Mitral stenosis: hemodynamics and clinical presentation

Causes and pathomorphology

The primary cause of this condition is a prior rheumatic infection. The valve cusps thicken and fuse, forming adhesions (commissures), while the valvular apparatus may become calcified and displaced. As a result, the orifice narrows and often acquires a characteristic "fish-mouth" appearance.

Less commonly, stenosis is caused by severe atherosclerosis with calcification of the mitral annulus or is a congenital anomaly.

Hemodynamic changes

The pathophysiological cascade in mitral stenosis spreads retrogradely: from the left heart chambers to the right through the lungs.

• First barrier (left heart chambers): The orifice area decreases, causing the left ventricle to receive insufficient blood. The entire load falls on the left atrium: the pressure within it rises, and it undergoes hypertrophy and dilation.
• Pulmonary circulation: Pressure from the atrium is transmitted to the pulmonary veins (venous hypertension). If pulmonary capillary pressure exceeds the oncotic pressure, the liquid portion of the blood transudates into the alveoli, leading to pulmonary edema.
• Second barrier (arterial response): To protect the lungs from edema, pulmonary arterioles undergo spasm. This reduces blood flow to the left heart, but at the cost of developing pulmonary arterial hypertension.
• Right heart chambers: Due to high vascular resistance in the lungs, the right ventricle becomes overloaded. It hypertrophies and then dilates, which ultimately leads to increased pressure and enlargement of the right atrium.

The severity of the abnormalities depends on the orifice area and blood flow volume. During physical exertion, blood flow increases, raising the pressure gradient across the valve and sharply aggravating pulmonary congestion.

Clinical presentation

For a long time, the disease may be asymptomatic and discovered incidentally. Symptoms typically debut at 40–50 years of age. Without treatment, patients can live for more than 10 years from the onset of symptoms.

Symptoms during decompensation:

• Dyspnea (initially upon exertion, later at rest).
• Nocturnal attacks of cardiac asthma.
• Palpitations and irregular heart rhythm (atrial fibrillation).
• Hemoptysis (due to rupture of pulmonary capillaries under high hypertension).

Decompensation is frequently triggered by fever, pregnancy, or surgery.

Objective symptoms and auscultation

In severe stenosis, the patient acquires a specific appearance — facies mitralis. The person looks younger than their years, a cyanotic "mitral flush" appears on the cheeks, and the lips, tip of the nose, and fingers are bluish (acrocyanosis).

Palpation and percussion:

• The hypertrophied right ventricle pulsates in the epigastric region and the area of absolute cardiac dullness.
• A diastolic thrill — "cat's purr" — is palpated at the apex.
• The cardiac borders are shifted upward (due to the left atrium and pulmonary artery) and to the right (due to the right heart chambers).

Auscultation (key diagnostic method): Auscultation should be performed at the apex, with the patient in the left lateral position, preferably after slight exertion. Characteristic findings include:

1. Loud, snapping first heart sound — the left ventricle is underfilled and its walls are relaxed during diastole, tensing sharply during systole to produce a loud sound.
2. Opening snap of the mitral valve (opening snap).
3. Diastolic murmur.

Briefly: answers to topical questions

What else to study on this topic

• Chronic structural changes in the lungs and redistribution of blood flow
• Mechanisms of low cardiac output syndrome in mitral stenosis
• Late complications: relative tricuspid and pulmonary valve regurgitation
• Effect of fever and pregnancy on hemodynamics in valvular heart disease

Other topics in the "Cardiovascular system" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.