Acute myocardial infarction of LVOT : An unrecognised cause for refractory hypotension
Posted Feb 06 2010 1:23am
Hypotension is one of the dreaded complication of acute STEMI.
It can be due to either a mechanical complication or hypovolemia.
The hypotension in inferoposterior MI is often related to enhanced vagal tone and easily correctable with atropine and fluid administration.
RVMI is the classical example of hypotension that may improve with fluid resuscitation
Hypotension, if not reversible within 12 hours , is more likely to represent a more sinister mechanism like pump failureMR or ventricular septal tear etc .
A new mechanism for persistent hypotension is increasingly recognised.
This is due to the
1.Loss of LVOT dynamic activity.
2.Excessive dynamism of LVOT.
LVOT contractile and ejectile falure
Even though LV outflow tract contain less contractile myocytes it has an important mechanical job to do. We know it’s primary job is that of a conduit but it also has to eject the blood into aorta with sufficient force. In factit is thought much of the acceleration of blood velocity occur in LVOT . SoLVOT plays a key role in maintaining the cardiac index. An excessively dynamic LVOT will impede the forward blood flow as in HCOM. Similarly less dynamic contraction of LVOT results in low velocity propulsion that interferes with proper delivery of blood from LV cavity into the aorta .
These factors get amplified in acute MI as it is a compromised situation with fluctuating HR and contractility. So a properly functioning LVOT conduit is absolutely mandatory.
STEMI due to a proximal LAD obstruction located can involve the septal .If the first septal branch happens to be a major one, there will be definite impact on the LVOT function.