I am a second year internal medicine resident in the metro detroit area interested in a pulmonary/critical care fellowship. I am from a smaller community based program so my resources, mentorship and guidance is minimal. Would love advise on what steps to take. I'll list some things below that I'm struggling with and looking for guidance from current fellows and/or attendings.

1. Research and case reports. We have ZERO guidance or help regarding any form of research. I've attempted reaching out to bigger programs but no luck. I'd love to join existing research or case reports and help complete the work. I am not looking for a free case report, I will be more than happy to do majority of the work.
2. What could I add to my CV to help improve my chances when applying.
3. Overall mentorship would be appreciated. I'd love a situation where I could pick a fellows brain but there could be some sort of clinical aspect I could contribute to benefit the fellow as well. Even if that means completing the majority of the work for case studies and/or research.

Really any genuine input would be appreciated.

Hey all - I’m a CVICU nurse and I received a patient today who was pretty acidotic coming out of the OR (7.2 / CO2 high 40s / Bicarb 20). Their lactate was also elevated in the high 5s.

Our MD ordered 150 mEq of Bicarb and upon pushing them our patient had intermittent hypotension with MAPs in the 40s - what’s the physiology behind this? I’ve never experienced it before.

Also - I’ve heard before that Bicarb doesn’t really effect mortality based on some study done - is this true? If so, we do we even use it for lactic acidosis?

Edit - I have learned a lot from this but not much about this paradoxical hypotension from pushing bicarb :(

It's an issue that generates heated controversy at every institution I've practiced, and I can't take the uncertainty anymore - does a used guidewire go in the sharps or regular biohazard container?

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PCCM fellow here

We have in-house IP but it's only 1 physician so my exposure to IP is based around a sample size of one. I was hoping the greater reddit community could give me a better understanding of what the field is like.

What is the work life balance during fellowship? As an attending?

Are there private practice IP attendings? I assume since it's a relatively small and specialized field (compared to just PCCM), you're typically working in an academic setting.

Is there a compensation difference?

Apart from enjoying procedures, what are some other things I should know about before consider applying to IP?

Any downsides of IP that I wouldn't be privy to as a fellow?

Hi all, why doesn’t vasopressin lead to decreased urine output when used as a pressor?

At DI concentrations, vasopressin reduces UOP. At higher pressor concentrations, clinically I don’t see a drop in UOP (often an increase in low UOP shock states), despite ostensibly still acting on V2 in addition to V1a.

Thanks!

Hey y’all ms4 here applying for residency this fall. My absolute favorite rotation in med school has been the ICU ( with EM and PEM close 2nd and 3rd). I’m dead set on doing CC and have thought a lot about the ways to get there. Didn’t really love anesthesia so much and IM while great learning and cerebral problem solving did not have enough procedures for me. I was between EM and gen surg for most of my third year until I realized I didn’t absolutely love the OR and found it boring at times. EM is definitely my cup of tea and love the variety and craziness. I’ve gotten a lot of advice to consider IM more seriously if I want to do to CC bc obvi it’s a lot easier for hiring. But tbh I keep thinking what if fellowship doesn’t happen and I be an attending right after residency, what could I be happier with and it’s clearly EM>IM. So now with this uphill battle with intending to get CCM fellowship via EM, anything I should be doing or thinking about to best set myself up to follow down the EM/CC path?

Hey y’all. I’m an RN new to the MICU, have spent all of my career in the ER so I still have lots of questions. I had a patient last night, severe ARDS, not vent compliant, requiring proning. They had been giving her rocuronium during day shift, but stopped it after 0/4 on TOF. She had been off of the roc since 1730. My entire night shift she remained off of it, remained 0/4 on TOF,and with absent reflexes. She was alert and oriented prior to intubation and reflexes were all intact prior to starting roc. My understanding is that it can last a few hours, but not 15+ hours. She’s not a kidney patient, slightly overweight but not obese. Just curious if anyone has any wisdom for me!

I work in a CV-SICU and just recently I have seen way more of our patients post heart surgeries shunting on Cleviprex and Cardene, then we have to switch to Nipride for blood pressure control issue. I have read some researches about it too but it becomes more and more common at my work place now. Is it just our unit or do you see it at your work place too?

Hello US-based PCCM docs

I'm interested in learning more about typical work models in PCCM, and google just isn't cutting it.

What are examples of some practice models + compensation? Such as how many days per week working, split between ICU vs consult vs clinic, PTO, overall compensation / average hourly?

And as a bonus - would you choose PCCM again, or even better IM?

Thanks everyone!

A little background about me: I come from a lower acuity icu from a small community hospital, I see mainly pt’s you would see on micu. I have an interview for a cvicu position. I don’t have a lot of experience with crrt or ecmo, & cardiac surgeries. So that will all be new to me.

Any tips or advice on what they might ask or how to prepare for the interview is appreciated!

I'm a relatively new nurse in MICU and I just had a patient with acute pancreatitis 2/2 hypertriglyceridemia. The treatment being used was a dextrose-containing infusion and an insulin drip on a set rate. I'm having some difficulty understanding how this treatment modality works. From what I read online, the dextrose infusion is supposed to induce an anabolic state so that there is decreased production of free fatty acids, which will also decrease triglyceride levels. The insulin drip is to control hyperglycemia from the dextrose. Is this correct? The patient's triglycerides continued to trend upwards, so the resident increased the rate of the insulin. However, shouldn't they have increased the rate of the dextrose if I'm understanding the mechanism of action? Thank you for your help!

Can someone explain to me or link me a resource that explains:

1. Why can beta blockers cause hypoglycemia
2. Why can they mask hypoglycemic symptoms
3. How does glucagon work for BB overdose

I never understood the mechanism of these things.

Hello

What kind of standard sedation/analgesia are you using for your patients? Let's say for the ones that are freshly admitted or the ones that you still need rass -2 or below for some reason. I am not talking about cases where concomitant paralysis is needed but even then it would be interesting to know.

I am working in a general adult ICU and we are using propo/remi . I've read that an opioid is not always used as a standard practice, it would be interesting for me to hear about different practices.

Hey all!

I've been trying to find an answer for this online but can't seem to.

I understand that Alpha 1 (A1) will cause vasoconstriction and Beta 2 (B2) among other things will cause vasodilation. So, when we administer medications such as Levo (Norepinephrine) that hits both of these receptors ( plus A2 & B1 ), how does the Alpha 1 overshadow B2 to prevent that vasodilatory effect? Is B2's vasodilation just negligent? Because I also understand that with medications like Dobutamine, hypotension is one of the side effects as well. However, this is not the case for Levo. Why is that so?

Do you see what I mean?

​

I hope this question makes sense, please help me learn! :)

Hey all, I’m a trauma NP now with CVICU experience as an NP. I’m going to be transferring to a SICU only position. I’m somewhat familiar with ICU management, but also realize that I have some deficits. Any recommended ICU books to study up on? I’ve seen Marino’s book which looks pretty good, but can only see a little bit without purchasing.

Thanks!

hi everyone, any recommendations for a good stethoscope to use in a cardiac ICU?

Helllo all, Hope yall are having a good day. Wondering if anyone has any advice on good resources when switching from adult to pediatric ICU. My background is about a year in a step down and a year in neuro-trauma ICU. I’m moving to a new city/hospital and will also be making the switch to cardio AND pediatric nursing. Needless to say, I will very much be out of my comfort zone and would appreciate any resources anyone has to offer. Thank you so much in advance.

Hello all!

So I recently switched over from neuro to a cardiothoracic ICU and just finished up my first week. Overall, HARD but amazing experience. However, I’m really hard on myself. My preceptor says I’m doing good and I have good time management as well as making sure everything gets done but I do need to brush up on hemodynamics. Also, last shift was incredibly busy and I had no time to re write my report sheet so when I was giving report it was just a disaster (the other times I had everything written down it flowed smoothly). My preceptor is amazing and says to give myself a break since it’s only my first week, and that some days will be so busy I will not have time to write down much but will still need to give important information such as what rhythm they’ve been in during my shift, general HR and hemodynamic values. This is such a huge change from neuro that I might have underestimated it. And although my preceptor says I’m doing good and everyone comments on how good I’m doing … idk why I keep telling myself I’m not good enough? I know I’ve only worked 3 shifts so far but I guess when things don’t “click” immediately I get frustrated and discouraged. Anyone else switch specialties to cardiac and had to deal with imposter syndrome or something similar? Hearing similar stories would really help!

Is giapreza less harmful to the kidneys in AKI than neo?

Is a temporary hemodialysis catheter the same thing as a central venous catheter?

If the ECMO machine is oxygenating their blood, why are most ECMO patients I’ve seen also intubated?

I’ve seen those waiting for lung transplant 2/2 to fibrosis (meaning their lungs don’t work that well) on ECMO and intubated.

Has anyone ever seen this done? I didn't know it was a possibility, but there was a patient on my MICU that it was being considered for. Younger guy in severe ARDS secondary to an aspiration. All of his lung lobes were whited out except one. The attending on rounds brought up it up on rounds. I guess he wanted different peep for different lungs. It never ended up happening. They consented his family for ECMO and a bronchoscopy, and he was doing well enough after the bronchoscopy. Well, an improving blood gas at 16 of peep, flolan running, and 80% fio2. Can someone explain a bit more about dual ventilation?

Hey Y'all!.

Quick question: why are fresh liver transplant patients placed on an insulin gtt ?

Thanks !

I am trying to understand the pathophysiology behind this case. it happened about 6 months ago, and it still boggles me this day. To preface this, my background is as a trauma/Cardiac/Transplant ICU nurse, in a hospital with a dedicated Neuro ICU that would typically manage these cases by a very smart and dedicated neurointensivist. The neurointensivist in the case prefaced by saying the entirety of the shock state was neurological in nature, but my biases in my experience had me believe it was cardiac in origin. I want to have better answers because this was so far removed from my day to day experiences with hemodynamic instability that i could stand to learn a lot about the hemodynamic changes occurring in a large vessel occlusion.

The Case:

This was a 50M with a past history of a-fib on eliquis and metoprolol. Family found him at the dinner table unresponsive after they had a meal and went out for a few hours; patient reported feeling unwell for a week prior to that. Family endorsed upper respiratory symptoms.

EMS scoops him and BVMs him because his O2 is 60%. arrives to the ED where he is promptly intubated. Immediate post-intubation, an ABG is drawn that shows PaCO275 HCO323, ph 7.1, SaO270% and PaO2 50s. Vital signs were: Afib rate 80s, BP260s/130s, afebrile.

The patient was taken for a CT chest (which i did not ever look at) and them sent to the MICU, where it was received by the night shift. The Patient was promptly started on a Nicardipine drip, which was quickly maxed out at 15mg/hr with a target BP of 180 SBP. 1 hour post intubation ABG reveals respiratory acidosis resolved down to PaCO2 of 35, and further hypoxemia is not evident both on SPo2 readings nor on SaO2. Vent fiO2 was adjusted to 35% at this time and the vent rate was dropped. There is some concern this may be neurological. A STAT CT head revealed a Basilar Stroke. At this point they were probably close to 13 hours out from LKW, and I’m not 100% sure why a thrombectomy was not decided on or attempted, but medical management was pursued at this point. At this point, I assumed care of this patient at shift change. Family reveals he ran out of eliquis a week ago, and was going to pick up his next dose soon.

Neuro assessment revealed a positive weak cough, and large 6mm equal, very sluggishly reactive pupils. BP still high, but managing to get right at 200/100BPs on maxed out cardene drip. The patients heart is beating out of their chest, a-fib rate 90-100.

I am slowly coming down on the drip at this point without having transitioned to anything. No other sedation on. The first hours I’ve cut the cardene in half, meeting goal BP @180. The second hour I’ve completely turned it off for a SBP of 160, sustained. A fib RVR rate 120s. Red flags just got redder. Patient is febrile to 105F, I contact neuro PA and we put him on TTM to achieve normothermia.

Cardiology comes by. 25mg Metoprolol by NGT then reassess. SBP at this point is around 105/70s. I mention this to the cardiologist at bedside, and the decision is made to still give it because it wasn’t a large dose. I assess neuron status and pupils are dilated and airway reflexes are lost. Troponin in mildly elevated, BNP is also only mildly elevated.

I call Neuro-Intensivist because this patient’s shock index is rapidly rising. PA is sent down to evaluate and we agree this patient may require levo, as the blood pressure is dropping in front of our eyes. I start levo, with a decent response, and the PA leaves after being satisfied.

About thirty minutes after, the patient remains in a-fib RVR rate 120s from a conduction standpoint, but the Pulsox reveals a mechanical pulsatility at the fingertips to be around 40 bpm. whereas before I could see this patients heart beating out of their chest, this was no longer the case. I flag down a resident I know to quietly quickly probe his chest so I can see what the patients heart is doing, so I have cause for concern. EF looked about 30% at best, and the heart was effectively beating about 40 bpm. Views were affected by the TTM cooling pads so while disconcerting for cause, not the most accurate view. Sluggish cap refill and cold extremities (although TTM may have contributed).

Neuro PA puts an art line in, art line rate correlates with pulsox, BP is in the dirt, max out levo, and start vasopressin, he says. Neurointensivist comes to the bedside, says this shock state is all Neuro, and asks to transfer the patient upstairs to his ICU, and also that the patient is very fucked.

Chem8 drawn off the art line revealed normal sodium of 140 unchanged from arrival, a rising chloride and dropping bicarb to about 17, with no change in anion gap from prior labs. Hypertonic saline was not given during the time frame. Urine output dropped off steeply when the hemodynamic instability started. At some point I had gotten a VBG off a new central line, which showed a low SvO2, but I don’t remember specifics. It did also correlate a developing NAGMA.

I transferred the patient, and I would’ve walked away from that case thinking that the patient probably want into cardiogenic shock from the perfusion demand the brain was placing on the heart if the intensivist hadn’t said this case of shock was 100% Neuro. I did get one last set of numbers from a FloTrack monitor that was placed on arrival to the unit (ours were broken or in use). CI was 1.8-2.0, and SVR was about 2500 if I recall correctly.

My experience with neurogenic shock has largely been the loss of sympathetic tone in newly brain dead patients, characterized by bradycardia both mechanically and conductively. I have very little understanding of this Neuro-cardiac relationship outside of my typical experience and what we learned in nursing school (peanuts in comparison to what we learn on the job).

When I brought this case up to my wife, who is a stroke coordinator, she merely shrugged and said “Brain No Worky” and said that from a Neuro standpoint, this is more common than you think. She also outlined a similar case a few weeks prior that was attributed to a rapid correction of BP with cardene, which precipitated the shock state.

I can’t claim to know enough about this. But I was curious enough to reach out, because how does one differentiate these shock states? It seems like the devil is in the fine details, and comparing what is expected of true cardiogenic shock to what is presented. For all intents and purposes, if this patient was plopped down in front of me with zero context, my immediate reaction would’ve been separate cardiogenic shock precipitated by the loss of brain perfusion in the stroke setting and now with a low cardiac output state, the two are spiraling one another. Albeit, lungs were dry, and only mild JVD was present.

I’m interested to know what others think. The last time I posted a case here, I had so many comments lead me down a rabbit hole of education I didn’t know that I needed to know, and it helped me out clinically.

Hi all, beyond excited to start pulmCCM fellowship in the next couple months. Would love if the community could share some wisdom that you wish you knew when you began fellowship

What is a good way to distinct RBBB/LBBB especially on a 5 lead telemetry monitor? I feel like the pictures of what it should look like NEVERA looks like that and since most leads are placed around v2 or v3 I find it hard to recognize it at all. Any guidance?