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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You can call me lazy but if a patient is admitted to the ICU with pneumonia (& this CXR), is diaphoretic, breathing 50/min, has HR 150/min & O2 Sat 88% on "FiO2 100%", I don't calculate the ROX index or the HACOR score. I just intubate...
The ROX (Respiratory rate-OXygenation) index was introduced in 2016 as a prediction tool to identify the need for IMV in pneumonia patients w AHRF treated wHFNC. It's calculated as [(SpO2/FiO2)/Respiratory Rate] & is typically assessed at 2, 6, & 12 hours after HFNC initiation
The HACOR (Heart rate, Acidosis, Consciousness, Oxygenation, & Respiratory rate) score is a tool for predicting NIV failure in pts with AHRF. It demonstrates good predictive power for NIV failure, w higher scores (>5) having a strong diagnostic accuracy in predicting NIV failure
Dexmedetomidine (D) (Precedex in 🇺🇸) is one of my favorite ICU drugs. It is a highly selective α-2 adrenoreceptor agonist, w sedative/analgesic/ anxiolytic properties & minimal resp depression. Its main side effects are hypotension & bradycardia
Herein I chose 10 less known D's effects/associations with:
1. Hypertension (the opposite from what you would expect): likely due to initial stimulation of peripheral a-1 or a-2b receptors. It is usually transient, mild, & does not require treatment. However, I have seen severe
D withdrawal after abrupt stop of prolonged infusion presenting w severe hypertension (plus tachycardia / diaphoresis / agitation). It went unrecognized for a while & was attributed to "prolonged alcohol withdrawal"
We divide patients with circulatory shock into 3 primary hemodynamic phenotypes, namely hypovolemic, vasodilatory/distributive, & cardiogenic (including obstructive)
But we all witness/manage "mixed" shock, an entity lacking a uniform, evidence-based definition
By analogy to the cardiorenal syndromes, Jentzer et al categorize mixed shock into 3 principal groups, each defined by the sequence & nature of the insult (ie, primary vs secondary hemodynamic process): cardiogenic-vasodilatory, vasodilatory-cardiogenic, & primary mixed shock:
The conceptual model of mixed shock etiology & pathogenesis describes "two-hit" & "single insult" scenarios:
We are all familiar w the concept of "protective ventilation": aiming for normal blood gases entails significant risk
What if we apply the same idea in hemodynamics & try to limit the damage associated w excessive vasoconstriction?
The CLEAR approach is not intended to be a series of
sequential steps but rather key elements that should be addressed simultaneously, depending on the clinical context and patient’s needs
In this recently published article, the authors propose a classification of different cardiovascular phenotypes potentially observed in septic shock into 3 profiles of LV-centric dysfunction, promptly recognizable by critical care echocardiography (CCE):
The figure speaks for itself, but we have to highlight a few points made throughout the paper...
1. Cardiovascular profiles are dynamic; patients may move from one to another according to fluid administration, correction of LV afterload & evolution of the disease. Therefore, CCE has to be repeated to personalize therapy