15.4
Mitral Kapak Yetmezliği: Giriş
Mitral kapak yetmezliği, sistol sırasında sol ventrikülden sol atriuma kanın geri kaçması ile karakterizedir. Sistol, kalbin kasıldığı ve kanı odacıkl…
Mitral yetersizliği veya MR, mitral kapağın sistol sırasında tamamen kapanmadığı ve kanın sol ventrikülden sol kulakçıka geriye doğru sızmasına neden olduğu bir kalp rahatsızlığıdır.
Etiyolojisi iki tipe ayrılır.
Primer MR, mitral kapak prolapsusu, romatizmal ateş ve dejeneratif değişiklikler dahil olmak üzere doğrudan mitral kapak anormalliklerinden kaynaklanır.
Sekonder MR, iskemik kalp hastalığı ve enfektif endokardit gibi indirekt faktörlerden kaynaklanır.
MR'ın patofizyolojisi, mitral kapakta veya yaprakçıklar, korda tendineae, annulus veya papiller kaslar dahil olmak üzere destekleyici yapılarında işlev bozukluğunu içerir ve bu da geriye doğru kan akışına ve hacim aşırı yüklenmesine yol açar.
Bu aşırı yüklenme sol atriyal genişlemeye ve sol ventrikül hipertrofisi ve genişlemesine neden olur.
Bu telafi edici değişiklikler sonunda sistolik disfonksiyona neden olabilir.
Sol kulakçıkta artan basınç, akciğer tıkanıklığına ve hipertansiyona neden olabilir, sağ ventrikülü zorlayabilir ve kalp debisinin azalmasına ve kalp yetmezliği semptomlarına yol açabilir.
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Q1: What happens to blood flow when the mitral valve fails to close properly?
When the mitral valve fails to close entirely during systole, blood leaks backward from the left ventricle into the left atrium instead of being pumped forward. This abnormal backward circulation reduces the efficiency of cardiac output and forces the heart to work harder to maintain adequate blood flow throughout the body.
Q2: What are the two main categories of mitral regurgitation causes?
Primary mitral regurgitation originates from direct valve abnormalities such as mitral valve prolapse, rheumatic fever, and degenerative changes affecting the leaflets and chordae tendineae. Secondary mitral regurgitation results from indirect factors like ischemic heart disease, myocardial infarction, and infective endocarditis that damage supporting structures or alter ventricular geometry.
Q3: How does mitral regurgitation affect the structure of the heart chambers?
The regurgitated blood creates volume overload in the left atrium and ventricle, causing them to enlarge and stretch. Initially, this adaptive response of hypertrophy and dilation helps maintain cardiac output, but chronic volume overload eventually leads to progressive ventricular dilation and systolic dysfunction.
Q4: What role do the mitral valve's supporting structures play in regurgitation?
The mitral valve's supporting structures include the leaflets, chordae tendineae, annulus, and papillary muscles. Dysfunction or damage to any of these components prevents complete valve closure during systole, leading to incomplete valve closure and blood regurgitation into the left atrium.
Q5: How does increased pressure in the left atrium affect the lungs and right heart?
Increased pressure in the left atrium due to regurgitated blood leads to pulmonary congestion and pulmonary hypertension. This back pressure strains the right ventricle, potentially causing right-sided heart failure and reducing overall cardiac output, which manifests as fatigue and exertional dyspnea.
Q6: What is the relationship between chronic mitral regurgitation and heart failure?
Chronic volume overload and increased atrial pressures result in progressive ventricular dilation and dysfunction, culminating in systolic heart failure. The heart's pumping efficiency decreases over time, reducing cardiac output and causing symptoms such as reduced exercise tolerance and breathing difficulties.
Q7: How do rheumatic fever and degenerative changes cause primary mitral regurgitation?
Rheumatic fever causes scarring and deformation of the mitral valve leaflets, while degenerative changes cause the leaflets and chordae tendineae to thicken and become fibrotic. Both conditions impair the valve's ability to close completely, resulting in blood leakage during systole.