Echocardiography Board Review: 500 Multiple Choice Questions With Discussion

Chapter 11

Questions

1.  201. Principal determinants of LV end systolic circumferential wall stress include all of the following except:

1.  A. Left ventricular (LV) end systolic dimension

2.  B. Left ventricular (LV) end systolic pressure

3.  C. Left ventricular (LV) systolic wall thickness

4.  D. Left ventricular (LV) pressure at mitral valve closure

2.  202. Increase in LV end systolic wall stress is likely to reduce all of the following except:

1.  A. Ejection fraction

2.  B. Fractional shortening

3.  C. Velocity of circumferential shortening

4.  D. LV positive dp/dt

3.  203. The response of LV end systolic volume to an increase in LV end systolic wall stress would be:

1.  A. An increase

2.  B. A decrease

3.  C. No change

4.  204. In a person with LV dysfunction, compared to a normal individual, a graph showing end systolic wall stress (ESWS) on the x-axis and end systolic volume (ESV) on the y-axis, would be:

1.  A. Steeper

2.  B. Flatter

3.  C. None of the above

5.  205. In response to dobutamine infusion, the ESV–ESWS curve will shift:

1.  A. Down

2.  B. Upward

3.  C. No shift

6.  206. The factor least likely to affect the mitral E/A ratio is:

1.  A. Tau

2.  B. Modulus of LV chamber stiffness

3.  C. Left atrial pressure

4.  D. LV elastic recoil

5.  E. Cardioversion for atrial fibrillation performed 2 h ago

6.  F. Pulmonary artery pressure

7.  207. Factors affecting LV isovolumic relaxation time (IVRT) are all of the following except:

1.  A. Tau

2.  B. Left atrial pressure

3.  C. Heart rate

4.  D. Moderate aortic regurgitation

8.  208. The factor least likely to diminish mitral A-wave amplitude is:

1.  A. Recent cardioversion

2.  B. Myopathic left atrium

3.  C. An acute rise in LV end diastolic pressure

4.  D. Severe aortic stenosis with mild LV hypertrophy and normal LV ejection fraction

9.  209. Both high left atrial (LA) pressure and atrial mechanical failure result in a high E/A ratio. The following is least likely to help in the differential diagnosis in this situation:

1.  A. E-wave deceleration time

2.  B. Amplitude and duration of AR-wave

3.  C. Pulmonary vein S/D time velocity integral ratio

4.  D. Mitral annular velocity with tissue Doppler imaging

10. 210. Which of the changes are least likely to occur in a patient with acute severe aortic regurgitation:

1.  A. Reduction of A-wave amplitude

2.  B. Premature presystolic closure of the mitral valve

3.  C. Diastolic mitral regurgitation

4.  D. Increased amplitude and duration of pulmonary AR-wave

5.  E. A decrease in mitral Em-wave amplitude

11. 211. A late peaking systolic velocity signal is found in which of the following conditions?

1.  A. Mitral valve prolapse causing late systolic mitral regurgitation (MR)

2.  B. MR due to systolic anterior motion of the mitral leaflet

3.  C. LV cavity obliteration

4.  D. Acute severe MR

12. 212. The following condition causes a reduction in the acceleration time of pulmonary arterial flow:

1.  A. Pulmonary stenosis

2.  B. Pulmonary hypertension

3.  C. Dilated pulmonary artery

4.  D. Right ventricular (RV) dysfunction

13. 213. Increased respirophasic variations in transvalvular flows may occur in all of the following conditions except:

1.  A. Status asthmaticus

2.  B. Constrictive pericarditis

3.  C. Cardiac tamponade

4.  D. A large RV infarct

5.  E. Hypovolemic shock

14. 214. Intrapericardial pressure is increased in all of the following conditions except:

1.  A. Cardiac tamponade

2.  B. Acute massive pulmonary embolism

3.  C. Acute traumatic rupture of tricuspid valve, causing acute tricuspid regurgitation

4.  D. Acute RV infarct

5.  E. Severe aortic stenosis with normal LV function

15. 215. A patient with a St. Jude mitral valve no. 29 has a mean diastolic gradient of 3 mmHg and a pressure half-time of 70 ms at a heart rate of 70 beats/min. This is consistent with:

1.  A. Normal prosthetic valve function

2.  B. Prosthetic valve thrombosis

3.  C. Significant pannus growth

4.  D. Severe MR

16. 216. A patient with a St. Jude mitral prosthetic valve no. 29 has a mean diastolic gradient of 7 mmHg at a heart rate of 70 beats/min and a pressure half-time of 30 ms. This is consistent with:

1.  A. Normal prosthetic valve function

2.  B. Prosthetic valve thrombosis

3.  C. Significant pannus growth

4.  D. Severe MR

17. 217. A patient with prosthetic mitral valve no. 29 has a mean diastolic gradient of 10 mmHg at a heart rate of 70 beats /min and a pressure half-time of 200 ms. This is consistent with:

1.  A. Normal prosthetic valve function

2.  B. Prosthetic mitral valve stenosis

3.  C. Severe anemia with high output failure

4.  D. Severe MR

18. 218. The A2–OS snap interval corresponds to:

1.  A. Isovolumic relaxation time

2.  B. Isovolumic contraction time

3.  C. Pre-ejection period

4.  D. All of the above

19. 219. In a patient with mitral valve stenosis, the A2–OS interval may be shortened by all of the following except:

1.  A. Severe mitral stenosis

2.  B. Severe MR

3.  C. Tachycardia

4.  D. Abnormal LV relaxation

20. 220. An abnormal LV relaxation pattern is consistent with:

1.  A. Mean LA pressure of 10 mmHg and LV end diastolic pressure (LVEDP) of 22 mmHg

2.  B. Mean LA pressure of 22 mmHg and LVEDP of 10 mmHg

3.  C. Mean LA pressure of 10 mmHg and LVEDP of 12 mmHg

4.  D. Mean LA pressure of 28 mmHg and LVEDP of 30 mmHg

5.  E. Mean LA pressure of 28 mmHg and LVEDP of 40 mmHg

Answers for chapter 11

1.  201. Answer: D.

Systolic wall stress is the force that myocardial fibers have to overcome in order to affect circumferential shortening. It is proportional to LV size and intracavity pressure and inversely proportional to wall thickness. There are three types of wall stresses operating on the myocardium. These are circumferential, radial, and meridional.

2.  202. Answer: D.

The first three measures are afterload dependent and positive dp/dt is preload dependent. LV end systolic wall stress (ESWS) is a good measure of afterload, whereas LV end diastolic wall stress is a good measure of preload.

3.  203. Answer: A.

An increase. ESWS/ESV is a good load-independent measure of LV systolic performance; a decrease suggests reduced performance, as this indicates a larger ESV for a given ESWS.

4.  204. Answer: A.

An increment in ESV in response to an increase in ESWS is greater in a person with LV dysfunction, making this relationship steeper. Contractile responses to changes in afterload may also be studied by using ejection fraction or fractional shortening in place of ESV. However, the response will be in the opposite direction. Also, noninvasively derived LV end systolic pressure (from cuff pressure and carotid pulse tracing) is a reasonable surrogate for ESWS.

5.  205. Answer: A.

Dobutamine brings out the LV contractile reserve, causing a reduction in LV end systolic volume for a given ESWS.

6.  206. Answer: F.

Tau is an invasive measure of LV relaxation, impairment of which will reduce the E/A ratio. Modulus of LV chamber stiffness is a measure of LV late diastolic stiffness. This affects the A-wave amplitude. High LA pressure increases the E-wave amplitude. Increased elastic recoil as it occurs in a hypercontractile state increases the E-wave amplitude through a suction effect. Atrial mechanical failure is common after cardioversion for atrial fibrillation and may take 1–20 days for full recovery.

7.  207. Answer: D.

Impaired relaxation prolongs IVRT through slowing the LV pressure decay between aortic valve closure and mitral valve opening. High LA pressure and a large left atrial V-wave will result in earlier opening of the mitral valve at a higher pressure. Fast heart rate diminishes IVRT partly through an improvement of LV relaxation.

8.  208. Answer: D.

Myopathic atrium and recent cardioversion result in reduced A-wave amplitude due to reduced atrial mechanical function. Acute rise in LVEDP results in an acute increase in atrial afterload, diminishing its ejection function, just like any other pumping chamber. Atrial output during its contraction depends upon its preload, afterload, and contractility. In aortic stenosis with LV hypertrophy due to abnormal relaxation, there is reduced early LV filling and a compensatory increase in contribution from left atrial contraction.

9.  209. Answer: C.

High LA pressure results in short IVRT, reduced E-wave deceleration time, and an increase in pulmonary vein AR-wave duration and amplitude. Mitral E/mitral annular Em ratio is a good indicator of LA pressure. Atrial mechanical failure results in diminution of pulmonary AR reversal and absence of atrial relaxation, which causes a left atrial suction effect and will result in diminution of S-wave amplitude. The S-wave amplitude is diminished in high LA pressure due to increased LA operating stiffness during LV systole, when there is no LA emptying.

10. 210. Answer: E.

Acute atrial regurgitation causes a rapid increase in LV end diastolic pressure, diminishing A-wave amplitude, or eliminating it due to acutely increased atrial afterload. This may also prematurely close the mitral valve. Atrial contraction on a closed mitral valve will result in exaggerated flow reversal in the pulmonary vein during atrial contraction. None of these phenomena directly affect early diastolic LV mechanics, LV relaxation, or early diastolic LV lengthening (Em-wave).

11. 211. Answer: C.

Causes flow acceleration in late systole due to a severe reduction in flow area that occurs in end systole. Although in mitral valve prolapse and hypertrophic obstructive cardiomyopathy the regurgitant volume may be more towards end systole, the shape of the signal is dictated only by the LV–LA pressure gradient and not by the volume of MR. The LV–LA pressure gradient tends to be maximum in early to midsystole. In acute severe MR, a large V-wave causes late systolic deceleration of the signal, a so-called “V-wave cutoff sign.”

12. 212. Answer: B.

This is thought to be because of faster return of the reflected pressure waves because of increased operative stiffness of the pulmonary arterial tree, which causes early deceleration of the flow.

13. 213. Answer: E.

In status asthmaticus, exaggerated respiratory variation in intrapleural pressures causes marked variation in venous returns both to the right and left heart during the respiratory cycle. In constriction and tamponade, there is exaggerated interventricular interaction due to septal shifts during respiration, causing an exaggeration of normal flow variations across the valves during the respiratory cycle. RV infarct causes acute RV dilation and invokes pericardial constraint and physiology similar to constrictive pericarditis.

14. 214. Answer: E.

In addition to pericardial fluid accumulation, any phenomenon that acutely increases the intrapericardial volume invokes pericardial constraint and hence elevation of the intrapericardial pressure. Massive pulmonary embolus and RV infarct cause acute RV dilation. Any acute regurgitant lesion causes acute chamber dilation and hence invokes pericardial constraint. Intrapericardial pressure also increases when intrapleural pressure is increased as in PEEP and tension pneumothorax.

15. 215. Answer: A.

Both the mean gradient and pressure half-time are useful in assessing and monitoring prosthetic mitral valve function.

16. 216. Answer: D.

Reduced pressure half-time is suggestive of high LA pressure, and an increased gradient at a normal heart rate is suggestive of an increased flow across the mitral valve; this combination is highly suggestive of mitral regurgitation.

17. 217. Answer: B.

Stenotic prosthetic valve hemodynamics is similar to native mitral valve stenosis. An increase in gradient is accompanied by an increase in pressure half-time, indicating reduced effective orifice area. High output causes an increase in gradient with a normal or reduced pressure half-time depending upon left atrial pressure.

18. 218. Answer: A.

IVRT is the interval between the aortic component of the second heart sound and mitral valve opening.

19. 219. Answer: D.

High left atrial pressure that occurs in mitral stenosis or MR will cause earlier opening of the mitral valve, thus causing a shortening of the A2–OS interval. Tachycardia improves LV relaxation and shortens this interval. Abnormal LV relaxation, by reducing the rate of pressure decay between aortic valve closure and mitral valve opening, would lengthen this interval.

20. 220. Answer: A.

Abnormal relaxation generally has normal LA pressure but an elevated LVEDP because of a combination of increased contribution of LV filling during atrial systole and possibly increased LV late diastolic stiffness by the same process that caused abnormal LV relaxation. Very high mean LA pressures result in pseudonormal or restrictive LV filling patterns.