Aortic stenosis: hemodynamics and clinical presentation

Concept of obstruction and etiology of the defect

Aortic stenosis represents a specific, yet most common, instance of a broader clinical concept — left ventricular outflow tract obstruction. Several variants of such obstruction are distinguished:

• Valvular stenosis: an acquired defect that is the main cause of narrowing.
• Subvalvular and supravalvular stenosis: categorized as congenital heart defects.
• Muscular obstruction: a specific condition developing in hypertrophic cardiomyopathy.

By origin, the narrowing of the aortic orifice is divided into congenital and acquired. Among the causes of acquired stenosis, rheumatic heart disease, infective endocarditis, and degenerative changes in elderly patients (atherosclerosis and valve calcification) are the leaders. An important differential diagnostic sign: if aortic stenosis is combined with a mitral valve defect, this strongly suggests its rheumatic origin.

Using rheumatic disease as an example, the pathomorphological picture appears as thickening and fusion of the cusps. The main functional defect consists of a drastic decrease in cusp mobility, making their complete opening impossible during the left ventricular systole phase.

Hemodynamics and compensation mechanisms

The primary hemodynamic disorder in stenosis aortica is a mechanical obstacle to blood ejection from the left ventricle into the aorta. Because of this, a pathological pressure difference is formed — a pressure gradient between the ventricular cavity and the aorta, which should normally be absent. The diagnostic criterion for the defect is a gradient exceeding 20 mmHg, and in severe narrowing, this indicator can reach 100 mmHg.

To overcome such high resistance and maintain a normal cardiac output, the main compensatory mechanism is engaged — concentric hypertrophy of the left ventricle. The increase in muscle mass allows for maintaining an adequate cardiac output for a long time both at rest and during physical exertion.

However, myocardial hypertrophy has negative consequences. The thickened muscle loses its elasticity and compliance, leading to impaired relaxation — diastolic function suffers. As a result, the end-diastolic pressure in the ventricular cavity rises, which, as the pathology progresses, causes retrograde overload of the left atrium.

Myocardial ischemia and the stage of decompensation

Patients with aortic valve stenosis frequently develop relative coronary insufficiency, even if the coronary arteries themselves remain intact (clean). The pathogenesis of ischemia, which is localized predominantly in the subendocardial layers, is due to two factors:

1. Increased oxygen demand: the significantly enlarged mass of the hypertrophied myocardium requires an increased blood supply.
2. Impaired blood flow: the powerful systolic contraction of the thickened muscle mechanically compresses the intramural coronary arteries.

Prolonged hemodynamic overload and chronic ischemia inevitably lead to dystrophic changes in the myocardium. The stage of decompensation sets in. The left ventricle loses its tone, its cavity enlarges (dilatation develops). Cardiac output begins to drop, first during exertion and then at rest — left ventricular failure forms. In the latest stages, due to developing pulmonary hypertension, right ventricular failure joins the process.

Clinical presentation and objective findings

For many years, the defect may manifest no symptoms thanks to compensatory hypertrophy. The diagnosis is often established incidentally during routine auscultation (a systolic murmur is heard in the 2nd intercostal space on the right). Symptoms manifest only during critical narrowing, when the orifice area is less than a quarter of normal.

The classic clinical picture includes three groups of complaints:

• Angina pectoris: typical retrosternal anginal pain due to relative ischemia.
• Cerebral symptoms: dizziness and syncope. During exertion, they are associated with a fixed stroke volume and cerebral hypoperfusion, and at rest — with rhythm disturbances (ventricular tachycardia, transient AV block, atrial fibrillation).
• Left ventricular failure: dyspnea, orthopnea, episodes of cardiac asthma, and pulmonary edema.

On objective examination, "aortic pallor" of the skin draws attention — a consequence of compensatory arteriolar spasm due to low output. The pulse becomes small, slow (pulsus parvus et tardus), and soft. Blood pressure is characterized by a decrease in systolic pressure and a reduction in pulse pressure. On palpation, the apex beat is intensified, and in late stages, shifted to the left and downward. To the right of the sternum in the 2nd intercostal space, a systolic thrill is clearly palpable.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Pathogenesis of resting cardiac rhythm disturbances: from atrial fibrillation to AV blocks.
• Features of retrograde left atrial overload in severe diastolic dysfunction.
• Differential diagnosis of valvular, subvalvular, and supravalvular stenoses.
• Specifics of the development of systolic thrill and murmur in the 2nd right intercostal space.
• The role of left ventricular dilatation in the transition from the compensation stage to total heart failure.

Other topics in the "Cardiovascular system" section

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