HY lecture notes:
Atrial septal defect (ASD) you’d hear wide, fixed splitting of S2. Usually due to patent foramen ovale.
S2 denotes the closure of the semilunar valves (aortic + pulmonic) and the onset of diastole. A2 normally closes 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 = 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 –> 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.
When you’ve got an ASD, blood is constantly moving L –> R from LA –> RA (pressure is always greater on the left side). So the effects of inhalation/exhalation are minimized in terms of the A2-P2 split bc you’ll always have more right-sided preload. This causes a wide, fixed-splitting.
Bottom line is “fixed splitting of S2” is exceedingly HY for ASD. If you memorize it as “wide, fixed splitting,” that’s okay too, but for the USMLE only the fixed part matters.
Bicuspid aortic valve is autosomal dominant and is the most important cause of aortic stenosis (AS) in the population. Valve should normally have three leaflets. Will calcify in middle age as opposed to elderly age, leading to stenosis. But can also easily cause AS in young patients.
Bc it’s AD and runs in families, do transthoracic echo (TTE) to diagnose. If present, monitor with yearly TTE. If cross-sectional area falls below 1.0cm2, do aortic valve replacement. One of the NBME surgery questions had 0.8 as the cross-sectional area, and the answer was aortic valve replacement, so this isn’t just some pedantic detail I’m romanticizing.
AS and hypertrophic obstructive cardiomyopathy (HOCM) are both crescendo-decrescendo systolic (aka mid-systolic) murmurs auscultated best over the second intercostal space, right sternal border. USMLE wants you to know how to differentiate.
HOCM and MVP (mitral valve prolapse) are the two murmurs that get worse with LESS volume in the heart; all other murmurs get worse with more volume in the heart.
So if you do a clinical maneuver that decreases volume (Valsalva, going from supine to sitting/standing, nitrate administration), HOCM should get worse, and AS better or no change.
If you do a clinical maneuver that increases volume (lying down, squatting, leg raise while supine, hand grip), HOCM should get better / no change, and AS worse. (Hand grip actually increases afterload, which then prevents ejection of blood, which in turn actually keeps more blood in the heart; but using the word “preload” to describe hand grip’s effect on keeping volume in the heart would be misleading and inaccurate.)
The USMLE will slam you on this. They’re going to say young athlete (“oh em gee, sudden death in young athlete = HOCM!”), who has a 2/6 mid-systolic murmur, and then they’ll tell you that there’s no change with Valsalva maneuver.
If there’s no change with Valsalva, then that’s AS, not HOCM. The answer would simply be “bicuspid aortic valve,” as they expect you to know that’s synonymous with AS. And once again, you don’t need to be older with a calcific valve for it to cause AS.
Myxomatous degeneration of mitral valve = mitral valve prolapse on the USMLE. It’s a type of connective tissue degeneration, seen classically in Marfan and Ehlers-Danlos syndromes.
Don’t confuse myxomatous degeneration with atrial myxoma, which is usually an adult-onset heart tumor that will cause a “ball-in-valve” murmur effect. That is, they’ll say there’s a diastolic rumble that disappears when the patient is positioned in an unusual way, e.g., lying down on his or her right side. Kids with tuberous sclerosis get cardiac rhabdomyoma, not myxoma.
Carney complex can cause myxoma in kids = perioral melanosis (hyperpigmentation around the lips), endocrine hypersecretion (usually granular, bilateral zona fasciculata hyperplasia leading to Cushing syndrome, but can be hyperthyroidism or acromegaly), and cardiac myxoma (not rhabdomyoma). I promise this is on the USMLE as low-yield as that sounds. No USMLE resource mentions it. But I’m mentioning it.
Remember, MVP gets WORSE with less volume in the heart (same as HOCM). MVP = mid-systolic click.
You can also get an “ejection click” sometimes with aortic stenosis. Or they’ll say a “late-peaking” systolic murmur. But most of the time, you’ll see just mid-systolic murmur for AS.
MVP is most common murmur in the population overall and is usually just a benign, incidental finding in otherwise healthy people.
Mitral valve prolapse syndrome = “fleeting” and sharp left-sided chest pain that will occur in people teens to 30s, and they’ll have many episodes (i.e., at least 30) in their history. You don’t treat it generally, even when symptomatic. This was a question on one of the 2CK NBMEs somewhere, where you’d think you’d give propranolol to slow heart rate and increase diastolic filling, but the answer was no Tx necessary.
Rheumatic heart disease (rheumatic fever, RF) causes mitral regurg (MR) acutely but mitral stenosis (MS) later in life.
Almost all mitral stenoses are due to previous rheumatic heart disease. But when the infection with S. pyogenes (Group A Strep) actually occurs, it’s MR, not MS.
MR = holosystolic murmur at the 4th intercostal space, left-midclavicular line, with radiation to the axilla; but USMLE can just as easily say left sternal border, or not even mention radiation.
MS = opening snap with a mid-late diastolic descrescendo rumble; same location as MR without the radiation.
Rheumatic heart disease = JONES = joints (polyarthritis), O (supposed to look like the heart; carditis); nodules (subcutaneous); erythema marginatum (not multiforme, which is instead caused by drugs or infection); Sydenham chorea (abnormal movements).
Caused by S. pyogenes M-protein. Immune system makes antibodies against it, which cross-react with mitral valve (molecular mimicry; type II hypersensitivity).
12-year-old, sore throat, salmon maculopapular body rash + strawberry tongue = Scarlet fever = give penicillin to prevent RF.
If this 12-year-old gets a murmur, answer = MR, not MS.
But ten years later, answer is MS, not MR.
MS often shows up in pregnancy. Increased preload by second trimester (plasma volume expands >50%) hits threshold by which MS becomes symptomatic and dyspnea occurs. In contrast, dyspnea usually later in pregnancy, circa parturition, is peripartum cardiomyopathy, which is antibody mediated. But just making a point that MS both in real life and on the USMLE will often surface in pregnancy in second trimester.
MS can rarely be seen in situations like Libman-Sack endocarditis in SLE causing anti-phospholipid syndrome secondary to lupus anticoagulant. But once again, almost all MS is due to previous RF.
RF will never occur following skin infection (e.g., impetigo, cellulitis, erysipelas), but instead will occur following Strep pharyngitis. Post-streptococcal glomerulonephritis (type III hypersensitivity) frequently occurs following Strep skin infections however. Treat skin with oral dicloxacillin or oral cephalexin for cellulitis and erysipelas. Use topical mupirocin for impetigo. Orals can be used for impetigo, but topical is first-line.
