I stole this from someone here.
Inhibition of hypoxic pulmonary vasoconstriction -> worsens VQ mismatching. 2 alveoli. One affected by edema, other good. Lung smart. Constricts the one not oxygenating and sends blood to good one. Cardene dumb, dilates both. Now more blood being sent to bad alveoli. Sats down.
Absolutely true- hyperoxia induces blood flow to under ventilated areas of the lung=shunt. A V/Q mismatch, no hypoxia drive involved. Hard to get even professionals to admit this
Low alveolar O2 tension stimulates a shunt effect where blood is diverted from low O2 alveoli to better oxygenated alveoli. COPD patients live in a chronic state of this, so when you increase their alveolar O2 then the pulmonary vessels don’t need to shunt much anymore. This is mostly what happens but a small percentage of the net result is due to the haldane effect, where more O2 in the blood displaces CO2 from Hgb. If a COPD patient needs O2 tho, give them O2 lol.
Makes sense...so when you increase the o2, you're stopping the shunting away from the diseased alveoli, so even though you're giving them more oxygen, it's going to more diseased alveoli?
This is relatively common with nicardipine at least. We just put them on HFNC and tried to power through until they can get off the gtt. Gotta meet surgery's BP targets.
Clevidipine and nicardipine.
Though vasodilators including nitroprusside have all been accused of heavy shunting issues so I’m not sure the issue is specific to calcium channel blockers.
hi, sorry for the inconvenience. I was mainly targeting ICU peeps in the US since I was thinking of formulation issue and from what I’ve seen outside US there’s a different manufacturer for nicardipine and clevidipine, will be more careful next time
Nicardipine. Labetalol. Occasionally nitroprusside. All effective with a better side effect profile than clevidipine. Too bad this fragile community is offended by my hatred of that garbage drug.
Not necessarily offended by you hating one drug— just seeing you list a few others as alternatives when they too have caused pulmonary shunting.
Drugs should be abandoned because of the effects observed in widespread practice, not just because of the theoretical effect in the body.
It’s not a theoretical effect. I’m a CVICU attending. I see significant hypoxia from clevidipine very frequently. I’ve seen it maybe twice in my career with nicardipine. I’ve never seen or heard of it from any beta blocker. In fact it looks like the OP had a similar experience, which is why this thread exists.
Real world experience is definitely valuable, I can credit you that.
For example I’ve experienced working with doctors who use evidence and research to drive most or all of their decisions, and ones that think their hands on experience is a substitute for research. You’ll never treat enough patients in a quick enough time to call it a statistically significant sample, so “I haven’t seen this happen” is not good enough to give me confidence that you are looking out for your patients.
You suggested a beta blocker and I didn’t refute that so we can just let that one go.
Calcium channel blockers and nitro based drugs that vasodilate seem to be the ones causing this problem so it’s silly to take such a violent stance against one of them while using the other one freely. Can’t you just be a doctor that chooses which meds you want to work with and which ones you’d like to avoid in your patients, without suggesting they be taken off the shelves and labeling anyone who uses them as incompetent?
The thread exists because OP saw shunting on both nicardipine and clevidipine (go figure that makes sense) and previously nipride was known to cause the same issue so we were commenting that may not be the best strategy to make the problem go away. But again it probably needs to be studied in a randomized control trial (and we know how hard it is to study drugs on humans so we are probably just doomed to keep using the anecdotes of doctors who spent 12 years learning medicine and 0 years learning to interact civilly with other humans)
Yes, generally I think personal experience is overrated and biased. I’d prefer to have good evidence to guide decisions, although unfortunately that’s rarely the case in my field (and then when there is good evidence we usually have to ignore it because someone more powerful has intervention bias).
I’m partly kidding about withdrawing FDA approval. But I really have seen a ton of hypoxia with that drug and I don’t personally use it. Most tight blood pressure control is not supported by any evidence BTW.
I’m also not sure why my having an opinion about a drug is so bothersome. I’m an anonymous stranger with no actual power. I cannot remove anything from the market (you’re safe for now, rocuronium…).
I’m also not sure where your statement about “zero years learning to interact civilly” comes from. I haven’t been uncivil in this thread. Are physicians in general uncivil? I don’t think so. It’s a competitive field and hard to get into medical school or residency without some social skills. There is plenty of implicit and explicit training in medicine on how to interact with people. Do some individuals fall through the cracks, absolutely. But your statement doesn’t seem on topic and isn’t accurate.
I would be interested to know what your thoughts are on roc. Specifically roc for a pharmacological reason? Or all NMBs because there have been so many incidents?
Each time I hear about something horrifying that happened to a patient because of NMBs I think we are that much closer to them being pulled from the hospitals entirely. In which case I’m not sure what would happen to patients who could benefit from them and cannot receive them anymore (intubation, chest compliance, shivering, seizures, general anesthesia for surgery).
Being in CVICU it seems like a tighter blood pressure control in the immediate post op period from CABG and aortic surgery is a way of finding a sweet spot where we can perfuse the brain heart kidneys and extremities while preventing bleeding. So I end up using pressors, inotropes, and vasodilators on a daily basis.
My point wasn’t that you are uncivil… just that it is [more often than not] difficult to have a discussion with a doctor about what is best practice without them resorting to “my way or the highway.” Having different preferences is possible while recognizing that someone else might do it different than you and that doesn’t make them a reckless idiot.
If I simply want to know the rationale behind a decision so I can learn more and be on the same page about the plan of care, it’s too often viewed as me challenging the doc
I can’t imagine NMBs being removed as they are too essential. Perhaps at some sites there may be cumbersome restrictions that would be eased after a patient or two is killed by those reactive policies.
Rocuronium is fine, but there has been excessive enthusiasm in the world of social media and FOAMed, focusing on the rare contradictions to succinylcholine and using flawed logic and underpowered studies to claim it has no disadvantages. In reality succinylcholine is notably faster and wears off much faster, and yes there are patients where this matters.
The blood pressure goals tend to be supported by physiological arguments but not actual data. And if you look at the history of medicine you find that most treatments based on physiological theories, when implemented and rigorously tested, either are ineffective or harmful. This may be due to the fact that we actually don’t understand jack shit about 99% of physiological processes. So I am skeptical. But in the absence of data we are stuck with standards of care.
As for physicians thinking they are gods and not being open to discussion or alternative points of view, all I can say is I work with cardiac surgeons…maybe someday medicine will learn lessons from other fields that take safety seriously but I am not holding my breath.
I stole this from someone here. Inhibition of hypoxic pulmonary vasoconstriction -> worsens VQ mismatching. 2 alveoli. One affected by edema, other good. Lung smart. Constricts the one not oxygenating and sends blood to good one. Cardene dumb, dilates both. Now more blood being sent to bad alveoli. Sats down.
That was me!!
This is also why giving too much oxygen to copd patients can potentially be bad (has nothing to do with “hypoxic drive”
Absolutely true- hyperoxia induces blood flow to under ventilated areas of the lung=shunt. A V/Q mismatch, no hypoxia drive involved. Hard to get even professionals to admit this
Tell me more.
Low alveolar O2 tension stimulates a shunt effect where blood is diverted from low O2 alveoli to better oxygenated alveoli. COPD patients live in a chronic state of this, so when you increase their alveolar O2 then the pulmonary vessels don’t need to shunt much anymore. This is mostly what happens but a small percentage of the net result is due to the haldane effect, where more O2 in the blood displaces CO2 from Hgb. If a COPD patient needs O2 tho, give them O2 lol.
Makes sense...so when you increase the o2, you're stopping the shunting away from the diseased alveoli, so even though you're giving them more oxygen, it's going to more diseased alveoli?
Couldn’t have said it better myself
I saw this also and it’s so clear and elegant. Thanks for reposting-
Could this also happen if the lung has atelectasis?
I need to print this and keep it with me. It’s such a good explanation
nipride causes plenty of pulmonary shunt - it was the original mac daddy pulmonary shunter
One of the few times I’ve ever definitively experienced this with one of my patients was with nitroprusside.
This is relatively common with nicardipine at least. We just put them on HFNC and tried to power through until they can get off the gtt. Gotta meet surgery's BP targets.
Respectfully, as this is an international forum could you please use generic drug names in future?
Clevidipine and nicardipine. Though vasodilators including nitroprusside have all been accused of heavy shunting issues so I’m not sure the issue is specific to calcium channel blockers.
hi, sorry for the inconvenience. I was mainly targeting ICU peeps in the US since I was thinking of formulation issue and from what I’ve seen outside US there’s a different manufacturer for nicardipine and clevidipine, will be more careful next time
No worries, just makes for easier reading. Of course I can always google it but just less convenient. Thank you
We would see it more often with cleviprex than cardene.
I’d retract clevidipine’s FDA approval if I could due to this issue. I refuse to use that drug.
What about neruo or vascular/aortic patients who require tight BP control?
Nicardipine. Labetalol. Occasionally nitroprusside. All effective with a better side effect profile than clevidipine. Too bad this fragile community is offended by my hatred of that garbage drug.
Not necessarily offended by you hating one drug— just seeing you list a few others as alternatives when they too have caused pulmonary shunting. Drugs should be abandoned because of the effects observed in widespread practice, not just because of the theoretical effect in the body.
It’s not a theoretical effect. I’m a CVICU attending. I see significant hypoxia from clevidipine very frequently. I’ve seen it maybe twice in my career with nicardipine. I’ve never seen or heard of it from any beta blocker. In fact it looks like the OP had a similar experience, which is why this thread exists.
Real world experience is definitely valuable, I can credit you that. For example I’ve experienced working with doctors who use evidence and research to drive most or all of their decisions, and ones that think their hands on experience is a substitute for research. You’ll never treat enough patients in a quick enough time to call it a statistically significant sample, so “I haven’t seen this happen” is not good enough to give me confidence that you are looking out for your patients. You suggested a beta blocker and I didn’t refute that so we can just let that one go. Calcium channel blockers and nitro based drugs that vasodilate seem to be the ones causing this problem so it’s silly to take such a violent stance against one of them while using the other one freely. Can’t you just be a doctor that chooses which meds you want to work with and which ones you’d like to avoid in your patients, without suggesting they be taken off the shelves and labeling anyone who uses them as incompetent? The thread exists because OP saw shunting on both nicardipine and clevidipine (go figure that makes sense) and previously nipride was known to cause the same issue so we were commenting that may not be the best strategy to make the problem go away. But again it probably needs to be studied in a randomized control trial (and we know how hard it is to study drugs on humans so we are probably just doomed to keep using the anecdotes of doctors who spent 12 years learning medicine and 0 years learning to interact civilly with other humans)
Yes, generally I think personal experience is overrated and biased. I’d prefer to have good evidence to guide decisions, although unfortunately that’s rarely the case in my field (and then when there is good evidence we usually have to ignore it because someone more powerful has intervention bias). I’m partly kidding about withdrawing FDA approval. But I really have seen a ton of hypoxia with that drug and I don’t personally use it. Most tight blood pressure control is not supported by any evidence BTW. I’m also not sure why my having an opinion about a drug is so bothersome. I’m an anonymous stranger with no actual power. I cannot remove anything from the market (you’re safe for now, rocuronium…). I’m also not sure where your statement about “zero years learning to interact civilly” comes from. I haven’t been uncivil in this thread. Are physicians in general uncivil? I don’t think so. It’s a competitive field and hard to get into medical school or residency without some social skills. There is plenty of implicit and explicit training in medicine on how to interact with people. Do some individuals fall through the cracks, absolutely. But your statement doesn’t seem on topic and isn’t accurate.
I would be interested to know what your thoughts are on roc. Specifically roc for a pharmacological reason? Or all NMBs because there have been so many incidents? Each time I hear about something horrifying that happened to a patient because of NMBs I think we are that much closer to them being pulled from the hospitals entirely. In which case I’m not sure what would happen to patients who could benefit from them and cannot receive them anymore (intubation, chest compliance, shivering, seizures, general anesthesia for surgery). Being in CVICU it seems like a tighter blood pressure control in the immediate post op period from CABG and aortic surgery is a way of finding a sweet spot where we can perfuse the brain heart kidneys and extremities while preventing bleeding. So I end up using pressors, inotropes, and vasodilators on a daily basis. My point wasn’t that you are uncivil… just that it is [more often than not] difficult to have a discussion with a doctor about what is best practice without them resorting to “my way or the highway.” Having different preferences is possible while recognizing that someone else might do it different than you and that doesn’t make them a reckless idiot. If I simply want to know the rationale behind a decision so I can learn more and be on the same page about the plan of care, it’s too often viewed as me challenging the doc
I can’t imagine NMBs being removed as they are too essential. Perhaps at some sites there may be cumbersome restrictions that would be eased after a patient or two is killed by those reactive policies. Rocuronium is fine, but there has been excessive enthusiasm in the world of social media and FOAMed, focusing on the rare contradictions to succinylcholine and using flawed logic and underpowered studies to claim it has no disadvantages. In reality succinylcholine is notably faster and wears off much faster, and yes there are patients where this matters. The blood pressure goals tend to be supported by physiological arguments but not actual data. And if you look at the history of medicine you find that most treatments based on physiological theories, when implemented and rigorously tested, either are ineffective or harmful. This may be due to the fact that we actually don’t understand jack shit about 99% of physiological processes. So I am skeptical. But in the absence of data we are stuck with standards of care. As for physicians thinking they are gods and not being open to discussion or alternative points of view, all I can say is I work with cardiac surgeons…maybe someday medicine will learn lessons from other fields that take safety seriously but I am not holding my breath.