VALVES
Stenosis - valve can't open Regurgitation - valve can’t close
The bicuspid valve is a congenital anomaly. A two-valve setup is structurally unsound. After 40 years of microdamage, the valves will have accumulated enough traumatic calcification to obstruct blood flow through the valve.
A note on Aortic Stenosis. The symptoms of aortic stenosis are exertional. “So what,” you may be thinking, “lots of cardiac diseases are exertional.” This may be true, but I want to highlight a pattern here. While angina causes exertional chest pain, and CHF causes exertional dyspnea, Aortic stenosis causes exertional chest pain / dyspnea / lightheadedness / syncope. Activity will cause very dramatic symptoms in AS!
MURMURS
Murmurs are hard. They’re confusing, described poorly in test questions, hard to hear in real life, and examiners love to ask about how certain maneuvers will change the quality of the murmur. That’s a lot of variables to account for, and don’t get me started on the Valsalva maneuver. Here’s the quick and dirty.
Almost all murmurs get louder as blood flow through the heart increases (lying down, elevating their legs). Maneuvers that decrease blood flow through the heart include standing up, hand grips and the Valsalva maneuver. A notable exception to this rule is Hypertrophic Obstructive Cardiomyopathy, because as the heart gets emptier the swollen wall creeps closer to the LV outlet.
All diastolic murmurs are scary. They are also much less common. And actually much harder to hear. All diastolic murmurs require a cardiology workup. In comparison, many systolic murmurs are transient. You will see systolic murmurs in many kids and pregnant women. The high flow murmur is a common phenomenon whenever the blood moves fast enough (anemia, hyperthyroidism, tachycardia).
Focus on the mitral and aortic valve. The right sided valves are pretty low-yield, with the exception of recognizing that IV drug users tend to get right sided endocarditis. And thankfully, Aortic murmurs sound equivalent to Pulmonic murmurs, and mitrals sound like tricuspids.
Murmurs
Gallops
SPLIT HEART SOUNDS
This diagram illustrates the complexity of the mitral valve. Each piece can fail.
RHEUMATIC FEVER
Strep throat’s revenge
Rheumatic Fever is an autoimmune complication that occurs 2 to 4 weeks after a strep throat. The body mistakes the M protein on Streptococcus pyogenes with myosin proteins in the heart. This is a type 2 hypersensitivity.
RheuMATic heart disease affects the Mitral > Aortic >> Tricuspid valves. Here’s the classic case. Early on, the patient develops Mitral regurgitation, and decades later on they develop Mitral stenosis. You diagnose Rheumatic fever based on the presence of anti-Streptolysin O antibodies (ASO) and the J♥NES criteria:
Joint pains that migrate all over the body
♥ (pancarditis)
Nodules in the skin
Erythema marginatum (redness on the margin of the splotchy rash)
Sydenham chorea
Rheumatic fever only occurs when strep throat isn’t treated (with a Penicillin). So Rheumatic fever is uncommon in the US. The patient in the stem will probably be an immigrant.
Rheumatic Fever Pancarditis (affecting all 3 layers). Don’t sweat these histology details, but I included them here if you’re interested.
ENDOCARDITIS
Valve vegetation
Endocarditis is a bacterial infection of the endocardial, almost always involving the valves. Valves are the most fragile piece of the endocardium. Valves occasionally fissure due to movement and high pressure, causing small clots to form. If there’s bacteremia, then the bacteria can latch onto the sticky clots, and set up shop on the valve by coating themselves in a protective biofilm. These vegetations are relatively safe from the WBCs, since the inside of the heart is such a hostile environment. From there, the microbe can set up a permanent home, causing a constant low-grade infection. Endocarditis is the only cause of a fever + new heart murmur. There are a boatload of other symptoms, which are due to septic emboli (see diagram above).
Bacteremia is defined as the presence of bacteria in the blood. If it’s serious, sepsis occurs. If it’s not serious, then the WBCs can immediately clean up the infection (transient bacteremia). Transient bacteremia commonly happens during dental procedures, surgery and IV drug use. The biggest risk factor for endocarditis is having pre-existing valvular disease. The second biggest risk is IV drug use. By introducing bacteremia into the veins, they expose the first valve (Tricuspid) to bacteria.
There are two classic presentations. One is “acute,” the other is “subacute.” Acute (Staph) is much more severe, Subacute (Strep) is insidious and mild.
Strep viridans is the most common cause. Thankfully, it’s low virulence (subacute). It normally lives in the mouth, enters the blood during dental procedures, and only attacks valves that have previously been damaged. It builds small vegetations that don’t damage the valve further.
Staph aureus is the second most common cause. This one is devastating (acute). Staph is found on the skin, enters the blood with IV drug use and attacks both damaged and healthy valves. It builds large vegetations that damage the valve further.
Staph epidermidis is the biggest nosocomial cause. It loves plastic (IV lines, prosthetic valves).
Enterococcus faecalis and Strep bovis are part of the gut flora. But when someone has serious bowel disease (colorectal cancer or UC), these guys can migrate across the gut lining into the blood. Surprisingly high-yield.
The HACEK organisms are gram (-) bugs that don’t grow on traditional blood cultures. They comprise about 2% of all endocarditis infections. They normally live in the mouth. HACEK is an acronym for Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella and Kingella. Low-yield.
Endocarditis is surprisingly hard to diagnose. The gold standard is multiple blood cultures from multiple IV sites drawn at least 30 minutes apart. One of the reasons you go to that much trouble is that most of the relevant bacterial pathogens already live in our body, and are common contaminants for blood cultures in general (e.g., the Staph aureus on the nurse’s skin gets into the culture). Drawing multiple cultures minimizes that risk. They’re drawn from multiple IV sites because staph epidermidis like to live on IV lines. The culture data is considered in conjunction with what you see on the ultrasound of the heart (Duke Criteria).
Treatment - prolonged abx, usually Vancomycin plus or minus some Gram negative coverage. Surprisingly complex topic fyi.
Prevention - people with known valve disease should take a dose of prophylactic Ampicillin before surgery or a dental procedure (some new research is throwing doubt onto this practice).
Libman-Sacks Endocarditis - this is the only major valvular vegetation that is unrelated to infection. Seen with Lupus, and more specifically with Antiphospholipid Syndrome. The Lupus immune complexes deposit in the endocardium. Tends to hit the mitral valve. Interestingly, the vegetation will be on both sides of the leaflet (not seen in bacterial endocarditis).