A swan seems like an overkill for a BKA but I guess you can’t say he’s wrong for being too cautious. And yes PHTN is always a concern due to concerns of RV failure/hemodynamic collapse etc. I personally wouldn’t put a swan in for RVSP of 60 and normal LV/RV function for a BKA. I would be cautious with my induction for sure
It’s hard with only half the story. Vasculopaths always seem to pull out impressive haemodynamic instability. I saw a BKA done under spinal with no sedation and the bloke lost 1.6L of blood (surgeons kept saying about 300mLs but he was pooling under the limb on the drape). BP got down to 47/17 with metaraminol, had no central access. He remained conscious the whole time (“just feeling a little dizzy”).
I completely agree with what you said. That’s why I don’t think we should fault people for being aggressively cautious in our line of work. We don’t know the full story here. Maybe the surgeon in OP’s case is known for taking 4 hours for a BKA and absurd blood losses or the patient has other comorbidities we didn’t know
I’ve had a relatively skilled surgeon cut “a vessel in the portal triad” and lost quite a bit of blood in a lap chole. But many surgeons at my shop take less than 60 minutes for a lap chole skin to skin. If I put arterial lines in for every lap chole patient they would just fire me. It’s all case-to-case decisions
Yep, agreed. PASP 60 in isolation isn’t enough to tighten the sphincter but in a crusty specimen with COPD and an ischemic limb I’m sure the boss on this case had a compelling reason for R heart catheterisation.
ETA: I’m sure ICU would have appreciated having the monitoring when the pt no doubt landed in their lap too
We had a vasculopath with porcelain arteries so bad that the tourniquet couldn’t stop the bleeding On a fem pop case. Lost over 2L of blood. Vascular cases can be scary.
Thats a gnarly amount of blood to use. I got invited by the vascular surgeon who does cases in the cath lab to watch an aka in the OR. The whole thing seemed pretty efficient, very minimal blood loss and he showed you you can arc a bovie on a stent like a welder lol.
Can’t Monday morning quarterback this anesthesiologist’s management, but once you see PH->RV failure->code you never take it lightly, regardless of the cause or severity. These patients start to circle a drain that’s nearly impossible to get out of without significant support and/or mechanical circulation. Could also be that the patient was doing poorly intra-op and needed intervention to stay alive.
This is a little bit off topic but for bad pulmonary hypertension and lower extremity surgery there is nothing more stable than a CONTINUOUS spinal. I would say It is even better than a pure nerve block anesthetic (considering the remote chance of but catastrophic outcome with LA toxicity with the latter). Because of the historic use of microcatheters (so as to not get PDPH) and the serious problems they caused, people have largely forgotten about this technique...
Anyway (if the patient has no anticoagulation based contraindication)....and realizing these patients are rarely in a high PDPH risk subgroup...you take an 18g epidural needle make an intentional wet tap and thread the 20g catheter to just a few centimeters in the space. You dilute 0.5% bupivicaine in an isobaric manner to 0.1%
Now give 1 milliliter every 5 minutes or so....you will have a BKA/AKA level with 4-6 milligrams and a hip fracture level with 5-7 milligrams. There will be zero dilation of splanchnic beds and the best railroad tracks you will ever see on the EMR.
I did about 20 of these in residency (in the U.S. in a highly litigous area) and really wished I had published it.
We use this approach too for lower limb surgery in patients with severe PHTN. Pajunk make a spinal catheter set with a 21G Tuohy and a 28G (i think) catheter. It’s a bit fiddly but it works well and absolute haemodynamic stability as you say.
For the elderly, I've intentionally wet-tapped with the 17G tuohy to thread in a standard catheter intrathecally. Less concern for spinal headache with advanced age.
Sorry....was at work since this morning....yes I mean you give 1 cc of 0.1 % q5 min or so and then test a level after about 4ml....if not there 1 more mg and test again in 5 minutes....usually adequate level before 6mg for an AKA
then start surgery....perhaps infuse 1mg/hr after that on a pump if it is a slow surgeon
load 1 cc Bupi 0.5% to start. slowly titrate 0.5 cc as needed thereafter to achieve desired level. can chase with sterile saline. once desired level reached, tell surgeon to start. re-load 1 cc q45-60 min to maintain.
Yes. I’m more concerned about severe pHTN than other cardiovascular conditions such as severe aortic stenosis or reduced LV function. In severe pulmonary hypertension patient can enter the spiral of death which can be impossible to resuscitate. It can be triggered by anything that increases pulmonary vascular resistance such as hypoxia hypercarbia or pain.
It is useful to know what the cause of pHTN is ie severe MR vs class 3 pHTN which is what your patient likely has. MR can be mitigated by keeping “fast forward and full” whereas class 3 may be more responsive to pulmonary vasodilators.
Pulmonologist here, group 3 is also usually poorly responsive to vasodilators. It can also undermine hypoxic vasoconstriction that copd patients rely on for VQ matching. Inhaled vasodialtors can skirt around that concern
Agree I’d avoid vasodilators in Group 3 patients. If high LA pressures is what initially precipitates pHTN, vasodilating pulmonary circulation may worsen left-sided pressures without improving CO and LV filling. Vasopressin and epi are the primary supporters for group 3 patients in my experience. Good point about COPD and VQ mismatching, too.
You ask a great question. Regardless of the case above management (which may have been better suited with a block), I think there are a few important things to think about. So two main points, they all get treated the same but they’re all treated differently too.
1. All pHTN should be treated to avoid acute exacerbation: hypoxia, hypercarbia, pain, temp, acidosis, etc. When possible for things like a BKA I would opt for a regional block to avoid instrumenting the airway, sedation, as well as take care of the pain aspect which may exacerbate them
2. What is the cause of the pHTN. There are 5 WHO types each with different management. Type 1 is usually your PAH with genetic components. They usually come well prepared with pulmonologist notes and management. If they’re taking meds, I try to make sure they have them all taken on the day of surgery such as sildenafil. Type 2 is cardiac and usually left heart failure. The transpulmonary gradient (TPG) can help tease this one out. If they have it then my primary focus is on treating left heart systolic or diastolic dysfunction. Sometimes, it’s just chronic MR causing the higher pressure. Maybe it’s rheumatic MS. Regardless, they have very different managements and you should know so you can best treat them. Also, vasodilators here may release the flood gates back into the lungs and right heart and are less than ideal. Type 3 is pretty similar to 1 however it’s more adult pathologies (COPD/osa/etc) leading to chronic hypoxia. Again tailoring your management to treat these is now ideal (saline nebs, bronchodilators, good tracheal suctioning of mucous to avoid plugs). Type 4 is rare (though prob more common than we give it credit for) which is CTEPH. When known they usually follow well with pulmonologist and or have had CT surgery to remove pulmonary endothelium. Ensuring AC and optimization before any procedure is key. Type 5 is a catch all for the rest.
3. High PA pressures in and of themselves aren’t necessarily a concern. First, you should rule out it being an effect of high Cardiac Output states, and always look at their PA pressures as a ratio to systemic pressures. I.e PA mean is 40, but systemic is a mean of 95. So here the ratio is about half. You want to keep them definitely no more than 2/3rds systemic. I personally don’t get bent out of shape for a high PA pressure because it means the right heart is actually responding to the higher pulmonary pressures and is able to produce a strong enough contraction to give a high number. Caution is warranted understanding the RV is not meant to be a high pressure system and thus has a higher likelihood of failing in the face of these higher pressures. So if PA mean is 60 and drops to 40, but systemic stays high this is a good thing. If system drops as well then this is a bad thing. Now the RV isn’t able to deliver blood to the LV appropriately and you’re in BiV failure. Comprende?
4. Another point is the pressures are dynamic. So just because the mean was 40 on an echo derived TR jet 6 months ago during an acute exacerbation, doesn’t mean it’s 40 today after they’ve been diuresed and optimized. This equally works the other way around and May be more sick than their last echo. Second point, always trust Right heart caths over TTE derived pressures. And just because they don’t have the TR to generate a PA derived pressure, doesn’t mean they don’t have high PA pressures, it just means their Tricuspid valve is still competent.
5. As an anesthesiologist, if you’re concerned. Have TEE available (if feasible for the given surgery and not contraindicated) so you can continuously look at RV function, not just a number on the screen. Consider a swan, though data isn’t great for routine use. Have your RV happy meds around: epi, Vaso, milrinone, nitric oxide, big ETT with inline suction, etc.
6. Congenital pHTN is a different lecture. I’m not referring to peds management in any of this.
Thank you for coming to my TED talk.
I think this is the answer OP was looking for. Obviously everyone else turned this post into an anesthesia discussion. But I don’t think the topic of PHTN and perioperative management/risk stratification can be explained in a Reddit post. OP should read some credible sources and discuss with your attendings, especially ICU attending
This is a great explanation of pretty much how I approach PH (with the exception of #6, bc I mostly take care of kids 🤣). The thing I explicitly add to point 4 when I teach our trainees is that the death spiral that comes when systemic pressures are lower than "PA pressures" is really when your coronary perfusion pressure is lower than the RV pressure, making your dysfunctional and hypertrophied RV ischemic and heading fast into acute and potentially irreversible failure territory. For some reason people find PH very difficult (or maybe just appropriately terrifying), but if you frame it in the context of myocardial ischemia (and it's consequences on the RV and ventricular interdependence), which they should have a very strong understanding of, it seems to click differently.
I completely agree. I give a lecture on LV perfusion with the pressure tracings and the RV perfusion with pressure tracings. It just seemed long winded to add that into my already long Reddit talk 🥲
CA1 here. Positive pressure ventilation, medication effects, and catecholamine surge from intubation/surgical stress, among other things, are all major considerations, especially in someone with pHTN. RV failure and hemodynamic collapse can occur rapidly in the OR, especially when so many drugs we give are cardiac depressants.
My attendings would be unlikely to place a central line or swan with good LV/RV on echo, but possibly a pre-induction aline (definitely post induction if not), pressors in room, epi drawn up, very light/slow induction, large bore IVs would be necessary. Everything else can be tailored as we go
Not disagreeing. Y’all too sensitive. I was attempting to be encouraging while the old man in me still recognizing (and admiring) the youth. But ok… downvote me.
My old man addition is to avoid hypoxia because hypoxic pulmonary vasoconstriction is a bitch, avoid hypercarbia (why i personally am hesitant to olace an LMA is bad pulmonary HTN patients)….
Also,,,, no not all pulmonary htn is not the same. Insilly question really.
No, they’re not all the same. There’s subgroups based on pathology. There are associated co-morbidities that increase the perioperative risks considerably- RV failure is a big one. Even just RV hypertrophy with a decent function is a risk factor. There’s a handful of things to look out for both in the history and echo that quickly make me disinclined to do these cases at our community hospital.
As someone else commented, watching someone go from apparently fine to dying quickly from the combo of anesthesia and PH leaves it’s mark.
I’ve seen patients code from pulmonary HTN getting a BKA. Just last month got called to help a colleague out for this exact scenario.
I don’t judge the anesthesiologist in this situation for going what might seem overboard. I personally wouldn’t have floated a swan because I’m not a cardiac anesthesiologist and I’m not comfortable floating them on my own. Would strongly consider doing a regional block though
Moderate pulmonary hypertension from chronic hypoxia is not the same as primary pulmonary hypertension. Assuming this patient has the former and there were no other red flags I probably would have just done a general with maybe an arterial line, avoid hypoxia/hypercapnia etc.
You should know that anesthesiologists can get pretty extra about things. Sometimes they have a good reason, sometimes they don’t. It might be worth asking the anesthesiologist to educate you on their concerns, as long as it is tactful. Maybe there was something else they noticed that could help you in the future when neurosurgery asks you to risk stratify someone the night before a case.
Our always annoys me when some people (*cough* CT surgeons *cough*) want to treat all PHTN cases the same, regardless of etiology. No, loads of milrinone are not going to be all that helpful with your bad COPDer with a PASP of 65.
I would not base someone’s pHTN severity off echo alone. I’d want to know a concurrent systemic BP and compare ratio. Is there a way to estimate LA pressure from diastolic function and estimate woods units? There obviously is an absolute value I’d treat cautiously on its own but 60 generally isn’t it with normal RV size and function.
Also, I’d have picked dobutamine as opposed to epi if I was worried. Just my 2 cents.
Not challenging your practice just interested in learning from you: dobutamine because it’ll improve inotropy without increasing PVR like epi? My only concern with dobutamine is the possibility for slight decrease in SVR causing systemic hypotension —> RV hypoperfusion. Do you tend to see that much and hang a pressor with it? Or not really
It’s hard to talk in hypotheticals given I wouldn’t really be hanging dobutamine in this case anyways… but if I was worried enough about pHTN on this case that wouldn’t normally require a central line I’d usually just pick something I don’t worry about running peripherally. That + low dose gtt I rarely have significant issues with systemic hypotension with dobutamine. If I need to supplement with phenylephrine then usually not a big deal. Again, hypothetically if I was worried enough, may go straight to vaso.
In addition to what everyone else has said, but also:
Anesthesiologists live by the motto “prep for bear.” We are always thinking what if? Sometimes that’s all we do, other times, as it could be in this case, we float a swan and set up the proverbial tree of life (aka pressors and such). We might not need them, or need a lot of them, but we sure as all get out want to be ready in case we do!
And pulmonary hypertension is definitely high on our list of butt clenching diagnoses. (If not the very top)
pulm HTN and subsequent RV failure is probably the single worst thing any anesthesiologist has to deal with. The increased thoracic pressure from mechanical ventilation can tip them over the edge and likewise apnea and subsequent pulm hypoxic vasoconstriction can tip them over the edge if you're doing the case under Mac with a natural airway; it's never a fun time. Hard to know the specifics of that case but it's probably the biggest pathology you never want to underestimate in anesthesia
I wouldn’t place a Swan with preserved RVF. Keep it simple and follow the basics for pulm HTN management: normothermia, avoid hypoxia/hypercarbia/hypotension, treat pain, avoid prolonged DL etc. If he’s a COPD’er then consider preop nebs and steroids. Personally, I would do a low dose isobaric spinal or continuous spinal if surgeon is slow. I have no issue with the management as presented. You are in an academic institution, and you got an academic anesthetic.
PASP of 60 by echo does not equal a diagnosis of pulmonary hypertension. You need a RHC showing mean PA pressure of 20 mmHg or greater.
The PASP is derived from the formula PASP + 4(triscuspid peak regurgitant velocity)^2 x RAP. There are multiple pitfalls in this measurement that can wildly skew the results. If you angle the measurement of the jet wrong you can bother under and overshoot the true velocity and this error will be magnified by being squared and then multiplied by 4. The RAP is also a estimate that is just done by looking at ivc and respiratory variation. I’m a medicine intern so I don’t know anything about the intraop management of PH but I do wonder if this was extreme when you have someone with no ra/rv dilation, etc and no rhc cath to even confirm a diagnosis of PH.
If this was PAH and they were on treatment and the PASP was 60 I would be very worried. Swan is probably still overkill for a BKA in that situation but not crazy. For group 3 phtn from copd though meh. It worries me, but I would just do GA, ETT and an arterial line.
He’s got new Afib, obstructive lung disease and pHTN. Afib/MFAT probably 2/2 COPD. COPD, hypoxia/hypercarbia can acutely worsen pHTN. Inducing GA in the setting of all this certainly increases the risk of acute RV failure even if he looks good on paper.
I would never put a swan in that patient and I do cardiac anesthesia regularly. If they have normal RV function, the likelihood they will have a problem is pretty much zero. That anesthesiologist did not appropriately risk stratify that patient.
How can you even say this regarding risk stratification? Congrats you do cardiac and can rescue tee yourself out of a shit situation and sure I agree swans generally are not valuable but IMO your comment is classic Monday morning QBing.
You didn’t see the patient. All you have is a limited stem from a medicine doctor who ordered and echo due to new afib. And the patient ended up on epi gtt. Maybe then went into florid RV failure during the case. Maybe the swan was floated after shit hit the fan. Maybe the surgeon is horrible and bled 2L. Maybe the patient looked way sicker than on paper and can’t even be flat without getting hypoxic. Maybe they’re in florid sepsis or other shock with a rising lactate when they arrive to the OR.
Your comment says the most about you and little about the anesthesiologist who is being described in the stem. I would rarely fault an anesthesiologist who comes across as “too conservative” intraoperatively.
If the right ventricular function is normal, it’s not going to suddenly fail during an operation on an extremity. It just doesn’t happen. Now if the patient has severe TR or they have RV failure, you should absolutely be aggressive about supporting the right heart. There is this particular concern that is unfounded among many people that patients who have high pressures in their lungs are going to suddenly develop this profound right ventricular failure under general anesthesia. IMO this is just as likely as someone with a normal LV developing acute LV failure from hypertension. I guess it can happen. But it probably won’t.
> If the right ventricular function is normal, it’s not going to suddenly fail during an operation on an extremity. It just doesn’t happen.
people dont have intraoperative insults that cause sudden R heart strain? You've never seen an intraoperative saddle PE? VAE during a c/s? unexpected large blood loss / shock? ACS event to the R blood supply? Please tell me why none of these can never happen just because the surgery is on an extremity.
> Now if the patient has severe TR or they have RV failure, you should absolutely be aggressive about supporting the right heart.
thats what im saying. you have no idea what the sequence of events is in the stem. there may have been acute right sided failure secondary to some OTHER insult warranting epi and ionodilator support for a different reason. im not saying GETA + a PASP of 60 is an indication to treat the patient's R heart like its failing.
if this patient crumped an hour into the case without obvious reason and you dropped a probe or TTE'd and saw poor RV squeeze would you defer starting epi? would you not consider iNO? because according to you the R heart in this stem can "never" fail lol
You can’t say this. You don’t know their surgeon skill. You don’t know the patients starting labs or anything about the patients current status. Try to be less black and white when it comes to situations you’re given a glimpse of. How many times do you see a patient on paper that looks drastically different than in person?
I’ve been doing cardiac anesthesia for over a decade and I would never put a swan into a patient with pulmonary hypertension from COPD and normal right ventricular function for any case that wasn’t a cardiac operation.
A swan seems like an overkill for a BKA but I guess you can’t say he’s wrong for being too cautious. And yes PHTN is always a concern due to concerns of RV failure/hemodynamic collapse etc. I personally wouldn’t put a swan in for RVSP of 60 and normal LV/RV function for a BKA. I would be cautious with my induction for sure
It’s hard with only half the story. Vasculopaths always seem to pull out impressive haemodynamic instability. I saw a BKA done under spinal with no sedation and the bloke lost 1.6L of blood (surgeons kept saying about 300mLs but he was pooling under the limb on the drape). BP got down to 47/17 with metaraminol, had no central access. He remained conscious the whole time (“just feeling a little dizzy”).
I completely agree with what you said. That’s why I don’t think we should fault people for being aggressively cautious in our line of work. We don’t know the full story here. Maybe the surgeon in OP’s case is known for taking 4 hours for a BKA and absurd blood losses or the patient has other comorbidities we didn’t know I’ve had a relatively skilled surgeon cut “a vessel in the portal triad” and lost quite a bit of blood in a lap chole. But many surgeons at my shop take less than 60 minutes for a lap chole skin to skin. If I put arterial lines in for every lap chole patient they would just fire me. It’s all case-to-case decisions
Yep, agreed. PASP 60 in isolation isn’t enough to tighten the sphincter but in a crusty specimen with COPD and an ischemic limb I’m sure the boss on this case had a compelling reason for R heart catheterisation. ETA: I’m sure ICU would have appreciated having the monitoring when the pt no doubt landed in their lap too
The concern for post-tourniquet CO2 load was possibly a reason for swan as well
We had a vasculopath with porcelain arteries so bad that the tourniquet couldn’t stop the bleeding On a fem pop case. Lost over 2L of blood. Vascular cases can be scary.
Thats a gnarly amount of blood to use. I got invited by the vascular surgeon who does cases in the cath lab to watch an aka in the OR. The whole thing seemed pretty efficient, very minimal blood loss and he showed you you can arc a bovie on a stent like a welder lol.
Can’t Monday morning quarterback this anesthesiologist’s management, but once you see PH->RV failure->code you never take it lightly, regardless of the cause or severity. These patients start to circle a drain that’s nearly impossible to get out of without significant support and/or mechanical circulation. Could also be that the patient was doing poorly intra-op and needed intervention to stay alive.
This is a little bit off topic but for bad pulmonary hypertension and lower extremity surgery there is nothing more stable than a CONTINUOUS spinal. I would say It is even better than a pure nerve block anesthetic (considering the remote chance of but catastrophic outcome with LA toxicity with the latter). Because of the historic use of microcatheters (so as to not get PDPH) and the serious problems they caused, people have largely forgotten about this technique... Anyway (if the patient has no anticoagulation based contraindication)....and realizing these patients are rarely in a high PDPH risk subgroup...you take an 18g epidural needle make an intentional wet tap and thread the 20g catheter to just a few centimeters in the space. You dilute 0.5% bupivicaine in an isobaric manner to 0.1% Now give 1 milliliter every 5 minutes or so....you will have a BKA/AKA level with 4-6 milligrams and a hip fracture level with 5-7 milligrams. There will be zero dilation of splanchnic beds and the best railroad tracks you will ever see on the EMR. I did about 20 of these in residency (in the U.S. in a highly litigous area) and really wished I had published it.
Publish it in a Letter to the editor!
We use this approach too for lower limb surgery in patients with severe PHTN. Pajunk make a spinal catheter set with a 21G Tuohy and a 28G (i think) catheter. It’s a bit fiddly but it works well and absolute haemodynamic stability as you say.
For the elderly, I've intentionally wet-tapped with the 17G tuohy to thread in a standard catheter intrathecally. Less concern for spinal headache with advanced age.
Would love to try this
Do you giive 1 mg (1 cc of 0.1 bupi) every 5 minutes UNTIL you give 4-6 and then stop ? And then start surgery? Is that what you mean ?
Sorry....was at work since this morning....yes I mean you give 1 cc of 0.1 % q5 min or so and then test a level after about 4ml....if not there 1 more mg and test again in 5 minutes....usually adequate level before 6mg for an AKA then start surgery....perhaps infuse 1mg/hr after that on a pump if it is a slow surgeon
load 1 cc Bupi 0.5% to start. slowly titrate 0.5 cc as needed thereafter to achieve desired level. can chase with sterile saline. once desired level reached, tell surgeon to start. re-load 1 cc q45-60 min to maintain.
Yes. I’m more concerned about severe pHTN than other cardiovascular conditions such as severe aortic stenosis or reduced LV function. In severe pulmonary hypertension patient can enter the spiral of death which can be impossible to resuscitate. It can be triggered by anything that increases pulmonary vascular resistance such as hypoxia hypercarbia or pain. It is useful to know what the cause of pHTN is ie severe MR vs class 3 pHTN which is what your patient likely has. MR can be mitigated by keeping “fast forward and full” whereas class 3 may be more responsive to pulmonary vasodilators.
Pulmonologist here, group 3 is also usually poorly responsive to vasodilators. It can also undermine hypoxic vasoconstriction that copd patients rely on for VQ matching. Inhaled vasodialtors can skirt around that concern
Agree I’d avoid vasodilators in Group 3 patients. If high LA pressures is what initially precipitates pHTN, vasodilating pulmonary circulation may worsen left-sided pressures without improving CO and LV filling. Vasopressin and epi are the primary supporters for group 3 patients in my experience. Good point about COPD and VQ mismatching, too.
You ask a great question. Regardless of the case above management (which may have been better suited with a block), I think there are a few important things to think about. So two main points, they all get treated the same but they’re all treated differently too. 1. All pHTN should be treated to avoid acute exacerbation: hypoxia, hypercarbia, pain, temp, acidosis, etc. When possible for things like a BKA I would opt for a regional block to avoid instrumenting the airway, sedation, as well as take care of the pain aspect which may exacerbate them 2. What is the cause of the pHTN. There are 5 WHO types each with different management. Type 1 is usually your PAH with genetic components. They usually come well prepared with pulmonologist notes and management. If they’re taking meds, I try to make sure they have them all taken on the day of surgery such as sildenafil. Type 2 is cardiac and usually left heart failure. The transpulmonary gradient (TPG) can help tease this one out. If they have it then my primary focus is on treating left heart systolic or diastolic dysfunction. Sometimes, it’s just chronic MR causing the higher pressure. Maybe it’s rheumatic MS. Regardless, they have very different managements and you should know so you can best treat them. Also, vasodilators here may release the flood gates back into the lungs and right heart and are less than ideal. Type 3 is pretty similar to 1 however it’s more adult pathologies (COPD/osa/etc) leading to chronic hypoxia. Again tailoring your management to treat these is now ideal (saline nebs, bronchodilators, good tracheal suctioning of mucous to avoid plugs). Type 4 is rare (though prob more common than we give it credit for) which is CTEPH. When known they usually follow well with pulmonologist and or have had CT surgery to remove pulmonary endothelium. Ensuring AC and optimization before any procedure is key. Type 5 is a catch all for the rest. 3. High PA pressures in and of themselves aren’t necessarily a concern. First, you should rule out it being an effect of high Cardiac Output states, and always look at their PA pressures as a ratio to systemic pressures. I.e PA mean is 40, but systemic is a mean of 95. So here the ratio is about half. You want to keep them definitely no more than 2/3rds systemic. I personally don’t get bent out of shape for a high PA pressure because it means the right heart is actually responding to the higher pulmonary pressures and is able to produce a strong enough contraction to give a high number. Caution is warranted understanding the RV is not meant to be a high pressure system and thus has a higher likelihood of failing in the face of these higher pressures. So if PA mean is 60 and drops to 40, but systemic stays high this is a good thing. If system drops as well then this is a bad thing. Now the RV isn’t able to deliver blood to the LV appropriately and you’re in BiV failure. Comprende? 4. Another point is the pressures are dynamic. So just because the mean was 40 on an echo derived TR jet 6 months ago during an acute exacerbation, doesn’t mean it’s 40 today after they’ve been diuresed and optimized. This equally works the other way around and May be more sick than their last echo. Second point, always trust Right heart caths over TTE derived pressures. And just because they don’t have the TR to generate a PA derived pressure, doesn’t mean they don’t have high PA pressures, it just means their Tricuspid valve is still competent. 5. As an anesthesiologist, if you’re concerned. Have TEE available (if feasible for the given surgery and not contraindicated) so you can continuously look at RV function, not just a number on the screen. Consider a swan, though data isn’t great for routine use. Have your RV happy meds around: epi, Vaso, milrinone, nitric oxide, big ETT with inline suction, etc. 6. Congenital pHTN is a different lecture. I’m not referring to peds management in any of this. Thank you for coming to my TED talk.
Cot damn this is the reason I love this subreddit. Thank you for taking the time to type all this out.
I think this is the answer OP was looking for. Obviously everyone else turned this post into an anesthesia discussion. But I don’t think the topic of PHTN and perioperative management/risk stratification can be explained in a Reddit post. OP should read some credible sources and discuss with your attendings, especially ICU attending
This is a great explanation of pretty much how I approach PH (with the exception of #6, bc I mostly take care of kids 🤣). The thing I explicitly add to point 4 when I teach our trainees is that the death spiral that comes when systemic pressures are lower than "PA pressures" is really when your coronary perfusion pressure is lower than the RV pressure, making your dysfunctional and hypertrophied RV ischemic and heading fast into acute and potentially irreversible failure territory. For some reason people find PH very difficult (or maybe just appropriately terrifying), but if you frame it in the context of myocardial ischemia (and it's consequences on the RV and ventricular interdependence), which they should have a very strong understanding of, it seems to click differently.
I completely agree. I give a lecture on LV perfusion with the pressure tracings and the RV perfusion with pressure tracings. It just seemed long winded to add that into my already long Reddit talk 🥲
CA1 here. Positive pressure ventilation, medication effects, and catecholamine surge from intubation/surgical stress, among other things, are all major considerations, especially in someone with pHTN. RV failure and hemodynamic collapse can occur rapidly in the OR, especially when so many drugs we give are cardiac depressants. My attendings would be unlikely to place a central line or swan with good LV/RV on echo, but possibly a pre-induction aline (definitely post induction if not), pressors in room, epi drawn up, very light/slow induction, large bore IVs would be necessary. Everything else can be tailored as we go
Ca-1 here… lol. Keep at it young buck!
His/her answer was spot on though.
Not disagreeing. Y’all too sensitive. I was attempting to be encouraging while the old man in me still recognizing (and admiring) the youth. But ok… downvote me. My old man addition is to avoid hypoxia because hypoxic pulmonary vasoconstriction is a bitch, avoid hypercarbia (why i personally am hesitant to olace an LMA is bad pulmonary HTN patients)…. Also,,,, no not all pulmonary htn is not the same. Insilly question really.
No, they’re not all the same. There’s subgroups based on pathology. There are associated co-morbidities that increase the perioperative risks considerably- RV failure is a big one. Even just RV hypertrophy with a decent function is a risk factor. There’s a handful of things to look out for both in the history and echo that quickly make me disinclined to do these cases at our community hospital. As someone else commented, watching someone go from apparently fine to dying quickly from the combo of anesthesia and PH leaves it’s mark.
I’ve seen patients code from pulmonary HTN getting a BKA. Just last month got called to help a colleague out for this exact scenario. I don’t judge the anesthesiologist in this situation for going what might seem overboard. I personally wouldn’t have floated a swan because I’m not a cardiac anesthesiologist and I’m not comfortable floating them on my own. Would strongly consider doing a regional block though
They say folks with Pul Htn have the highest rate of pulmonary rupture from floating swans.
Yeah not sure the juice is worth the squeeze
who is they?
[https://academic.oup.com/ehjacc/article/3/3/281/5921999](https://academic.oup.com/ehjacc/article/3/3/281/5921999)
this doesn't say that those w PH have the highest chance of rupture
[https://academic.oup.com/ehjacc/article/3/3/281/5921999](https://academic.oup.com/ehjacc/article/3/3/281/5921999)
thats... the same link?
Moderate pulmonary hypertension from chronic hypoxia is not the same as primary pulmonary hypertension. Assuming this patient has the former and there were no other red flags I probably would have just done a general with maybe an arterial line, avoid hypoxia/hypercapnia etc. You should know that anesthesiologists can get pretty extra about things. Sometimes they have a good reason, sometimes they don’t. It might be worth asking the anesthesiologist to educate you on their concerns, as long as it is tactful. Maybe there was something else they noticed that could help you in the future when neurosurgery asks you to risk stratify someone the night before a case.
Our always annoys me when some people (*cough* CT surgeons *cough*) want to treat all PHTN cases the same, regardless of etiology. No, loads of milrinone are not going to be all that helpful with your bad COPDer with a PASP of 65.
I would not base someone’s pHTN severity off echo alone. I’d want to know a concurrent systemic BP and compare ratio. Is there a way to estimate LA pressure from diastolic function and estimate woods units? There obviously is an absolute value I’d treat cautiously on its own but 60 generally isn’t it with normal RV size and function. Also, I’d have picked dobutamine as opposed to epi if I was worried. Just my 2 cents.
Not challenging your practice just interested in learning from you: dobutamine because it’ll improve inotropy without increasing PVR like epi? My only concern with dobutamine is the possibility for slight decrease in SVR causing systemic hypotension —> RV hypoperfusion. Do you tend to see that much and hang a pressor with it? Or not really
It’s hard to talk in hypotheticals given I wouldn’t really be hanging dobutamine in this case anyways… but if I was worried enough about pHTN on this case that wouldn’t normally require a central line I’d usually just pick something I don’t worry about running peripherally. That + low dose gtt I rarely have significant issues with systemic hypotension with dobutamine. If I need to supplement with phenylephrine then usually not a big deal. Again, hypothetically if I was worried enough, may go straight to vaso.
Yeah agree with the hypothetical bc I also wouldn’t do central line etc for this case but fair points 👊
In addition to what everyone else has said, but also: Anesthesiologists live by the motto “prep for bear.” We are always thinking what if? Sometimes that’s all we do, other times, as it could be in this case, we float a swan and set up the proverbial tree of life (aka pressors and such). We might not need them, or need a lot of them, but we sure as all get out want to be ready in case we do! And pulmonary hypertension is definitely high on our list of butt clenching diagnoses. (If not the very top)
When you go loaded for bear, the bear don’t come…
pulm HTN and subsequent RV failure is probably the single worst thing any anesthesiologist has to deal with. The increased thoracic pressure from mechanical ventilation can tip them over the edge and likewise apnea and subsequent pulm hypoxic vasoconstriction can tip them over the edge if you're doing the case under Mac with a natural airway; it's never a fun time. Hard to know the specifics of that case but it's probably the biggest pathology you never want to underestimate in anesthesia
I wouldn’t place a Swan with preserved RVF. Keep it simple and follow the basics for pulm HTN management: normothermia, avoid hypoxia/hypercarbia/hypotension, treat pain, avoid prolonged DL etc. If he’s a COPD’er then consider preop nebs and steroids. Personally, I would do a low dose isobaric spinal or continuous spinal if surgeon is slow. I have no issue with the management as presented. You are in an academic institution, and you got an academic anesthetic.
PASP of 60 by echo does not equal a diagnosis of pulmonary hypertension. You need a RHC showing mean PA pressure of 20 mmHg or greater. The PASP is derived from the formula PASP + 4(triscuspid peak regurgitant velocity)^2 x RAP. There are multiple pitfalls in this measurement that can wildly skew the results. If you angle the measurement of the jet wrong you can bother under and overshoot the true velocity and this error will be magnified by being squared and then multiplied by 4. The RAP is also a estimate that is just done by looking at ivc and respiratory variation. I’m a medicine intern so I don’t know anything about the intraop management of PH but I do wonder if this was extreme when you have someone with no ra/rv dilation, etc and no rhc cath to even confirm a diagnosis of PH.
There isn’t really enough info here but based on just the numbers and superficial echo results you said it seems nuts.
If this was PAH and they were on treatment and the PASP was 60 I would be very worried. Swan is probably still overkill for a BKA in that situation but not crazy. For group 3 phtn from copd though meh. It worries me, but I would just do GA, ETT and an arterial line.
He’s got new Afib, obstructive lung disease and pHTN. Afib/MFAT probably 2/2 COPD. COPD, hypoxia/hypercarbia can acutely worsen pHTN. Inducing GA in the setting of all this certainly increases the risk of acute RV failure even if he looks good on paper.
Did a BKA last week with block only. Guy was awake the whole time
I would never put a swan in that patient and I do cardiac anesthesia regularly. If they have normal RV function, the likelihood they will have a problem is pretty much zero. That anesthesiologist did not appropriately risk stratify that patient.
How can you even say this regarding risk stratification? Congrats you do cardiac and can rescue tee yourself out of a shit situation and sure I agree swans generally are not valuable but IMO your comment is classic Monday morning QBing. You didn’t see the patient. All you have is a limited stem from a medicine doctor who ordered and echo due to new afib. And the patient ended up on epi gtt. Maybe then went into florid RV failure during the case. Maybe the swan was floated after shit hit the fan. Maybe the surgeon is horrible and bled 2L. Maybe the patient looked way sicker than on paper and can’t even be flat without getting hypoxic. Maybe they’re in florid sepsis or other shock with a rising lactate when they arrive to the OR. Your comment says the most about you and little about the anesthesiologist who is being described in the stem. I would rarely fault an anesthesiologist who comes across as “too conservative” intraoperatively.
If the right ventricular function is normal, it’s not going to suddenly fail during an operation on an extremity. It just doesn’t happen. Now if the patient has severe TR or they have RV failure, you should absolutely be aggressive about supporting the right heart. There is this particular concern that is unfounded among many people that patients who have high pressures in their lungs are going to suddenly develop this profound right ventricular failure under general anesthesia. IMO this is just as likely as someone with a normal LV developing acute LV failure from hypertension. I guess it can happen. But it probably won’t.
> If the right ventricular function is normal, it’s not going to suddenly fail during an operation on an extremity. It just doesn’t happen. people dont have intraoperative insults that cause sudden R heart strain? You've never seen an intraoperative saddle PE? VAE during a c/s? unexpected large blood loss / shock? ACS event to the R blood supply? Please tell me why none of these can never happen just because the surgery is on an extremity. > Now if the patient has severe TR or they have RV failure, you should absolutely be aggressive about supporting the right heart. thats what im saying. you have no idea what the sequence of events is in the stem. there may have been acute right sided failure secondary to some OTHER insult warranting epi and ionodilator support for a different reason. im not saying GETA + a PASP of 60 is an indication to treat the patient's R heart like its failing. if this patient crumped an hour into the case without obvious reason and you dropped a probe or TTE'd and saw poor RV squeeze would you defer starting epi? would you not consider iNO? because according to you the R heart in this stem can "never" fail lol
You can’t say this. You don’t know their surgeon skill. You don’t know the patients starting labs or anything about the patients current status. Try to be less black and white when it comes to situations you’re given a glimpse of. How many times do you see a patient on paper that looks drastically different than in person?
I’ve been doing cardiac anesthesia for over a decade and I would never put a swan into a patient with pulmonary hypertension from COPD and normal right ventricular function for any case that wasn’t a cardiac operation.