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Ross Prager

@ross_prager

Aug 10

(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.

(3/x) I started the usually therapy, phenylephrine pushes, levophed, vaso pushes, and epi infusion.

No response.

I started bolusing aliquots of 20-50mcg of epinephrine ... no response. We intubated while this was going on.

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Ross Prager

@ross_prager

Jul 29

(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 💩🪭

(2/x) Next, I start perform a very quick (<15 seconds) scan of the patient

Essentially quickly checking the ABCs

This involves:
Reviewing the monitor for current vitals
Looking at the patient's skin colour
Looking for mottling
Looking at the Work of Breathing
Looking for LOC
Approaching the patient and briefly feeling their feet or hands for temperature and pulse characteristics

My goal here is to determine whether we need to go straight into resuscitation within seconds (cardiac arrest) or peri-arrest, or whether I can take a bit more detailed handover from the team that's already caring for the patient.

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Ross Prager

@ross_prager

Jul 28

(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.

(2/x) Optimizing volume status is crucial to weaning patients.

For neuromuscular weakness patients, even having 500 mL of pleural effusion adds a pound of weight onto each diaphragm.

When multiplied over the thousands of breaths per day, this significantly contributes to weaning failure.

Optimize your patient's volume status to help them wean!

Read 8 tweets

Ross Prager

@ross_prager

Jul 23

(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.

Tip 2: When you first meet a patient or family, listen more than you speak.

Ask the patient and family lots of questions about their values, functions, and what's important to them in their life.

Try to get to know them as a person before they became into the ICU.

Taking time to ask the patient and family these questions up front will actually answer a lot of questions for you down the road and save time in conversations.

It also builds rapport, shows that you are committed to their loved one, and will often get you useful clinical information that helps solve any diagnostic puzzles you have

Avoid launching into a medical update within the first 5 minutes of meeting a family.

Often they are not yet primed to hear this information, and spending a bit of time building rapport ahead of time is invaluable.

Read 11 tweets

Ross Prager

@ross_prager

Jul 22

(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.

(2/x) Second: we should start acetazolamide early when we diurese patients.

This prevents alkalosis that may limit diuresis and acetazolamide is CHLORIDE SPARING.

Why does this matter?

Hypochloremia is a potent activator of diuretic resistance. Acetazolamide might attenuate this.

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Ross Prager

@ross_prager

Jul 21

(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.

(3/x) Patients with septic shock can have any of the following patterns hemodynamics (which we will explore in more detail):

1. Distributive shock with high cardiac output and low filling pressures (‘warm’)

2. Distributive shock with low cardiac output and low filling pressures (‘cold’ or sometimes referred to as ‘hypovolemic’ à not a volume issue but rather a low filling pressure)

3. Distributive shock with high cardiac output and HIGH filling pressures (‘high output failure’)

4. RV failure (high or low CO)

5. LV failure (high or low CO)

6. Biventricular failure (high or low CO)

7. Pericardial Effusions

8. Venous Congestion (this can be layered on to any of the phenotypes with higher filling pressures)

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