ARDMS AE-Adult-Echocardiography - AE Adult Echocardiography Examination

In interrupted aortic arch, the normal continuity between the ascending and descending aorta is disrupted. The patent ductus arteriosus (PDA) provides a vital conduit for blood to flow from the pulmonary artery to the descending aorta, maintaining systemic circulation distal to the interruption.

Persistent left superior vena cava and left carotid artery do not provide this flow. The foramen ovale is an atrial-level shunt and does not compensate for interrupted aortic arch.

This clinical anatomy is described in the "Textbook of Clinical Echocardiography, 6e", Chapter on Congenital Aortic Arch Anomalies【20:135-140†Textbook of Clinical Echocardiography】.

The image is a parasternal long axis M-mode echocardiographic tracing demonstrating the interventricular septum and posterior left ventricular wall. The arrow points to the septal “bounce” or “shudder,” which is an abnormal early diastolic septal motion.

This septal bounce is a classic echocardiographic finding in constrictive pericarditis, caused by rapid early diastolic filling with abrupt cessation due to pericardial constraint, resulting in paradoxical septal motion.

Cardiac tamponade usually shows pericardial effusion with chamber collapse but not septal bounce. Pulmonary embolism and pulmonary hypertension have different echocardiographic signs such as right ventricular dilatation and pressure overload but no septal bounce.

These features are well described in the "Textbook of Clinical Echocardiography" and ASE pericardial disease guidelines【16:Textbook of Clinical Echocardiography, 6e†p.280-285】【12:ASE Pericardial Disease Guidelines†p.300-305】.

In the early stages of aortic stenosis, the left ventricle adapts to increased afterload by concentric remodeling, which is characterized by increased wall thickness without a proportional increase in chamber size. This adaptation helps normalize wall stress.

As the disease progresses, concentric hypertrophy develops with thickened walls and decreased compliance. Eccentric hypertrophy and global systolic dysfunction occur later with decompensation and ventricular dilation.

This progression is explained in the "Textbook of Clinical Echocardiography, 6e", Chapter on Left Ventricular Adaptations to Pressure Overload【20:365-370†Textbook of Clinical Echocardiography】.

Decreasing the color scale (velocity range) improves the sensitivity of color Doppler for detecting low-velocity flow, such as shunting across the interatrial septum (e.g., patent foramen ovale). A lower scale allows subtle flow jets to be visualized.

Decreasing color gain would reduce sensitivity, increasing color sector size can degrade frame rate and resolution, and increasing the wall filter may remove low-velocity signals.

This optimization is discussed in the "Textbook of Clinical Echocardiography, 6e", Chapter on Color Doppler Imaging Techniques【20:100-105†Textbook of Clinical Echocardiography】.

Comprehensive and Detailed Explanation From Exact Extract:

Tetralogy of Fallot (TOF) is a congenital heart defect characterized by four key anatomical abnormalities: an outlet (malalignment) ventricular septal defect (VSD), an overriding aorta that receives blood from both ventricles, right ventricular outflow tract (RVOT) obstruction (commonly infundibular stenosis), and resultant right ventricular hypertrophy. These defects cause cyanosis due to right-to-left shunting and impaired pulmonary blood flow.

Option A describes Ebstein anomaly, characterized by a displaced tricuspid valve and atrialization of the right ventricle.

Option B describes features more consistent with Shone complex or other left heart obstructive lesions.

Option C describes atrioventricular septal defect (AVSD), seen in conditions like Down syndrome.

In unrepaired TOF, echocardiography demonstrates the large malalignment VSD, overriding aorta, RVOT obstruction, and hypertrophied right ventricle. These are classic textbook findings described in adult and pediatric echocardiography literature, including “Textbook of Clinical Echocardiography” (Chapter on Congenital Heart Disease) and ASE guidelines【16:Textbook of Clinical Echocardiography, 6e†p.560-565】【12:ASE Adult Congenital Guidelines†p.400-410】.

Comprehensive and Detailed Explanation From Exact Extract:

Mitral regurgitation (MR) Doppler signals tend to be longer in duration because MR occurs throughout systole, often spanning most or all of ventricular systole, resulting in a prolonged jet on continuous wave Doppler.

Aortic stenosis (AS) velocities can be high but may vary and are not necessarily always higher than MR velocities. The density of waveforms is not a reliable discriminator. MR only happens in systole, not diastole, which makes option C incorrect.

Therefore, the duration or length of the Doppler signal (longer for MR) is the best differentiating feature.

This differentiation is explained in the "Textbook of Clinical Echocardiography, 6e", Chapter on Doppler Assessment of Valvular Disease【20:320-325†Textbook of Clinical Echocardiography】.

Comprehensive and Detailed Explanation From Exact Extract:

The echocardiographic image shows an apical four-chamber view of the left ventricle. The arrows point to the lateral wall of the left ventricle, which in this view corresponds to the anterolateral wall. The anterolateral wall is located opposite the septum and posterior to the left atrium.

Anteroseptum and inferoseptum refer to different segments of the interventricular septum. The inferior wall is visualized better in other views.

This segmental wall nomenclature and identification are described in ASE chamber quantification and stress echocardiography guidelines【12:ASE Chamber Quantification Guidelines†p.90-95】【16:Textbook of Clinical Echocardiography, 6e†p.140-145】.

Pulmonic stenosis is a congenital valve abnormality often seen in genetic syndromes with cardiac manifestations. Among these, Noonan syndrome is the most frequently associated with pulmonic stenosis. Noonan syndrome is a genetic disorder characterized by distinctive facial features, short stature, and congenital heart defects, with pulmonic valve stenosis being the predominant cardiac lesion. The stenosis is usually valvular and caused by dysplastic pulmonary valve leaflets, leading to obstruction of right ventricular outflow.

Other syndromes listed do not typically present with pulmonic stenosis:

Turner syndrome is more commonly linked with bicuspid aortic valve and coarctation of the aorta, not pulmonic stenosis.

Eisenmenger syndrome refers to the advanced phase of congenital heart defects with significant pulmonary hypertension and is not a genetic syndrome.

Marfan syndrome is predominantly associated with aortic root dilation and mitral valve prolapse, but not with pulmonic stenosis.

This association is well documented in adult echocardiography guidelines and texts, such as the "Textbook of Clinical Echocardiography" by Catherine Otto, which clearly identifies Noonan syndrome as the syndrome most commonly associated with pulmonic stenosis among congenital heart defects【16:Chapter on Congenital Heart Disease†Textbook of Clinical Echocardiography, 6e】.

TAPSE measures the longitudinal systolic excursion of the tricuspid annulus towards the apex and is a widely used echocardiographic parameter of right ventricular systolic function. It is not a measure of diastolic function nor an indirect measure of left ventricular function.

TAPSE is relatively angle independent because it is measured in M-mode from the apical four-chamber view aligned with annular motion.

The lower normal limit for TAPSE is generally accepted as 16 mm, but 13 mm is sometimes cited as a threshold below which right ventricular systolic dysfunction is suggested.

This information is presented in the "Textbook of Clinical Echocardiography, 6e", Chapter on Right Ventricular Function Assessment【20:320-325†Textbook of Clinical Echocardiography

Rupture of a papillary muscle leads to acute mitral regurgitation, producing a holosystolic murmur heard throughout systole. This murmur results from backward flow of blood from the left ventricle to the left atrium during systole.

Ejection systolic murmurs are typically due to outflow obstruction like aortic stenosis. Early or late systolic murmurs occur in specific valve lesions but not with papillary muscle rupture.

This is covered in the "Textbook of Clinical Echocardiography, 6e", Chapter on Mitral Valve Disease and Mechanical Complications of Myocardial Infarction【20:430-435†Textbook of Clinical Echocardiography】.