1. What causes the obstruction in hypertrophic obstructive cardiomyopathy (HOCM)?
ANS: The obstruction is usually caused by the combination of a hypertro-phied septum, which bulges into the LV outflow tract during systole, and an abnormal anterior motion of the anterior leaflet of the mitral valve. The outflow tract, which is the space between the septum and the anterior leaflet of the mitral valve, becomes narrowed when a freely mobile portion of distal mitral valve is pulled toward the septum by a Bernoulli effect.
Note: a. Occasionally, even a distal portion of posterior leaflet can swing forward to cause obstruction to outflow. b. All patients with significant outflow tract obstruction have some MR by Doppler studies. 2. In HOCM, when in systole does the obstruction begin? ANS: Just prior to mid-systole.
3. When does the ejection murmur begin in HOCM?
ANS: The murmur usually begins early because even though the obstruction is delayed to slightly beyond the time of onset of aortic valve opening, the tremendously rapid early ejection characteristic of HOCM can cause early turbulence. In the normal heart only about 50% of ventricular volume is ejected during the first half of systole, but in HOCM 80% or more is ejected during this period .
4. How can raising the blood pressure by a vasopressor agent or by having the patient squat help to differentiate between the ejection murmur of valvular AS and that of HOCM?
ANS: A vasopressor agent will produce a bradycardia by the vagal effect of suddenly raising blood pressure. The bradycardia gives more time for diastolic filling, which will increase the volume and make the murmur of valvular AS louder. However, in HOCM the increase in pressure against the mitral leaflet will push the leaflet away from the septum and decrease the loudness of the murmur.
Normal mean pressure High mean pressure
Normal mean pressure High mean pressure
5. What tends to make an HOCM obstruction worse, making the LV cavity smaller or making it larger? Why?
ANS: Making it smaller allows the hypertrophied septum to obliterate the outflow tract space more easily.
6. How can a Valsalva maneuver help to differentiate the ejection murmur of valvular AS from that of HOCM?
ANS: During the Valsalva maneuver the venous return is decreased, thus decreasing the stroke volume and the ejection murmur of valvular AS.
However, in a patient with HOCM, the decreased venous return produces a smaller LV and therefore more obstruction and a louder murmur.
Note: The Valsalva maneuver may not always work, because the obstruction may already be so severe that the Valsalva maneuver cannot produce any significant increase in obstruction.
7. How can amyl nitrite inhalation differentiate the ejection murmur of valvular AS from that of HOCM?
ANS: The blood pressure will drop immediately with amyl nitrite inhalation, but flow does not increase until about 20 s later. Therefore, the murmur of valvular AS, which is dependent on flow, will not begin to increase for about 20 s. The murmur of HOCM, on the other hand, will become louder within a few beats after inhalation, because as soon as the blood pressure drops (which occurs almost immediately), the loss of resistance to outflow causes a loss of support for the anterior leaflet of the mitral valve as the ventricle contracts. (See Chapter 14 for the hemodynamic effects of amyl nitrite.)
8. How will squatting differentiate between the murmur of HOCM and that of valvular AS?
ANS: Squatting, especially for the first few beats, will diminish the murmur of HOCM because it causes both increased venous return for a few beats and then a persistent increase in peripheral arterial resistance. In the presence of valvular AS, the increase in venous return will tend to increase the murmur.
Note: a. In standing after squatting, the systolic murmur sometimes doubles in intensity. The second or third repetition of squatting and standing may show more changes than first trial of squatting and standing.
b. The physician should sit with the patient standing facing him. The patient should support himself or herself by a hand on the examining bed.
c. In patients unable to squat, similar circulatory changes can be induced by bending the patient's knees on his abdomen while supine.
d. The increased peripheral resistance on squatting is probably due to "kinking" of the femoral arteries as well as some isometric contraction effect.
9. What is peculiar about the site of greatest loudness of the HOCM murmur that may help to differentiate it from the murmur of valvular AS?
ANS: It is usually loudest near the apex, but occasionally it is loudest at the left lower sternal border.
Note: a. When septal hypertrophy is so great that it also produces RV outflow (infundibular) obstruction (rare), the murmur may be louder at the base than elsewhere (as in other forms of pulmonic stenosis). b. The term asymmetric septal hypertrophy of the heart is often used to describe the heart in HOCM because the septum is dispro-portionately hypertrophied in relation to the hypertrophy of the free wall.
10. Why is there usually some MR with HOCM?
ANS: The hypertrophied septum may distort the direction in which the papillary muscles pull on the cusps.
Note: a. Mitral valve prolapse may occur in as many as 75% of patients with HOCM.
b. Occasionally a short apical early to mid-diastolic low-frequency murmur may be heard in HOCM, simulating mitral stenosis.
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