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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Elderly patient with multiple medical problems (HFpEF / A fib / HTN / PE / obesity etc) was admitted w CHF exacerbation. Improved w diuresis but developed left upper extremity edema; diagnosed with extensive DVT for which Interventional Radiology (IR) was consulted
IR found severe L subclavian stenosis at the intersection of the clavicle & 2nd rib & upstream LUE extensive DVT. Performed successful image-guided LUE DVT mechanical thrombectomy & stenotic site angioplasty with near complete resolution of clot burden & improvement of stenosis
Towards the last hour of the procedure, patient developed hypotension that did not improve with fluid boluses. Had received fentanyl & midazolam & and this was thought to play a role. Transferred to the ICU and
Assessment of the efficacy (stroke volume) and tolerance (left ventricular filling pressures) of blood volume expansion using Doppler echocardiography:
The 1st fluid challenge resulted in a large ⬆️ in LV stroke volume (38 to 65 mL), whereas the 2nd was unsuccessful (65 to 69 mL). The mitral Doppler profile progressed from “abnormal relaxation” to “restriction to filling” consistent with a gradual ⬆️ in left cardiac pressures
From:
Philippe Vignon and Michel Slama in:
"Hemodynamic Monitoring Using Echocardiography in the Critically Ill"; DOI 10.1007/978-3-540-87956-5
There is not such a thing as a “normal” cardiac output (CO). A CO of 3.5 l/min may be adequate for a 90 years’ old, 100 pounds sedated patient but inadequate for a 40 years’ old, 250 pounds patient with septic ARDS. Ideally,
any CO value should be accompanied by an assessment of the adequacy of perfusion (clinical: mental status, urine output etc or laboratory: central venous O2 saturation, lactate etc)
Many times, we don’t time/energy/means to measure CO, and we employ workarounds to convince ourselves that CO is adequate even when we don’t know what its actual value is. One of them is ScvO2, the O2 saturation in a venous blood sample drawn from a catheter in the SVC;
This is a recently published, information-dense document. It may be a bit technical for the average POCUS user but if you manage patients who harbor a right heart, consider reading it:
It is a 40+ pages' document, so I will just highlight some of the most useful points:
Approach to acquisition of the RA- & RV-focused views:
To obtain the RV-focused apical 4Ch view, place the transducer @ the apex, & rotate until the maximal RV chamber dimension is obtained. Often, the transducer must be positioned more laterally & tilted upward toward the RV