Edel Part 2

A persistant elevation of the systolic BP 140 and over and elevation of the diastolic BP up to and greater than 90 mmHg. These BP's must be obtained on three separate occations at leat 1 week apartl

-cerebrovascular accident
-kidney disease
-coronary heart disease
-congestive heart failure
-peripheral vascular disease
-arotic dissection

LV ventricular failure as they become dialted & hypocontractile.

-left ventricular hypertrophy
-increased left ventricular bulk
-left atrial enlargemetn (usually mild)
-possible aortic dilatation or dissection

-an abnormal mitral inflow pattern featuring an A wave greater thant the E wave and prolonged deceleration that indicates decreased LV relaxation
-arotic regurgitation (in the presence of aortic dilatation)

Pulmonary hypertension denotes a pulmonary artery pressure greater than 30 mmHg. It has many causes, including idiopathic, chronic mitral stenosis or regurgitation, pulmonary embolism and Eisenmenger's syndrome (Eisenmenger's syndrome is defined as the process in which a left to right shunt caused by a congenital heart defect in the fetal heart causes increased flow through the pulmonary vasculature, causing pulmonary hypertension, which in turn causes increased pressures in the right side of the heart).

-an enlarged right atrium and ventricle
-right ventricular hypertrophy
-thickening of the interventricular septum
-flattening of the interventricular septum
-flattening of the interventricular septum in the short axis view
-an absent "A" wave and a mid-systolic closure of the pulmonic valve (flying W) in M-mode

2. The "A" wave occurs when the atrial contraction causes the RV pressure to increase, thereby deforming the closed pulmonic valve. In pulmonary hypertension, the PA pressure is so high that, even during atrial contraction, the pulmonic leaflets do not move. Therefore, no "A" wave is produced.

Flattening of the interventricular septum will be seen in both volume and pressure overloaded right ventricles. In fact, there is never a purely volume or pressure overloaded situation- there is always some combination of the two.

One way to determine which is dominant, volume or pressure is to watch the septal motion throughout the cardiac cycle. Most of the time the septum sill return to normal in systole (round up) when volume overload is predominate. The septum will stay falttened during systole when the problem is due to pressure.

1. RV systolic pressure (RVSP) can be calculated by adding the tricuspid regurgitation velocity (converted to mmHg by 4V² and the estimated RA pressure.

2. The pulmonarty artery pressure can be calculated from the pulmonary artery Doppler spectral trace by measuring the systolic acceleration time. The normal systolic asseleration time is greater than 120 msec, as measured from the onset of flow to peak velocity.
In patients with pulmonary ypertension, the acceleration time is decreased. In general, an acceleration time of less the 75 msec indicates at least moderate pulmonry hypertension (in adults).

1. RV systolic pressure (RVSP) can be calculated by adding the tricuspid regurgitation velocity (converted to mmHg by 4V² and the estimated RA pressure.

2. The pulmonary artery pressure can be calculated from the pulmonary artery Doppler spectral trace by measuring the systolic acceleration time. The normal systolic asseleration time is greater than 120 msec, as measured from the onset of flow to peak velocity.
In patients with pulmonary hypertension, the acceleration time is decreased. In general, an acceleration time of less the 75 msec indicates at least moderate pulmonry hypertension (in adults).

-hypertrophic (with or without obstruction)
-dilated (congestive)
- restrictive (infiltrative)

2. In hypertrophic cardiomyopathy, the ventricular walls are thickened (symmetrically or asymmetrically) and the ventricular chambers are reduced in size.

In dilated cardiomyopathy, the ventricles are enlarged, and contractility is decreased. One or both chambers may be affected.

In restrictive cardiomyopathy, the ventricles are hypertrophied, the cardiac chambers are nearly normal in size, and the myocardium appears bright.

1. The most common cause of hypertrophic is genetic.

Over half of all patients with such cardiomyopathy hae an autosomal diminant gene trait. In other patients, the disease appears to occur sopntaneously.

2. SAM of the MV is caused by the Venturi effect. The left ventricular outflow tract is narrowed by septal hypertrophy. As ejection occurs, the velocity in the narrowed outflow tract increases, creating a lower pressure region above the mitral, drawing the mitral leaflets toward the septum.

1. -dyspnea on exertion; this is the most common symptom, occuring in 90% of symptomatic patients
-angina (75%)
-syncope
-sudden death


ASH = asymmetric septal hypertrophy
HCM = hypertrophic cardimyopathy
HOCM = hypertrophic obstructive cardiomyopathy
IHSS = idopathic hypertrophic suaortic stenosis

1. The murmur will increase
It is usually harsh systolic, crescendo-decresendo type. Located between the cardiac apex and left sternal border.

2. Increases. like amyl nitrite. Increases systolic murmur associated with HOCM.

-left ventricular hypertrophy (symmetric or asymmetric)
-a samll ventricular cavitry
-systolic anterior motion of the MV

2D shoes the extent of the hypertrophy better than M-mode especially in asymmetric. You can also see apical hypertrophy better.

2D:
-ground glass
-calcification
-fibrosis of the mitral annulus
-MV thickening
-Septal scarring where the leaflets strike the IVS

1. PW Doppler is performed from the apical window, localizes the site of obstruction. When the sample volume is moved from the cardiac apex toward the aortic valve an obstruction is encountered, the flow velocity increases and changes from laminar to trubulent on the Doppler spectral trace.

2. CW Doppler records the peak gradient both at rest and after provocation with the Valsalva maneuver amyl nitrite. The spectral trace often shows the late peaking systolic jet typical of obstructive cardiomyopathy.