Aortic Valve Insufficiency
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Aortic Valve Insufficiency
Causes and symptoms
insufficiency(in?su-fish'en-se) [ L. insufficientia, insufficiency]
acute adrenocortical insufficiency
aortic insufficiencyAbbreviation: AI
Chronic aortic insufficiency produces a gradual volume overload of the heart and eventual congestive heart failure. It may occur in patients with poorly controlled hypertension, tertiary syphilis, Marfan's disease, or other disorders that affect aortic valve competence. Management often includes antihypertensive vasodilators such as nifedipine. If congestive heart failure becomes severe enough, valve replacement may be recommended for patients who are good operative candidates. Surgery usually is recommended to be done before EF falls below 55%.
Chronic AI may be asymptomatic until heart failure (HF) occurs. With HF, patients often report difficulty breathing, e.g., during exercise or sleep, and lower extremity swelling. Patients may occasionally report palpitations or a subjective awareness of their heart beating.
The murmur of AI occurs in diastole, is high-pitched (best heard using the diaphragm of the stethoscope), and is usually described as “blowing” and “decrescendo.” It is best heard at the left second to fourth intercostal spaces, radiating to the apex and sometimes the right sternal border, after the patient exhales and sits leaning forward, holding his or her breath. Patients with AI often have a widened pulse pressure with a waterhammer pulse and may have head bobbing, bobbing of the uvula, or visible movement of blood under the nails when the tips of the nails are gently compressed (Quincke pulse). The patient may experience dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and fatigue.
A history of related cardiac illnesses and symptoms is obtained. Fever and other signs of infection are noted. Vital signs, weight, and fluid intake and output are monitored for indications of fluid overload. Activity tolerance and degree of fatigue are assessed regularly, and the patient is taught to intersperse periods of activity with rest.
Desired outcomes include adequate cardiopulmonary tissue perfusion and cardiac output, reduced fatigue with exertion, and ability to manage the treatment regimen.
aortic valve insufficiencyAortic insufficiency.
cardiac insufficiencyHeart failure.
ileocecal insufficiencyIleocecal incompetence.
mitral insufficiencyMitral regurgitation.
insufficiency of ocular muscles
primary adrenal insufficiencyAddison disease.
pulmonary valvular insufficiency
secondary adrenal insufficiency
tertiary adrenal insufficiency
valvular insufficiencyValvular incompetence.
Aortic Valve Insufficiency
|Mean LOS:||3.3 days|
|Description:||MEDICAL: Cardiac Congenital and Valvular Disorders without Major CC|
Aortic valve insufficiency (AI) is the incomplete closure of the aortic valve leaflets, which allows blood to regurgitate backward from the aorta into the left ventricle. The retrograde blood flow occurs during ventricular diastole when ventricular pressure is low and aortic pressure is high. The backflow of blood into the ventricle decreases forward flow in the aorta and increases left ventricular volume and pressure. In compensation, the left ventricle dilates and hypertrophies to accommodate the increased blood volume. Eventually, the increase in left ventricular pressure is reflected backward into the left atrium and pulmonary circulation. Risk of premature death from AI, as well as complications and the chronic need for medication because of congenital heart disease, is approximately 50%.
Most patients with AI experience left ventricular failure. If heart failure is serious, the patient may develop pulmonary edema. If the patient is overtaxed by an infection, fever, or cardiac dysrhythmia, myocardial ischemia may also occur.
AI may result either from an abnormality of the aortic valve or from dilation and distortion of the aortic root. AI can be congenital or acquired. Congenital abnormalities are associated ventricular septal defect, bicuspid aortic valve, subvalvular aortic stenosis, dysplasia of valve cusps, or the absence of two or three aortic valve leaflets. Acquired AI results from conditions such as endocarditis, trauma, systemic diseases such as rheumatic fever or systemic lupus erythematosus, and connective tissue syndromes.
Dilation or distortion of the aortic root may be due to systemic hypertension, aortic dissection, syphilis, Marfan’s syndrome, and ankylosing spondylitis. Rheumatic heart disease and endocarditis cause the valve cusps to become thickened and retracted, whereas an aortic aneurysm causes dilation of the annulus (the valve ring that attaches to the leaflets). Chronic high blood pressure causes an increased pressure on the aortic valve, which may weaken the cusps. All of these conditions inhibit the valve leaflets from closing tightly, thus allowing backflow of blood from the high-pressure aorta.
AI can occur as a feature of several genetic diseases, including Marfan’s syndrome, Turner’s syndrome, and velocardiofacial syndrome. Alternations in the aortic valve structure, such as bicuspid aortic valve, have been shown to be heritable. Mutations in the NOTCH1 gene can lead to aortic valve calcification, among other congenital aortic valve defects, in an autosomal dominant inheritance pattern.
Gender, ethnic/racial, and life span considerations
Symptoms do not usually occur until age 40 to 50. AI is more common in males unless it is associated with mitral valve disease, when it is then more common in women. Mild aortic regurgitation is probably quite common in the elderly but is usually overlooked. Ethnicity and race have no known effect on the risk of AI.
Global health considerations
Rheumatic heart disease and subsequent valvular disease is a continuing problem in developing nations, where up to 60% of all admissions for cardiovascular illnesses are related to the condition. Prevalence may be as low as 1 per 100,000 children in Costa Rica to as high as 150 per 100,000 children in China. Areas of particular concern are Southeastern Asia, Central America, North Africa, and the Middle East.
A history of rheumatic fever suggests possible cardiac valvular malfunction; however, many patients who have had rheumatic fever do not remember having the condition. The most common symptom of AI is labored breathing on exertion, which may be present for many years before progressive symptoms develop. Angina with exertion, orthopnea, and paroxysmal nocturnal dyspnea are also principal complaints. Patients with severe AI often complain of an uncomfortable awareness of their heartbeat (palpitations), especially when lying down.
Inspection of the thoracic wall may reveal a thrusting apical pulsation. Palpation of the precordium reveals the apical pulse to be bounding and displaced to the left. Auscultation of heart sounds reveals the classic decrescendo diastolic murmur. The duration of the murmur correlates with the severity of the regurgitation. Auscultation of breath sounds may reveal fine crackles (rales) if pulmonary congestion is present from left-sided heart failure. The pulmonary congestion will vary with the amount of exertion, the degree of recumbency, and the severity of regurgitation. Assessment of vital signs reveals a widened pulse pressure caused by the low diastolic blood pressure (often close to 40 mm Hg). The heart rate may be elevated in the body’s attempt to increase the cardiac output and decrease the diastolic period of backflow.
The symptoms of AI usually develop gradually. Most people have already made adjustments in their lifestyle to adapt, not seeking treatment until the symptoms become debilitating. Assess what the patient has already done to cope with this condition.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Cardiac catheterization and aortic angiography||Normal aortic valve||Diastolic regurgitant flow from the aorta into the left ventricle; increased left ventricular end-diastolic volume/pressure||Aortic valve is incompetent, and during diastolic phase, blood flows backward into the left ventricle|
|Transthoracic echocardiography||Normal aortic valve||Incompetent aortic valve, thickening and flail of valve structures||Aortic valve is incompetent, and during diastolic phase, blood flows backward into the left ventricle|
Other Tests: Echocardiography to assess aortic valve’s structure and mobility electrocardiogram; chest radiography, magnetic resonance imaging, color-flow Doppler, pulse-flow Doppler, continuous-flow Doppler, computed tomography
Primary nursing diagnosis
DiagnosisActivity intolerance related to imbalance between oxygen supply and demand
OutcomesEndurance; Energy conservation; Self-care; Ambulation: Walking; Circulation status; Cardiac pump effectiveness; Rest; Respiratory status; Symptom severity; Nutritional status: Energy
InterventionsActivity therapy; Energy management; Circulatory care; Exercise therapy: ambulation; Oxygen therapy; Self-care assistance; Nutrition management
Planning and implementation
medical.Medical management focuses initially on treating the underlying cause, such as endocarditis or syphilis. Patients are encouraged to limit strenuous physical activity. Fluid restrictions and diuretics may be ordered to reduce pulmonary congestion. Supplemental oxygenation will enhance oxygen levels in the blood to decrease labored breathing and chest pain.
surgical.Most patients can be stabilized with medical treatment, but early elective valve surgery should be considered because the outlook for medically treated symptomatic disease is poor. Surgical repair or replacement is the most common treatment of AI.
The incompetent valve can be repaired (valve-sparing techniques) or replaced with a synthetic or biological valve, such as a pig valve. The choice of valve type is based on the patient’s age and potential for clotting problems. The biological valve usually shows structural deterioration after 6 to 10 years and needs to be replaced. The synthetic valve is more durable but also more prone to thrombi formations.
|Medication or Drug Class||Dosage||Description||Rationale|
|Digoxin||0.25 mg PO qd||Cardiotonic||Increases force of contraction in people with left ventricular dysfunction|
|Vasodilators such as nifedipine, hydralazine, prazosin, nitroprusside||Nifedipine, 10–30 mg tid PO or SL||Calcium channel blocker; systemic vasodilators||Decrease afterload (pressure that the left ventricle has to pump against) and decreases regurgitant blood flow|
|Diuretics||Varies with drug||Thiazides; loop diuretics||Enhance pumping ability of the heart|
Other Medications: If the incompetent valve is replaced surgically with a synthetic valve, patients are prescribed long-term anticoagulation therapy such as warfarin (Coumadin) to prevent thrombi from forming on the synthetic valve. Initially, heparin is given along with the warfarin, and the prothrombin time (PT) is monitored. As the PT value becomes therapeutic, the heparin is discontinued. The use of beta blockers is controversial and under investigation. If the patient is critically ill prior to surgery, he or she may receive a positive inotrope, such as dopamine or dobutamine, and a vasodilator, such as nitroprusside.
Physical and psychological rest decreases cardiac workload, which reduces the metabolic demands on the myocardium. Physical rest is enhanced by providing assistance with activities of daily living and encouraging activity restrictions. Most patients with advanced AI are placed on activity restrictions to decrease cardiac workload. If the patient is on bedrest, advise her or him to use the bedside commode, because research has shown it creates less workload for the heart than using the bedpan. If the patient can tolerate some activities, those that increase isometric work, such as lifting heavy objects, are more detrimental than activities such as walking or swimming.
Encourage the patient to avoid sudden changes in position to minimize increased cardiac demand. If the patient is hospitalized, instruct the patient to sit on the edge of the bed before standing. If pulmonary congestion is present, elevate head of bed slightly to enhance respiration.
Reducing psychological stress is a challenge. Approach the patient and family in a calm, relaxed manner. Decrease the fear of the unknown by providing explanations and current information and encouraging questions. To help the patient maintain or reestablish a sense of control, permit the patient to participate in decisions about aspects of care within his or her knowledge. If the patient decides to have valve surgery, offer to let her or him speak with someone who has already had the surgery. Seeing and talking with someone who has undergone surgery and lives with a replacement valve is usually very therapeutic.
Evidence-Based Practice and Health Policy
Lowenthal, A., Tacy, T.A., Behzadian, F., & Punn, R. (2013). Echocardiographic predictors of early postsurgical myocardial dysfunction in pediatric patients with aortic valve insufficiency. Pediatric Cardiology, 34(6), 1335–1343.
- Investigators explored predictors of early postsurgical myocardial dysfunction in a sample of 40 pediatric patients undergoing surgical repair of moderate to severe aortic valve insufficiency.
- In this sample, preoperative left-ventricular global longitudinal strain (GLS) values < 15.4 and strain rate (GLSr) values < −0.79/second predicted postoperative myocardial dysfunction (p < 0.0001).
- Preoperative GLS and GLSr values may help identify higher postoperative risks in patients with aortic valve insufficiency and should be used to inform planning during the immediate postoperative period.
- Physical findings: Diastolic murmur, bounding apical pulse, rales in the lungs, presence or absence of pain, quality of pulses
- Response to diuretics, cardiotonics, vasodilators, and inotropic agents
- Reaction to activity restrictions, fluid restrictions, and cardiac diagnosis
- Presence of complications: Chest pain, bleeding, fainting