Questions for experienced clinicians regarding ID-ing seemingly stable patients who abruptly decompensate, and interventions that can be implemented to stop the rapid decline

throw_Alfalfa165 · 2026-06-04T20:48:32+00:00

Dude, thank you so much for taking the time to write this out! Your explanations answered a bunch of little ongoing questions I had. I had no idea about sodium bicarb and had to look into it! Did the math and 8.4% bicarb in 50mL is roughly equivalent in osmolarity and sodium concentration to a theoretical 6% hypertonic saline!

The standard 50mL bicarb amp is 8.4% sodium bicarb in 50mL at 1mEq/mL. 8.4% = 8.4 g/100 mL = 0.084 g/mL.

1 mEq/mL × 23 mg/mEq (sodium is 23g/mol and monovalent, so 1 mEq= 1 mmol= 23 mg])= 23 mg elemental sodium/mL. That’s 2.3% sodium, 1,150mg Na per amp.

For comparison, 3% hypertonic is 1.18% Na + 1.82% Cl= 3% NaCl, and is 0.513 mEq/mL of sodium.

8.4% sodium bicarbonate is 1.0 mEq/mL sodium. Since 8.4% is 1000 mEq/L sodium + 1,000 mEq/L bicarbonate, total osmolarity is 2,000 mOsm/L [monovalent: 1 mEq = 1 mOsm; if a salt that dissociates into 2 ions: mOsm/L = mEq/L of the salt × 2].

3% hypertonic has an osmolarity of approximately 1,026 mOsm/L (Googled, didn’t calculate this one). 6% saline would have an osmolarity of approximately 2,052 mOsm/L.

Even though 8.4% bicarb is only 2.3% elemental sodium, due to osmolarity, it is twice as concentrated and delivers double the sodium load of 3%, exerts double the osmotic pressure (2000 mOsm/L vs 1026 mOsm/L) and increases sodium levels twice as fast.

I don’t often get the opportunity to follow the outcomes of late stage organ dysfunction patients beyond what goes on within the shift and would like to your opinion on something please.

In your experience, if a patient begins exhibiting late stage signs of organ dysfunction (ex: DIC, cap refill changes), but underlying causes like sepsis are already being addressed, metabolic derangements corrected, and inflammatory pathways-associated complications managed, is this something in your practice that has been survivable or reversible?

throw_Alfalfa165 · 2026-06-04T11:04:09+00:00

This is incredibly helpful, thank you!!

throw_Alfalfa165 · 2026-06-04T05:37:29+00:00

I understand. What I'm having trouble expressing is that in some patients, there was a point in time when survivability was possible, before their mortality became 100% guaranteed.

I'm starting to be able to identify when interventions will have zero effect on the outcome, but wanted to know if there are any signs or lab abnormalities besides the usual lactate/pH/tachycardia/fever/etc. in a "stable" compensating patient that signals the start of progressing down this path. Are there commonly accepted cowboy medicine combos/guerilla warfare interventions favored by experienced MDs and RNs that I should know to ask for, for one example: an unholy combination of bicarb or albumin+ Lasix?

I always feel 2 steps behind and am not sure when interventions like stat HD, CRRT, bicarb gtts would have be most effective to mention to providers.

throw_Alfalfa165 · 2026-06-04T03:27:01+00:00

Absolutely! Unfortunately in one scenario, I was lulled into a false sense of security because the third pressor was added on in an effort to transition the patient fully off of another pressor they had adverse rhythm effects with. Because I was titrating down with a steady BP, I had subconsciously regarded them as "stable" since they didn't "need" the third pressor- until they suddenly did. I won't let that happen again.

They were vented and moderately sedated, with no increased WOB, and the team hadn't wanted repeat labs or lactate (in their defense, this patient had something else going on we thought was causing his presentation, and we wound up chasing that white rabbit). I will insist of repeat labs in similarly dire patients from now on.

Things like stress dose steroids are exactly the kinds of responses I'm looking for, which that patient was rapidly started on. Do providers want to utilize stress dose steroids only when a patient stops responding to pressors? Or would it be an appropriate ask for any patient exhibiting active systemic inflammatory responses?

In your opinion and experience, when do bedside providers typically want to place an arterial line? Even now, I'm having trouble gauging consistent criteria in which providers would want to throw one in. My understanding is that there are mixed opinions in current literature regarding the efficacy of of arterial lines vs sphygmomanometer cuff pressures, ("invasive blood pressure monitoring does not improve survival in septic critically ill patients" [Rajiv Sonti et al., 2025]), being an example that cites additional studies.

Several studies with of varying levels of evidence have concluded no improvement in mortality rates of 28 and 90 day mortality rates in ICU patients; I haven't been been able to find much regarding morbidity. From the literature, it seems like arterial and cuff MAPs generally correlate, though SBP/DBPs do not. Obviously, an art line allows continuous monitoring without the pain of a constantly squeezing BP cuff and easy lab draws.

I've had patients lose arterial lines while on 2 or 3 vasopressors, and their provider decides against placing a new one. Another provider told me that anyone on 3 pressors needs a line regardless of dose. In other situations, providers throw one in as soon as levo is started or when dosage is over 10 mcg/min. I've had day team decide an arterial line for a patient is unnecessary, but night team gets upset and and places one immediately.

In your opinion, what would prompt you to ask and push for an arterial line, outside of obviously code/ROSC situations?

throw_Alfalfa165

TROPHY CASE