Changed AE-Adult-Echocardiography Exam Questions

The proximal isovelocity surface area (PISA) method estimates the effective regurgitant orifice area (EROA) in mitral regurgitation by measuring the radius of the hemispheric flow convergence region (aliasing radius) and incorporating the aliasing velocity and the peak velocity of the MR jet.

The equation for EROA is:

EROA = (2π × r² × Va) / Vmax

Where:

r = radius of the PISA hemisphere (aliasing radius)

Va = aliasing velocity (the velocity at which color aliasing occurs)

Vmax = peak MR velocity obtained by continuous wave Doppler

This calculation does not involve the mitral annular diameter, time velocity integral of mitral annulus, or left ventricular outflow tract diameter.

Thus, the third necessary parameter after aliasing radius and velocity is the maximum MR velocity measured by continuous wave Doppler, which allows determination of flow rate through the regurgitant orifice.

This formula and its clinical application are well established in adult echocardiography literature and ASE valvular regurgitation guidelines【12:ASE Valvular Regurgitation Guidelines†p.210-220】【16:Textbook of Clinical Echocardiography, 6e†Chapter on Mitral Regurgitation Assessment】.

Comprehensive and Detailed Explanation From Exact Extract:

The left ventricular dP/dt is a measure of the rate of rise in left ventricular pressure during isovolumic contraction, which reflects systolic function. It is derived from Doppler echocardiography by measuring the time interval between mitral regurgitant jet velocities of 1 m/s and 3 m/s. Using the simplified Bernoulli equation, the pressure gradient at each velocity is calculated, and the rate of pressure rise (dP/dt) is calculated by dividing the pressure difference by the time interval between these velocities.

A normal left ventricular dP/dt is generally considered to be greater than 1200 mmHg/s. Values lower than this indicate impaired systolic function, as the ventricle is slower to generate pressure during contraction.

For example, a measured time interval of 36 milliseconds (0.036 seconds) between the MR velocities of 1 and 3 m/s corresponds to a dP/dt of approximately 889 mmHg/s, which is mildly reduced, indicating some systolic dysfunction.

The exact extract from the "Textbook of Clinical Echocardiography, 6e" states that normal dP/dt values are typically above 1000 mmHg/s, with >1200 mmHg/s considered a robust indicator of normal systolic function. This measure is useful but requires a measurable mitral regurgitation jet and consistent alignment of the ultrasound beam. Variability in measurement can occur based on technical factors, but the dP/dt remains a useful parameter to quantify systolic function noninvasively.

Comprehensive and Detailed Explanation From Exact Extract:

Constrictive pericarditis is characterized by thickening and fibrosis of the pericardium which restricts diastolic filling of the ventricles. Key echocardiographic features include a characteristic interventricular septal "bounce" or shift during early diastole due to the abrupt cessation of ventricular filling imposed by the rigid pericardium. This septal bounce reflects rapid early diastolic filling followed by a sudden halt as filling pressures equalize, a hallmark of constriction physiology.

Additionally, Doppler studies show marked respiratory variation in mitral and tricuspid inflow velocities (>25%), with an inspiratory increase in tricuspid inflow and a decrease in mitral inflow velocity, reflecting ventricular interdependence caused by the noncompliant pericardium. The mitral inflow typically shows a large E-wave with a small or absent A-wave and a steep deceleration slope, but importantly these velocities vary significantly with respiration, which is not the case in restrictive cardiomyopathy.

Hepatic vein Doppler often reveals a prominent a-wave and a deep y-descent with increased diastolic flow reversal during expiration, indicating elevated right atrial pressures and constrictive physiology.

The inferior vena cava (IVC) is usually dilated and shows no inspiratory collapse (i.e., no normal collapse with sniff test) because of elevated right atrial pressure and impaired venous return.

Therefore:

Option A is incorrect because mitral inflow in constrictive pericarditis shows significant respiratory variation, not absence of it.

Option B is incorrect because the hepatic vein is typically dilated with abnormal flow patterns, not normal size.

Option C is incorrect because the IVC is dilated and does NOT collapse normally with inspiration/sniff in constrictive pericarditis.

Option D is correct because the interventricular septal bounce is a classic feature reflecting ventricular interdependence and constrictive physiology.

These findings are summarized in the "Textbook of Clinical Echocardiography, 6e" (Catherine M. Otto, MD), Chapter 10 (Pericardial Disease), pages 280–285, with key illustrations showing septal bounce, Doppler inflow variations, hepatic vein flow patterns, and IVC findings in constrictive pericarditis. The "Mayo Clinic criteria" for echocardiographic diagnosis also emphasize ventricular septal shift as a critical feature, often combined with tissue Doppler annular velocity patterns and hepatic vein diastolic flow reversal for high diagnostic accuracy.

Comprehensive and Detailed Explanation From Exact Extract:

A continuous murmur is a heart murmur that occurs throughout both systole and diastole. Among the options, a ruptured sinus of Valsalva aneurysm produces a continuous murmur due to persistent flow between the aorta and a cardiac chamber (usually the right atrium or ventricle) during both systole and diastole.

Aortic regurgitation causes a diastolic murmur, mitral stenosis causes a diastolic murmur, and a muscular ventricular septal defect typically causes a holosystolic murmur but not continuous.

Ruptured sinus of Valsalva aneurysm causes a continuous shunting of blood, resulting in the characteristic continuous murmur, often described as “machinery-like.”

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