ICU stories: Middle-aged pt with cirrhosis presented to the ED with abd pain and underwent Hartmann's procedure (colectomy - end-colostomy). Next am, pt was hypotensive on rising levo gtt (0.24 from 0.1) and ⬆️lactate (3.4 -> 6.7). S/he was positive 8 liters in 12 hours 😱
After reading the chart, I was almost certain that pt would be congested/fluid intolerant (after 8 liters+ fluid balance...). When I first walked in the room, BP was 90-100/30-40 (radial a-line), HR 120-130 and this is what the monitor showed:
I did POCUS: hyperdynamic LV, no pericardial effusion, RV OK, IVC very small (images not shown). I threw some color Doppler in the LV and this happened:
"A lot of color"! -> high velocity signals in the LV cavity and probably the LVOT. US windows not good (pt on the vent; subcostal views impossible given recent laparotomy), so I tried some continuous Doppler in the LVOT:
☝️Voila! A dagger-shaped signal with max velocity of 6 m/sec. I was not interested in finding exactly where the obstruction was. I bolused ivf, started vasopressin 0.04 and gave 5 mg iv metoprolol. In a few hours, lactate was normal and levo was ⬇️by 2/3.
Patient seemed to benefit from being managed as one with LV outflow tract obstruction. I would have never tried iv metoprolol in a pt on industrial doses of pressors. In the past, I might have tried esmolol that can be dc/ed fast. POCUS makes us smarter at the bedside. To be fair
the initial monitor view gave me pretty much the diagnosis or at least raised my suspicion of it. Do you see how weird it looks? Do you see the 2 systolic inflections?
Let's look closer. The obstruction to the ejection of blood from the left ventricle creates the 2nd systolic peak
This is what happened after fluids were given and heart rate was controlled. The dynamic obstruction to ejection of blood from the left ventricle disappeared
Take home messages: 1. Looking at the arterial/CVP waveforms can be sometimes very helpful, in fact more helpful than the exact BP/CVP values 2. We should not automatically equate a positive fluid balance, even a significant one, with fluid intolerance or venous congestion
3. We should always consider LV outflow tract obstruction in hemodynamically unstable patients
DOI 10.1007/s12630-009-9174-y
Thanks for reading!
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I know you know them, but let’s remind ourselves of some additional basic hemodynamic "secrets":
16. Volume status is a nebulous term, but I don’t foresee stop using it anytime soon
17. The ultimate goal of hemodynamic management is adequate tissue perfusion (TP). TP may suffer even if the macrohemodynamic markers look good. This scenario is called “hemodynamic incoherence”. Sadly,
I know you know them, but let’s remind ourselves of some basic hemodynamic "secrets":
1. Pressure ≠ volume, even though volume can affect pressure
2. CVP (central venous pressure) is not a marker of “volume status” since it can be affected by non-volume related disorders (eg, tricuspid regurgitation/stenosis, pericardial pressure etc)
Elderly 👴 w interstitial🫁disease was admitted -on NIV- from the ED to StepDown unit w "pneumonia": bil infiltrates/low-grade fever. PF ratio 140. Since I was in the ICU, I asked how he looked. Reply: needs high FiO2 but pulls good tidal volumes
When I saw him:
This is not an uncommon scenario: a "low" expired tidal volumes (Vt) makes the staff worried during NIV initiated for hypoxemic respiratory failure but a "high" Vt (even if accurately measured) is left unabated...
In fact, high Vt during NIV has been associated with NIV failure and poor outcomes
The American Thoracic Society (ATS) updated its recommendations on some aspects of the diagnosis and management of community-acquired pneumonia (CAP)
This guideline update focuses only on immunocompetent adult patients with a standard diagnosis of CAP
It addresses four clinically relevant questions:
The guideline underwent peer review by 16 experts (4 from ATS; 11 from Infectious Diseases Society of America (IDSA). It Is not clear to me why IDSA did not approve it. I copy from the supplement: "The IDSA chose to withdraw rather than approve the final version of the guideline"
Have you ever managed a septic patient & ordered antibiotics to be given stat only to discover hours later that they were still infusing? If yes, stay tuned
Among several controversies in sepsis management, the early administration of antibiotics
is one of the least debatable ones. Time is life in sepsis!
Even though it's hard to believe that every hr of delay in antibiotics ⬆️ mortality by 8% (this is a different topic...), it's one of my pet peeves when it takes for ever to give antibiotics to a septic shock patient
The most commonly ordered combination in 🇺🇸 hospitals (EDs/ICUs) is piperacillin-tazobactam (Zosyn in 🇺🇸) + vancomycin (V). If the usual practice is followed, giving a dose of Zosyn & a dose of vanco can take close to 3 hours. This should not be the case!
Is there anything regarding UGIB that has not been already done, studied or tweeted about? Not much, but all of the following are things I witnessed happening (or not happening…) in two UGIB cases I recently saw in the ICU
Here it begins:
1. If a patient does not have an obvious UGIB as in the clip above, she has just presented with melena & it is still unclear if this is due to upper or lower GIB, a quick & dirty trick is to check the blood urea nitrogen/creatinine (BUN/creat) ratio. There are various published
cut-offs in the literature (don’t sweat about them…) but, in general, a ratio of >30 suggests UGIB. This is due to the small bowel absorption/digestion of blood protein which is subsequently metabolized to urea. There are confounding factors, but the trick usually works well