Pulmonary and tricuspid valve diseases are right heart diseases. Pulmonary valve diseases are the least common heart valve disease in adults.

Pulmonary valve stenosis is often the result of congenital malformations and is observed in isolation or as part of a larger pathologic process, as in Tetralogy of Fallot, Noonan syndrome, and congenital rubella syndrome . Unless the degree of stenosis is severe individuals with pulmonary stenosis usually have excellent outcomes and treatment options. Often patients do not require intervention until later in adulthood as a consequence of calcification that occurs with aging.

Pulmonary valve insufficiency occurs commonly in healthy individuals to a very mild extent and does not require intervention. More appreciable insufficiency it is typically the result of damage to the valve due to cardiac catheterization, aortic balloon pump insertion, or other surgical manipulations. Additionally, insufficiency may be the result of carcinoid syndrome, inflammatory processes such a rheumatoid disease or endocarditis, or congenital malformations. It may also be secondary to severe pulmonary hypertension.

Tricuspid valve stenosis without co-occurrent regurgitation is highly uncommon and typically the result of rheumatic disease. It may also be the result of congenital abnormalities, carcinoid syndrome, obstructive right atrial tumors (typically lipomas or myxomas), or hypereosinophilic syndromes.

Minor tricuspid insufficiency is common in healthy individuals. In more severe cases it is a consequence of dilation of the right ventricle, leading to displacement of the papillary muscles which control the valve's ability to close. Dilation of the right ventricle occurs secondary to ventricular septal defects, right to left shunting of blood, eisenmenger syndrome, hyperthyroidism, and pulmonary stenosis. Tricuspid insufficiency may also be the result of congenital defects of the tricuspid valve, such as Ebstein's anomaly.

The symptoms associated with MI are dependent on which phase of the disease process the individual is in. Individuals with acute MI are typically severely symptomatic and will have the signs and symptoms of acute decompensated congestive heart failure (i.e. shortness of breath, pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea), as well as symptoms of cardiogenic shock (i.e., shortness of breath at rest). Cardiovascular collapse with shock (cardiogenic shock) may be seen in individuals with acute MI due to papillary muscle rupture, rupture of a chorda tendinea or infective endocarditis of the mitral valve.

Individuals with chronic compensated MI may be asymptomatic for long periods of time, with a normal exercise tolerance and no evidence of heart failure. Over time, however, there may be decompensation and patients can develop volume overload (congestive heart failure). Symptoms of entry into a decompensated phase may include fatigue, shortness of breath particularly on exertion, and leg swelling. Also there may be development of an irregular heart rhythm known as atrial fibrillation.

Findings on clinical examination depend on the severity and duration of MI. The mitral component of the first heart sound is usually soft and with a laterally displaced apex beat, often with heave. The first heart sound is followed by a high-pitched holosystolic murmur at the apex, radiating to the back or clavicular area. Its duration is, as the name suggests, the whole of systole. The loudness of the murmur does not correlate well with the severity of regurgitation. It may be followed by a loud, palpable P, heard best when lying on the left side. A third heart sound is commonly heard.

In acute cases, the murmur and tachycardia may be the only distinctive signs.

Patients with mitral valve prolapse may have a holosystolic murmur or often a mid-to-late systolic click and a late systolic murmur. Cases with a late systolic regurgitant murmur may still be associated with significant hemodynamic consequences.

Historically, the term mitral valve prolapse syndrome has been applied to MVP associated with palpitations, atypical chest pain, dyspnea on exertion, low body mass index, and electrocardiogram abnormalities in the setting of anxiety, syncope, low blood pressure, and other signs suggestive of autonomic nervous system dysfunction.

Occasionally, supraventricular arrhythmias observed in MVP are associated with increased parasympathetic tone.

Upon auscultation of an individual with mitral valve prolapse, a mid-systolic click, followed by a late systolic murmur heard best at the apex is common. The length of the murmur signifies the time period over which blood is leaking back into the left atrium, known as regurgitation. A murmur that lasts throughout the whole of systole is known as a holo-systolic murmur. A murmur that is mid to late systolic, although typically associated with less regurgitation, can still be associated with significant hemodynamic consequences.

In contrast to most other heart murmurs, the murmur of mitral valve prolapse is accentuated by standing and valsalva maneuver (earlier systolic click and longer murmur) and diminished with squatting (later systolic click and shorter murmur). The only other heart murmur that follows this pattern is the murmur of hypertrophic cardiomyopathy. A MVP murmur can be distinguished from a hypertrophic cardiomyopathy murmur by the presence of a mid-systolic click which is virtually diagnostic of MVP. The handgrip maneuver diminishes the murmur of an MVP and the murmur of hypertrophic cardiomyopathy. The handgrip maneuver also diminishes the duration of the murmur and delays the timing of the mid-systolic click.

Both valsalva maneuver and standing decrease venous return to the heart thereby decreasing left ventricular diastolic filling (preload) and causing more laxity on the chordae tendineae. This allows the mitral valve to prolapse earlier in systole, leading to an earlier systolic click (i.e. closer to S), and a longer murmur.

Signs/symptoms of tricuspid insufficiency are generally those of right-sided heart failure, such as ascites and peripheral edema.

Tricuspid insufficiency may lead to the presence of a pansystolic heart murmur. Such a murmur is usually of low frequency and best heard low on the lower left sternal border. As with most right-sided phenomena, it tends to increase with inspiration, and decrease with expiration. This is known as Carvallo's sign. However, the murmur may be inaudible indicating the relatively low pressures in the right side of the heart. A third heart sound may also be present, also heard with inspiration at the lower sternal border.

In addition to the possible ausculatory findings above, there are other signs indicating the presence of tricuspid regurgitation. There may be giant C-V waves in the jugular pulse and a palpably (and sometimes visibly) pulsatile liver on abdominal exam. Since the murmur of tricupsid regurgitation may be faint or inaudible, these signs can be helpful in establishing the diagnosis.

Signs and symptoms of mitral stenosis include the following:

- Heart failure symptoms, such as dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea (PND)

- Palpitations

- Chest pain

- Hemoptysis

- Thromboembolism in later stages when the left atrial volume is increased (i.e., dilation). The latter leads to increase risk of atrial fibrillation, which increases the risk of blood stasis (motionless). This increases the risk of coagulation.

- Ascites and edema and hepatomegaly (if right-side heart failure develops)

Fatigue and weakness increase with exercise and pregnancy.

A mild diastolic murmur can be heard during auscultation caused by the blood flow through the stenotic valve. It is best heard over the left sternal border with rumbling character and tricuspid opening snap with wide-splitting S1. It may increase in intensity with inspiration (Carvallo's sign). The diagnosis will typically be confirmed by an echocardiograph, which will also allow the physician to assess its severity.

Symptoms related to aortic stenosis depend on the degree of stenosis. Most people with mild to moderate aortic stenosis do not have symptoms. Symptoms usually present in individuals with severe aortic stenosis, though they may occur in those with mild to moderate aortic stenosis as well. The three main symptoms of aortic stenosis are loss of consciousness, anginal chest pain and shortness of breath with activity or other symptoms of heart failure such as shortness of breath while lying flat, episodes of shortness of breath at night, or swollen legs and feet. It may also be accompanied by the characteristic "Dresden china" appearance of pallor with a light flush.

In many cases, a bicuspid aortic valve will cause no problems. People with BAV may become tired more easily than those with normal valvular function and have difficulty maintaining stamina for cardio-intensive activities due to poor heart performance.

The annulus of the valve is still in the normal position. The valve leaflets, however, are to a varying degree, attached to the walls and septum of the right ventricle. A subsequent 'atrialization' of a portion of the morphologic right ventricle (which is then contiguous with the right atrium) is seen. This causes the right atrium to be large and the anatomic right ventricle to be small in size.

- S3 heart sound

- S4 heart sound

- Triple or quadruple gallop due to widely split S1 and S2 sounds plus a loud S3 and/or S4

- Systolic murmur of tricuspid regurgitation = Holosystolic or early systolic murmur along the lower left sternal border depending on the severity of the regurgitation

- Right atrial hypertrophy

- Right ventricular conduction defects

- Wolff-Parkinson-White syndrome often accompanies

Bicuspid aortic valves may assume three different types of configuration:

1. "Real" bicuspid valves with two symmetric leaflets

2. A tricuspid architecture with a fusion of two leaflets

3. A tricuspid architecture with a fusion of three leaflets

Symptoms of aortic insufficiency are similar to those of heart failure and include the following:

- Dyspnea on exertion

- Orthopnea

- Paroxysmal nocturnal dyspnea

- Palpitations

- Angina pectoris

- Cyanosis (in acute cases)

Among some of the symptoms consistent with pulmonary valve stenosis are the following:

- Heart murmur

- Cyanosis

- Dyspnea

- Dizziness

- Upper thorax pain

- Developmental disorders

In regards to the cause of pulmonary valve stenosis a very high percentage are congenital, the right ventricular flow is hindered (or obstructed by this). The cause in turn is divided into: valvular, external and intrinsic (when it is acquired).

Mitral insufficiency (MI), mitral regurgitation or mitral incompetence is a disorder of the heart in which the mitral valve does not close properly when the heart pumps out blood. It is the abnormal leaking of blood backwards from the left ventricle, through the mitral valve, into the left atrium, when the left ventricle contracts, i.e. there is regurgitation of blood back into the left atrium. MI is the most common form of valvular heart disease.

An enlargement of the aorta may occur; an increased risk of abnormality is seen in babies of women taking lithium during the first trimester of pregnancy (though some have questioned this) and in those with Wolff-Parkinson-White syndrome.

Major symptoms of Lutembacher's syndrome as a result of ASD and MS can range from heart failure to pulmonary congestion.

- Right ventricular overload and Right-sided heart failure: Both are caused by a large ASD and MS (moderate to severe).

- Palpitations: This is caused by blood flowing from left atrium to the right atrium causing a higher left atrial pressure and leading to mitral stenosis. Both atria will be dilated (stretched or open)leading to future atrial arrhythmias or atrial fibrillation (Riaz).

- Pulmonary congestion: When blood or fluid pools within the lungs; this is usually a symptom of mitral stenosis and a small ASD.

- Loud mitral S1 and wide fixed split of pulmonary S2: The loud sound of the mitral S1 and the wide fixed split of pulmonary S2 is a symptoms of mitral stenosis. The sounds often are caused by a reduced pressure gradient in the mitral area that was caused from decompression of the left atrium from the ASD and a displacement (moving from normal position) of the left ventricular lower portion of the heart to the a large right ventricle. The second heart sound (S2) split is caused by the increase right heart blood flow through the ASD causing a late closing of the pulmonary component of the S2 as well as decreased left ventricular and aortic blood flow.

- III/IV mid diastolic murmur, early systolic murmur: This heart murmur is caused by an increase blood flow through the tricuspid valve due to ASD; it is heard best in the left lower sternal area or the bottom of the heart (apex).

There have been seven described variations of the quadricuspid aortic valve. They are classified on a scale from A to G and describe the variations in size of the four cusps. The most common variation is that of B – three equal-sized cusps and one smaller cusp. There is no correlation between the anatomy and functional status of the aortic cusps.

Mitral stenosis is a valvular heart disease characterized by the narrowing of the orifice of the mitral valve of the heart.

Valvular heart disease is any disease process involving one or more of the four valves of the heart (the aortic and mitral valves on the left and the pulmonary and tricuspid valves on the right). These conditions occur largely as a consequence of aging, but may also be the result of congenital (inborn) abnormalities or specific disease or physiologic processes including rheumatic heart disease and pregnancy.

Anatomically, the valves are part of the dense connective tissue of the heart known as the cardiac skeleton and are responsible for the regulation of blood flow through the heart and great vessels. Valve failure or dysfunction can result in diminished heart functionality, though the particular consequences are dependent on the type and severity of valvular disease. Treatment of damaged valves may involve medication alone, but often involves surgical valve repair (valvuloplasty) or replacement (insertion of an artificial heart valve).

Angina in setting of heart failure also increases the risk of death. In people with angina, the 5-year mortality rate is 50% if the aortic valve is not replaced.

Angina in the setting of AS occurs due to left ventricular hypertrophy (LVH) that is caused by the constant production of increased pressure required to overcome the pressure gradient caused by the AS. While the muscular layer of the left ventricle thickens, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may not receive enough blood supply to meet its oxygen requirement. This ischemia may first be evident during exercise when the heart muscle requires increased blood supply to compensate for the increased workload. The individual may complain of anginal chest pain with exertion. At this stage, a cardiac stress test with imaging may be suggestive of ischemia.

Eventually, however, the heart muscle will require more blood supply at rest than can be supplied by the coronary artery branches. At this point there may be signs of "ventricular strain pattern" (ST segment depression and T wave inversion) on the EKG, suggesting subendocardial ischemia. The subendocardium is the region that is most susceptible to ischemia because it is the most distant from the epicardial coronary arteries.

Tricuspid insufficiency (TI), a valvular heart disease also called tricuspid regurgitation (TR), refers to the failure of the heart's tricuspid valve to close properly during systole. This defect allows the blood to flow backwards, reducing its efficiency.

Regurgitation may be due to a structural change of components of the tricuspid valve apparatus, a lesion can be primary (intrinsic abnormality) or secondary (right ventricular dilatation).

A quadricuspid aortic valve (QAV) is a rare congenital heart defect characterized by the presence of four cusps, instead of the usual three found normally in the aortic valve. It is a defect that occurs during embryological development of the aortic trunk during gestation. There is an increased risk of developing post-natal aortic regurgitations and other heart-related diseases; therefore patients with the condition should be carefully monitored.

Heart valve dysplasia is a congenital heart defect which affects the aortic, pulmonary, mitral, and tricuspid heart valves. Dysplasia of the mitral and tricuspid valves can cause leakage of blood or stenosis.

Dysplasia of the mitral and tricuspid valves - also known as the atrioventricular (AV) valves - can appear as thickened, shortened, or notched valves. The chordae tendinae can be fused or thickened. The papillary muscles can be enlarged or atrophied. The cause is unknown, but genetics play a large role. Dogs and cats with tricuspid valve dysplasia often also have an open foramen ovale, an atrial septal defect, or inflammation of the right atrial epicardium. In dogs, tricuspid valve dysplasia can be similar to Ebstein's anomaly in humans.

Mitral valve stenosis is one of the most common congenital heart defects in cats. In dogs, it is most commonly found in Great Danes, German Shepherd Dogs, Bull Terriers, Golden Retrievers, Newfoundlands, and Mastiffs. Tricuspid valve dysplasia is most common in the Old English Sheepdog, German Shepherd Dog, Weimaraner, Labrador Retriever, Great Pyrenees, and sometimes the Papillon. It is inherited in the Labrador Retriever.

The disease and symptoms are similar to progression of acquired valve disease in older dogs. Valve leakage leads to heart enlargement, arrhythmias, and congestive heart failure. Heart valve dysplasia can be tolerated for years or progress to heart failure in the first year of life. Diagnosis is with an echocardiogram. The prognosis is poor with significant heart enlargement.

Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.

VSD is an acyanotic congenital heart defect, aka a left-to-right shunt, so there are no signs of cyanosis in the early stage. However, uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis.

- Pansystolic (Holosystolic) murmur along lower left sternal border (depending upon the size of the defect) +/- palpable thrill (palpable turbulence of blood flow). Heart sounds are normal. Larger VSDs may cause a parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally over time, as the heart enlarges). An infant with a large VSD will fail to thrive and become sweaty and tachypnoeic (breathe faster) with feeds.

The restrictive VSDs (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur). Larger defects may eventually be associated with pulmonary hypertension due to the increased blood flow. Over time this may lead to an Eisenmenger's syndrome the original VSD operating with a left-to-right shunt, now becomes a right-to-left shunt because of the increased pressures in the pulmonary vascular bed.