fireflymedic Posted September 5, 2008 Posted September 5, 2008 Okay DA is going to prevent proper blood flow and oxygenation throughout the heart producing murmurs and central cyanosis which we seem to be seeing. If severe enough, can also cause oliguria. This is most likely a result of a congenital defect is my guess. I also can't help though but wonder if this fluid overload isn't now causing some kidney issues making the baby reluctant to feed? See where that takes me. One point to ponder though is - aren't we wanting to close the DA to create a proper pathway through heart as is the case with preemies/neonates? NSAIDS are used for that purpose. So just a thought to ponder....
ericenglund Posted September 5, 2008 Posted September 5, 2008 In addition, what were some of the indicators that the patient was getting ready to deliver? Take care, chbare. 28 years old 10/10 abdominal pain that comes and goes(can anyone say contractions) Urge to urinate G5P5 "I can't be pregnant, I had one less than a year ago." (a little ignorance?) This should have been pretty obvious, letting her sit on the toilet may not have been the wisest of things. At least we played catch and saved face.
chbare Posted September 5, 2008 Author Posted September 5, 2008 Okay DA is going to prevent proper blood flow and oxygenation throughout the heart producing murmurs and central cyanosis which we seem to be seeing. If severe enough, can also cause oliguria. This is most likely a result of a congenital defect is my guess. I also can't help though but wonder if this fluid overload isn't now causing some kidney issues making the baby reluctant to feed? See where that takes me. One point to ponder though is - aren't we wanting to close the DA to create a proper pathway through heart as is the case with preemies/neonates? NSAIDS are used for that purpose. So just a thought to ponder.... A good question to ask. Like Ncmedic309 stated, we may want to strongly consider something to keep the PDA open. Obviously, this is a very hard concept to understand. However, PDA is not this patients primary problem. However, it will need to be repaired at some point. I think we can agree we have some sort of cyanotic heart defect. In the case of a cyanotic defect, oxygen rich blood may not be going where it needs to go. For example, in transposition of the great vessels, the pulmonary artery is attached to the left ventricle while the aorta is attached to the right ventricle. Obviously, this condition would result is rapid deterioration and death of the baby. However, if a PDA is present, at least some of the blood can mix and some oxygenated blood can be pumped out to the body. In many of the cyanotic defects, a PDA must be present for the patient to have any change of survival. Luckily, PDA is a fairly common problem and often associated with other defects. This can be a very difficult concept to understand and I urge anybody who is rusty on neonatal disorders to brush up on this subject. So, yes we are correct in wanting to maintain a patent PDA. PGE1 is a medication that can be used to prevent closure of the PDA. What serious side effects should we anticipate with PGE1 administration? Anybody make sense of those heart tones? Yes, we have a very progressive EMS system. Again, it is more about learning and hitting the books/net to research congenital defects and possibly, I recently had a patient who was status post repair of the said defect causing me to make up this scenario. Take care, chbare.
ncmedic309 Posted September 5, 2008 Posted September 5, 2008 In regards to the heart sounds - we're hearing a diastolic murmor and I'm assuming an S2 split? If this is the case, it's probable that we have some heart valve abnormalities and the heart sound would indicate a ASD or VSD. I've got a couple of the less common CHDs in mind on this one. The PGE1 medications can have some serious side effects. It's possible that we can see hypotension and bradycardia along with arrhythmias. We also want to be concerned about respiratory depression and metabolic imbalances. It's not something I would want to be administering in the out-of-hospital environment, but at the moment we're going to be working hard to keep this kid alive.
chbare Posted September 5, 2008 Author Posted September 5, 2008 Think about the right axis deviation and right ventricular hypertrophy seen on the XII lead. Why is this little guy's right ventricle enlarged? Let me give you a bit more to go on: Following PGE1 administration, the patient improves rapidly. However, tachycardia and tachypnea is still noted. Take care, chbare.
VentMedic Posted September 5, 2008 Posted September 5, 2008 chbare, Pardon me for dropping in here, but: How about the differentials between R to L and L to R shunting? How about elaborating on O2 (mentioned in earlier post) as a medication? What it does in cyanotic heart disease and in PPHN? Actually same action but different outcomes. And the differential for PPHN and cyanotic heart disease which have similar presentation but with a couple of distinquishing features. The difference in O2 therapy? Crackles? TTN or CHD? With adults, you can screw them up from the wrong treatment but usually not much more than they already are from their own habits. However, the first few hours of treatment for a newborn will determine if the child will have a somewhat normal life or be part of the trach and peg section in the cabbage patch class. Physical differential assessment of the newborn for CHD, PPHN and RDS is very systematic and it wouldn't hurt for a Paramedic or EMT to review the processs. Probably some already have now that you have brought the subject up. Some will not because they don't believe they will ever see a baby like this. And, then there are those that wonder why they can't do more "skills' on a Neo/Pedi transport team when they have never bothered to look up some of this stuff. It might then be evident to them why it is a specialty transport.
Mateo_1387 Posted September 5, 2008 Posted September 5, 2008 The Split heart sounds would be due to pressure against the right ventricle, as well as the factor of hypertrophy. Transposition of the great arteries could cause the hypertrophy. The right ventricle would be pumping into the aorta. It would have to pump faster, and would have to increase size in order to compensate for decreased cardiac output. In the case of transposition, this is how I figure the blood flow goes. Blood from the veins go to the right atrium, to the right ventricle and into the aorta, to the body, and then back around. The blood goes from the left ventricle into the pulmonary artery, to the lungs, returns through the pulmonary veins, and into the left atrium. The blood then goes to the left ventricle, and then back through the pulmonary artery. The increased pressure of the pulmonary artery due to the size of the left ventricle forces the oxygen rich blood through the PDA and into the arterial circulation. So switching the great vessels would fix the problem, and eliminate the need for a PDA.
chbare Posted September 5, 2008 Author Posted September 5, 2008 Ventmedic: A tall order for 11:00 pm . Let me at least throw out some basic information: Left to Right shunt: Essentially some condition that causes a shunting of blood from the left to the right side of the heart. This is generally considered a non-cyanotic defect because some oxygen rich blood remains and is pumped out by the left ventricle. The right sided pressures do not overcome the left and deoxygenated blood is not mixed with oxygenated blood. Right to Left Shunt: Essentially a condition that causes a shunt of blood from the right to the left side of the heart. A greater right sided pressure gradient leads to mixing of oxygenated and deoxygenated blood. Hence, these problems are usually cyanotic. Oxygen: A good topic to consider. We are often told to simply give oxygen if we think somebody needs oxygen. However, think about a patient who may depend on maintaining a patent PDA? What is involved in the natural closure of the DA following birth? How could this effect our patient? Is it possible that some patients may need to be transported on very low FiO2's and lower than normal saturations to assist in maintaining an open DA? Allow me to elaborate on PPHN? PPHN or persistent pulmonary hypertension involves increased pulmonary vascular resistance and pulmonary vessel changes. You will find both a PDA and patent foramen ovale in these patients. PPHN can mirror the signs and symptoms of congenital heart defects. However, PPHN usually is the result of another problem such as diaphragmatic hernia and meconium aspiration. This is a condition where you hear about inhaled nitric oxide therapy being used. However, would PGE1, nitro, and nitroprusside be good options to treat this condition? Finally, TTN or transient tachypnea of the newborn: I think some people also call this infant wet lung? This is usually a condition that will resolve within a few days of presentation and is caused by impaired clearance of fluids from the lungs. Hence the question regarding crackles. I agree that this is a very complicated topic and I really hope people google and research this one to death. I am by no means a neonatal specialist; however, I really want people to realize what a complex area this can be. Mateo: Think about the left side of the heart. Could this be a left sided heart problem? Take care, chbare.
streethealer535 Posted September 5, 2008 Posted September 5, 2008 How about this? It does not get much more complicated then this... and if you think this is bad you should see the 3 stage surg done to corect it! stay safe. JJ
streethealer535 Posted September 5, 2008 Posted September 5, 2008 Basicaly when all is said and done there is only one lower chamber and the IVC and SVC atatch directly to the pulmanary arteries and the Aorta is attatch to the RV Stay safe JJ
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