Pathogenesis and hemodynamic disorders
The development of pathological changes in VSD is based on a tremendous pressure difference between the heart chambers. During systole, the contraction of the powerful left ventricular myocardium creates a high pressure gradient relative to the right ventricle.
Key stages of intracardiac blood flow disturbance:
- Blood rushes along the pressure gradient, forming a left-to-right shunt (a shunt from the left ventricle to the right).
- An excess volume of blood enters the pulmonary artery, causing pronounced hypervolemia of the pulmonary circulation.
- The increased volume of venous return from the lungs initially leads to volume overload of the left ventricle.
- As the defect progresses, total overload of both ventricles occurs, which serves as the substrate for severe heart failure.
Physical examination
The classical presentation of the defect is clearly manifested during physical examination of the patient, primarily during palpation and auscultation of the heart.
The main auscultatory phenomenon is a harsh systolic murmur. It has a number of specific characteristics:
- Epicenter of the sound: the murmur is maximally pronounced in the area of absolute cardiac dullness, localized directly at the sternal border.
- Respiratory dependence: the loudness of the murmur noticeably increases on expiration.
- Palpatory equivalent: due to high flow turbulence, the murmur is often accompanied by a pronounced systolic thrill over the chest, which in classical propedeutics received the figurative name «cat's purr» (thrill).
Instrumental diagnostic methods
Routine instrumental examinations are used to confirm the diagnosis and visualize hemodynamic shifts:
- Chest X-ray. Allows visualization of the consequences of pulmonary hypervolemia: the images show dilation of the pulmonary trunk and increased pulsation of the pulmonary roots.
- Echocardiography (EchoCG) with Doppler mapping. This is the gold standard, as it provides direct visualization of the pathological blood flow (shunt) through the defect from the left ventricle into the right.
Evolution of the defect and late stages
With the long-term presence of the defect, continuous overload of the pulmonary circulation triggers irreversible changes in the pulmonary vessels. Severe pulmonary hypertension develops, fundamentally altering the hemodynamics and clinical picture.
This stage is known as Eisenmenger syndrome (shunt reversal). Due to critical resistance growth in the pulmonary vessels, the pressure in the right ventricle begins to exceed the pressure in the left. As a result:
- The direction of the blood shunt changes to right-to-left.
- Venous blood enters the systemic circulation, which clinically manifests as the appearance of cyanosis.
- The auscultatory picture transforms: the classic gradient disappears, and the initial harsh murmur becomes atypical or fades away.
Briefly: answers to topical questions
What congenital and acquired defects are included in the differential diagnosis of VSD?
The differential diagnosis of VSD according to the provided materials is described for the clinical picture with cyanosis, dyspnea, tachycardia, and a harsh systolic murmur to the left of the sternum. In this case, VSD is differentiated from other congenital anomalies:
- atrial septal defect (ASD);
- patent ductus arteriosus (PDA);
- coarctation of the aorta.
Differential diagnosis of VSD with acquired heart defects is not described in the provided sources.
The image will help remember auscultation: "VSD is a harsh cat at the sternal border." The cat "purrs" (systolic thrill), and its voice sounds harsh and is better heard on expiration.
Class and exam questions
Why is the left ventricle the first to be overloaded in a ventricular septal defect?
Due to the left-to-right shunt, pulmonary hypervolemia occurs. All this excess blood volume returns via the pulmonary veins back to the left heart chamber, causing its diastolic overload.
Where is the epicenter (punctum maximum) of the murmur in VSD?
The murmur is best auscultated in the area of absolute cardiac dullness, directly at the left sternal border.
What is Eisenmenger syndrome?
This is the terminal stage of the defect, in which, due to severe pulmonary hypertension, the pressure in the right ventricle becomes higher than in the left, leading to shunt reversal (right-to-left shunt) and the appearance of cyanosis.
What else to study on this topic
- Mechanisms of pressure gradient formation between the ventricles
- Physical nature of the "cat's purr" phenomenon
- X-ray signs of pulmonary hypervolemia
- Doppler evaluation of blood flow directions
- Pathogenesis of cyanosis during shunt reversal
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