One of the leaflets of the mitral valve does not completely close. The pressure when the left ventricle contracts forces the leaflet to billow into the the left atrium and some blood back flows into the left atrium. Moderate posteriorly mitral regurgitation is degree of back flow and the direction of the regurgitation (gives an indication which leaflet and height helps determine degree which has been classified as moderate.
Regurgitation with the tricuspid does not indicate a prolapse of leaflets, but the regurgitation can be due to an enlarged orifice (opening), etc.
Moderate should be closely monitored, but usually doesn't require intervention unless there are symptoms.
Pulmonary pressure is the pressure the right ventricle pumps against (40 mmHg is slightly high).. Left side pumps against system resistence normal is 120/80.
Kenkeith, thank you. I have a ? for you based on your response. The pulmonary artery pressure I am referring to is noted in my Echo at the Tricuspid Valve. It specifically says Ticuspid Vale then mentions the regurgitation.
It then says Pulmonary artery pressure is estimated at 40 mm HG. Everything I have read that says this amt. of Pulmonary artery pressure indicates Pulmonary Hypertension. "Pulmonary (PULL-mun-ary) arterial hypertension (PAH) is continuous high blood pressure in the pulmonary artery. The average blood pressure in a normal pulmonary artery is about 14 mmHg when the person is resting. In PAH, the average is usually greater than 25 mmHg." Quoted from the Pulmonary Hypertension Assn. Website.
Do I have all this right? Also, is there some web site that shows heart blood flow A- Z. Thanks.
Diagnosis of PAH requires the presence of pulmonary hypertension with two other conditions. Pulmonary artery occlusion pressure must be less than 15 mm Hg (2000 Pa) and pulmonary vascular resistance (PVR) must be greater than 3 Wood units (240 dyn•s•cm-5 or 2.4 mN•s•cm-5).
Although pulmonary arterial pressure can be estimated on the basis of echocardiography, pressure measurements with a Swan-Ganz catheter provides the most definite assessment. Pulmonary hypertension (PAH) and pulmonary vessel (PVR)vresistance cannot be measured directly with echocardiography. "A diagnosis of PAH requires right-sided cardiac catheterization. A Swan-Ganz catheter can also measure the cardiac output, which is far more important in measuring disease severity than the pulmonary arterial pressure".
Your report doesn't specify but mean pulmonary artery pressure (mPAP) should not be confused with systolic pulmonary artery pressure (sPAP), which is often reported on echocardiogram reports. "A systolic pressure of 40 mm Hg typically implies a mean pressure more than 25 mm Hg. Roughly, mPAP = 0.61•sPAP."
Normal pulmonary arterial pressure in a person living at sea level has a mean value of 12–16 mm Hg ). Pulmonary hypertension is present when mean pulmonary artery pressure exceeds 25 mm Hg at rest or 30 mm Hg with exercise.
To complicate the issue pulmonary hypertension can be of five major types, a series of tests must be performed to distinguish pulmonary arterial hypertension from venous, hypoxic, thomboembolic, or miscellaneous varieties. and pulmonary hypertension can be associated with left heart disease, atrial or ventricular disease, valvular disease (e.g. mitral stenosis).
Pulmonary hypertension associated with lung diseases and/or hypoxemia is insufficient oxygen in the blood, chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD)
Sleep-disordered breathing, alveolar hypoventilation
Chronic eposure to high altitude
Developmental lung abnormalities
Pulmonary hypertension due to chronic thrombotic and/or embolic disease
Pulmonary embolism in the proximal or distal pulmonary arteries
Embolization of other matter, such as tumor cells or parasites
Miscellaneous: WHATEVER THE INITIAL CAUSE pulmonary arterial hypertension involves the vasoconstriction or tightening of blood vessels (PVR...resistence) connected to and within the lungs. This makes it harder for the heart to pump blood through the lungs, much as it is harder to make water flow through a narrow pipe as opposed to a wide one. Over time, the affected blood vessels become both stiffer and thicker, in a process known as fibrosis. This further increases the blood pressure within the lungs and impairs their blood flow. In addition, the increased workload of the heart causes thickening and enlargement of the right ventricle, making the heart less able to pump blood through the lungs, causing right heart failure. As the blood flowing through the lungs decreases, the left side of the heart receives less blood. This blood may also carry less oxygen than normal. Therefore it becomes harder and harder for the left side of the heart to pump to supply sufficient oxygen to the rest of the body, especially during physical activity. The condition if left untreated will cause an enlarged heart (cardiomegaly).
Pathogenesis in pulmonary venous hypertension is completely different. There is no obstruction to blood flow in the lungs. Instead, the left heart fails to pumps blood efficiently, leading to pooling of blood in the lungs. This causes pulmonary edema and pleural effusions.
In hypoxic pulmonary hypertension the low levels of oxygen are thought to cause vasoconstriction or tightening of pulmonary arteries. This leads to a similar pathophysiology as pulmonary arterial hypertension.
In chronic thromboembolic pulmonary hypertension the blood vessels are blocked or narrowed with blood clots. Again, this leads to a similar pathophysiology as pulmonary arterial hypertension.
Other forms of PAH are far more common. In scleroderma the incidence has been estimated to be 6 to 60% of all patients, in rheumatoid arthritis up to 21%, in systemic lupus erythematosus 4 to 14%, in portal hypertension between 2 to 5%, in HIV about 0.5%, and in sickle cell disease ranging from 20 to 40%.
Diet pills such as Fen-Phen produced an annual incidence of 25-50 per million per year.
Pulmonary venous hypertension is exceedingly common, since it occurs in most patients symptomatic with congestive heart failure.
Up to 4% of people who suffer a pulmonary embolism go on to develop chronic thromboembolic disease including pulmonary hypertension.
Only about 1.1% of patients with COPD develop pulmonary hypertension with no other disease to explain the high pressure. Sleep apnea is usually associated with only very mild pulmonary hypertension, typically below the level of detection. On the other hand Pickwickian syndrome (obesity-hypoventilation syndrome) is very commonly associated with right heart failure due to pulmonary hypertension.