Mehl. Cardio Aortic reg/sten; ASD, VSD 04-02 (2) Flashcards
M. Aortic stenosis. What murmur, definition?
Mid-systolic murmur, or just “systolic” murmur; can also be described as “late-peaking systolic murmur with an ejection click.
M. Aortic stenosis. radites to?
Radiates to the carotids. This descriptor shows up quite frequently on NBME (way more than radiation to the axilla for MR).
M. Aortic stenosis. causes what pulse? definition?
Causes slow-rising pulses, aka “pulsus parvus et tardus” (don’t confuse with bounding pulses of AR).
M. Aortic stenosis. SAD - abbreviation?
SAD -> Syncope, Angina, Dyspnea; classic combination seen in AS, albeit not mandatory. If you get a question where they say systolic murmur but you’re not sure of the diagnosis, if they say chest pain or fainting, you know it’s AS.
M. Aortic stenosis. often caused by what?
Often caused by bicuspid aortic valve.
M. Aortic stenosis.
The patient need not have Turner syndrome and often won’t. Bicuspid valve is usually inherited as an autosomal dominant familial condition.
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M. Aortic stenosis. The bicuspid valve need not calcify in middle-age prior to the AS forming.
Bicuspid valve can present with AS murmur in child or high schooler.
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M. Aortic stenosis.
Do aortic valve replacement on 2CK if 1) cross-section of valve is ?
cross-section of valve is <1.0 cm2,
M. Aortic stenosis.
Do aortic valve replacement on 2CK if 2) …?
2) there is SAD = syncope, angina, dyspnea
M. Aortic stenosis.
Do aortic valve replacement on 2CK if 1) cross-section of valve is <1.0 cm2, or 2) there is SAD. They ask both of these as separate Qs where they want valve replacement.
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M. Aortic stenosis.
“Supravalvular aortic stenosis” can occur in …. syndrome?
“Supravalvular aortic stenosis” can occur in Williams syndrome (rare AD disorder with elfin-like facies).
M. Aortic regurgitation. Murmur?
Decrescendo holo-diastolic (pan-diastolic) murmur.
Can also be described as “early diastolic murmur,” or “diastolic murmur loudest after S2.”
M. Aortic regurgitation. what pulse pressure?
Causes wide pulse pressure (i.e., big difference between systolic and diastolic pressures, e.g., 160/50, or 120/40) -> results in head-bobbing and bounding pulses (don’t confuse with slow-rising pulses of aortic stenosis).
M. Aortic regurgitation. CP?
head-bobbing and bounding pulses (don’t confuse with slow-rising pulses of aortic stenosis).
M. Aortic regurgitation.
The bounding pulses can be described on NBME as “brisk upstroke with precipitous downstroke.” In turn, they can just simply say, “the pulses are brisk,” meaning the systolic component is strong.
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M. Aortic regurgitation.
I would say 4/5 times bounding pulses means AR. The other 1/5 will be PDA and AV fistulae (discussed below). Bounding pulses occur when blood quickly leaves the arterial circulation. In AR, the blood quickly collapses out of the aorta back into the LV. In PDA, it leaves the aorta and enters the ductus arteriosus; in AV fistulae, it leaves for a vein.
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M. Aortic regurgitation. what HF?
Can lead to volume overload on the LV and eccentric hypertrophy.
M. Aortic regurgitation. HY cause on usmle?
Highest yield cause on USMLE is aortic dissection -> can retrograde propagate toward the aortic root causing aortic root dilatation and AR.
M. Aortic regurgitation. in what diseases?
Even though MVP is most common in Marfan and Ehlers-Danlos,
AR is second most common in these patients, since if they get aortic dissection, this can lead to AR.
M. Aortic regurgitation.
Peds shelf can give you random 2-year-old with robust decrescendo diastolic murmur (answer = AR). Student says, “What’s causing it though?” Great question. It’s still what shelf will do. You could be aware that congenital bicuspid valve also can cause AR in peds, not just AS.
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M. Atrioventricular septal defect. Seen in what syndrome?
Down syndrome
M. Atrioventricular septal defect.
Between the atrium and ventricle, aka “endocardial cushion defect,” although this latter term can also apply to ASD and VSD in Downs.
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M. Ventricular septal defect. what murmur, where?
Holosystolic (aka pan-systolic) murmur at lower left sternal border.
M. Ventricular septal defect.
Can be associated with a diastolic rumble or enlarged left atrium (if more blood going L->R across VSD, then more blood is returning to the LA from the lungs -> LA dilatation).
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M. Ventricular septal defect. seen as part in what?
Seen as part of tetralogy of Fallot (VSD, RVH, overriding aorta, pulmonic stenosis).
M. Ventricular septal defect.
If a VSD is repaired, USMLE wants arrows LV, RV, LA pressures?
incr. LV pressure
decr. RV pressure
decr. LA pressure
M. Ventricular septal defect. whats about cyanosis?
VSD does not cause cyanosis at birth.
M. Ventricular septal defect.
Only years later after the higher blood flow to the lungs results in pulmonary hypertension, followed by right ventricular hypertrophy and reversal R->L (Eisenmenger) does the patient become cyanotic.
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M. Ventricular septal defect.
Murmur can be silent or soft at birth, followed by loud at 7 days of life.
The USMLE will ask why the murmur is louder now -> answer = decreased pulmonary vascular resistance – i.e., the lungs open up during the first week of life, resulting in decreased RV pressure and an increase in the L -> R pressure gradient (louder murmur).
M. Ventricular septal defect.
Conversely, if they ask why the murmur was softer at birth compared to now, the answer is “increased pulmonary vascular resistance,” where the lungs were still closed at the time, so there was a lesser gradient L->R (softer murmur).
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M. Ventricular septal defect.
Similar to ASD Qs, USMLE loves giving you diagrams with changes in O2 between the chambers and then making you infer we have a VSD.
v. cava sup. ir right atrium 73 proc. -> RV and Pulm artery 85 proc. —> pulm vein. 99 proc. –> LA, LV and aorta 96 proc.
NBME loves this style of Q. You can see O2 somehow increased from RA to RV. The only way this is possible is if we have a VSD where oxygenated blood moves from LVàRV.
M. Ventricular septal defect.
v. cava sup. ir right atrium 73 proc. AND RV and Pulm artery 73 proc. —> pulm vein. 99 proc. –> LA 96 proc. -> LV and aorta 85 proc.
This one might initially appear a little more difficult. This is Eisenmenger syndrome, where we have a reversal of flow from RV->LV across the VSD. The NBME is known to show this diagram as well.
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M. Atrial septal defect. whats about S2?
Fixed splitting of S2
M. Atrial septal defect.
Can sometimes be associated with a systolic flow murmur, since more blood L->R from the LA->RA means more blood flow across the pulmonic valve. So Q might say “fixed splitting of S2 and a systolic murmur.”
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M. Atrial septal defect.
Sometimes can be seen in Qs as “wide, fixed splitting.” I only mention this because some students get pedantic / ask about this. “Wide splitting” just means right ventricular hypertrophy. So if the Q says “wide, fixed splitting,” they’re saying the patient has RVH due to an ASD.
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M. Atrial septal defect.
Patent foramen ovale = ?
ASD on USMLE. Don’t confuse with patent ductus arteriosus (discussed below).
M. Atrial septal defect.
USMLE loves asking questions showing you change in oxygen in the chambers of the heart and making you choose ASD, VSD, etc.
Suop. vena cava 73proc -> RA, RV, Pulm artery 85 proc. -> pulm vein 99 proc. -> LA, LV, aorta 96 proc.
For example, you can see above that somehow O2 increases from the SVC to the RA, which is ordinarily impossible. The only way this could occur is if an ASD is present, where oxygenated blood moved from LA->RA.
M. Aortic regurgitation. ADULTS. When valve replacement?
Valve is replaced if patient has EF <50%, there is significant left ventricular dilatation, or if severe endocarditis has obliterated the valve.
M. Atrial septal defect.
ASDs can sometimes be responsible for “paradoxical emboli,” where a DVT leads to stroke. This is ordinarily impossible, since a clot embolizing to the lungs via the venous circulation has no way of reaching the arterial circulation. But if an ASD is present, the clot can go RA -> LA -> LV -> up to the brain, causing stroke.
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M. Atrial septal defect. Tx?
ASDs do not need to be repaired unless patient has evidence of pulmonary hypertension, RVH, arrhythmia (usually AF), or paradoxical embolus.
M. Ventricular septal defect.
If you’re wondering why oxygen % goes from 99 to 96 from the pulmonary circulation to the LA, this is because of thebesian veins draining the myocardium itself, which open into the different heart chambers, including the LA. If you think that’s weird, take it up with NBME, not me, since they have the 99 to 96 drop-down on their diagrams.
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M. Ventricular septal defect. VSDs are repaired if ?
If patient develops pulmonary hypertension, RVH, arrhythmia, Eisenmenger syndrome, recurrent endocarditis (turbulence of blood due to VSD can incr. risk of valve infections), or aortic regurgitation (if VSD located near the aortic valve).
