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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Noninvasive ventilation (NIV) has been standard of care treatment for acute exacerbation of COPD (AECOPD) for > 30 years. In this article, the authors describe an evidence-based algorithm of the initiation, titration, monitoring, and weaning of NIV in AECOPD
An interesting study was recently published in @yourICM and the authors made some sensible - IMHO - suggestions about how to use echocardiography to guide fluid management in critically ill patients
They recognized 3 scenarios where echo can predict fluid responsiveness (FR):
1. Do NOT fill
2. Fill
3. Optional fill
I tried to tabulate their scenarios and recommendations/limitations extracting only information from their paper and not adding any thoughts of mine
ICU ID Secrets (following up on my post* from last week):
Ten things to remember about methicillin-resistant Staphylococcus aureus (MRSA) polymerase chain reaction (PCR) nasal swabs:
1. The MRSA nasal PCR is mostly helpful in patients with pneumonia or at least high suspicion of it since nasal colonization correlates with MRSA presence in the rest of the respiratory tract
2. The MRSA nasal PCR is mostly useful for its high negative predictive value (NPV) for MRSA pneumonia. The NPV number to remember is 95%. The use of MRSA PCR screening in pneumonia can reduce length of stay and antibiotic costs
Patient underwent laparoscopic colectomy complicated by R paracolic abscess (s/p drainage) & fascial dehiscence. On post-op day 8, at 20:30, he called out for his nurse stating he was having trouble breathing & back pain. He was diaphoretic w O2 sat in 70s at 2 l/m.
He was placed on 6 l/m nasal cannula w O2 sat 92%. A rapid response was called at 20:45. Pt was then placed on a non-rebreather mask; stat chest x-ray, ECG & blood gases ordered. CXR was later read as "small L basilar atelectasis". ECG (was read as "no acute MI"):
Assuming we are at end-expiration (the phase where CVP is least affected by the intra-thoracic pressure), at which point should we measure it?
There are other options: v, mean etc. However, most would measure CVP at the base of the "c" wave, especially if they wanted to use CVP as a surrogate of '"preload". OK, now we are in a slippery slope, since "preload" & "fluid responsiveness" are vague concepts. Having said that,