 First step is the four chamber view. Of course, for the purists, they will argue with me that there is something else before you even look at the heart, that is the abdominal siteus. Yes, I of course do that and we should do that, but I am just talking from a very, very basic perspective of a lot of people who are listening to me who can simplify the whole process and make sure that the anomalies which we should not miss are not missed. So the four chamber view is a very, very important view of the fetal heart. The specific reason why I say so is because the four chamber view can be used to separate heart defects which can be offered complete correction by way of surgery after birth. If there are two ventricles, then all those defects can be corrected with good results. However, if there is a hyperplasia of one of the ventricles or one of the atrioventricular valves, then you are looking at a very complex heart defect and these cannot be offered a complete surgical correction. They can only be palliated. So that means that they need multiple procedures and hence their long-term results are less than optimal. So that's the reason why the four chamber view has got a great prognostic value as far as the evaluation of fetal heart is concerned. Now when I list out the four chamber anomalies, so this is something which for the theoretical aspect for people, students who are listening, we can actually have a clear approach. When you look at the four chamber view, you need to look at different parts of the four chamber view to make sure that you don't miss anything. So on the left side, the left heart anomalies, the most important and the most severe one is a hyperplastic left heart syndrome. Then you have aiotic stenosis and then we have an entity called ventricular disproportion or asymmetry where one ventricle, typically the left one is a bit smaller than the right. So we will discuss the differential diagnosis of that hyperplastic left heart very soon. On the right hand side, right side of the heart you have abnormalities of the tricuspid valve, typically causing tricuspid regurgitation. Then we have this entity called pulmonary atresia with intact ventricular septum. Some people also call it hyperplastic right heart syndrome and then have tricuspid atresia. Then the third group is septic defects and the abnormalities of the crux of the heart and of this most common and the most significant one is atrioventricular septal defect. AST and VST are not perhaps so important in the fetal life because you know it's something which is totally correctable. So the focus is perhaps not on picking small VSDs and in fetus. Congenitally corrected transposition or CCTGA has got a very distinctive four chamber view variation so we'll just mention that as well. Then we have intra-cavatory lesions of which we have most important group is cardiac tumors and typically multiple cardiac tumors called raptor myomas. A very common problem is ecogenic focus which this I'm not going to cover because of lack of time. Then you look at area around the heart for pedicardia diffusion, area behind the heart which we will be seeing in one of these cases towards the end of the lecture. Then abnormal cardiac rhythm which is going to be covered in my next lecture and abnormal contractility which is essentially cardiac function and which is not be covered in this lecture. So essentially I'll be talking about left heart anomalies, right heart anomalies and septal defects in this group of four chamber anomalies. So let us first start with the most obvious anomalies which is the left heart abnormalities. So in this I'm going to show you three examples. Hypoplastic left heart syndrome, iotics genosis and asymmetry or disproportion of the left heart structures. So first let us see this picture and this is actually a movie. So sometimes in these sessions in peak hours there could be a slow running movie. Nevertheless even if you see the picture it should be all right. Watch this picture carefully and since it's a webinar and I'm relying on internet for getting this data across, I mark all the pictures as left and right, L is left and the R is right. So you can see also the icon on top which is showing anterior posterior left and right as well just to orient you and this is a color of the same picture, a same lesion. So in this case we can see that the left side of the heart particularly the left ventricle over here is really small and we small and as we see in this color flow there is no filling of the left ventricle at all. The entire blood is coming to the left atrium goes across the foramen ovale to the right atrium and then to the right ventricle. So obviously this is a very severe condition and this is what is called hypoplastic left heart syndrome and when we go to the three vessel view in color on the same lesion the pulmonary artery is marked as PA and iota is marked as AO and you can see that in the PA we see the blue flow which flow away from the heart towards the pulmonary artery while in the iota we see a retrograde flow that is blood flowing back into the iota through the ductus arteriosus and this signifies that there is a complete atresia of the iotic valve and thus the flow into the iota is completely sort of maintained by the ductus arteriosus. This is also shown very elegantly in the sagittal view of the iotaic arch. The AA is ascending iota, D is the ductus arteriosus and we can see that the entire blood flow into the iota is retrograde and not andigrate and these features suggest a critical circulation after birth and which is dependent on the patency of the ductus arteriosus. So these two images clearly tell a very severe end of the spectrum perhaps the most extreme type of heart defect which is hypoplastic left heart syndrome. Now there is a specific entity now in the previous picture I showed that the only way blood can exit the left atrium in hypoplastic left heart syndrome is through the foramanoval and in this picture we can see that the foramanoval is actually intact there is no opening at all and in fact you can see that the foramanoval is bulging towards the right side and in this case when you look at the pulmonary veins as seen by the arrows you can see that they are quite chunky the very big fat pulmonary veins. The reason is because the mitral valve is atritic so blood cannot go from the left atrium to the left ventricle so the only exit path was the foramanoval and that too is restrictive so the blood cannot exit the left atrium left atrial pressure will increase and the back pressure will reflect on the pulmonary veins causing dilatation and engulfment and this can be identified using by pulse wave Doppler and if you put normal pulse wave Doppler into the pulmonary vein this is what you see you see a systolic wave there are two waves the S wave and the D wave and a very small atrial reversal wave which is shown by this arrow however if you have hypoplastic left heart syndrome with restricting foramanoval the pulmonary vein pressure is high and now you look at the atrial reversal wave here it's very very prominent that's because the pressure is very high and in atrial systole the blood will reflect back into the pulmonary veins causing a prominent a reversal it's a bit high end but it's worth looking it's a very simple thing to do and just using Doppler to look at the pulmonary veins and it's useful in many other conditions as well and this suggests a very severe end of the spectrum so that's about hypoplastic left heart syndrome now let us see another case again the left and the right are marked for you and you can see that the left side ventricle is small while the right side of the ventricle is quite large but how do you differentiate this picture from the hypoplastic left heart syndrome which you saw before so in this the left ventricle even though it is small continues to form the apex of the heart while in hypoplastic left heart syndrome the left ventricle is so small that it doesn't form the apex of the heart the right ventricle forms the apex of the heart in etchelitis so in ventricular disproportion one factor which differentiates the anatomy is that the lv continues to form the apex of the heart while in hypoplastic left heart syndrome the rv will be apex forming and also the second factor is that when you look at the squeeze the contractility in this condition the ventricle still contracts while in hypoplastic left heart syndrome the ventricle is often hypo contracted the second feature is by color Doppler and here we are putting the color Doppler and as we can see here in hypoplastic left heart syndrome there is no flow across the mitral valve there is typically mitral atresia so all the blood from the left atrium has to go across the foramanoval to the right atrium however in ventricular disproportion the mitral valve is patent and as we can see here in this movie the blood will flow from left atrium to the left ventricle so many a time when you see a smallish left ventricle you have this tendency to label this condition as hypoplastic left heart syndrome and please do not do that because the meaning of etchelitis is very severe the prognosis is bad while a ventricular asymmetry is often a very common condition particularly in the trimester of pregnancy and if you label it as hypoplastic left heart syndrome you are implying a very poor prognosis and that is wrong and then the decisions may be taken in a very inappropriate manner so these clues should help you in making the distinction between a true hypoplastic left ventricle versus a disproportionate left ventricle now i'm just going to show this single slide for iotics stenosis because i'm this is obviously left and the right ventricles are marked and in this movie you can see that the left ventricle is in fact quite severely dilated and when you look at the contractility the lv is hardly moving the right ventricle is moving well contracting well by the left ventricle is dysfunctional and if you look carefully there are bright patches on the ventricular septum suggesting endocardial fibroelastosis as well the reason is that as we can see here the left ventricular outflow tract there is a severe stenosis of the iotic valve there is some anti-grade flow but the valve is severely stenotic now i don't want to dwell more into the management options here this is these are situations where some people perform in-utero intervention by doing a in-utero iotic valve dilatation it's of course a very major procedure and we will have to talk about this in a different kind of aesthetic