Definition

Aortic regurgitation (AR): Incompetence of the aortic valve resulting in a large volume of blood flowing back into the left ventricle during diastole. Mitral stenosis (MS): Constriction of the mitral orifice with an increase in turbulent flow across the reduced valve area.

History

Symptoms

MS: Crackles throughout the lung fields are present when pulmonary edema ensues. The presence or absence of lung findings bears no relationship to the degree of pulmonary hypertension.

Cardiovascular

AR: Apical impulse is displaced laterally. A high pitched blowing decrescendo diastolic murmur is best heard along the left sternal border in the third inter space. Augmented by asking the patient to lean forward while sitting and exhale. An S3 gallop is present in later stages and a diastolic rumble of regurgitant blood striking the mitral valve may be present (Austin Flint murmur). An increase in the murmur can be heard with squatting and forced expiration while leaning forward. The murmur exhibits no change with valsalva maneuvers and decreases with deep inspiration and vasodilators.

MS: The Sl is loudest at the apex and is the first sign of MS. The most conclusive sign of mitral stenosis is an opening snap. This is a high pitched sound occurring shortly after S2 and is best heard at the apex. An S3 is usually not present in MS and, if present, is of much lower pitch. The murmur of MS is decrescendo-crescendo and occurs immediately after the opening snap. This pattern occurs as the blood volume from a filled atrium empties and is then augmented by atrial contraction. If pulmonary hypertension has developed, an accentuated P2 may be heard and a right ventricular heave apparent in the epigastrium. The murmur decreases with standing as the preload is reduced and increases with squatting.

Gastrointestinal

AR: Right upper quadrant tenderness of the abdomen with hepatomegaly and hepatojugular reflux may be present if biventricular failure has developed.

MS: As right ventricular dysfunction becomes more prominent, ascites, hepatomegaly, and hepatojugular reflux typically appear.

Extremities

AR: Bounding pulses are often felt distally and capillary pulsations may be seen in the nail beds. Peripheral edema develops with the failure of the right ventricle.

AR: Those attributed to CHF, such as dyspnea, dyspnea on exertion, paroxysmal nocturnal dyspnea, nocturia, fatigue, and edema in later stages. Angina may develop at endstage.

MS: Dyspnea on exertion is pherphas the earliest symptoms. As the disease progress orthpnea , fatigue and palpitations are prominent.Systemic emboil are common on patient with AF who are not anticoagulated .

General

AR:

Most commonly due to rheumatic fever (75 percent), endocarditis, and calcific aortic stenosis.

MS: True MS is almost always due to rheumatic disease. An atrial myxoma or thrombus may produce a similar murmur.

Age

AR: Often seen in the middle to older age groups when due to rheumatic disease. Traumatic AR may occur at any age.

MS: The initial rheumatic episode occurs in childhood and the patient is asymptomatic from 15 to 25 years. Atrial thrombi and myxoma may occur at any time.

Onset

AR: Usually occurs over many years and is insidious. Acute AR is usually due to trauma, aortic dissection, or ongoing bacterial endocarditis.

MS: Usually gradual with dyspnea on exertion the first symptom. Some develop acute decompensation when higher demands on the system are required.

Duration

AR: Symptoms may occur so gradually that the patient compensates and does not present until very ill. Symptoms may not become apparent for 5 to 10 years after regurgitation begins. Survival past 2 years is low once CHF develops.

MS: Survival is limited to 10 to 12 years in untreated MS from time of symptom onset.

Intensity

AR: Mild symptoms in the early stages; often unnoticed by the individual.

MS: Mild progression of symptoms over the prolonged disease course.

Aggravating Factors

AR: Dietary indiscretion with high sodium intake, lack of fluid restriction, non compliance with medications (if patient has refused Surgery when recommended early). Concomitant atherosclerotic heart disease with angina may decrease contractility further and hasten the development of CHF.

MS: Pregnancy, exercise, infections, and AF can all place additional burden on an overloaded left atrium and pulmonary vasculature.

Alleviating Factors

AR: Valve replacement surgery.

MS: Rest and compliance with the prescribed medical regimen are the only factors that may be of benefit to the patient.

Associated Factors

AR: When due to rheumatic fever mitral valvular disease is almost always present.

MS: Left ventricular enlargement may be present when accompanied by mitral regurgitation (MR). An enlarged left atrium is almost always present. Atrial fibrillation (AF) common.

Physical Examination

AR: Patient may be asymptomatic early on but later will appear in moderate to severe distress as symptoms of pulmonary edema develop.

MS: Patient may be asymptomatic or be confused from hypoxia associated with pulmonary edema.

Vital Signs

AR: Widened pulse pressure due to peripheral vasodilitation as a compensatory mechanism for the loss of forward flow. Diastolic pressure is often less than 60. Tachycardia often present in later stages and tachypnea reflects the degree of hypoxia.

MS: Pulse may be regular to irregularly irregular; respiratory pattern may be normal to tachypneic.

Heent

AR: Carotid upstroke is rapid and sharply descends. Jugular venous distention seen later and associated with the development of endstage disease and CHF.

MS: Jugular venous disention is present when right ventricular involvement has progressed due to pulmonary hypertension. Carotid upstroke is preserved until the right ventricle fails to fill the left atrium; biventricular failure is then apparent. Flushed cheeks and perioral cyanosis are sometimes seen.

Pulmonary

AR: May be clear to auscultation with early asymptomatic disease. Later when CHF is present, crackles will be heard throughout the chest.

MS: Crackles throughout the lung fields are present when pulmonary edema ensues. The presence or absence of lung findings bears no relationship to the degree of pulmonary hypertension.

Cardiovascular

AR: Apical impulse is displaced laterally. A high pitched blowing decrescendo diastolic murmur is best heard along the left sternal border in the third interspace. Augmented by asking the patient to lean forward while sitting and exhale. An S3 gallop is present in later stages and a diastolic rumble of regurgitant blood striking the mitral valve may be present (Austin Flint murmur). An increase in the murmur can be heard with squatting and forced expiration while leaning forward. The murmur exhibits no change with valsalva maneuvers and decreases with deep inspiration and vasodilators.

MS: The Sl is loudest at the apex and is the first sign of MS. The most conclusive sign of mitral stenosis is an opening snap. This is a high pitched sound occurring shortly after S2 and is best heard at the apex. An S3 is usually not present in MS and, if present, is of much lower pitch. The murmur of MS is decrescendo-crescendo and occurs immediately after the opening snap. This pattern occurs as the blood volume from a filled atrium empties and is then augmented by atrial contraction. If pulmonary hypertension has developed, an accentuated P 2 may be heard and a right ventricular heave apparent in the epigastrium. The murmur decreases with standing as the preload is reduced and increases with squatting.

Gastrointestinal

AR: Right upper quadrant tenderness of the abdomen with hepatomegaly and hepatojugular reflux may be present if biventricular failure has developed.

MS:As right ventricular dysfunction becomes more prominent, ascites, hepatomegaly, and hepatojugular reflux typically appear.

Extremities

AR: Bounding pulses are often felt distally and capillary pulsations may be seen in the nail beds. Peripheral edema develops with the failure of the right ventricle.

MS: May be cool as cardiac output falls. Edema invariably present once right sided failure occurs.

Pathophysiology

AR: Basic hemodynamic abnormality is volume overload of the left ventricle due to the regurgitant flow of blood through the aortic valve. Initially the left ventricle can compensate with dilatation. Once maximal dilatation is achieved, the left ventricle demonstrates decreased compliance and contractility and overt signs of CHF develop.

MS: Causes an obstruction to blood flow from the left atrium to the left ventricle. This obstruction results in a volume overload in the atrium and dilatation of the chamber. The increased pressure is reflected into the pulmonary vasculature and pulmonary hypertension eventually develops. These elevated pulmonary pressures impose an unreasonable after load on the rather thin right ventricle and cor pulmonale ensues.

Diagnostic Studies

Laboratory: Usually noncontributory unless the patient has deteriorated and shows evidence of end organ dysfunction.

Radiology

CXR:AR: Reveals a normal or enlarged cardiac shadow with elongation of the left ventricle. Aortic dilatation is not seen unless the AR is due to aortic dissection or Marfan syndrome.

MS: Reveals an enlarged left atria and displacement of the esophagus. The left ventricle is not enlarged. Full pulmonary vasculature and peribronchial cuffing signify elevations of the pulmonary pressures. Right ventricular enlargement occurs later in the disease.

Other

ECG: AR: May suggest left ventricular hypertrophy and S-T depression with negative T waves across the precordium.

MS: Left atrial enlargement can be seen in lead V1 in those patients without AF.

Echocardiogram: AR: Demonstrates the regurgitation and provides an estimate of the pressure gradient. Left ventricular compliance may also be estimated and other valvular abnormalities identified.

MS: Demonstration of valvular calcifications, leaflet motion abnormalities, calculation of the valve orifice and an estimation of the gradient across the valve are helpful in determining further studies and treatment.

Cardiac catheterization: AR: Indicated when surgery is recommended to visualize the regurgitant flow and coronary arteries. Left ventricular compliance and any other valvular abnormalities can also be demon strated.

MS: Visualization of the coronary arteries is important before surgical correction can be attempted.

Differential Diagnosis

Traumatic

AR: Penetration of the leaflets or laceration of the aortic wall. Acute aortic dissection.

Infectious

AR: Bacterial endocarditis may produce a sudden acute presentation.

MS: Almost always the result of rheumatic heart disease.

Metabolic

Thyroid disorders and hyperpyrexia. May, but usually do not produce diastolic murmurs.

Neoplastic AR:

Myxomatous transformation of the aortic valve has become a more common cause of AR.

MS: Left atrial myxoma will produce a murmur similar to MS. Look for fever and signs of systemic embolization.

Vascular

AR/MS: Venous and arterial stenosis and/or thrombus. Congenital

AR: Bicispid valve and annular distention due to a variety of cardiac malformations. Usually overshadowed by any number of cardiac malformations.

Acquired

AR: Marfan syndrome, connective tissue disorders, and infiltrative diseases. Chronic hypertension.

MS: Left atrial thrombus look for signs of systemic embolization, tachycardia is common; sometimes the murmur changes with body position.

Treatment

AR: In the symptomatic patient with severe AR, surgery should not be delayed. Those with mild symptomatic disease may be managed with conventional CHF therapy. Aortic valve replacement should occur before left ventricular compliance is decreased. All younger patients need valve replacement if severe stenosis is present whether symptomatic or not. It is important in the patient awaiting surgery that preloads on the left ventricle not be reduced to the point the left ventricle cannot maximally fill. A small reduction in stroke volume can and often does result in a severe reduction in blood pressure.

MS: Anticoagulation is required once AF develops and some authorities anticoagulate all patients with MS. Diuretics and digoxin are often employed during the early stages of the disease. Antibiotics are required for endocarditis prophylaxis.

Surgery should occur before pulmonary hypertension and right ventricular failure develop. Commissurotomy may be used in the younger patient if no calcifications are present. Mechanical valves are the replacement of choice except in the elderly or childbearing females.

Pediatric Consideration

Isolated pulmonary regurgitation (PR) or insufficiency is rare in children. It generally occurs in association with an abnormal pulmonic valve and pulmonic stenosis (PS), or following treatment of PS with balloon dilitation angioplasty or surgical valvulotomy. Although most cases are mild, severe forms can occur and may result in CHE AR or insufficiency is usually of a very mild degree. In severe AR, the left ventricle becomes dilated and may eventually result in decreased function. Treatment of severe cases consists of aortic valve replacement.

Tricuspid stenosis (TS) is very rare in children. Tricuspid atresia (incomplete formation of the valve) does occur and will present early in the infant’s life with CHF, cyanosis, and murmur.

MS rarely occurs in infants and children. MS does occur in adolescents and young adults as an acquired disorder secondary to rheumatic fever. Children with a documented occurrence of rheumatic fever should have a periodic cardiac assessment to rule out valvular heart disease. Treatment is similar to adults.

Obstetrical Considerations

Aortic Insufficiency: If the pregnant patient with aortic regulation also has associated CHF, conventional medical therapy is usually successful. The aortic valve may be replaced during the pregnancy if endocarditis develops or medical therapy becomes ineffective. Epidural anesthesia may be used safely.

MS: In a patient with known MS who desires to become pregnant, valvuloplasty is recommended. Otherwise, MS often worsens during the pregnancy due to the increased cardiac output that occurs naturally during pregnancy. This leads to increased atrial pressure that can cause pulmonary edema or AF with development of an atrial mural thrombus with possible embolization. Previously asymptomatic females may become symptomatic during the second trimester of pregnancy when the blood volume increases. Symptoms may improve slightly late in the third trimester as the blood volume usually diminishes during that period.

In pregnant patients with MS, rheumatic fever prophylaxis should be given during theconfinement, and subacute bacterial endocarditis prophylaxis should be administered at the time of delivery. Surgical valve repair or replacement, antlcoagulatlOn as needed (with avoidance of warfarin), and the usual cardiac regimens (digitalis, bedrest, and low-sodium diet) can be used when the condition necessitates treatment. It has also been reported that use of propranolol or atenolol improved the symptoms. Epidural block is the anesthetic of choice for delivery in these patients.

General Considerations: If anticoagulation is indicated, only heparin should be used. For rheumatic fever and subacute bacterial endocarditis prophylaxis sulfonamides, ciprofloxacin, and erythromycin should be used with caution during the pregnancy; tetracycline use is contraindicated.

Tagged under:angina atherosclerotic heart disease Cardiology fatigue hyperpyrexia tachypneic ulmonary hypertension valve repair valvular disease valvular heart disease

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Filed under: Cardiology