Free ARDMS AE-Adult-Echocardiography Practice Exam with Questions & Answers | Set: 4

Partial anomalous pulmonary venous return (PAPVR) is a congenital defect where some pulmonary veins drain into the right atrium or systemic venous circulation rather than the left atrium. It is frequently associated with sinus venosus atrial septal defect (ASD), a defect near the junction of the superior vena cava and right atrium.

Cleft mitral valve is commonly associated with atrioventricular septal defects. Persistent left superior vena cava is a separate venous anomaly not typically linked with PAPVR. Perimembranous ventricular septal defects are different congenital defects not related to pulmonary venous anomalies.

The association between PAPVR and sinus venosus ASD is well described in the "Textbook of Clinical Echocardiography, 6e", Chapter on Congenital Heart Disease and Shunt Lesions【20:120-130†Textbook of Clinical Echocardiography】

Cardiac catheterization with coronary angiography is considered the gold standard for the assessment and diagnosis of coronary artery disease (CAD). It provides direct visualization of coronary artery luminal stenosis and allows for therapeutic intervention if needed.

While cardiac magnetic resonance imaging (MRI), stress echocardiography, and myocardial perfusion imaging are valuable non-invasive modalities for ischemia detection and functional assessment, none replace the anatomical and interventional capabilities of invasive angiography.

This is well established in the "Textbook of Clinical Echocardiography, 6e", Chapter on Ischemic Heart Disease and Diagnostic Modalities【20:400-405†Textbook of Clinical Echocardiography】.

Sinus of Valsalva aneurysms typically rupture into the right heart chambers, most commonly the right atrium or right ventricle. This creates a left-to-right shunt and can lead to volume overload and heart failure if not treated.

Rupture into the pericardial space is less common and may cause tamponade. Rupture into the left atrium or coronary sinus is rare.

This clinical detail is described in the "Textbook of Clinical Echocardiography, 6e", Chapter on Aortic Root Pathology and Sinus of Valsalva Aneurysms【20:420-425†Textbook of Clinical Echocardiography】.

Systemic blood pressure should be documented during every echocardiogram because blood pressure influences cardiac loading conditions, hemodynamics, and interpretation of valvular lesions and ventricular function.

Blood pressure affects Doppler velocities, gradients across valves, and myocardial performance; therefore, it is essential to record it routinely to interpret echocardiographic findings accurately.

This guideline is stated in the "Textbook of Clinical Echocardiography, 6e", Chapter on Echocardiographic Examination Standards and Reporting【20:15-20†Textbook of Clinical Echocardiography】.

Comprehensive and Detailed Explanation From Exact Extract:

The video shows a parasternal long-axis view of the left ventricle and mitral valve with the anterior leaflet of the mitral valve moving abnormally toward the interventricular septum during systole. This systolic anterior motion (SAM) of the mitral valve is characteristic of hypertrophic obstructive cardiomyopathy (HOCM) and contributes to left ventricular outflow tract obstruction.

Aortic root dilatation and left atrial elongation are structural findings seen in other views. Mid-anteroseptal hypokinesis is a regional wall motion abnormality not clearly visualized in this clip.

This echocardiographic sign is critical in diagnosing and managing HOCM and is discussed extensively in ASE guidelines and clinical echocardiography texts【16:Textbook of Clinical Echocardiography, 6e†p.350-355】【12:ASE Cardiomyopathy Guidelines†p.120-130】.

The echocardiographic images show prominent trabeculations and deep intertrabecular recesses communicating with the left ventricular cavity, best seen on contrast-enhanced images. This finding is characteristic of left ventricular noncompaction (LVNC), a cardiomyopathy resulting from arrested myocardial compaction during embryogenesis.

LVNC is diagnosed by visualizing a two-layered myocardium with a thin compacted epicardial layer and a thicker noncompacted endocardial layer with deep trabecular recesses. The use of contrast echocardiography enhances endocardial border delineation and recess visualization, increasing diagnostic accuracy.

Loeffler syndrome (hypereosinophilic cardiomyopathy) often shows endomyocardial fibrosis and restrictive physiology but not prominent trabeculations. Hypertrophic cardiomyopathy shows asymmetric septal hypertrophy without deep recesses. Ischemic cardiomyopathy shows wall motion abnormalities but not characteristic trabecular patterns.

These diagnostic criteria and imaging features are well documented in the "Textbook of Clinical Echocardiography" and ASE guidelines on cardiomyopathies and use of contrast echo【16:Textbook of Clinical Echocardiography, 6e†Chapter on LV Noncompaction】【12:ASE Contrast Echocardiography Guidelines†p.180-190】.

Comprehensive and Detailed Explanation From Exact Extract:

Pulmonary capillary wedge pressure (PCWP) is obtained by advancing a balloon-tipped catheter into a small branch of the pulmonary artery and inflating the balloon to "wedge" the catheter, thereby occluding forward blood flow and measuring the pressure distal to the occlusion. The measured pressure reflects the pressure in the pulmonary venous system, which closely approximates left atrial pressure (LAP) under normal conditions.

Since the left atrium receives pulmonary venous return before the blood enters the left ventricle, PCWP is a surrogate for LAP, which in turn reflects left ventricular end-diastolic pressure (LVEDP) in the absence of mitral valve disease or pulmonary venous obstruction. PCWP is widely used in clinical and echocardiographic contexts to estimate left heart filling pressures.

It does not estimate right atrial, right ventricular, or left ventricular pressures directly. Right atrial pressure is measured via central venous pressure, right ventricular pressure by catheterization, and left ventricular pressure by direct catheterization.

This concept is extensively discussed in the "Textbook of Clinical Echocardiography, 6e", Chapter on Hemodynamics and Doppler Assessment, with specific emphasis on the use of PCWP to estimate left atrial pressure【20:200-210†Textbook of Clinical Echocardiography】.

The color Doppler jet in the apical four-chamber view is directed posteriorly toward the posterior left atrial wall, indicating a posteriorly directed mitral regurgitant jet.

Jet direction can provide insight into the mechanism of mitral regurgitation; for example, anterior leaflet prolapse often causes a posteriorly directed jet.

This analysis is outlined in the "Textbook of Clinical Echocardiography, 6e", Chapter on Mitral Regurgitation - Jet Direction and Mechanism【20:390-395†Textbook of Clinical Echocardiography】.

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】.

Mitral valve prolapse (MVP) occurs during ventricular contraction (systole). Specifically, during systole, the increased pressure in the left ventricle causes the mitral valve leaflets to billow or prolapse back into the left atrium. This abnormal systolic displacement of the mitral leaflets beyond the annular plane leads to mitral regurgitation in many cases.

The echocardiographic hallmark of MVP is systolic bowing or displacement of the mitral leaflets into the left atrium, best visualized in parasternal long-axis or apical views during ventricular contraction. MVP is not seen during ventricular filling phases such as early filling, atrial systole, or diastasis because the leaflets are normally open or positioned differently.

This is well-documented in the "Textbook of Clinical Echocardiography, 6e", Chapter on Mitral Valve Disease, explaining the pathophysiology of MVP and its timing during the cardiac cycle【20:390-395†Textbook of Clinical Echocardiography】.