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The question of whether to give oxygen is always interesting because the tendency with any blue baby of course would be to give oxygen. But to warn you that in some of our babies we are concerned about giving oxygen in that oxygen can decrease the pulmonary vascular resistance and in some of these babies we need the increased pulmonary vascular resistance to achieve increased systemic oxygen saturation. This is, for example in patients with hypoplastic left heart syndrome, where the systemic circulation is dependent upon the pulmonary circulation. We want to maintain a pulmonary resistance that will allow perfusion of the systemic circulation via the ductus from the pulmonary bed. So think about the oxygen before you administer to these babies with potential cyanotic congenital heart disease.
If our baby has tetralogy of Fallot, let’s think about what that means in terms of the pathology involved. The embryologic aberration is probably a single phenomenon and that’s of mal-distribution of the division of the conus so that the conal septum is deviated anteriorally, crowding out the pulmonary outflow tract, if you will, leaving a defect in the ventricle septum and also a disproportionately large overriding aorta. So as complicated as tetralogy may seem, it’s probably a single embryologic problem. The presentation of tetralogy of Fallot can be quite variable, often depending upon the age and of course the severity of the cyanosis. The presentation may be with a murmur with or without cyanosis. If the obstruction of the outflow tract is very mild then the patient may have little or no cyanosis and present only because of the presence of a murmur. On the other hand, some of the most severe tetralogy of Fallot may have little or no murmur but the severe cyanosis being the key to that potential diagnosis. A physical examination, depending upon the level or degree of obstruction to the right ventricular outflow tract, cyanosis or not. If there is cyanosis then there is likely … long standing cyanosis, then there will be clubbing of the digits. So we don’t usually see clubbing in very young infants and neonates but after a matter of some months we often can see clubbing of the digits in these babies. An increased right ventricular impulse in that this right ventricle is facing obstruction to the outflow tract, as well as systemic resistance via the overriding aorta allows heart sounds and harsh mid-systolic murmur. This is another picture showing clubbing. We rarely see clubbing to this extent anymore except to those of us who go to Peru or third-world-countries occasionally to see cardiac patients and this is still a very prominent finding. The proliferation of capillary beds is apparent too as we look at the conjunctiva and we see these very full capillary beds that look like conjunctivitis often.
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The murmur can be quite variable. Typically a harsh, mid-systolic murmur of varying lengths that we hear at the mid left sternal border, transmitted usually along the left sternal border. In fact the duration and the loudness – the intensity – of the murmur can be a clue as to how severe the obstruction to the outflow tract is. If the murmur is long, loud and harsh then usually that’s less severe obstruction to the outflow tract. In other words, the right ventricle is managing to get flow through this obstructive outflow through most of systole. If the murmur, on the other hand, is very short and relatively soft then it usually represents a more severe form of tetralogy of Fallot. In other words, the right ventricle is not affecting a significant outflow through the obstruction. And in fact the patient is usually bluer because of their right to left shunting into the overriding aorta, in the severe forms of obstruction. This becomes important in the follow-up of these patients. For example, when you are seeing patients as primary care physicians and happen to determine whether the tetralogy is becoming more severe. Cheap propecia 5 mg at Canadian pharmacy mall.

Let’s continue with the case presentation of our cyanotic newborn and what workup we might consider doing in helping us to focus first of all to distinguish this cyanotic congenital heart disease from other causes of cyanosis. Looking at these parameters, oxygen saturation, arterial blood gas, doing the hyperoxic test – some of the other laboratory studies that could be helpful would be hemoglobin in terms of oxygen carrying capacity. If a patient is severely anemic then he may not reflect the degree of desaturation by observation of his cyanosis. On the other hand, babies that are polycythemic sometimes look more cyanotic than they actually are de-saturated. The glucose and calcium are helpful as baselines as we will want to intervene and help this baby with its management. The chest x-ray can be a helpful clue in distinguishing the form of congenital heart disease with which we are dealing. To emphasize this, the early cardiac intervention; we are very concerned with babies with cyanotic congenital heart disease in that they can have a rapidly deteriorating course, as we will see in just a moment. The echocardiogram is an important part of the assessment, usually in the hands of the pediatric cardiologist. But we had transferred to us last night a baby with cyanotic congenital heart disease in whom the neonatologist had ordered the echo and made the appropriate diagnosis and fixed the baby up with the appropriate management and sent him off to us. This may be a typical course of this baby with cyanotic congenital heart disease. They often present late night, early morning, when you are the primary care person out there all by yourself, trying to figure out what’s going on. But let’s say this baby has an oxygen saturation of 72% when you first see him, with these arterial blood gases, but he progressively de-saturates with time. As he de-saturates he also becomes more acidemic. So again, not an unusual course for these babies with cyanotic congenital heart disease and therefore our stress on the urgency of recognizing them and early management.
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So what are the goals, as far as the primary care physician in early management of these babies with cyanotic congenital heart disease? Well, treatment goals are to decrease or at least to check the level from progression of hypoxemia and to decrease the acidemia. The question is, how can you as a primary care physician intervene to implement these treatment goals in this early management? With regards to the hypoxemia, to increase pulmonary flow, increase mixing or to increase oxygen transport, are the potential ways of managing the hypoxemia. With regards to the acidemia, so reduce the hypoxemia usually is key to reducing the acidemia. To support the cardiac output. Often as these babies become more hypoxemic the myocardium suffers and they have decreased cardiac output. So to support the cardiac output can be helpful in correcting the acidemia. Also, to directly work at correcting the base deficit may be an important part of the management.
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Now, how do you do these? How do you implement this management? Well, to increase pulmonary flow we can use prostaglandin E infusion to increase pulmonary flow. As a result of increasing pulmonary flow and any sorts of mixing, then you can potentially increase the systemic saturation as well. As far as oxygen transport is concerned, by hemoglobin, then if indicated certainly if the baby is a bit on the anemic side, then to give packed red blood cells. We use as sort of an indicator a hematocrit of 40. If the baby’s saturation is less than 80% then we try to achieve a hematocrit of at least 40% to enhance oxygen transport. If the baby, as a result of the hypoxemia and acidemia, is showing signs of compromised cardiac output then inotropic support, usually in the form of low-dose dopamine or dobutamine, can be very helpful in the early management. Correcting any deficits in terms of serum glucose or calcium -again, to enhance the myocardial function – can be important parts of the management as well. Sodium bicarb if indicated with severe acidemia and if you are not correcting the acidemia by these other measurements.
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As we think about the differential between peripheral cyanosis and central cyanosis, again a distinguishing feature with regards to the mucous membranes is that in peripheral cyanosis the mucous membranes are pink. In contrast to cyanotic mucous membranes in central cyanosis as with congenital heart disease or pulmonary disease. The pulse oximetry can be helpful in terms of peripheral cyanosis. The pulse oximetry can be very normal, whereas in central cyanosis the saturation is abnormal. But I must warn you – because this happened to me in my clinic just last week – the examination rooms were particularly cold that day and I had two children, both of whom had had Fontan’s, and Fontan’s often have some peripheral vasomotor instability. Pulse oximetry on those children were alarming as far as their digits were concerned; 70 and 80. But they were very very cold. We put the pulse oximetry on the earlobe and they were 94 to 96. So we have to be careful with this choice of differential of central versus peripheral cyanosis. Again, usually if it is peripheral cyanosis the extremities are cool, in contrast to central cyanosis where the extremities are often very warm and well perfused. If we want to try to distinguish further, central cyanosis – pulmonary versus cardiac – then some observations can be helpful. With crying, often the babies will pink up. If it’s pulmonary, as they take deeper inspirations, overload lungs fill up. Whereas with cardiac cyanosis, often with crying that cyanosis increases. The presence of respiratory distress can sometimes be helpful in distinguishing a baby who looks comfortable but is cyanotic, is having congenital heart disease, versus those babies who are cyanotic based on respiratory disease that show some other evidence of distress.
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The electrocardiogram may be helpful in that it may be abnormal in cardiac, but that is not an absolute, as we will point out as we go along with case discussion. The chest x-ray can be helpful if it’s normal. If it’s abnormal, as far as cardiomegaly or abnormal contour, then that may gear your thinking more toward cardiac cyanosis. If we look at blood gases, for example the PCO2 is often increased abnormally in pulmonary, whereas with cyanosis-related congenital heart disease the PCO2 is often normal. The hyperoxic test – giving the baby 100% oxygen or close thereto – usually with even significant pulmonary disease you get a positive response with increase in oxygen saturation and PO2. Whereas you may have little or no response to hyperoxic tests in the babies with cyanotic congenital heart disease.
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As we look at an x-ray, as another point of trying to help us focus on cyanotic congenital heart disease and the specifics of congenital heart disease, we look for patterns of pulmonary flow in addition to abnormal heart contour or size. If the pulmonary flow is increased then it is likely we are dealing with one of these three congenital heart diseases; cyanotic congenital heart disease, transposition, total anomalous or truncus arteriosus. If the pulmonary vascular flow is decreased then we are more likely dealing with these anomalies; tetralogy, pulmonary atresia, tricuspid atresia, or some other forms of complex congenital heart disease with either pulmonary atresia or pulmonary stenosis.
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If we focus on cyanotic congenital heart diseases and try to resolve the case presentation, if we think of the five T’s then we have included the majority of cyanotic congenital heart diseases that may be represented here in this patient; tetralogy of Fallot being the most common, representing about 10% of congenital heart disease. Viagra professional pharmacy. Transposition of great arteries representing about 5% of all congenital heart disease, tricuspid atresia representing only about 1-2% as is true also with truncus or a total anomalous pulmonary venous return. So if you guess tetralogy then you are probably going to be on the right track for the majority of patients. Generic pharmacy

With regards to chromosome 21 there is an association “Catch-22″. And the CATCH is an acronym for the defects that we commonly see here. This includes the cardiac anomalies, the facial abnormalities, the thymic hypoplasia, the cleft palate and the hypocalcemia as the components that we frequently associate with aberrations on chromosome 21. The cardiac anomalies are for the most part, the cono-truncal abnormalities. So patients with tetralogy of Fallot, truncus arteriosus. Tetralogy of Fallot again being associated independent of either of these syndromes with chromosome 22 aberrations as well. We list a couple of other associations here with specific chromosomes.
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Here again, as we talk about the other group of factors as etiology of congenital heart disease and think about environmental factors – teratogens, if you will – there are some specific associations of congenital heart disease with certain teratogens; fetal alcohol syndrome for example. Twenty-five to thirty percent of those babies will have ventricular septal defects, PDA’s or ASD’s. We’ll talk about, for example, transposition of great arteries, and there is an association of transposition, tetralogy of Fallot, hypoplastic left heart syndrome with anticonvulsants of the trimethadione group. Tricuspid atresia, for example, is one of the cyanotic congenital heart diseases and there is an association with maternal lithium intake with that particular form of congenital heart disease. So as we look through this list of potential teratogens we can see that there are some specific kinds of congenital heart disease that may be found in association.
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As we go back to the etiologic reference here of the different types of effects; genetic can account for only 5% or less of the congenital heart diseases as we know now. But as I mentioned, this is a growing category as we are learning more about genetic factors through our molecular biologists. Environmental factors that we listed in the previous slide account for really a very small percent of congenital heart disease. Again, the majority, as we know to date, there are probably some interplay between genetic factors and environmental interactions.
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Now we will talk about a case to help us focus on some of the lesions, especially the cyanotic congenital heart diseases, in terms of their presentations, the pathophysiology involved, and the treatment modalities. Particularly as it would relate to the primary care physician. Here’s a fairly common presentation of a child with potential cyanotic congenital heart disease. Here’s a well-developed, 4 kg male newborn who presents at term, uncomplicated pregnancy with Apgar scores of 8 and 8. So looking very good, other than being a little cyanotic, moderately cyanotic. As you might expect, being a little cyanotic he’s a little tachypnic as well. But really in no acute distress. His lungs are clear on auscultation. A fairly unremarkable precordium for a newborn. No signs of congestive heart failure and his peripheral perfusion and pulses are normal. Now, first to review; cyanosis in terms of this implication. Cyanosis is a bluish discoloration that we see in the skin or mucous membranes which is related to reduced or unsaturated hemoglobin in the peripheral circulation. Cyanosis can occur either based on central factors, as congenital heart disease, and pulmonary disease would present as peripheral. A lot of babies, as you know, tend to have some vasomotor instability that make them appear to be cyanotic peripherally but it’s important to look at the mucous membranes to discern central cyanosis that may represent pulmonary or cardiac disease. The other thing in assessing the cyanosis in the newborn – as we can do by x-ray – is to determine whether there is a problem of increased or decreased pulmonary blood flow.

We are going to talk about congenital heart disease. Congenital heart disease represents about 1% of all live-born children; 8:1,000 of live-born children will have some form of congenital heart disease of varying severity. Some cases are very very mild and cause no problems throughout the life-span. Others are very severe and cause some compromise at birth. We are actually aware of some children with congenital heart disease by fetal ultrasound. Of those congenital heart diseases, 1% of live-born children, approximately 20% of those babies with congenital heart disease will have a form of cyanotic congenital heart disease, and we are going to focus on that primarily during this discussion.
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In terms of etiologies, just doing some overview; as far as etiology of congenital heart disease, we think of primary genetic factors and of course this category is growing – and we are excited about that as the molecular biologists and geneticists are identifying more and more genetic factors with regards to etiology of congenital heart disease. There is a group where we know the etiology is related to some primary environmental factors and the largest category, however, are those diseases that we have no clear-cut genetic or environmental factor as etiology but perhaps some interplay of those two factors.
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Here are some associations with autosomal dominant syndromes and the type of congenital heart disease that we see in association. For example, we’ll talk about tetralogy of Fallot and tetralogy of Fallot is related to – or may be related to – Apert’s syndrome. As we look down this list we will see that … we will talk about coarctation for example and its association here. As we look through this list we can see that there are a number of associations with these known autosomal dominant anomalies. Another of these lists is related to these x-linked recessive and dominant syndromes, including Hunter’s and Hurler’s for example, where we may find coronary artery disease for example associated with Hunter’s. We have a patient in the hospital right now with Duchenne’s muscular dystrophy who has a severe cardiomyopathy. Again, some other associations that you might want to familiarize yourself with, looking through these tables.
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In this one we talk about some of the selective chromosomal aberrations and some that are familiar to you. Cri du chat for example, with the most common lesion being a ventricular septal defect, patent ductus being second, and ASD. These congenital heart diseases occur in about 25% of the patients with cri du chat. Trisomy 18 for example, the majority of these patients – 99% of them – will have some form of congenital heart disease and most commonly a ventricular septal defect. Trisomy 21, for example – you are very familiar with – about 50% of those patients will have congenital heart disease in the form of ventricular septal defect as the most common, atrial ventricular septal defect or AV canal or endocardial cushion defect and ASD, just to name some of the associations we see with these selected chromosomal aberrations. Do you recognize this child? This syndrome that he represents? DiGeorge syndrome. DiGeorge syndrome is one of a group of chromosomal or genetic defects that we can make some specific associations of congenital heart disease. For the most part DiGeorge is associated with cono-truncal abnormalities; tetralogy of Fallot, truncus arteriosus, etc.