Mitral Valve Prolapse PDF

1/24/24, 9:46 AM Realizeit for Student Introduction Structural, infectious, and inflammatory disorders of the heart present many challenges for the patient, family, and health care team. Various mechanisms, heart valve disorders, cardiomyopathies, and infectious diseases of the heart alter cardiac o...

1/24/24, 9:46 AM Realizeit for Student Introduction Structural, infectious, and inflammatory disorders of the heart present many challenges for the patient, family, and health care team. Various mechanisms, heart valve disorders, cardiomyopathies, and infectious diseases of the heart alter cardiac output. Treatments for these disorders may be noninvasive or invasive. Noninvasive treatments often consist of medication therapy, diet changes, and activity modification. Invasive treatments include valve repair or replacement, ventricular assist devices (VADs), total artificial hearts (TAHs), cardiac transplantation, or other surgical procedures. Nurses have an integral role in the care of patients with structural, infectious, and inflammatory cardiac conditions. Valves of the heart control the flow of blood through the heart into the pulmonary artery and aorta by opening and closing in response to blood pressure changes during each cardiac cycle (heart contraction and relaxation). Atrioventricular valves separate the atria from the ventricles and include the tricuspid valve, which separates the right atrium from the right ventricle, and the mitral valve, which separates the left atrium from the left ventricle. The tricuspid valve has three leaflets; the mitral valve has two. Both valves have chordae tendineae that anchor valve leaflets to papillary muscles of the ventricles. When any heart valve does not close or open properly, blood flow is affected. When valves do not close completely, blood flows backward through the valve, a condition called regurgitation. When valves do not open completely, a condition called stenosis, blood flow through the valve is reduced. Regurgitation and stenosis affect all heart valves. The mitral valve may also prolapse (i.e., stretching of the valve leaflet into the atrium during systole). Depending on the severity of symptoms, patients with valve disorders may not require treatment, or they may need to make lifestyle changes, take medications, or require surgical repair or replacement of the valve. Disorders of the mitral and aortic valve cause more symptoms, require treatment, and cause more complications than disorders of the tricuspid and pulmonic valves. Regurgitation and stenosis may occur at the same time in the same or different valves. Mitral Valve Prolapse https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f5… 1/13 1/24/24, 9:46 AM Realizeit for Student Mitral valve prolapse is a deformity that usually produces no symptoms. Rarely, it progresses and can result in sudden death (Han, Ha, Teh, et al., 2018; Nalliah, Mahajan, Elliott, et al., 2019). This condition occurs in up to 2.5% of the general population and twice as frequently in women as in men (Han et al., 2018). In most cases, there is no clear cause, but it has been associated with inherited connective tissue disorders, causing enlargement of one or both of the mitral valve leaflets (Asher, Chen, & Kallish, 2018; Wozniak-Mielczarek, Sabiniewicz, Drezek-Nojowicz, et al., 2019). The annulus often dilates; chordae tendineae and papillary muscles may elongate or rupture. Pathophysiology In mitral valve prolapse, a portion of one or both mitral valve leaflets balloons back into the atrium during systole. Rarely, ballooning stretches the leaflet to the point that the valve does not remain closed during systole. Blood then regurgitates from the left ventricle back into the left atrium. Although uncommon, mitral valve prolapse can result in mitral regurgitation, which can cause heart enlargement, atrial fibrillation, pulmonary hypertension, or heart failure (Ma, Igata, Strachan, et al., 2019). https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f5… 2/13 1/24/24, 9:46 AM Realizeit for Student https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f5… 3/13 1/24/24, 9:46 AM Realizeit for Student Figure 24-2 Pathophysiology. Left-sided heart failure as a result of aortic and mitral valvular heart disease and development of right ventricular failure. Clinical Manifestations Most people with mitral valve prolapse never have symptoms. A small number of patients will have fatigue, shortness of breath, lightheadedness, dizziness, syncope, palpitations, chest pain, or anxiety. To date, there has been no consensus about the cause of symptoms. Patients may report fatigue, regardless of activity level and amount of rest or sleep, as well as shortness of breath, palpitations, and chest pain (Althunayyan, Petersen, Lloyd, et al., 2019). Assessment and Diagnostic Findings Often, the first and only sign of mitral valve prolapse is an extra heart sound, referred to as a mitral click. A systolic click is an early sign that a valve leaflet is ballooning into the left atrium. In addition to the mitral click, a murmur of mitral regurgitation may be heard if the valve opens during systole and blood flows back into the left atrium. If mitral regurgitation exists, a patient may experience signs and symptoms of heart failure (see Chapter 25). Echocardiography is used to diagnose and monitor progression of mitral valve prolapse (Han et al., 2018). Medical Management Medical management is directed at controlling symptoms. If a patient who reports palpitations is found to have an arrhythmia, the patient may be advised to eliminate caffeine and alcohol from the diet and to stop the use of tobacco products as well as electronic nicotine delivery systems (ENDS), including e-cigarettes, e-pens, e-pipes, ehookah, and e-cigars. Most patients do not require medication, but some are prescribed antiarrhythmic medications. Prophylactic antibiotics are not recommended prior to dental or invasive procedures (Nishimura, Otto, Bonow, et al., 2017). Patients who have chest pain related to mitral valve prolapse rarely require medical therapies, such as nitrates, calcium channel blockers, or beta-blockers. Heart failure, if present, is treated as it would be for any other case of heart failure. Patients with severe mitral regurgitation and symptomatic heart failure may require mitral valve repair or replacement. Nursing Management The nurse educates the patient about the diagnosis and the possibility that the condition is hereditary. First-degree relatives (e.g., parents, siblings) may be advised to https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f5… 4/13 1/24/24, 9:46 AM Realizeit for Student have screening cardiac evaluations or echocardiograms. Because most patients with mitral valve prolapse are asymptomatic, the nurse explains the need to inform the patient’s primary provider about any symptoms that may develop. The nurse encourages the patient to read product labels, particularly on over-the-counter products such as cough medicine, because these products may contain alcohol, caffeine, ephedrine, and epinephrine, which may produce arrhythmias and other symptoms. The nurse also explores diet, activity, sleep, and other lifestyle factors that may correlate with symptoms. (Treatment of arrhythmias, chest pain, heart failure, or other complications of mitral valve prolapse is described in Chapters 22 and 25.) Women diagnosed with mitral valve prolapse without mitral regurgitation or other complications may complete pregnancies without close cardiac monitoring and can safely proceed with vaginal deliveries (Yuan & Yan, 2016). Mitral Regurgitation Mitral regurgitation is a condition in which blood flows from the left ventricle back into the left atrium during systole. Often, the edges of mitral valve leaflets do not close completely during systole because leaflets and chordae tendineae have thickened and become fibrotic, resulting in abnormal contraction. Mitral regurgitation may be chronic or, less commonly, acute. The most common causes of mitral valve regurgitation in developed countries are degenerative changes of the mitral valve (including mitral valve prolapse) and ischemia of the left ventricle (Harb & Griffin, 2017). The most common cause in developing countries is rheumatic heart disease and its sequelae (Negi, Mahajan, Rana, et al., 2018). Other conditions that lead to chronic mitral regurgitation include pathologic myxomatous changes, which enlarge and stretch the left atrium and ventricle, causing leaflets and chordae tendineae to stretch or rupture (Harb & Griffin, 2017). Infective endocarditis may cause acute mitral regurgitation through leaflet perforation, or scarring following an infection that may cause retraction of leaflets or chordae tendineae (Watanabe, 2019). Collagen vascular diseases (e.g., systemic lupus erythematosus), cardiomyopathy, and ischemic heart disease may result in changes in the left ventricle, causing papillary muscles, chordae tendineae, or leaflets to stretch, shorten, or rupture. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f5… 5/13 1/24/24, 9:46 AM Realizeit for Student These conditions are often referred to as functional, or secondary, mitral regurgitation (Dziadzko, Dziadzko, Medina-Inojosa, et al., 2019). Pathophysiology Mitral regurgitation may result from problems with one or more leaflets, chordae tendineae, the annulus, or the papillary muscles. A mitral valve leaflet may shorten or tear, and chordae tendineae may elongate, shorten, or tear. The annulus may be stretched by heart enlargement, as in functional mitral regurgitation, or it may be deformed by calcification. A papillary muscle may rupture, stretch, or be pulled out of position by changes in the ventricular wall (e.g., scar from a myocardial infarction, ventricular dilation). Papillary muscles may be unable to contract because of ischemia, a condition referred to as ischemic mitral regurgitation. Regardless of the cause, the effect is backward blood flow into the atrium during systole. In this disorder, each beat of the left ventricle pushes blood backward into the left atrium, adding to blood flowing in from the lungs. This excess blood causes the left atrium to stretch and eventually thicken, or hypertrophy, then dilate. Over time, blood coming in from the ventricle prevents blood flow from the lungs into the atrium. As a result, the lungs become congested, eventually adding extra strain to the right ventricle. During diastole, the increased blood volume from the atrium fills the ventricle. The volume overload causes ventricular hypertrophy. Eventually, the ventricle dilates, and systolic heart failure develops. Clinical Manifestations Chronic mitral regurgitation is often asymptomatic, but acute mitral regurgitation (e.g., resulting from a myocardial infarction) usually manifests as severe and sudden congestive heart failure (Harb & Griffin, 2017). Dyspnea, fatigue, and weakness are the most common symptoms. Palpitations, shortness of breath on exertion, and cough from pulmonary congestion also occur. Assessment and Diagnostic Findings The systolic murmur of mitral regurgitation is a blowing sound best heard at the apex. The murmur may radiate to the left axilla (Harb & Griffin, 2017). The pulse may be regular, or it may be irregular because of extrasystolic beats or atrial fibrillation. Echocardiography is used to diagnose and monitor progression of this disorder (Nishimura et al., 2017). Medical Management https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f5… 6/13 1/24/24, 9:46 AM Realizeit for Student Patients with mitral regurgitation who develop pulmonary congestion are managed with medications used for heart failure. Patients with mitral regurgitation and heart failure benefit from afterload reduction (arterial dilation) by treatment with angiotensinconverting enzyme (ACE) inhibitors (e.g., captopril, lisinopril) or angiotensin receptor blockers (ARBs) (e.g., losartan, valsartan), direct arterial dilators (e.g., hydralazine), and beta-blockers (e.g., carvedilol, metoprolol). Symptoms of heart failure also are an indication to consider surgical intervention by mitral valvuloplasty (i.e., surgical repair of the valve) or valve replacement (replacement of the dysfunctional valve with either a mechanical valve or a type of tissue valve; discussed later in this chapter) (Nishimura et al., 2017). Mitral Stenosis Mitral stenosis results in reduced blood flow from the left atrium into the left ventricle. It is usually caused by rheumatic endocarditis, which progressively thickens mitral valve leaflets and chordae tendineae, causing the leaflets to fuse together (Negi et al., 2018). Eventually, the mitral valve orifice narrows and progressively obstructs blood flow into the ventricle.. Pathophysiology Normally, the mitral valve orifice is as wide as the diameter of three fingers. In severe mitral stenosis, the orifice narrows to the width of a pencil. Because of increased resistance through the narrowed valve orifice, the left atrium is less able to push blood into the left ventricle. This results in increased residual blood volume in the left atrium, which over time causes left atrial hypertrophy and dilation. Decreased blood flow into the left ventricle leads to reduced ventricular filling and decreased cardiac output. A stenotic valve fails to protect pulmonary veins from backward flow of blood from the atrium, resulting in congestion of the pulmonary circulation. The right ventricle must then contract against abnormally high pulmonary arterial pressure and is subjected to excessive strain. Over time, the right ventricle hypertrophies, enlarges, and eventually fails. If the heart rate increases, diastole is shortened; thus, the amount of time for forward flow of blood decreases, and more blood backs into the pulmonary veins. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f5… 7/13 1/24/24, 9:46 AM Realizeit for Student Therefore, as the heart rate increases, cardiac output further decreases, and pulmonary pressures increase. Clinical Manifestations Often, the first symptom of mitral stenosis is dyspnea on exertion (DOE) caused by pulmonary venous hypertension. Symptoms do not usually develop until after the valve opening is reduced by one third to one half its usual size (Harb & Griffin, 2017). Patients may experience progressive fatigue and decreased exercise tolerance because of low cardiac output. An enlarged left atrium may create pressure on the left bronchial tree, resulting in a dry cough or wheezing. In cases of severe mitral stenosis with significant pulmonary congestion, patients may expectorate blood (i.e., hemoptysis) or experience palpitations, orthopnea, paroxysmal nocturnal dyspnea (PND), or repeated respiratory infections. Increased blood volume and pressure cause the left atrium to dilate, hypertrophy, and become electrically unstable, which may result in patients developing atrial arrhythmias (Negi et al., 2018). Assessment and Diagnostic Findings Patients with mitral stenosis will have a low-pitched, rumbling diastolic murmur, best heard at the apex. Patients may have a weak and irregular pulse if they develop atrial fibrillation and may have signs or symptoms of heart failure (Nishimura et al., 2017). Echocardiography is used to diagnose and quantify the severity of mitral stenosis. Electrocardiography (ECG), exercise testing, and cardiac catheterization with angiography may be used to help determine the severity of mitral stenosis. Prevention Since rheumatic heart disease may result in mitral stenosis, prevention is aimed at decreasing the risk of contracting and providing early treatment for bacterial infections (see prevention of endocarditis later in this chapter). Prevention of acute rheumatic fever depends on effective antibiotic treatment of group A streptococcal infection (Nishimura et al., 2017). Antibiotic prophylaxis for recurrent rheumatic fever with rheumatic carditis may require 10 or more years of antibiotic coverage (e.g., penicillin G intramuscularly every 4 weeks, penicillin V orally twice daily, sulfadiazine orally daily, or erythromycin orally twice daily) (Szczygielska, Hernik, Kolodziejczyk, et al., 2018). Medical Management Congestive heart failure is treated as described in Chapter 25. Patients with severe left atrial dilation in mitral stenosis may benefit from anticoagulant medications to decrease https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f5… 8/13 1/24/24, 9:46 AM Realizeit for Student the risk of developing atrial thrombi. If atrial fibrillation develops, cardioversion may be attempted to restore normal sinus rhythm. If unsuccessful, the ventricular rate is controlled with beta-blockers, digoxin, or calcium channel blockers; furthermore, patients will require anticoagulation for thromboembolism prevention (January, Wann, Calkins, et al., 2019). Patients with severe mitral stenosis are advised to avoid strenuous activities, competitive sports, and pregnancy, all of which increase heart rate (Nishimura et al., 2017). Surgical intervention consists of valvuloplasty, usually a commissurotomy (i.e., splitting or separating leaflets) to open the fused commissure of the valve. The commissure is the site where valve leaflets meet. Percutaneous transluminal valvuloplasty or valve replacement may be performed. Aortic Regurgitation Aortic regurgitation is backward flow of blood into the left ventricle from the aorta during diastole. It may be caused by a congenital valve abnormality (e.g., a bicuspid aortic valve), inflammatory lesions that deform aortic valve leaflets, or dilation of the aorta, preventing complete closure of the aortic valve. Chronic or acute aortic regurgitation may also be caused by infections such as rheumatic endocarditis or syphilis, or by a dissecting aortic aneurysm resulting in dilation or tearing of the ascending aorta, blunt chest trauma, or deterioration of a surgically replaced aortic valve (Akinseye, Pathak, & Ibebuogu, 2018; Nishimura et al., 2017). Pathophysiology During diastole, blood is normally delivered into the left atrium from the aorta. In aortic regurgitation, blood flows back into the left ventricle, which will dilate to accommodate increased blood volume. Over time, the left ventricle hypertrophies to expel more blood with above-normal force, thus increasing systolic blood pressure. Arteries attempt to compensate for higher pressures by reflex vasodilation; peripheral arterioles relax, reducing peripheral resistance and diastolic blood pressure. Clinical Manifestations Aortic regurgitation, also called aortic insufficiency, develops without symptoms in most patients. Some patients are aware of a pounding or forceful heartbeat, especially in the https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f5… 9/13 1/24/24, 9:46 AM Realizeit for Student head or neck. Patients who develop left ventricular hypertrophy may have visible or palpable arterial pulsations at the carotid or temporal arteries due to increased force and blood volume. As aortic regurgitation worsens, DOE and fatigue follow; there may eventually be signs and symptoms of progressive left ventricular failure including increased shortness of breath, orthopnea, or PND (Akinseye et al., 2018). Assessment and Diagnostic Findings A high-pitched, blowing diastolic murmur is heard at the third or fourth intercostal space at the left sternal border. The difference between systolic and diastolic pressures (i.e., the pulse pressure) may be widened in patients with aortic regurgitation. One characteristic sign is the water hammer (Corrigan’s) pulse, in which the pulse strikes a palpating finger with a quick, sharp stroke and then collapses (Pabba & Boudi, 2019). The diagnosis may be confirmed by echocardiography (preferably transesophageal), cardiac magnetic resonance imaging (MRI), or cardiac catheterization. Patients with symptoms usually have echocardiograms every 6 months, and those without symptoms have echocardiograms every 2 to 5 years (Nishimura et al., 2017). Prevention Prevention of aortic regurgitation is primarily based on prevention of and treatment for bacterial infections (see prevention of endocarditis later in this chapter). The same strategies aimed at preventing acute and recurrent rheumatic fever previously described for the patient with mitral stenosis apply to patients with aortic regurgitation. Medical Management A patient who is symptomatic or has developed a significant decrease in left ventricular function is advised to avoid physical exertion, competitive sports, and isometric exercise until the valve has been replaced (Gati, Malhotra, & Sharma, 2019). If arrhythmias and heart failure occur, they are treated as described in Chapters 22 and 25. Controlling high blood pressure in patients with aortic regurgitation can improve forward blood flow through the heart. ACE inhibitors and dihydropyridine calcium channel blockers may be recommended for management of hypertension; these are effective at reducing afterload. Beta-blockers are less commonly used, due to concern that a lower heart rate may actually increase blood pressure through negative chronotropic effects (Akinseye et al., 2018). Patients who are symptomatic should be instructed to restrict sodium intake to prevent volume overload and will require valve replacement (Nishimura, Otto, Bonow, et al., 2014). https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f… 10/13 1/24/24, 9:46 AM Realizeit for Student The treatment of choice is aortic valve replacement or valvuloplasty (described later), preferably performed before left ventricular failure occurs. Surgery is recommended for any patient with significant left ventricular dilation, regardless of the presence or absence of symptoms (Nishimura et al., 2014). Surgery is also recommended for any patient who is symptomatic (Flint, Wunderlich, Shmueli, et al., 2019). Aortic Stenosis Aortic valve stenosis is narrowing of the orifice between the left ventricle and aorta. In adults, stenosis is usually caused by degenerative calcification. Calcification may be caused by proliferative and inflammatory changes that occur in response to years of normal mechanical stress, similar to changes that occur in atherosclerotic cardiovascular disease (Joseph, Naqvi, Giri, et al., 2017). Congenital leaflet malformations or an abnormal number of leaflets (i.e., one or two rather than three) are less common causes. Rheumatic endocarditis may cause adhesions or fusion of the commissures and valve ring, stiffening of the cusps, and calcific nodules on the cusps. Pathophysiology Typically, aortic stenosis progresses gradually over several years to several decades. As the valve orifice narrows, the left ventricle overcomes obstruction by contracting more slowly and more forcibly. Obstruction to left ventricular outflow increases pressure on the left ventricle, so the ventricular wall hypertrophies. When these compensatory mechanisms are insufficient to allow for normal heart function, clinical signs and symptoms of heart failure will develop (Joseph et al., 2017). Clinical Manifestations Many patients with aortic stenosis are asymptomatic. Often, the first symptom to appear is DOE, caused by increased pulmonary venous pressure due to a dilating left ventricle. Over time, left ventricular failure may occur, causing orthopnea, PND, and pulmonary edema. Reduced blood flow to the brain may cause dizziness, and in more severe aortic stenosis, syncope. Patients may also report angina pectoris, which is caused by limited blood flow into the coronary arteries, decreased time in diastole to https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f… 11/13 1/24/24, 9:46 AM Realizeit for Student allow for myocardial perfusion, and simultaneously increased oxygen demand of the hypertrophied left ventricle. Blood pressure is usually normal but may be low. In the setting of decreased blood flow, there may be a low pulse pressure (30 mm Hg or less). Assessment and Diagnostic Findings On physical examination, a loud, harsh systolic murmur is heard over the aortic area (i.e., right second intercostal space) and may radiate to the carotid arteries and apex of the left ventricle. The murmur may be described as low pitched, crescendo– decrescendo, rough, rasping, and vibrating (Libby, Zipes, Bonow, et al., 2018). An S4 sound may be heard (see Chapter 21 for discussion of heart sounds). By having the patient lean forward during auscultation and palpation, especially during exhalation, the murmur may be accentuated. There may also be a palpable vibration extending from the base of the heart (second intercostal space next to the sternum and above the suprasternal notch) and up along the carotid arteries. The vibration is caused by turbulent blood flow across the narrowed valve orifice. Cardiac imaging is used to diagnose and monitor the progression of aortic stenosis. This may consist of echocardiography, cardiac MRI, or computed tomography (CT) scanning (Lindman, Dweck, Lancellotti, et al., 2019). Patients with symptoms usually have echocardiograms every 6 to 12 months, and those without symptoms have echocardiograms every 2 to 5 years, depending on how severely the orifice is narrowed (Lindman et al., 2019; Nishimura et al., 2014). Left ventricular hypertrophy may be seen on a 12-lead ECG or an echocardiogram. Once aortic stenosis has progressed sufficiently to consider surgical intervention, left-sided heart catheterization is needed to measure the severity of the valvular abnormality and to evaluate the coronary arteries. Pressure measurements are taken from the left ventricle and base of the aorta. The systolic pressure in the left ventricle is considerably higher than that in the aorta during systole. Graded exercise studies (stress tests) to assess exercise capacity are performed with caution for patients with severe aortic stenosis due to the high risk of inducing ventricular tachycardia or fibrillation, and should not be performed on symptomatic patients (Joseph et al., 2017). Prevention Prevention of aortic stenosis is primarily focused on controlling risk factors for proliferative and inflammatory responses—namely, through treating diabetes, hypertension, hypercholesterolemia, and elevated triglycerides, and avoiding tobacco products and ENDS. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f… 12/13 1/24/24, 9:46 AM Realizeit for Student Medical Management Medications are prescribed to treat arrhythmias or left ventricular failure. Definitive treatment for aortic stenosis is replacement of the aortic valve, which may be done surgically or nonsurgically. Nonsurgical valve replacement, known as transcatheter aortic valve replacement (TAVR), is described in more detail later in this chapter. Patients who are symptomatic and are not candidates for valve replacement may benefit from one- or two-balloon percutaneous valvuloplasty procedures, which can provide symptom relief (Sandhu, Krishnamoorthy, Afif, et al., 2017). https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zf9bYqJIJpnNRIib2GLEMttOlL1iweKeKZVedZdQtr6duWC%2f… 13/13