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The electrocardiogram is likely to show us right axis deviation and right ventricular hypertrophy. I’ll make a comment now that if you throw the EKG of babies with cyanotic congenital heart disease, tetralogy or transposition into a batch of newborn electrocardiograms, you may not - in the first few days of life - be able to distinguish these because the normal newborn has a predominance of right ventricular forces. Canadian soma
The treatment for the transposition, and especially what can be done from the point of view of the primary care physician, would be to implement the prostaglandin. What the prostaglandin does here in this setting is to increase the ductal flow so that you have increased pulmonary flow via the ductus, bringing increased volumes of flow back to the left atrium, sort of stretching open this foramen ovale or ASD so that you end up with more saturated blood shunted to the right atrium, which then carries the blood out to the aorta. So in this fashion you can increase the oxygen saturation in a baby with a transposition. It’s not a typical ductal-dependent lesion as, for example, tetralogy of Fallot. The atrial mixing becomes quite key as well. Another part of the management, usually once it gets into my hands or my colleague’s hands, is to assess the atrial communication and if it is compromised at all, then to use the catheterization to effect a balloon atrial septostomy.
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Then the surgery of choice these days is the arterial switch operation which allows transection of the great arteries and re-anastomosis so that they come off the appropriate ventricle. Along with this it is important for us as a cardiologist to alert the surgeons of the coronary artery anatomy so that they will be able to re-implant these coronary arteries with a near aorta without compromise to coronary flow.
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I put this up to remind you that before our surgeons were so skilled at arterial switch operations, we did venous switch and the names that are associated with the venous switch approach, i.e. redirecting the systemic venous flow to the pulmonary artery via the left ventricle, and redirecting the pulmonary venous flow to the right ventricle to the aorta; either by a stenting operation or a Mustard operation, and we still occasionally have reason to use one of these two approaches rather than arterial switch. If our baby has tricuspid atresia he might remind us that we are dealing with an atretic bicuspid valve here, no orifice, no communication from the right atrium to the right ventricle. And usually as a result, a very hypoplastic underdeveloped right ventricle, which is key to remember in your assessment of this baby with the potential of bicuspid atresia. They almost always present right in the early newborn period because of the cyanosis. One of the keys to your examination is the lack of a right ventricular impulse. In other words, these blue babies tend to have a predominant apical left ventricular impulse and they may or may not have murmurs. There’s nothing about the bicuspid atresia that presents a murmur. I really put this up for looking at the EKG because this is one of the blue babies where the EKG may be very helpful, in that this baby usually has a left axis deviation, a lack of the usual predominance of right forces that expect for a newborn, but in fact progression that looks more adult-like with a predominance of left ventricular forces. And that makes sense if you think about the fact that the right ventricle is hypoplastic; underdeveloped due to the lack of inflow.
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What can you do about these babies as a primary care physician? Again, to effect pulmonary flow or to enhance it with the use of prostaglandin. When you refer that baby to the pediatric cardiologist then again we will assess the atrial septum to be sure that the defect is adequate. That’s the only way we decompress the right atrium in this setting. Then if not, then we do the balloon atrial septostomy. Then these babies require surgical intervention in the newborn period. Usually in the form of a aorticopulmonary shunt and to allow the baby to grow to several months of age, at which time we would bring the baby in for a Glenn shunt. The Glenn shunt, being an anastomosis of the superior vena cava to the right pulmonary artery so that systemic venous flow goes directly into the pulmonary bed. The Fontan is the second stage of the surgery and it completes the return of system venous return directly to the pulmonary bed by some kind of tunnel, if you will, within or nowadays external to the right atrium so that all systemic venous return goes directly into the pulmonary bed. Of course the reason this is not done earlier in life is that the pulmonary resistance is still relatively high in young infants and we have to wait until the pulmonary vascular resistance drops, so that you have essentially a passive venous flow into the pulmonary bed.

This x-ray is actually from a newborn with tetralogy of Fallot but the point to make is that it does not often show the typical boot-shaped heart that we associate with tetralogy of Fallot. This, on the other hand, is an x-ray of an older child with tetralogy of Fallot and it does show the boot-shaped heart. Because of the overall heart size, which is actually normal, there is some up-tipping of the apex with the right ventricle hypertrophy and absence of the normal pulmonary outflow here that usually forms part of the left shoulder. This is actually due in part to a right aortic arch. The electrocardiogram can be helpful usually to show right axis deviation and to show right ventricular hypertrophy, as indicated in this tracing. So in blue babies the EKG can be helpful in certain of these congenital heart diseases but not always. So in this day of medical economics when you have to choose your tests the EKG may not be very helpful in suspected tetralogy of Fallot.
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The course of a patient with tetralogy of Fallot can be quite variable too. It can be very benign. The baby that, for example, you pick up in the neonatal period because of a murmur, that doesn’t look very blue and who may show progressive cyanosis over the first months of life and to the point of actually having hypercyanotic spells. We’ll come back to that a little bit later. For management of tetralogy of Fallot, especially in this newborn baby that we’ve described as our index case, the medical management might be just close follow-up. If the baby is mildly cyanotic or not cyanotic at all then we can just follow this baby very closely. If the baby, on the other hand, is very cyanotic then intervention with prostaglandin - especially if he’s showing a deteriorating course in those few hours - would be appropriate. Specifically the PGE in this case increases the pulmonary blood flow in a setting where the obstruction to pulmonary outflow is severe enough that the pulmonary vascular flow is decreased.
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The surgical interventions might be indicated in the young infant in terms of a shunt, a palliative procedure, tapping from the aorta or one of its branches to effect an aorticopulmonary shunt of various names and techniques. On the other hand, in many of the even newborns we can effect a repair if the anatomy of the outflow tract is favorable. The repair often involves a patch across the outflow tract or sometimes across the anulus of the pulmonary valve. And internally the ventricle septal defect that we can see here with the overriding aorta is patched. With reaming out, often, of some of the infundibulum sub-pulmonic muscle affecting obstruction. Cheap amoxicillin.
If this baby were tetralogy of Fallot, how might he appear to us? How might he present? Just to review. Transposition of great arteries; transposition indicating that the aorta arises here from the right ventricle, the pulmonary artery arises from the left ventricle and these are parallel circulations unless there is some mixing level. Most commonly that’s at the atrial level as a patent foramen ovale or a true atrial septal defect. These babies usually present in the newborn period with their cyanosis and the cyanosis and hypoxemia can progress as in our index case. With that progressive hypoxemia, metabolic acidemia. The physical examination usually shows a cyanosis of varying severity and that relates to how well he is mixing through that atrial communication or if there are other levels of mixing as a ventricle septal defect. Not so likely, mixing at the ductus. The ductus is good for other reasons in this setting. Other important features on physical examination; increased right ventricular impulse, a loud single heart second heart sound - because that aorta is sitting right under your stethoscope under the anterior chest. The pulmonary is more remote and not well heard. The patient may or may not have a murmur. There is nothing about transposition itself that produces turbulent flow, to produce a murmur. So the murmurs that we hear are usually associated with ductal flow or the presence of a ventricle septal defect or other anatomical problems associated with transposition. About 30% of transpositions have no murmurs at all. This is a fairly typical x-ray for a baby with transposition of great arteries, however we’d have a hard time distinguishing this x-ray from a baby with truncus arteriosus. And basically it’s that egg-on-end shape with a narrow waist, and a narrow waist because the aorta is right but almost directly anterior to the pulmonary artery, which is just a little bit left-ward. So it leaves us with a narrow cardiac waist. The pulmonary vascularity is usually normal to slightly increased.
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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.