HY lecture notes:
Which murmurs are holodiastolic (pandiastolic)? –> aortic regurgitation (aortic insufficiency; AR) + pulmonic regurgitation (pulmonic insufficiency; PR).
Which murmur is pandiastolic and loudest in early-diastole? –> classically AR (decrescendo holodiastolic murmur).
Important initial principle regarding heart murmurs –> all will get worse / more prominent with more volume in the heart, however MVP and HOCM are the odd ones out; they’ll get worse with less volume in the heart.
8F + sickle cell + fever + HR of 120 + normal BP + 2/6 mid-systolic murmur at upper right sternal border; Dx? –> transient, functional high-flow murmur secondary to tachycardia à murmur will subside once HR returns to baseline.
13F + Hb of 7 g/dL + HR of 120 + normal BP + 2/6 mid-systolic murmur at upper right sternal border; Dx? –> once again, transient, functional flow murmur –> I point this out because students often erroneously think there’s some heart abnormality when they see this type of murmur.
Aortic stenosis (AS) – what will you auscultate? –> mid-systolic (crescendo-decrescendo systolic) murmur classically at 2nd intercostal space, right sternal border, with radiation to the carotids; however will also show up as “late-peaking systolic murmur with an ejection click.” –> don’t confuse the latter with “mid-systolic click,” which is mitral valve prolapse (MVP).
Who gets AS? –> classically bicuspid aortic valve –> can be familial autosomal dominant; also seen in Turner syndrome (45XO) –> leads to early calcification of valve in the 40s onward; however a young patient without significant calcification can easily have AS.
What about if the patient doesn’t have bicuspid valve? –> AS can still occur in the general population with normal senile calcification seen typically age 70s-80s onward (i.e., incidental 1/6 or 2/6 mid-systolic murmur in otherwise healthy elderly patient).
If patient is diagnosed with bicuspid aortic valve, next best step in Mx? –> annual transthoracic echos –> if valve cross-sectional area falls below 1.0 cm2 then do aortic valve replacement; there’s a surgery NBME Q where they say cross-sectional area is 0.8 cm2 and the answer is straight-up “aortic valve replacement.”
How does AS classically present Sx-wise? –> SAD à Syncope, Angina, Dyspnea.
AS causes what kind of LVH? –> concentric hypertrophy due to pressure overload –> can also cause hypertrophic cardiomyopathy with an S4 heart sound (stiff LV). This is in contrast to aortic regurgitation (aortic insufficiency), which causes eccentric hypertrophy due to volume overload.
What kind of pulse is seen in AS? –> slow-rising pulse (“pulsus parvus et tardus”). Don’t confuse this with AR, which causes bounding pulses with head-bobbing (Q will often say for AR: “pulse has brisk upstroke with precipitous downstroke.”).
Any weird factoid about AS? –> Heyde syndrome is the combo of AS + angiodysplasia (painless rectal bleeding in elderly due to superficial tortuous vessels on the bowel wall) –> shows up on NBME.
What does HOCM sound like? –> same as AS (mid-systolic murmur, aka crescendo-decrescendo systolic murmur).
What causes HOCM? –> autosomal dominant mutation in beta-myosin heavy-chain gene.
What’s the structural change in the heart with HOCM? –> asymmetric septal hypertrophy that causes the anterior mitral valve leaflet to block off the LV outflow tract under states of lesser preload –> student says, “if the LV outflow tract is blocked off (i.e., where the aortic valve is), why is it the mitral valve leaflet that blocks it off then?” Yeah, I know, it’s weird. But the asymmetric septal hypertrophy causes this to happen.
What’s the cause of death in HOCM? –> ventricular fibrillation (really HY!!) –> the “sudden death in young athlete” is not due to an MI –> i.e., the patient has clean coronary arteries –> do not select coronary artery occlusion as the answer.
What about if the vignette is sudden death in middle-aged patient with heart disease? –> answer = ischemic heart disease (MI), not HOCM.
18M athlete + 2/6 mid-systolic murmur at right sternal border 2nd intercostal space + there is paradoxical splitting of S2 + there is no change in the murmur with Valsalva; Dx? –> ”bicuspid aortic valve” (AS), not HOCM –> students say “oh em gee young athlete! HOCM!” –> the USMLE will slam you on this and wants you to know that the key way to distinguish between AS and HOCM murmurs is that HOCM gets worse with lower volume in the heart; AS will soften or there will be no change. Don’t just automatically jump on HOCM because it’s a young athlete.
How to Tx HOCM –> can give propranolol to keep HR from getting too fast (the slower the HR, the more time the heart spends in diastole –> more diastolic filling –> greater preload –> less occlusion of LV outflow tract) –> should be noted tangentially that although beta-blockers increase preload, they decrease chronotropy + inotropy so the net effect is still decreased myocardial oxygen demand.
Can you explain “splitting of S2”? What does that even mean? –> the aortic valve normally shuts (A2) just before the pulmonic valve (P2), so A2 will occur slightly before P2 –> when we talk about changes in splitting of the S2 heart sound (i.e., wide splitting, paradoxical splitting, etc.), if pressure in a ventricle is greater, the sound will occur later / is protracted. So if RV pressure becomes greater for whatever reason –> P2 occurs later –> wider splitting. So pulmonary artery hypertension = wide-splitting. If LV pressure becomes greater –> A2 occurs later, and can even occur after P2 –> paradoxical splitting. So LVH = paradoxical splitting. When R or L ventricular pressure exceeds the pulmonic arterial and aortic pressure, respectively, the valves open. Then the ventricle will lose pressure as blood ejects, followed by isovolumetric relaxation marking the onset of diastole, and the pressure within the ventricle falls below the pressure distal to the valve –> valve shuts. Normally splitting oscillates with the respiratory cycle. Inhalation causes P2 to occur later –> decrease in intrathoracic pressure –> increased venous return to right atrium –> more blood in right ventricle –> more preload à more pressure –> time it takes for RV pressure to fall below pulmonic arterial pressure is greater –> P2 will occur slightly later with inhalation. With exhalation it’s the opposite. P2 occurs slightly sooner because increased intrathoracic pressure will attenuate venous return –> less preload in RV à less pressure in RV –> time it takes for RV pressure to fall below pulmonic arterial pressure is less –> pulmonic valve closes slightly sooner –> distance between A2 and P2 is less.
What is fixed splitting of S2? –> Super HY for atrial septal defect (ASD) –> sometimes can be written as “wide, fixed splitting of S2” –> it’s not the “wide” that matters; you need to remember fixed splitting.
What does “splitting of S1 mean”? –> highly unlikely to show up on the USMLE, don’t worry, but for the sake of some people who’d ask, it’s usually seen in right bundle branch block (BBB), which causes delayed closure of the tricuspid valve.
Maneuvers that decrease blood in the heart –> Valsalva; standing up from seated position; sitting up from supine position; administration of nitrates –> any of these will cause MVP + HOCM to get worse; all other murmurs will soften or not change.
Maneuvers that increase blood in the heart –> Lying down; leg raise while supine; squatting; hand-grip.
How does Valsalva decrease blood in the heart? –> attempted exhalation against a closed glottis –> robust increase in intrathoracic pressure –> decreased venous return –> decreased cardiac preload.
How do nitrates decrease blood in the heart? –> if administered venously –> increased venodilatation + venous pooling –> decreased venous return to the heart –> decreased cardiac preload. If administered arterially –> decreased afterload –> easier for the LV to eject blood –> decreased blood in the LV; it should be noted that it would be incorrect to say arterial nitrates decrease preload; this is an indirect effect in this case.
How does hand-grip increase blood in the heart? –> hand-grip increases afterload –> LV cannot eject blood as readily –> greater volume of blood left in the LV; it should be pointed out, however, that it would be incorrect to say hand-grip increases preload, as this effect is indirect.
How does respiration relate to left- vs right-sided murmurs –> inspiration makes right-sided murmurs worse; exhalation makes left-sided murmurs worse.
Why does inspiration make right-sided murmurs worse? –> inspiration –> decreased intrathoracic pressure –> easier for blood to return to the RA –> increased venous return –> more preload in right heart –> worsening of TR, TS, PR, PS.
Why does inspiration soften left-sided murmurs? –> decreased intrathoracic pressure –> increased pulmonary vascular compliance –> transient decrease in pulmonary venous return to the LA –> decreased LA preload; it should be noted that although RA preload increases, this effect does not carry over to the LA because of pulmonary vascular pooling.
Why does expiration soften right-sided murmurs? –> expiration –> increased intrathoracic pressure –> harder for blood to return to the RA –> decreased venous return –> less preload in right heart –> softening of TR, TS, PR, PS.
Why does expiration intensify left-sided murmurs? –> expiration –> increased intrathoracic pressure –> decreased pulmonary vascular compliance –> transient increase in pulmonary venous return to the LA –> increased LA preload; it should be noted that although RA preload decreases, this effect does not carry over to the LA because of pulmonary vascular compression.
