Published Jan 3, 2020
Alright y’all. This one really has me stumped. In the NICU when we have a baby with a congenital heart defect we usually keep their sat parameters lower than normal. 85-90% for example. A long time ago someone told me that the reason we do this is because oxygen is a vasoconstrictor and it would cause a shunt of unoxygenated blood to the left side of the heart. But now I’m reading in several places that oxygen is a vasodilator and everything I thought I knew has gone out the window! Please help with an explanation as to why we keep these kids sat parameters low!
adventure_rn, MSN, NP
I've got a background in NICU as well as Peds Cardiac ICU, so I can take a stab at explaining this concept; honestly, it's so complicated that I could talk about it for hours and it would still be a bit confusing, so bear with me. (Pardon my subtitles, I hope they help clarify the post...)
Oxygen is a Vasodilator
First of all, oxygen is always, always a vasodilator. Here's a completely NICU, non-cardiac example: That's why we set the O2 parameters for PPHN kids higher, and why we're ok with them high-sating. PPHN is, by definition, pulmonary vasoconstriction. The first-line treatment for PPHN is cranking up a kid's FiO2 because the O2 itself is a vasodilator (and has fewer adverse effects than other vasodilators like nitric oxide).
Different Conditions Have Different Sat Goals
Second, different conditions will have different sat goals; the cardiology team should recommend sat goals based on the baby's anatomy. Some conditions (i.e. critical coarctations) will have normal sat goals; some (i.e. AV canals, certain Tets) may have goals of > 80%; some (i.e. the ductal-dependent and/or 'single ventricle' lesions--HLHS, tricuspid atresia, aortic atresia) will have goals of 75-85%.
Why Cardiac Kids Have Lower O2 Sats
Many of these kids have lesions which allow or require mixing between the blood of the right heart (desaturated blood returning from the body to the lungs) and the blood of the left heart (oxygenated blood going from the lungs out to the body). The mixing can come from an ASD, a VSD, or at the level of the PDA.
The oxygenated blood in your left heart (the blood being pumped out to your body) has an O2 sat of 98-100% (i.e. a normal O2 sat). The O2 sat of your blood in your right heart (returning from your body to your lungs) isn't 0%--rather, it's got a sat of around 60-70%. Therefore, when kids have cardiac defects, the blood from their left heart (100%) and right heart (60%) mixes to create sats in the 80%-ish range. In the cardiac world, we call these kids 'mixers.'
This is where it gets super-confusing, so bear with me:
Blood Follows the Path of Least Resistance...
When you've got a cardiac lesion that allows mixing (i.e. an ASD, VSD, or PDA), your blood has two options--it can go towards the 'left' (out to your body and systemic circulation) or to the 'right' (to your lungs and pulmonary vasculature). A really good example is a Truncus: in this defect, the baby has a huge VSD (so there's mixing between the right and left heart) and there's a common artery that exists the heart. Instead of an aorta going to the body and pulmonary arteries going to the lungs, there's a huge super-vessel (the 'truncus') which does both.
So in this case, when the blood exists the heart through this huge, super-vessel, it has two options: it can go to the 'left' out of the aorta and into the body, or it can go to the 'right' into pulmonary circulation in the lungs.
In a perfect world, blood should go to the body and lungs in a 1:1 ratio, meaning that exactly as a much blood goes to the lungs as to the heart. (FYI, this is called the Qp:Qs ratio, i.e. p is pulmonary and s is systemic blood flow).
This makes sense, because you need balance: If you send too much blood to the lungs and not enough to the body, you end up with awful pulmonary edema (and in extreme cases, even relative hypotension). If you send too much blood to the body and not enough blood to the lungs, you end up with kids who are desaturated and poorly ventilated.
...Which is Why it Matters that Oxygen is a Vasodilator
The main reason we care so much about O2 sat goals in cardiac kids has to do with where their blood goes.
Let's say you've got an HLHS kid whose goal O2 sat is 75-85%, but you've cranked up their FiO2 and now they're sating 100%.
This can be FATAL, and I've seen cardiac kids die from hypotensive shock because of it.
Why? Because oxygen is a pulmonary vasodilator, so if you flood a cardiac baby's lungs with oxygen, then their pulmonary vascular resistance is going to rapidly drop. Therefore, the blood in their heart is going to preferentially go toward their lungs instead of their body.
This is a core concept in peds cardiac care, and it's called 'overcirculation.'
Recall how we said that the flow of blood to the lungs vs. body in a perfect world should be 1:1. If you give a cardiac baby too much oxygen, that ratio can quickly become 5:1, where 5 times as much blood is going to the lungs as is going to the body.
This is dangerous for two reasons: The first is more obvious, but less dangerous: it will cause severe pulmonary edema (which we all realize can be very problematic).
The second is less obvious, but far more dangerous: if 80% of the baby's blood volume is going to the lungs and only 20% is going to the body, the baby will present as though they have distributive hypovolemic shock.
The scary thing is that you literally can't fix it. Yes, this presents like 'hypovolemic shock,' but but unlike real hypovolemic shock, you can't treat it with volume because it will simply flood their lungs. The only way to treat this complication is by turning their FiO2 down to 21% (or in extreme circumstances, you can use subambient oxygen therapy where you literally give them less than 21%). However, that therapy takes a long time to work, and isn't helpful when a kid is already coding with a MAP of 15.
Goal Sats Matter
I don't mean to get on a soap box, but having seen both NICU and peds cardiac, this topic is really important to me.
In preemies, high-sating can cause ROP (which is important, but not always taken seriously in the moment). In certain cardiac kids, high-sating can literally cause cardiac arrest. My Peds Cardiac ICU would get transfers from NICUs that allowed their kids to sat too high, and like I said, I've seen kids die because of it. So if cardiology says that a kids goal should be 75-85, please don't let them sit in the 90s (or conveniently forget to change your alarm parameters because they're alarming too much).
This concludes my Peds Cardiac Nursing TED Talk.
Clear as mud?
Wow! Thank you! I couldn’t have asked for a better answer. This is so helpful.
To Adventure RN ....
Thanks so much for the detailed explanation about O2 sats and cardiac babies. ..... I’ve been NICU connected for 30 + years. ... Cardiac has always been my uncomfortable / weak area. ... I know for our cardiac infants, the peds cardiologists always want lower O2 sats, but I attributed it to the cardiologists just accepting “mixing” is going on, and the lower sats are the best we’ll get in these infants. ... I’m old school, so I struggle with wanting to see higher O2 sats, (even though I always keep the sats where the docs order them). This even translated to the revised NRP guidelines from a few years back. Starting a neonatal resuscitation at 21%, felt so counterintuitive to me. But you just gave me that “Ah hah!” moment. Now I get it! You’ve even helped me understand & have less fear of the cardiac patients I encounter. That was the best explanation I have ever had. You have a knack for explaining things. If you are not an Instructor, you should be! Your explanations are spot on! ... Thanks so much for all of your insight!
@PJG RN thank you for taking the time to write such a thoughtful response! I love NICU bedside, but I've been toying with the idea of moving into an educator role; fortunately my NICU offers opportunities to split your time and do both.
I honestly didn't understand cardiac very well until I was fully immersed in it in peds cards ICU. My hospital is a high-volume congenital cardiac center, and many of the cardiac preemies live with us for several months until they're ready for repairs. Now that I have a firm grasp on cardiac, I'm hoping that I can help our nurses better understand the ins and outs of the more complex defects that we see.
Adult ICU Nurse here. Thank you for the very enlightening education on how very different NICU & PICU Cardiac kiddos are compared to adults. As others have said, u genuinely have a teaching gift, and I hope you get a chance to utilize it to the fullest. You will save a lot of lives by educating other nurses & obviously at the bedside too♡ Your hospital and patients are blessed to have you☆
Can not thank you enough for this! My daughter has a 2month old DS infant with VSD who was just removed from home O2 and given instructions to allow desatting. Though I sort of 'got it', I didn't fully comprehend the specifics. Truthfully, I was/am always concerned that less care might be given to this baby because 'he already has developmental delays'...crazy, but I know some providers do 'go there'. Tough to not worry that the low SAT will have a negative effect on his brain. It's all a balancing act...and the providers would prefer to wait until Spring to do surgery in the hopes that risk of respiratory viral infections is less. Feel free to feed our brains more as we all work towards learning more about the medical nuances of this sweet, much-loved baby's status. Also, just confirmed no hearing in one ear...seems so 'no big deal' compared to VSD and pulm hypertension!
I''m so sorry for the long delay. I am not the original poster. But I am the NICU nurse who was so appreciative when adventure_rn, BSN explained the rational for allowing lower O2 sats in neonates who are born with cardiac anomalies. . . . First, Congratulations on the Birth of your Grandson and becoming a Grandmother! What an awesome time! . . . . Second, I understand your concern/skepticism about whether medical professionals attending to your grandson are giving him the "best care." Something important to remember. You keep being his advocate, and keep encouraging your daughter to be his advocate too. You are always entitled to a "second opinion," and if you question or feel uncomfortable with something being said, done, or planned for your grandson, definitely ask questions. If you don't get answers that make sense and allay your fears, (and they should make sure you understand and that fears/concerns are allayed), or if you experience a "blow-off" attitude from the medical staff, it's time to get that second opinion, & possibly new doctors / providers. . . . It is a balancing act. And I agree with the docs waiting until Spring for surgery. Respiratory viral infections can be particularly bad for children, and especially in children who are compromised. This Winter has seen a significant uptick in viral infections compared to last year. . . . Can you say "less social distancing" and "relaxing of mask requirements?". . . . . . If your grandson's docs could remove just "one risk factor" for his surgery and not compromise something else while waiting, then by all means wait. . . . . Sorry to hear about your grandson's hearing. But keep fighting and loving on him. I've seen doctors be amazed at how well some children can do, despite their challenges. And I think your grandson is going to wow many, because he has such a great Grandma in his corner advocating for him! Wish you, your daughter, and your grandson the best!
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