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
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IKYK that: i) blood pressure (BP) is the driving force for organ perfusion, but ii) hypotension does not always lead to hypoperfusion
One of my favorite reviews (PMID: 34392972) tries to reconcile the paradox and expand on the topic:
Fact:
Although an abundance of cohort studies have suggested an association between hypotension & unfavorable outcomes, several RCTs have failed to demonstrate consistently improved outcomes from maintaining a higher BP
Back to basics:
Arterial blood pressure is the result of multiple hemodynamic parameters:
When you prepare for the "average" intubation (no cardiac arrest, no active emesis), how do you pre-oxygenate the patient?
In PREOXI, a multicenter, randomized trial conducted in 24 🇺🇸 EDs and ICUs and published in 2024 (PMID: 38869091), 1,301 critically ill adults were randomly assigned to receive preoxygenation with either noninvasive ventilation (NIV) or an oxygen mask (O2M)
Hypoxemia (defined by O2 sat < 85% during the interval between induction of anesthesia & 2 minutes after tracheal intubation) occurred in 9.1% in the NIV group & in 18.5% in the O2M group (difference, −9.4%; 95% confidence interval [CI], −13.2 to −5.6; P<0.001)
For the average RSI - rapid sequence intubation (no cardiac arrest, no active emesis), do you provide bag-mask ventilation between induction and laryngoscopy (I & L)?
RSI flow(s):
In PreVent, a multicenter, randomized trial conducted in 7 academic 🇺🇸 ICUs and published in 2019, 401 critically ill adults were randomly assigned to receive either ventilation with a bag-mask device (BMV) or no ventilation (NoV) between I & L
In a multicenter study of 283 acute heart failure patients, changes in renal filtration markers (cystatin C or creatinine) with aggressive diuresis were not associated with changes in markers of renal tubular injury (NAG, NGAL, or KIM-1)
In this aggressively diuresed population (560 mg iv furosemide -> urine output of 8425 mL over 72h), both worsening renal function & increases in tubular injury biomarkers were not associated with adverse outcomes; rather, there was a trend towards improved outcomes
The data suggested that the small-moderate ⬇️in GFR that commonly occur during aggressive diuresis, colloquially referred to as "bumps in creatinine", may not primarily be a manifestation of renal tubular injury; rather, they represent clinically benign changes in filtration
Ten things that -for no good reason- we don't do in the ICU:
OK, in general a "less is more" approach is reasonable & there is a "rationale" behind many of the following but the truth is that they don't make sense if scrutinized
Here it begins:
1. Holding tube feeds or
any type of nutrition, because the glucose is "high"...
I see it often when I do morning rounds; the tube feeds were held at 2:00 am (and never restarted) because glucose was 400. Obviously, the right approach is to adjust the insulin regimen and keep feeding the patient.
2. Not starting or stopping TPN because the patient is bacteremic/septic...
Does this mean that if a patient cannot be fed enterally and remains bacteremic for 5-7 days (not uncommon scenario in S. aureus bacteremia), she cannot have any caloric intake for a week? 🤷♂️
77 yo patient admitted to the ICU from a nursing home w hyperglycemic-hyperosmotic state & acute kidney injury. On day 6, he spikes a temp 38.3. BP 96/59, HR 110/min. UA suggestive of urinary tract infection. The next day, urine culture grows Enterobacter cloacae
A day later, the blood culture grows Gram (-) rods (eventually proven to be the same bug). The susceptibility profile is:
You discuss with the team about treatment options: