 And one thing we want to discuss when we're talking about a cyanotic heart defect is Eisenmanger syndrome. What's Eisenmanger syndrome? It's essentially a reversal of the shunt in which a left-to-right shunt becomes a right-to-left shunt and we'll discuss in a second how that happens, but basically it's the consequence of a long-standing and uncorrected left-to-right shunt. So any kind of larger AST, BST, or patent ductus arteriosus could lead to Eisenmanger syndrome. And let's discuss the physiology of how this happens because this is really important to understand. We have an example of an atrial septal defect on the right side here. And again, as you'll recall, we have blood flowing down the pressure gradient from the left atrium to the right atrium into the right ventricle and then out through the pulmonary artery. And over time this increased amount of blood flow will lead to increased pressures in the pulmonary artery and eventually these patients will develop a pulmonary hypertension. And in response to the pulmonary hypertension, this right ventricle is pumping so hard against the pulmonary hypertension that it begins to hypertrophy in response. And eventually the pulmonary hypertension will become so bad that actually what will begin to see happen is the path of least resistance is no longer from the right ventricle to the pulmonary artery. It's now from the right ventricle back into the right atrium and into the left atrium. Okay, so the pressure gradient now favors the flow of blood from the right ventricle into the right atrium rather than the from the right atrium into the pulmonary artery. That's how you get Eisenmenger syndrome. And as you can see now, we have a right-to-left shunt rather than a left-to-right shunt. And again, what kind of patients are we going to see this in? It's in someone who's had a uncorrected shunt. So generally this would be a child or a yoga adult that may have had a known heart defect or was never diagnosed with one. And then what kind of symptoms are they going to have? Again, now we're dealing with a right-to-left shunt and that would cause the patient to develop some cyanosis. Again, they have even poor oxygenation of the blood as well. So they're going to have dyspnea. And again, in response to poor O2 saturation, you'll see some clubbing in their digits as well. And again, these patients are going to be evaluated with the echocardiogram. And on their labs, you might see some rethrocytosis. And the reason this happens is, again, you have poor O2 saturation in the blood. But the difference here is that it starts to develop gradually as Eisenmenger syndrome starts to develop. It's a slow process. So the bone marrow will adapt by increasing the production of red blood cells to try to maintain oxygenation of the peripheral tissues. And how do we treat these patients? Again, they're going to have pulmonary hypertension that causes them to develop Eisenmenger syndrome as well. They're going to have some symptoms of bright-sided congestive heart failure. So we can give them diuretics and medications for pulmonary hypertension to manage these symptoms. But eventually, Eisenmenger syndrome has quite a poor prognosis. So a heart transplant is going to be the definitive treatment for most of these patients. And they generally don't have very good outcomes. So this is why it's so important to identify these defects early. That's why we do a good physical exam on newborns, do the appropriate workup. So if there is a defect present, we can catch it and prevent the onset of Eisenmenger syndrome.