Valvular heart disease: Nursing

Valvular heart disease refers to damage or defect involving one or more heart valves, and it can be divided into stenosis or narrowing of the valvular orifice; as well as regurgitation or insufficiency, and prolapse, in which the valvular leaflets fail to close adequately.

Now, let’s go over some anatomy and physiology. If we take a look at a cross-section of the heart. Here, we can see the outer layer called the epicardium; the middle layer called the myocardium, and finally, a very thin inner layer called the endocardium.

Now, the endocardium folds over the heart openings, forming the valvular leaflets that separate the heart chambers, so the atria and ventricles.

There are two atrioventricular valves; the mitral valve separates the left atrium from the left ventricle, while the tricuspid valve separates the right atrium from the right ventricle. These valves are connected to the papillary muscles, and chordae tendinae of the heart.

So when the heart is relaxed during diastole, they are open, enabling the ventricles to fill up with blood. On the flip side, when the heart contracts during systole, the valves close, thereby preventing the blood flow from the ventricles back into the atria.

Then, there are two semilunar valves; the aortic valve separates the left ventricle from the aorta, while the pulmonary valve separates the right ventricle from the pulmonary artery.

Now, in contrast to the atrioventricular valves, the semilunar valves close after ventricular contraction during systole, when the heart starts to relax in diastole, thereby preventing the backflow of the blood from the arteries into the ventricles.

Alright, so valvular heart disease is caused by damage or defects involving one or more heart valves.
Rheumatic fever, which is a delayed inflammatory condition that typically occurs two to four weeks after a strep throat infection from Streptococcus pyogenes, also referred to as group A beta hemolytic streptococcus or GAS for short.

Other important causes of valvular heart disease include infective endocarditis, atherosclerosis, myocardial infarction, and dilated cardiomyopathy.

Finally, valvular heart disease can have congenital causes, such as congenital valve disease characterized by malformation defects during fetal life, as well as Marfan syndrome, which is an inherited connective tissue disorder that can affect a client’s skeleton, blood vessels, eyes, and lungs.

Now, risk factors for valvular heart disease include genetic predisposition and family history; as well as older age; and a history of strep throat or rheumatic fever, infectious endocarditis, cardiomyopathy, and valvular disease.

Other important risk factors include congenital heart diseases; autoimmune conditions, such as rheumatoid arthritis and systemic lupus erythematosus; and radiation exposure.

So the pathology depends on the type of valvular heart disease, as well as the affected valve. Let’s start with mitral stenosis. In mitral stenosis, the leaflets might fuse together, impairing the opening of the mitral valve.

The impaired opening will make it harder for blood to flow from the left atrium to the left ventricle. As a result, the pressure in the left atrium increases; so to compensate, the left atrium undergoes hypertrophy, as well as dilation to accommodate the extra blood.

Over time, this compensation won’t be enough, resulting in backflow of blood in the pulmonary circulation. This can result in pulmonary edema, as well as pulmonary hypertension, which can ultimately make it harder for the right ventricle to pump blood into the pulmonary artery. Over time, the right ventricle can undergo hypertrophy, and ultimately fail, which is also known as right-sided heart failure.

Next up is mitral valve regurgitation, in which the valves fail to close completely during systole. A type of mitral valve regurgitation is mitral valve prolapse, where the leaflets of the mitral valve bulge back into the left atrium during systole. As a result, blood flows back from the left ventricle into the left atrium. Over time, this volume overload leads to atrial dilation, and the buildup of blood in the pulmonary circulation. This results in pulmonary hypertension, which in turn increases the pressure in the right ventricle, causing it to undergo hypertrophy, and eventually leads to right-sided heart failure.

With aortic stenosis, the three leaflets of the aortic valve become stiff and often calcified. As a result, they can’t open fully, making it harder for blood to flow from the left ventricle into the aorta. To compensate, the left ventricle undergoes hypertrophy and dilation to accommodate the extra blood. Over time, this compensation won’t be enough, resulting in left ventricular failure, which is followed by subsequent accumulation of blood in the left atrium and pulmonary circulation.

Finally, in aortic regurgitation, the valve doesn’t properly close during diastole, therefore blood leaks back from the aorta into the left ventricle. To compensate, the left ventricle undergoes hypertrophy and dilation. Over time, when the left ventricle cannot compensate anymore, the client develops left ventricular heart failure.

Initially, valvular heart disease may not have clinical manifestations, so clients are generally asymptomatic for a long period, even for decades. But, when symptoms do develop, they usually include dyspnea, orthopnea, fatigue, and angina.

Upon auscultation, clients may present various heart murmurs depending on the affected valve and disease.

Mitral stenosis is characterized by a low-pitched mid to late diastolic murmur; while in mitral valve prolapse, there’s a mid-systolic click, sometimes followed by a systolic murmur. On the other hand, in mitral regurgitation, there’s a pansystolic murmur, often referred to as a high-pitched holosystolic murmur, and an audible S3 heart sound.

Next up, aortic stenosis is characterized by a systolic crescendo-decrescendo murmur and decreased S2 sound; and lastly, aortic regurgitation is associated with a decrescendo diastolic murmur. In severe cases, clients might develop complications like heart failure, leading to peripheral edema or syncope; while others may experience atrial fibrillation, and even cardiogenic shock.

The diagnosis of valvular heart disease starts with the client’s history and physical assessment, including electrocardiogram or ECG assessment, and exercise tolerance testing, or ETT for short. Other important diagnostic methods include chest X-ray, as well as a Doppler, transthoracic or transesophageal echocardiography, as well as a stress echocardiography, or cardiac catheterization to evaluate the affected valve.

Now, the treatment of valvular heart disease can involve three approaches.

First, pharmacological therapy includes anticoagulants, and severe cases may require medications used in the treatment of heart failure, such as ACE inhibitors and beta-blockers.

Second, minimally invasive procedures include percutaneous transluminal balloon valvuloplasty for valvular stenosis, in which the valve is dilated using a balloon; and percutaneous valve replacement, in which the affected valve is replaced with a new one.