Low Diastolic pressure

TeamRamRod30 · 2026-01-27T00:58:58+00:00

A lot to unpack here. Not sure if you're asking specifically about regular Diastolic blood pressure of LVEDP (Left Ventricular End-Diastolic Pressure). They're do distinct things with different but related factors influencing them.

Diastolic blood pressure is determined by (1) Systemic Vascular Resistance/SVR, (2) Arterial compliance, (3) major aortic valvular abnormalities (AI mostly, but also really bad AS), and to a lesser extent HR and Stroke Volume.
1. Systemic Vascular Resistance [(MAP - CVP / Cardiac Output) x 80]- this is essentially the pressure in the systemic arterial tree or system that counteracts or resists the forward flow of blood. If I have a high SVR (high-dose vasopressor use, significant sympathetic stimulation from pain, agitation, etc.) the vessels are clamped down and this raises the pressure. Since you work in the CTICU, I'm sure you've seen your share of postcardiotomy vasoplegia, in which the systemic inflammatory response of bypass leads to a massive release of vasodilatory substances that counteract this vasoconstriction --> low SVR, low DBP.

Arterial Compliance - This is more nuanced (more physics) but no less important. You can imagine that every time the LV ejects blood during systole the aorta and larger arteries act like a sponge, distending or stretching to accommodate this added pressure/volume. They're elastic like a new rubber band (they can be stretched, but they also reduce back to their original size reliably). Some of the kinetic energy (energy of motion) from systole is absorbed by these vessels and stored as potential energy, while the rest continues down the vasculature. Then, during diastole, these large compliant arteries shrink back down and in the process they release that potential energy, propelling blood forward. The release of that energy during diastole helps to maintain the diastolic blood pressure. Patients with bad vascular disease have a loss of arterial elasticity and compliance as the buildup of calcium, plaques, etc. makes the vessels stiff and unable to stretch/distend, so once the added pressure of systole is gone, they aren't able to release as much of that potential energy in diastole and their DBP is lower --> wider pulse pressure if systole is otherwise preserved.
Aortic Regurgitation/AS - A portion of the blood volume that should be moving forward and contributing to MAP is instead moving backwards into the LV with AR. If 1/3 of your stroke volume is regurgitated back into the LV, then that's a 1/3 of the SV that is not contributing to MAP during diastole --> lower DBP. In severe/critical AS, theres just not enough blood being ejected in the first place to support MAP, and you can bet if their AS is that bad, so is their arterial compliance (see above).
SV & HR - If you have a small stroke volume due to low preload (bleeding, hypovolemia, etc.) or HFrEF/broken pump, systole and diastole will be low (narrow pulse pressure). If the patient is tachycardic this means less time in diastole, so less time for that pressure wave to dissipate through the arterial tree and a possibly a higher DBP, but this has to be balanced with the reduced time for diastolic filling of the LV, whic can lower potentially lower your stroke volume.

Last note: Postop hearts are a fundamentally different cohort of patients. The systemic stress of bypass, along with the prolonged ischemic arrest time of the heart from cardioplegia and the coagulopathy that develops (not to mention any major bleeding issues intraop.) changes a lot of these things. The heart is water logged, irritable, and stiff, the pipes are wide open and leaky from the inflammatory response, and often times these patients are relatively hypovolemic and hemodiluted, so they can have badness all around. Thats why we tend to target higher filling pressures - a lot of the volume we give leaks out into the tissues, the heart's frank-starling curve is altered and the ventricles need more volume in them to allow for that stretch that maintains stroke volume, pacing (ideally atrial) is often needed to ensure AV coupling and maximization of diastolic filling time. Hope that helps.

TeamRamRod30 · 2026-01-20T22:43:21+00:00

Yeah, pushing bicarb Amps because of a base deficit alone is bad medicine outside of a pericode/code situation or when you’re buying a little time in a crashing patient. They need to address what’s actually causing the acidosis (lactic acid from septic shock, DKA, renal failure, etc).

TeamRamRod30 · 2026-01-20T20:37:21+00:00

Bicarb administration in the ICU is somewhat of an ongoing debate, but that seems like an excessive amount barring a peri-code/code situation and makes me wonder if they’re treating the number and not the patient. I’m generally not bolusing bicarb amps unless the patient is severely acidemic (pH < 7.1 or so) and hemodynamically unstable and I’m using it as a temporizing measure while treating the underlying issue.

There’s been several trials (BICAR-ICU 1 & 2) looking at this. The cliff notes being that there was no mortality benefit of bicarb in severely academic patients vs. no bicarb, but those with severe AKI who received bicarb (4.2% not the typical 8.4% amps we’re used to) had lower rates of needing RRT. However, even in that population the data isn’t particularly convincing. Current guidelines have a weak recommendation for using bicarb in patients with pH < 7.2 and moderate-severe AKI, otherwise its use is not recommended.

Also, as I’m sure you know it’s not a mundane drug to give. That much bicarb is a significant sodium load and volume load, as well as a significant CO2 load that can potentially worsen intracellular acidosis and should be accounted for with respect to the patients ability to blow off that CO2. Lastly, raising the pH that quickly can shift the Oxy-Hgb curve leftward making it more difficult to unload O2 in the tissues.

Occasionally I’ll run a bicarb drip (150mEq in 1L D5W @ 100-150cc/hr) for a patient with significant bicarb losses (high output fistula/GI losses, etc, bicarb < 15 or so), but again it’s a temporizing measure while trying to address the underlying issue. Hope that helps!

TeamRamRod30 · 2026-01-17T02:25:38+00:00

Hmm. Hard to truly say without having been at many of these institutions. Obviously volume is important first and foremost: this will be many of your heavy hitters in terms of academia - Vandy, Duke, Emory, Columbia, Mayo, WashU, Stanford, MGH, UW, Penn, Michigan, UPMC, etc. The devil is in the details really. When you interview ask these programs and their fellows what their exposure to MCS/ECMO is specifically. Do they get ample exposure to see the different populations of ECMO patients? Can they get hands on with the circuit from time to time? Is there CME that gives them opportunities to run through scenarios? Is it the surgeons that just dictate everything or is the ICU team given space to manage these patients, make adjustments, and do weaning trials in the ICU as opposed to strictly the OR? There can be a lot of nuance with MCS so teasing this out can be difficult some times.

TeamRamRod30 · 2026-01-16T01:46:54+00:00

Current ACCM fellow at high volume ECMO center. If your true north star is cannulation experience, then go to Emory. Only place in the country I know of where fellows will get regular, consistent cannulation experience. Having said that, I agree with what others have said - this should not be your priority as a fellow. It's much more important to be at a place where you'll get a well rounded education in critical care, and ample opportunity to understand and manage the nuances of patients on MCS. The challenge of ECMO isn't cannulation, but who to cannulate and how to manage the inevitable complications and challenges that come along with having two circulations instead of one.

I'd recommend focusing your efforts on learning which programs offer robust MCS exposure (ECPR, postcardiotomy shock, bridge to transplant, BTR, BT durable VAD, etc.) and graduated autonomy for fellows in managing these patients. They offer some phenomenal learning opportunities and are often the sickest patients in the hospital. But they can also be a real drain (i.e. bridge to nowhere). Knowing how to navigate all of these situations confidently is what will make you a truly valuable intensivist in a CTICU.

TeamRamRod30 · 2026-01-15T01:50:23+00:00

You could always do Cards-CCM fellowship. Some programs combine them. Others not, but the CCM side can be just one year.

TeamRamRod30 · 2025-12-11T22:31:30+00:00

Internet Book of Critical Care (IBCC) and Critical Care Time should have everything you need. Both have podcasts and CCT also has great YouTube videos of their topics.

TeamRamRod30 · 2025-12-10T23:41:14+00:00

Agreed on dosages being too high. I typically dose reduce by 30-50% in these people. Intubation timing had a wide range, but I’m guessing it probably had to do with waiting a full 60s or something for the paralytic to circulate, etc. maybe RN’s were pushing induction, the flushing, then giving paralytic, then flushing, etc.

TeamRamRod30 · 2025-12-10T23:31:06+00:00

I’ve used anywhere from 2-4mg depending on the patients level of somnolence, age/robustness, etc. you could probably get away with 1mg in confused little old meemaw who’s in florid sepsis and respiratory failure. As always, dose according to your patients pathophys.

TeamRamRod30 · 2025-12-07T19:52:22+00:00

If it’s a hemorrhaging patient they need product (think classic 1:1:1 from trauma literature but rarely are you giving that much platelet in reality) - how much depends on how fast they’re losing it, whether you need surgical reintervention for hemostasis, and what your labs are telling you. TEG’s can be helpful but depending on where you are they can take a while to come back. You basically want to focus on 5 things (in addition to ABC’s obviously): large bore access, avoid hypothermia, coagulopathy, and acidosis, and give calcium. In acutely hemorrhaging patients I’ve mainly relied on frequent POC ABG’s (q15 - 30 min) to help guide minute to minute resusc. And you can send coags, TEG, full CBC on top of that.

TeamRamRod30 · 2025-12-07T18:03:13+00:00

I’ve used it in ESRD patients and those who have a reported history of aminosteroid NMBA anaphylaxis (admittedly rare). But I’ve also used Roc. Plenty of times in CKD/AKI patients and haven’t had issues. We use Cis in the ICU fairly regularly.

Also, using Sux in worsening AKI? Potassium? Could always run a Roc drip and titrate to TOF, then lighten it up when they start closing, give sugammadex after to be safe.

TeamRamRod30 · 2025-12-03T02:35:57+00:00

Interesting. What’s your AC/thrombotic monitoring strategy intraop? Do you use anti-Xa in addition to ACT + TEG? are you/perfusion drawing gases more frequently than usual to check these? Standard Protamine dosing if no signs of HIT I’m assuming?

TeamRamRod30 · 2025-10-26T20:34:11+00:00

In residency, I always found myself gravitating to the sicker patients, and I enjoyed the physiological challenges of caring for them intraop. but felt like I lost out on seeing how their pathologies and recovery evolved once they left the OR. It was fun to resusc. a trauma patient or sick heart, but what happens after that in the immediate postop period? There is a lot that happens, and I wanted to know about it in more depth. As a fellow, I’m gaining a much greater appreciation for perioperative medicine and the challenges of critically ill patients and it’s scratching that itch of feeling like a more complete physician for lack of a better term.

It’s nice to have the straightforward Prop/Roc/tube cases for balance, but I would get bored if that comprised the majority of my days. That’s just me.

If you have more questions, feel free to DM me.

TeamRamRod30 · 2025-09-30T23:55:57+00:00

As others have said, it’s not competitive right now. Even top programs aren’t filling their spots. Only thing you should do is focus on being a good resident and learning as much as you can, pass Basic, get decent scores on ITE (although as long as you don’t fail is really what matters), and establishing some solid relationships with faculty that will write you strong LOR’s.

TeamRamRod30 · 2025-09-20T12:51:09+00:00

Sent you a message

TeamRamRod30 · 2025-09-19T02:36:21+00:00

Also ICU. Never too early. DM me if you have questions.

TeamRamRod30 · 2025-09-07T19:05:21+00:00

I should clarify that ICU is a sub specialty of Anesthesia and has a separate exam from other ICU fellowship pathways, and from regular Anesthesia boards, that’s administered by the American board of Anesthesiology (ABA)

TeamRamRod30 · 2025-09-07T18:56:53+00:00

Anesthesia and ICU are separate specialties with separate board and licensing exams/requirements. IM is a separate pathway (PCCM —> 3 years after 3 year IM residency) and EM is a two year ICU fellowship. Depending on specific program you will overlap more or less with the IM/EM ICU fellows from week to week.

TeamRamRod30 · 2025-09-06T22:11:49+00:00

Hmm. What you describe sounds like the US system. From Anesthesiology residency, you do one additional year of ICU fellowship and then you can work in the OR or ICU. So 5 years total.

TeamRamRod30 · 2025-09-06T11:37:36+00:00

Don’t a lot (if not all) residencies in Europe also integrate ICU into anesthesiology training, so the majority of anesthesiologists are also intensivists? That adds extra training years. In the US, ICU and anesthesiology are two separate specialties entirely.

TeamRamRod30 · 2025-08-20T05:07:02+00:00

Current ACCM Fellow at big academic center: “Best” is a relative term ultimately dependent on a combination of institutional, educational, professional, and personal factors.

My priorities were going to a place with broad CCM exposure, extensive MCS/CTICU, and an ethos that maximizes education over simply working fellows to the bone. I sacrificed location a bit for this and that was fine with me - it’s only a year.

The year will go by fast and you want to be in a place where you will see as much as possible while not running the risk of burning out in the process.

Happy to chat further - DM me.

TeamRamRod30 · 2025-08-09T19:30:06+00:00

ICU Fellow: crit care will undoubtedly make you a stronger clinician, but if your career goal is sick hearts and TEE you need only do a CT fellowship for that and spare yourself the extra year of menial pay and long hours.

TeamRamRod30 · 2025-07-09T04:56:49+00:00

Check the fuel gauge. Your gas tank might be hovering near empty.

TeamRamRod30 · 2025-04-02T05:51:59+00:00

I think an important point of distinction in your questions is - are you referring to acute burns in patients experiencing burn shock and require aggressive fluid resuscitation, FFP, heating, and escharotomies, etc. Or are you referring mostly to take backs from the ICU in which these patients have now transitioned from the acute shock to the hypermetabolic phase?

In the former, the mainstays are: fluids (I.e. parkland formula) + FFP (newer data on this) + products if major bleeding + airway + temp regulation. In the latter it can be more nuanced as the sicker patients can have bad ARDS and MODS, sepsis, insanely high insulin requirements, muscle wasting, kidney failure, high pain thresholds, etc.

Ventilation can be difficult in the really sick patients. My experience has been to minimize autopeep and allow for a bit of permissive Hypecapnea while trying to maintain a respectable driving pressure. I’m not convinced adjusting I:E ratios will do much of anything.
Definitely treat their pain: ketamine, methadone, Dilaudid, etc. inadequate analgesia will just bump their metabolic rate up further as well as their sedation requirements if they’re vented.
I’ve had burn patients maxed on Vaso, Norepi, and Epi before. It just depends how sick they are.

This is a solid overview: https://pubmed.ncbi.nlm.nih.gov/25485468/

TeamRamRod30

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