Left ventricular outflow tract (LVOT) obstruction is a potentially catastrophic etiology for hypotension due to several etiologies: idiopathic hypertrophic subaortic stenosis (IHSS), hypertrophic obstructive cardiomyopathy (HOCM), systolic anterior motion (SAM) of the mitral valve, and even mid-cavity obstructive hypertrophic cardiomyopathy. These obstructions can be dynamic in nature and consequently vary based on cardiac parameters like preload, afterload, contractility, heart rate, etc.
For a specific example, let’s look at systolic anterior motion (SAM) of the mitral valve causing a dynamic LVOT obstruction. Risk factors for this process include a narrowed LVOT diameter from a thick intraventricular septum (IVS), an elongated anterior mitral valve leaflet which gets “sucked” into the LVOT with high blood velocities during systole (Venturi effect), and papillary muscles positioned more apically moving the mitral plane towards the IVS. In LVOT obstructions from any of the aforementioned etiologies, we have several hemodynamic goals to reduce the obstruction and improve forward flow.
Here are the abbreviations in the diagram: systolic anterior motion (SAM) of the mitral valve, pulmonary artery (PA), left atrium (LA), left ventricle (LV), ALMV/PLMV (anterior and posterior leaflet of the mitral valve, respectively), aortic valve (AV), left ventricular outflow tract (LVOT)
In general, we aim to increase ventricular volume (“preload“) and reduce contractility. We can accomplish this by administering fluids, elevating the legs to increase venous return, and using agents like beta blockers for the dual benefit of negative inotropy and negative chronotropy. By keeping the heart rate on the low-normal side, we prolong diastole and allow the heart to fill more to alleviate the LVOT obstruction.
Here are some transesophageal echo (TEE) clips I acquired of SAM. The first shows the tissue movement of the anterior leaflet of the mitral valve into the LVOT during systole and the second shows the doppler consequences, namely mitral regurgitation with a posteriorly directed jet.
Now consider this example around the time of inducing general anesthesia. We routinely administer medications like succinylcholine, nondepolarizing neuromuscular blockers, and antibiotics which can cause anaphylaxis at the beginning of surgery. How does anaphylaxis present in a patient under general anesthesia? Typically hypotension and tachycardia. How does a dynamic LVOT obstruction present? Typically hypotension and tachycardia.
Okay, but why does that matter?
Epinephrine is the mainstay treatment for true anaphylactic reactions to stabilize mast cell degranulation and support hemodynamics. However, epinephrine will drastically increase a patient’s contractility and heart rate… a bad idea in dynamic LVOT obstruction. The presentations are the same. The treatments are different. This is the benefit of bedside echocardiography to differentiate between the two! 🙂
Drop me a comment below with questions! 🙂