Podcast: Play in new window | Download (Duration: 9:54 — 13.9MB)
Subscribe: Apple Podcasts | Spotify | RSS
Welcome back to the tasty morsels of critical care podcast.
Today we’re going to verge into challenging territory for an audio podcast in that we’re going to the discuss the very visual topic of dynamic LV outflow tract obstruction. This is something fairly dependent on echocardiography for diagnosis which as you can imagine translates poorly to audio format. This also means you’ll be denied my interpretative dance as i simulate the mitral valve leaflets being pulled over towards the septum via the Venturi effect. But alas i digress.
In essence dynamic LVOTO occurs when the closure point and tips of mitral valve tips are pulled into the left ventricular outflow tract during systole forming an anatomic obstruction to LV outflow thus reducing SV, CO, perfusion etc… This is reflected in poor blood pressure to which we respond by giving more catecholamines which makes this whole thing worse in a horrible cycle of nastiness.
Perhaps it’s best to start by identifying contexts where we should be on the look out for this. We’ll start with sepsis. Sepsis is a state of low systemic vascular resistance leading to reduced preload and afterload in the heart. The LV receives less than usual volume to stretch it and the low afterload makes it incredibly easy for the LV to empty itself of this load. This results in a small cavity LV where the LVOT and the mitral valve find themselves in much closer proximity than they are normally used to. If it gets out of hand bits of the mitral valve find themselves in the LVOT itself causing all kinds of bother.
The incidence of dynamic LVOTO in those with septic shock is remarkably high and is reported to be 20% in one study from ICU echo guru Michel Slama. Even if it’s not that common it’s yet another reason why the super shocked patient should get a timely echo.
So let’s say we’re worried about our septic patient: within that cohort who is at risk? Classically it would be the older person with LVH or a thickened septal bulge, sometimes called a sigmoid septum. Going with that is a stiff ventricle that fills poorly and has diastolic dysfunction.
As noted at the beginning it’s clear that echo is a key part of the diagnosis here and if you do one you may see some of the baseline features just mentioned but with the addition of SAM or systolic anterior motion of the mitral valve. Most dynamic LVOTO has SAM but not all SAM has LVOTO. SAM can be quite a common out patient echo finding and so in addition to SAM you might want to look for flow acceleration. Just as a river approaching a narrow point accelerates and becomes turbulent so does blood flow in the LVOT approaching an unwelcome and intrusive mitral apparatus. This flow acceleration can be easily measured with doppler and produces characteristic patterns that get echo nerds like me all hot under the collar and is largely beyond the scope of the podcast.
Before we get onto management I want to mention another at risk cohort. These are usually easy to spot as they return from theatre with a big sternotomy following an AV replacement or mitral valve repair. To take the example of the aortic valve. Aortic stenosis leads to severe LVH as the LV has to generate an enormous pressure to get the crusty calcified stenotic valve to open. The heart slowly adapts and learns to live with this very high afterload. Then one day someone opens their chest and pops in a nice shiny new valve that opens like a dream. The LV is not used to this and continues to eject blood like pompeii on a bad day. This hyperdynamic contraction in an LV not used to it has a tendency to drag the mitral apparatus into the LVOT forming an obstruction. Patients following MV repair are also at risk as the change in shape of the annulus and final position of the coaptation point at end repair can also lead to the MV getting pulled into the LVOT. If you’ve ever done the TOE board examinations you will curse yourself learning the 8 echocardiographic risk factors for SAM post MV repair…
So we’ve talked about what it is, and a few at risk populations (sepsis and cardiac surgery). The clinical appearance is typically rapidly worsening shock and rising pressors, hypotension and rising lactate. Let’s say you’ve even managed to diagnose it using echo. How should you manage the thing?
Increasing the preload can help, typically best done with volume expansion. Part of the mechanism here is an empty LV so filling it up can help. You can of course increase preload with noradrenaline but it comes with the unfortunate side effect of inotropy which is how we got into this mess in the first place. As such you find yourself having to do something quite uncomfortable and reduce or stop your catecholamines even when you think they might be keeping the patient alive. If that’s not bad enough, you probably want to swap them out for…. eughhh, and i struggle to say this… phenylephrine… Much derided and neglected it may well have a role here and it does hold the title of “pure alpha” and as such gives pressor effect without inotropy. Vasopressin is of course a reasonable option but as you know it is not the most titratable drug.
The next step might make you even more uncomfortable. Understandably these patients are often very tachycardic. This tachycardia leaves less time for diastole, less time for cardiac filling, again worsening the LVOTO. As such beta blockers become a very attractive option. Even though beta blocking a very sick patient seems like a slightly insane idea. But of course you’ll only be doing this after a high quality, well interpreted echo that shows a hyperdynamic LV so that should give you a little reassurance. Esmolol is probably the agent of choice here given it’s titratability. The dosing can be tricksy as it’s in the mcg/kg/min range and is not a daily use drug for most of us. I tend to skip the loading dose. In other words look it up.
Usually with filling and removal of inotropy and chronotropy you can ride it out and you should see some improvement in your haemodynamics. A failure to respond to treatment should make you question your diagnosis, that high lactate may well be due to dead gut rather than low output due to LVOTO.
References
- Chapter 13, Oxford Textbook of Advanced Critical Care Echocardiography covers this nicely.
- Chauvet, J.-L. et al. Early dynamic left intraventricular obstruction is associated with hypovolemia and high mortality in septic shock patients. Critical Care 19, 1–8 (2015).
- Slama, M., Tribouilloy, C. & Maizel, J. Left ventricular outflow tract obstruction in ICU patients. Current Opinion in Critical Care 22, 260–266 (2016).
- Pollick, C., Shmueli, H., Maalouf, N. & Zadikany, R. H. Left ventricular cavity obliteration: Mechanism of the intracavitary gradient and differentiation from hypertrophic obstructive cardiomyopathy. Echocardiogr Mt Kisco N Y 37, 822–831 (2020).
- Deranged Physiology. (Also contains mention of the wonderfully named Brockenbrough–Braunwald-Morrow phenomenon, which seems ripe for morning ward round pontification)