Mitral Regurgitation
What is the timing for MR? BE SPECIFIC!
Holosystolic (both isovolumic periods, and all of systole)
MVP is defined as leaflet movement >___mm superior to the mitral annulus on closure.
>2mm
Name 2 etiologies of AI.
Aortic root dilation (HTN, connective tissue disorders, bicuspid AV, AS, sinus of valsalva aneurysms)
Cusp abnormalities (rheumatic, degenerative, bicuspid or other congenital valve, IE)
Loss of commissural support (VSD, Ao dissection, trauma)
What is almost always the cause of PS?
Congenital
What is the gold standard exam for identifying occluded coronary arteries?
Coronary Angiography
Name two causes of acute MR.
MI, or trauma (stabbing, car accident, etc)
Which leaflet is usually affected in patients with a cleft MV?
AMVL
What is the treatment for severe acute AI? Name one etiology of acute AI.
IMMEDIATE valve replacement--this is a medical emergency.
MI, IE, trauma, dissection
What is the most common site of obstruction with PS (subvalvular, valvular, or supravalvular)?
Valvular
Where do the coronary arteries originate? What are their names?
The aortic root. Left Main Coronary Artery, Right Coronary Artery
What are the two phases of chronic MR and describe each phase.
Compensated- initial phase where heart uses compensatory mechanisms to maintain CO.
Decompensated- eventual phase where the heart can no longer compensate and the patient will go into HF.
What mechanism causes SAM? How is the timing of this MR different from primary MR?
ASH. MR occurs in mid-late systole, rather than being holosystolic.
What is the value for mild AI pressure half time? Severe?
>500ms
<200ms
What is the best criteria to visually assess PI?
Jet width or height
What is a viability study and why are they done?
A stress echo. They are done to differentiate between viable myocardium and irreversible myocardial death (doctors what to know if the heart muscle can be saved with reperfusion).
Name 3 etiologies of primary MR.
MVP, MS, MAC, MV prosthesis, cleft MV, IE, flail leaflet
What is the EROA for mild MR? Severe?
<0.2cm2
>/=0.4cm2
What is the vena contracta AND EROA for mild AI? Severe?
Mild <3mm, 0.1cm2
Severe >6mm, >/=0.3cm2
What is the peak gradient for mild PS? Severe?
<36mmHg
>64mmHg
There are four main causes of paradoxical septal motion. Name 2.
LBBB
Pericardial disease
Post open-heart surgery
Disease of the IVS (CAD/MI)
What two echo measurements do we need to calculate EROA of the MV?
PISA radius, MR VTI.
Where is MR vena contracta measured (upstream, at valve level, or downstream)? What is mild? Severe?
Narrowest diameter of the flow downstream from the MV (LA side).
Mild <0.3cm
Severe >/= 0.7cm
What is pressure half time? Why does it decrease (get steeper) with more severe cases of AI (describe the hemodynamics)?
The time for the initial diastolic gradient between the LV and Ao to drop to 1/2 it's original value.
With AI, the LV pressure INCREASES more quickly that normal in diastole because the LV receives blood from the AI and the LA. The Ao pressure DECREASES more quickly than normal because the Ao is losing blood to the LV and to the body. This causes the gradient between LV and Ao to drop FASTER throughout diastole than normal.
How do we calculate SPAP in the presence of hemodynamically significant PS?
What is the difference between ischemia and infarction? What is the typical cause of each?
Ischemia-reduced CA perfusion to myocardium, caused by stenotic CA
Infarction-absent CA perfusion to myocardium, caused by occluded CA