[LoveICU]

Hi. I am starting a new job in Pediatric CVICU at a Level I Trauma and Level IIIc Neonatal facility. They do everything: ECMO, HFOV, CRRT,etc. I have been studying up on the congenital heart defects and would like info regarding the different HD that the use of oxygen is dangerous. Could you list the defects and what o2 sats are acceptable (just the ones that are affected detrimentally)? Thanks.

I bought the AACN Core Curriculum for Pediatrics, ECG Interpretation of Pediatric, Illustrative Field Guide to Congenital HD and repair, PALS, and pediatric assessment book, and lol, Hazinski's Manual of Pediatric...think that's enough?

[janfrn]

Are you planning on carrying all those books around with you? I hope you have a strong back!

When you think about congenital heart defects and oxygen, think about what oxygen does to the fetal circulation right after birth. The change from placental gas exchange to pulmonary gas exchange increases the paO2 in the blood which leads to constriction of the ductus arteriosus and dilatation of the pulmonary vasculature directing more blood to the lungs. The increased oxygen saturation from about 55% in the descending aorta of the fetus to the close-to-normal sat in the 90's of the blood flowing to the lungs produces vasodilatation of the pulmonary vascular bed. This pressure change also decreases the amount of mixing between arterial and venous circulations. At the same time the pulmonary vascular resistance is falling, the systemic vascular resistance is increasing; in the normal neonate, this is the desired effect. The blood flows from the right side of the heart to the lungs and then back to the left side of the heart. But for conditions such as pulmonary stenosis, coarctation of the aorta, transposition of the great arteries, tetralogy of Fallot (dependent on degree of pulmonary stenosis), interrupted aortic arch and tricuspid and/or pulmonary atresia, it's essential that there be some mixing of oxygenated blood with deoxygenated blood that can only be accomplished by preserving an open (patent) ductus. Sometimes this is the only source of oxygenated blood to the systemic circulation. So keeping the PVR high and the paO2 lower would be of great benefit. Prostaglandin E1 infusions are used to maintain the ductus until the baby can be assessed further and definiteve treatment started.

Children with hypoplastic left or right heart following Norwood and Glenn procedures will also have lower saturations due to their single ventricle physiology and the method of circulating blood to the lungs and back to the heart. Fontan circulation when it's not fenestrated, will have normal sats. There are some great interactive videos of cardiac defects at www.cincinnatichildrens.org that will help make sense of all this. Take a look and tell me what you think...

[LoveICU]

After reading one of your other posts the other day, I read the info at cincinatti's website. It was very helpful. I understand the explanation you were stating. I am moving from the adult world and know that it is completely different. It's gonna take some effort to get used to 55 % sats...wow. It makes sense though bc the increased sat will close the DA. So, if the child is getting the medication to keep it open longer...do you still accept a sat that low or do allow it to be higher?

[janfrn]

You'll have specific orders about where the docs will want the sats. Our orders often read "keep sats between 70 and 85%" or something along that line. You'll see maybe 75% on the monitor and maybe 68% on an ABG, and that would be acceptable. It's a bit of a culture shock to ignore sats in the 70's but you get used to it! Another thing you'll notice is the very high H&H these kids have. That's how they compensate for the lower paO2... I'm trying to remember what kind of sats I see with our pre-op babies on Prostin, and I'm thinking that they're still kept on the lower side. Prostaglandin causes severe apnea in many babies so they're always pre-emptively intubated beofre being started on PGE1. There are other side-effects that figure into just how much the baby should get, so anything that will help achieve the goal is a good thing. We don't usually get the babies pre-op, they go to our NICU and we get them after the OR. Some (very few) kids we'll keep on Prostin for a day or so post-op, the arterial switches and the TAPVDs, I'm thinking.

There's another good reason not to overoxygenate neonates... and that's the effect of O2 on the developing retina. It can cause neovascularization of the retina and visual defects. When you see a toddler wearing glasses, you can probably safely bet your mortgage that they spent some time in NICU on supplemental oxygen.

Welcome to the exciting and often bewildering world of pediatric critical care. Come back anytime with questions. We have some great resources here.

[LoveICU]

Thank you. Your response was very helpful! I feel better knowing that there will be a parameter designated by CV surgeon. Our neonates don't come to the unit until after surgery (unless on ECMO)...I think.

[janfrn]

I'd expect the parameters to come from an intensivist, unless your CV surgeons are the attendings in your PICU. In our unit, we aren't allowed to take orders from any physician but our intensivist or resident/fellow. Other physicians may suggest, but we aren't expected to blindly follow an order from a CV surgeon who might not have clapped eyes on the kid since the OR 18 hours previous. It it's something reasonable the intensivist will sign off on it and we're good to go.

We very occasionally get the babies pre-op and NOT on ECMO, but rarely. We do a lot more intensive hemodynamic tweaking and use a lot of drugs taht NICU won't, so we might get a kid for those kinds of issues. Otherwise they stay in the land of the little people until they go to the OR.

[Ventjock]

Originally Posted by LoveICU

Thank you. Your response was very helpful! I feel better knowing that there will be a parameter designated by CV surgeon. Our neonates don't come to the unit until after surgery (unless on ECMO)...I think.

another note.

subambient oxygen therapy.
this is mainly used for patients with ductal-dependent lesions in order to prevent "overoxygenation". an fio2 of less than 21% is administered to limit the pulmonary vasodilatory effects of oxygen. by reducing the fio2 in theory one can keep the PVR elevated. another way to accomplish this is to administer CO2, usually 2-5%. by creating a respiratory acidosis the PVR should remain elevated.

there are also what are known as the "rules of 40".
for example a kid with a hypoplastic left heart who had a norwood performed. these kids have profound hemodynamic instability and require mechanical ventilation. many require an fio2 of less than or equal to 21%. the lungs can flood if too much oxygen is given causing PVR to decrease. thus this is a general rule:
(the "rule of 40s”) - keep ABG in the following range: pH > 7.40, PaO2 ~ 40, PaCO2 ~ 40

LoveICU,
if you can find a book called Perinatal and Pediatric Respiratory Care by Czervinske, that would also be another good reference for the PICU. There is a good chapter in there that covers CHD including diagrams of the surgical procedures. i also recently bought the AACN Core Curriculum for Pediatrics last month. i skimmed through a few chapters and it looks like a great book. I took PALS last november and the "guide" (book) is great.

also ROP can be avoided, not by watching the kids Spo2/Sao2 or fio2 levels, but by monitoring the PO2. a PO2 below 80 can be considered safe for a premature infant.
term infants, correct me if im wrong Jan, have little to no risk of developing ROP.

[janfrn]

No ventjock, you're not wrong. ROP isn't usually seen in term infants. We can't assume though that all of our patients are going to be term infants so some awareness isn't a bad thing. It is a bit difficult to monitor paO2 in those prems who are in the intermediate care nursery and may only have one CBG a week... sats are a fairly reasonable guide in that situation.