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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ICU Snapshots - Ventilator waveforms (from a patient I just saw):
Patient on "volume control" (or: VC-CMVs). Please notice the significant change in the pressure waveforms while the flow waveforms remain "mostly" unchanged
What happened?
What happened between breath (A) and breath (D)?
In breath (A), there is severe work shifting (what we called "flow starvation" or "flow asynchrony" or "air hunger") with the pressure falling below the set PEEP level & the pressure waveform being deformed due to the presence of Pmus (patient's effort)
Did you ever admit to the ICU a patient with COPD exacerbation who came from the ED on NIV? Or who went home on NIV? If you are a pulmonologist, you will not learn anything from this post but the rest of us
from different specialties (I am Internal Medicine) should remember that NIV settings are not just inspiratory/expiratory pressure (IPAP/EPAP) and FiO2
We have to admit that not every COPD patient will do well with “10 over 5” *. So what else should we pay attention to?
Trigger: beginning of inspiratory support and switch from EPAP to IPAP
Rise time: the time to get from EPAP to IPAP (aka pressurization time)
Inspiratory time: duration of inspiratory support
Cycle: end of inspiratory support and return from IPAP to EPAP
ICU Physiology Secrets - Return to Basics Edition:
If you are placing Swan-Ganz (SG) catheters or you like reading/interpreting their waveforms, this is for you:
You walk in a patient’s room exactly when your fellow intensivist tries to “wedge” a newly placed SG catheter:
At which point - approximately – do you think that the pulmonary capillary pressure (Pcap) should be measured?
1. Please assume that the recording is taken during an expiratory hold while on mechanical ventilation 2. Please feel free to choose any point other than these choices
Why do we care about pulmonary capillary pressure? Because it is a primary determinant of fluid flux across the pulmonary capillary wall (normal: 8-10 mmHg). It is determined by the mean pulmonary artery pressure, pulmonary vascular resistance, and total blood flow
Every 2 y this time of the year I have to provide my hospital-employer w proof of ACLS recertification. I usually take an on-line course which I finish in a few hours. Sadly, this biennial ritual is also a reminder that we keep following the same #CPR
choreography year in & year out without moving the needle. I am not opposing standardization of such a critical intervention as CPR is, if it was not for the persistently dismal outcomes (that are even worse in out-of-hospital (OHCA) compared w in-hospital cardiac arrest (IHCA)
A glimpse of hope was the introduction of #POCUS in the management of IHCA but, if you work in the trenches, POCUS (let alone #TEE!) is not an option. I am actually thrilled if there is a waveform capnogram in place to provide some information about the adequacy of resuscitation