygenated ECMO blood and deoxygenated lung blood mix is everything.

If it occurs too proximal to the heart then blood going into the carotids (and to the brain!) may be deoxygenated.

If not recognized, Harlequin Syndrome can cause hypoxic brain injury 🧠

'Problem representation' is one of the most fundamental skills of clinical diagnosis, yet is often taken for granted.

Here's how to get it right.

A 🧵

(1/x) (2/x) Here's a case stem:

45 y.o. F with fever, nuchal rigidity, and headache --> we might immediately think of meningitis

If I chose to include (or omit) other relevant details for the same case:

45 y.o. female with nuchal rigidity, thunderclap headache, low grade fever, and a 1stdegree relative with aneurysm --> we might immediately think of aneurysmal subarachnoid hemorrhage.

Our choice of what we include in the problem representation influences the perceived diagnosis, yet is very subjective.

So how do you decide what to include?

Night shifts are associated with a higher risk of death ☠️👇

Here are some evidence based approaches to maintaining healthy while working shifts. A 🧵
(1/x) (2/x) Exercise is key - but should you do cardio or weight training?🏋️🏃

Cardio (150min/week) of moderate intensity reduces mortality, insulin resistance, and all-cause mortality.

Weight training may offer additional reduction in mortality beyond cardio by around 9% (HR=0.91 (95% CI 0.88 to 0.94). (PMID 36167669)

The key? Combined cardio + weight for optimal health outcomes.

Below is the hazard ratio for long term death based on cardiovascular fitness --> there is no upper limit on the benefit from fitness in terms of mortality! (PMID: 30646252)

@KwadCast @kwadwo777 has been advocating for this for years and is totally right. It isn't an either or, but BOTH.

(1/x) A simple approach to severe hypoxemia 🫁

A 🧵

(there is only 1 mechanism to know) (2/x) Severe hypoxemia may be challenging to manage, however, the approach to its diagnosis is actually quite simple.

Severe hypoxemia (if on high FiO2) is caused by shunt.

All other causes of hypoxia (diffusion, deadspace, hypoventilation etc.) are overcome by increasing the FiO2 delivered to the patient.

When you encounter a patient in the ICU (or anywhere) with severe hypoxemia they are shunting.

The question is where? 🫀vs 🫁

Rapid atrial fibrillation is common in the ICU.

How do you decide whether Afib is driving hypotension or simply an innocent bystander?

A 🧵

(1/x) (2/x) Atrial Fibrillation is one of the most common complications for ICU patients.

The big question that comes up --> is atrial fibrillation the cause of the hypotension or simply a bystander resulting from some other cause of shock.

Here's how I approach this 👇