Pulmonary valve regurgitation

Pulmonary valve regurgitation, if trivial to mild, is so common that it is considered physiologic.

Mild pulmonary regurgitation is extremely useful echocardiographically, as the Doppler velocity of the regurgitant trace may be used to predict mean and end-diastolic pulmonary artery pressures.

Pulmonary valve regurgitation is commonly noted in adults, and recognized originating from the pulmonic valve as turbulent flow traveling into the ventricular outflow tract during diastole.

There are several pathologic causes of pulmonary valve regurgitation, including its association with pulmonary valve stenosis.

Dilation of the pulmonary annulus, which can be idiopathic or due to pulmonary artery dilation, amplitude (less than 6 mm) with thickening of the leaflets.

Pulmonic valve regurgitation can be caused by numerous cardiac pathologies, including:
*Pulmonary hypertension
*Bacterial endocarditis
*Pulmonary valvotomy
*Congenital defects
*Carcinoid heart disease
*Trauma
Pulmonary valve regurgitation

Pulmonary stenosis

The majority of pulmonary stenosis are conginetal. It cause by abnormal formation of the pulmonary valve leaflets during fetal cardiac development. Rarely, rheumatic heart disease, malignant carcinoid, or extrinsic compression by a tumor or sinus of valsalva aneurysm may lead to pulmonary stenosis.

Pulmonary stenosis can be valvular, subvalvular or supravalvular. Valvular pulmonary stenosis is the most common, accounting for 90% cases.

Subvalvular pulmonary stenosis can occur as part of a conginetal heart complex such as tetralogy of Fallot or as a result of hypertrophic obstructive cardiomyopathy involving the right side of the heart.

Patients with pulmonary stenosis may live for extended periods completely without symptoms and frequently survive past the age of 70 years without surgical intervention, when they do occur, include tachypnea, syncope, angina or hepatomegaly and peripheral edema.
Pulmonary stenosis

Pulmonary insufficiency

In pulmonary insufficiency, blood ejected into the pulmonary artery during systole flows back into the right ventricle during diastole, causing a fluid overload in the ventricle and ventricular hypertrophy; it may ultimately result in right-sided heart failure.

Pulmonic insufficiency is frequently very difficult to appreciate on physical exam, particularly if the pulmonary pressures are normal.

In the fetus, severe pulmonary inefficiency causes hydrops and death.

Alternately, pulmonary insufficiency may be well-tolerated functional disturbance until late adulthood or come to medical attention because of a dilated main pulmonary artery detected on a routine chest x-ray.

The causes of pulmonary insufficiency may be the result of a rare congenital lesion or the stretching of the valvular ring by long lasting pulmonary hypertension. Rarely, prolonged use of a pressure-monitor catheter in the pulmonary artery will lead to this disorder.
Pulmonary insufficiency

Pulmonary venous hypertension

Pulmonary hypertension may occur from blockage of the left atrium by a myxoma or thrombus.

Congenital and acquired heart lesions can cause pulmonary venous hypertension.

Congenital causes include hypoplastic left heart syndrome, aortic coartation, interrupted aortic arch, anomalous origin of a coronary artery, valvular aortic stenosis, cor triartrium, total anomalous pulmonary connection below the diaphragm and pulmonary vein stenosis or atresia.

Pulmonary venous hypertension necessitates a passive rise in pulmonary systolic pressure to maintain a driving force across the vasculature.

Volume overloaded cause shear force injury to the vascular endothelium, which leads to vascular remodeling and luminal narrowing.

Pulmonary venous hypertension may be identified on radiographs, pulmonary angiogram or nuclear medicine perfusion scans.

Pulmonary venous hypertension is considered mild with wedge pressures of 10 to 13 mm Hg, moderate with equalization of upper and lower lobe blood flow and wedge pressures of 14 to 16 mm Hg.
Pulmonary venous hypertension