Mitral Regurgitation

Think of the mitral valve like a one-way door between the left atrium (LA) and left ventricle (LV). During systole, the LV squeezes and that door is supposed to snap shut, forcing all the blood out through the aorta. In mitral regurgitationRegurgitation = backward flow. The valve does not seal, so blood leaks backward into the LA instead of forward to the aorta during every heartbeat., the door does not close properly. Every squeeze of the LV sends some blood backward into the LA instead of forward into the body.

The result: the LV has to pump the same blood twice. Over time this volume overload stretches the LV and LA. The LA dilates. A dilated LA is a chaotic electrical nightmare, which is exactly how AFib sets up camp.

Because the LV ejects blood in two directions (aorta plus back into LA), the ejection fractionEF = stroke volume divided by end-diastolic volume. In MR, EF is falsely elevated because the LV ejects into both the aorta AND the LA. An EF of 55% in MR is actually worse than it sounds. looks falsely preserved for a long time. This is the sneakiest thing about chronic MR: the patient can be asymptomatic with a "normal" EF of 60% while the LV is quietly decompensating.

Here is why MR is holosystolic (meaning it runs all the way from S1 to S2 without a break): as soon as systole starts, the LV pressure shoots above LA pressure. Since the mitral valve does not close properly, blood starts leaking backward immediately at the start of systole and keeps leaking until the aortic valve closes at S2. The pressure gradient between LV and LA exists for the entire duration of systole, so the murmur fills the entire window.

Contrast this with aortic stenosis, which only gets loud once the LV builds enough pressure to force blood through the narrowed aortic valve, creating a crescendo-decrescendo (diamond) shape.

Radiation: MR radiates to the left axilla (and sometimes the back) because the regurgitant jet squirts backward and lateral, following the direction of the jet. It does NOT radiate to the carotids (that is AS).

Intensity: Graded 1 through 6. Grade 4 and above has a palpable thrill. S3 gallopS3 = a third heart sound in early diastole. In MR, so much blood rushes from the overfilled LA into the LV that it causes a low-pitched thud. S3 in MR = volume overload is severe. is often heard in significant MR because a huge volume of blood rushes from the overfilled LA into the LV in early diastole.

LA dilation is not just a size problem. A stretched left atrium becomes electrically chaotic. Think of a guitar string: when it is tuned to the right tension, it vibrates at one clean frequency. Stretch it unevenly and it produces noise instead of notes. The LA works the same way. Stretch the walls enough and the electrical signals that coordinate atrial contraction become a disorganized mess, and AFibAtrial fibrillation: loss of coordinated atrial contraction. The atria quiver uselessly while the AV node lets through irregular impulses to the ventricles. Results in irregular pulse, reduced cardiac output, and thrombus risk. sets in.

Once AFib is present, things get worse fast. Without coordinated atrial kick, the LV loses the "last top-off" of blood before systole, reducing preloadPreload = the volume of blood in the LV at the end of diastole. Atrial kick contributes about 20% of LV filling. In AFib, this is lost. In MR, the LV is already volume-overloaded, so this loss matters less initially but accelerates decompensation. by about 20%.

The dilated LA also creates a clot factory: stagnant blood pools in the appendage, forms thrombus, and that thrombus can embolize to the brain. AFib in MR means anticoagulation conversation is required.

Acute MR is like suddenly punching a hole in a water pipe. The water (blood) has nowhere to go but back into the LA, which has not had time to stretch. Pressure skyrockets. Pulmonary edema follows within hours. This patient is crashing and needs emergency surgery.

Chronic MR is like a slow, small leak in the same pipe. The LA gradually enlarges over years, accommodating more and more volume without raising pressure dramatically. The patient is asymptomatic for a long time. The LV undergoes eccentric hypertrophy, meaning it adds sarcomeres in series (gets bigger in volume capacity, not wall thickness), to handle the extra load. Eventually, even this adaptation fails.

In chronic MR, the LV handles a constantly elevated end-diastolic volume. To cope, it undergoes eccentric hypertrophy: sarcomeres are added in series (lengthened), which increases chamber size without proportionally thickening the wall. The LV becomes a big, stretchy, compliant chamber that can hold more blood without a dramatic rise in filling pressures.

This sounds like a win. But there is a critical threshold: when the LV begins to decompensate, the EF falls below 60% (remember, in MR the EF is inflated because the LV ejects into the low-resistance LA, so 60% in MR is actually like 50% in a normal heart) and the left ventricular end-systolic diameter (LVESD) exceeds 40mm. Once these thresholds are crossed, surgery must happen before irreversible LV dysfunction sets in.