an asymptomatic adult human presents with these findings...
should you institute therapy or repeat lytes?
EKG shows classic findings of hypoK (ST depression & pronounced U-wave that produce a "wavy baseline" pattern). so the hypokalemia is real - treatment should start immediately.
(more on EKG findings of hypoK:hqmeded-ecg.blogspot.com/search?q=hypokโฆ )
the patient is hypovolemic, what fluid is best for volume resuscitation?
0.9% saline is probably ideal.
- will reduce the serum bicarbonate level
- may increase the K level due to pH/K shifting
there's nothing *wrong* with LR or PL here, but they won't help the electrolytes. saline actually will help.๐คฏ
the primary life threat is probably the risk of torsade de pointes (one form of polymorphic VT). hypoK & hypoMg both promote this arrhythmia, with the combination causing synergistic badness. prolonged QT/U duration on the EKG is a bit ominous here.
(emcrit.org/ibcc/tdp/)
the patient has a single functional IV line. what do you order first?
4 grams of IV Mg sulfate will immediately raise the Mg level and reduce the risk of torsade de pointes. In contrast, it's largely impossible to *rapidly* fix the potassium deficit (rapid & high doses of IV potassium are dangerous & avoided in asymptomatic/stable pts)
the patient's sodium is 122, do you think this requires specific therapy (eg 3% NaCl)?
nope. KCl has the same effect on tonicity (and sodium concentration) as NaCl does. so as KCl is given to improve the hypokalemia, this will increase the sodium. if anything, there might be a risk of correcting the hyponatremia too *rapidly*!
the potassium is 1.4 mM with EKG changes. do you need to insert a central line?
no solid data on this, but since the patient was asymptomatic and able to take PO we combined aggressive IV magnesium with aggressive oral potassium repletion (with a bit of IV K to get things started as well). #zentensivist
(more: emcrit.org/ibcc/hypokalemโฆ)
case conclusion - the patient got better, nothing too exciting happened. no procedures were needed, providing the physicians with additional time to scroll twitter.
Waveform capnography! I've been meaning to cover this for years. Finally posted an IBCC chapter on it. The chapter is pretty long (filled with subversion, physiology, and zentensivism), so here is a thread with some key points.๐งต emcrit.org/ibcc/co2/
end tidal CO2 (etCO2) will ~always be lower than the arterial CO2 (b/c dead space dilutes CO2 as the patient exhales). the gap between the etCO2 and the arterial CO2 varies depending on lung function. in normal lungs, the CO2 gap is usually ~2-5 with an upper limit of ~10-15
Imagine that we intubate a healthy patient for airway protection 2/2 intoxication. A safe pH for this patient might be ~7.2-7.5 (no good data!). To achieve this, we need an arterial pCO2 to be ~32-64 mm. So all we need to do is target an etCO2 of ~30-35 and we should be good.
oh, the life & times of remdesivir! - let's review the bizarre trajectory we've taken with this medication! with emoji's to represent each study ๐คฃ
we start with a retrospective series of patients treated with remdesivir under the banner of "compassionate use." most patients didn't die. this paper has so many flaws, at this point it's merely a case study in horrific research design ๐คฎ (commentary: bit.ly/2XBwnx1)
next: the 1st placebo-controlled trial. the primary endpoint (time to clinical improvement) was negative, as were most 2nd endpoints (including viral load). the only glimmer of benefit was faster clinical improvement in one slicing of the data ๐ฅด (bit.ly/3lIxnXZ)
fresh RCT on the effects of a continuous infusion of hypertonic saline for traumatic brain injury (#1/6) jamanetwork.com/journals/jama/โฆ
patients were randomized to an infusion of 20% NaCl for 48 hours. as shown here, the infusion was successful at pushing sodium levels to the mid-150s, with nice separation between groups (#2/6)
initially, patients receiving hypertonic infusions had fewer episodes of ICP elevation. however, their brain cells adapted rapidly to the higher tonicity... so when the hypertonic was stopped they had *rebound* elevation of ICP (#3/6)
if you don't immediately know why this paper is garbage, then read this explanation (bit.ly/3klwkek). in short, time-to-intervention studies are retrospective correlational junk which continue to infest the scientific literature (rantorial #1/4)
the data from this study actually suggest that early antibiotics in pneumonia are *bad*, but early antibiotics in septic shock are *good*. this obviously isn't true -it merely serves as an illustration of what happens when you conflate correlation with causality (rantorial #2/4)
the study is funded and largely performed by Shionogi (a company producing - you guessed it - antibiotics!). this may explain their unbridled enthusiasm with the conclusion that early antibiotics will save the world (rantorial #3/4)
three short chapters on gastrointestinal hypo-motility in critical care.
๐ฃthis topic often gets *ignored* until there's a serious complication
๐ฃearly attention to motility can avoid iatrogenesis & facilitate recovery...
(thread #1/4)
ICU gastroparesis
๐คฎ manifests as tube feed intolerance (but don't assume that feeding intolerance = gastroparesis!)
๐คฎ a post-pyloric feeding tube can treat this nicely. otherwise erythromycin +/- metoclopramide
๐คฎ treat this- don't just watch/wait (#2/4) emcrit.org/ibcc/gastroparโฆ
ICU ileus
๐คฎprevention is key- avoid opioids, early enteral nutrition, early mobility๐
๐คฎNG drainage *only* if needed for symptomatic relief
๐คฎprokinetic meds don't work, but *oral* naloxone might help among patients on significant opioid doses (#3/4) emcrit.org/ibcc/ileus/