SAM & the Wicked Case of Obstructive Shock

SAM

• Movement of mitral valve leaflets, more commonly the anterior leaflet, into the LVOT during systole
• Most common condition that causes SAM is hypertrophic cardiomyopathy (HOCM), the incidence of which is 1/500 in the general population
• If LV wall thickness during diastole is > 15 mm, then the patient likely has HOCM

How to measure

• In the parasternal long-axis view, line M mode across the tip of the anterior mitral valve leaflet and the septum
• Systole and diastole can be differentiated based on RV and LV wall movement (inward contraction during systole, outward dilation during diastole) OR by simultaneously running an ECG tracing on the ultrasound. If the mitral valve moves anterior during systole, then SAM is present

Hemodynamically significant SAM

• SAM may be present, but not affect hemodynamics
• If the mitral leaflet(s) spends >30% of systole in the LVOT, then there is likely a hemodynamic consequence of the SAM
• Continuous-wave doppler can be placed across the LVOT in the five-chamber view and if the pressure gradient (provided by the ultrasound machine) is > 50 mmHg then the SAM is hemodynamically significant

Conditions that worsen SAM

• Tachycardia (less time for LV filling)
• Increased inotropy
• Decreased preload (volume-depleted)
• Decreased afterload (exacerbates the pressure gradient and possible Venturi and drag effects leading to the mitral valve leaflets spending more time in the LVOT)

How to treat SAM

• Fluid resuscitation (increase preload)
• Increase afterload (i.e. phenylephrine is vasopressor of choice)
• Avoid inotropes
• Treat any conditions causing sympathetic surge (i.e. pain)
• Beta-blocker (i.e. esmolol) to reduce heart rate and allow more time for LV filling