Obese, hypoxic, Down's pt for TEE

[excalibur]

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My case for tomorrow...

31 year old Downs female pt is scheduled for TEE tomorrow. 5'6'', 153 kg. She presented to the hospital with SOB and her initial ABG on admission was 7.36/48/55 on 2L NC. She is not on home O2, but uses BIPAP at night with 15 PS, 5 PEEP, 35% FIO2, and 10 rate.

Pt has a history of SOB at rest, but has never had a history of cardiac problems per mom. BNP was 350 and CXR shows pulmonary edema bilaterally. No signs of infection. CBC, BMP, coags normal.

Pt also has a history of hypothyroidism and has been on Synthroid for 3 years. TSH, T4 wnl. Cardiology attempted TTE, which was a technically poor study, but estimated an EF of 60%. ECG: sinus tach (101), low voltage QRS, poor R wave progression.

Exam:
104/53, 65, RR 19 and respirations are not labored, 94% on 3L NC
MP II, very short neck, wide neck, small mouth opening, big tongue, good neck extension, >3FB
CTAB, RRR

Most recent ABG on 3L NC is 7.43/60/60/39

*C-spine film pending to evaluate atlanto-occipital joint instability*

What would be your anesthetic plan?

Please provide me with backup plans in case plan A does not work as in the thread Jet posted with the facial abscess.

I'll let you know the plan(s) my attending and I had, and thn let you know how it went

 

[Fastrach]

Assuming pt won't cooperate with a true awake fiberoptic, I think you still have plenty of options:

For induction:
Ketamine blow dart if she won't cooperate with an IV, otherwise go with Dexmedetomidine +/- Midaz for a sedated yet spontaneously breathing approach, +Glyco (or scope may be better if she's tachy) to dry things up, +topicalization if tolerated

Optimize positioning c shoulder roll/ramp

Then for tubage:
Plan A: Oral fiberoptic
Plan B: Nasal fiberoptic
Plan C: Gently slide in LMA, keep spontaneously breathing but throw on some Sevo, and do wire-guided LMA/ETT exchange
Plan D: Rapid sequence & gentle DL with in-line stabilization

Extubate awake at the end and hook up to bipap asap.

 

[jetproppilot]

My case for tomorrow...

31 year old Downs female pt is scheduled for TEE tomorrow. 5'6'', 153 kg. She presented to the hospital with SOB and her initial ABG on admission was 7.36/48/55 on 2L NC. She is not on home O2, but uses BIPAP at night with 15 PS, 5 PEEP, 35% FIO2, and 10 rate.

Pt has a history of SOB at rest, but has never had a history of cardiac problems per mom. BNP was 350 and CXR shows pulmonary edema bilaterally. No signs of infection. CBC, BMP, coags normal.

Pt also has a history of hypothyroidism and has been on Synthroid for 3 years. TSH, T4 wnl. Cardiology attempted TTE, which was a technically poor study, but estimated an EF of 60%. ECG: sinus tach (101), low voltage QRS, poor R wave progression.

Exam:
104/53, 65, RR 19 and respirations are not labored, 94% on 3L NC
MP II, very short neck, wide neck, small mouth opening, big tongue, good neck extension, >3FB
CTAB, RRR

Most recent ABG on 3L NC is 7.43/60/60/39

*C-spine film pending to evaluate atlanto-occipital joint instability*

What would be your anesthetic plan?

Please provide me with backup plans in case plan A does not work as in the thread Jet posted with the facial abscess.

I'll let you know the plan(s) my attending and I had, and thn let you know how it went

I agree with the backup plan concept, Ex.

Gotta remember though that this is a diagnostic, notta therapeutic endeavor....so I'm sure you're gonna lay her on her side and titrate in propofol until the TEE can be passed...pretty simple in spite of her pathology....

PLAN B (which you won't need...propofol will work) could include dex, ketamine, etc etc.

My point about this being diagnostic is.....you don't wanna raise the invasiveness of this anesthetic to the point where the risk outweighs the benefit....risk (anesthesiologist intervention), benefit (TEE results).

So do the propofol thing.

Plan B should be "OK, maybe we'll try another drug."

Thats it.

Changing drugs.....and if the drug-changing doesnt work,

CANCELAMUNDO.

Cancel.

Buh bye.

Wouldnt even consider intubating her for this.

Risk vs benefit.

Doctor Kevin Krane taught me a long time ago to know what the consultant is gonna say before you get the consult.

I'll bet the TEE shows her cardiac pathology is primarily right-sided secondary to pulmonary hypertension.

 

[jetproppilot]

Assuming pt won't cooperate with a true awake fiberoptic, I think you still have plenty of options:

For induction:
Ketamine blow dart if she won't cooperate with an IV, otherwise go with Dexmedetomidine +/- Midaz for a sedated yet spontaneously breathing approach, +Glyco (or scope may be better if she's tachy) to dry things up, +topicalization if tolerated

Optimize positioning c shoulder roll/ramp

Then for tubage:
Plan A: Oral fiberoptic No.
Plan B: Nasal fiberoptic No!
Plan C: Gently slide in LMA, keep spontaneously breathing but throw on some Sevo, and do wire-guided LMA/ETT exchange No.
Plan D: Rapid sequence & gentle DL with in-line stabilization No.

Extubate awake at the end and hook up to bipap asap.

No need for intubation for a TEE.

And if there is a need,

CANCEL.

 

[SleepIsGood]

had similar case...except had to do RF ablation of the heart for atach/afib

we tried to do MAC..using propofol,etc.

then we tried unsuccesfully to do awak Oral FOI. Finally we got the awake nasal FOI.

 

[Fastrach]

So do the propofol thing.

Why even try this without intubating, JPP? You're setting this up to go down in flames from the get-go. You know she has no reserve, and as soon as she stops breathing her sats are gonna go boop boooop booooooooop. I just don't think you can keep her sats up long enough for them to stuff a TEE probe in fast enough and get a decent study before you have to bail and bag.

Point being, if you know she'll crap out on you in advance, are you gonna just tell them up front "No echo for you" just because you think she shouldn't be intubated for it?

 

[jetproppilot]

had similar case...except had to do RF ablation of the heart for atach/afib

we tried to do MAC..using propofol,etc.

then we tried unsuccesfully to do awak Oral FOI. Finally we got the awake nasal FOI.

Thats not similar.

Diagnostic (TEE).

Therapeutic (RF ablation).

 

[jetproppilot]

Why even try this without intubating, JPP? You're setting this up to go down in flames from the get-go. You know she has no reserve, and as soon as she stops breathing her sats are gonna go boop boooop booooooooop. I just don't think you can keep her sats up long enough for them to stuff a TEE probe in fast enough and get a decent study before you have to bail and bag.

Point being, if you know she'll crap out on you in advance, are you gonna just tell them up front "No echo for you" just because you think she shouldn't be intubated for it?

I've done many, many anesthetics for TEE.

None required intubation. All MACs. Its done EVERY DAY across our great nation.

And to answer your question about why do this case without intubating,

please re-read my intitial post on this thread.

I think my reasoning is explained pretty clearly.

My question to you is: Why intubate for this diagnostic procedure? Why subject her to all the RISK a difficult airway brings, all for a TEE?

 

[Dejavu]

This patient definitely has a Ketamine deficiency.

 

[Noyac]

Yes Ketamine.
I did one like this the other day but not a Down's pt. He was 5'10" 450lbs with an EF of 15% for "diagnostic" TEE. CPAP, PHTN all that ****.
I topicalized his throat well with viscous lido until his gag was gone (use whatever you want here but I like the viscous b/c they swallow it). I started a low dose propofol infusion. Don't remember the rate but it was around 75 mcg/kg/min, i think. They started to pop him with small doses of ketamine. It went great. Just be patient with the sedation and it will work.
I find that most Down's folks do well with sedation b/c they have had many things done to them and they are not so worked up. But if this isn't the case the ketamine dart is great. Then continue with above. Since they tried to sedate b/4 I'll bet she is sedatable (new word). We also have these face masks for O2 with a hole in them for scoping. Use this or cut out a hole big enough for the scope in a regular FM.

The airway is a problem especially with C1/2 instability, if present. Usually I find that once the probe is down it stents the airway open enough for the pt to breath. NOw if she has sev PHTN and her PCO2 is 60 now, then you don't want it to climb much. But for this short procedure you "should" be fine.
So if airway is god awful and cards gives you one hell of a reason to do this procedure then I don't know what to do. Glidescope or DL both work fine in Down's pts. I would screw with FOB unless first two fail. But I'm pretty much with Jet here, don't intubate unless necessary

Oh finally, do this in the OR where you have good help and space and tools etc.

 

[seinfeld]

No need for intubation as well.

? does the pt have eisenmengers syndrome? I would guess that a vsd would have been diagnosed years ago but you never know so practically less of a concern about increasing Pulm HTN (hypoxia and hypercarbia) and increaseing shunt fraction.

I did have a case a year or so ago where i was called in the middle of the night by GI/Medical ICU fellow. 30 something year old Downs pt with eisenmengers and upper GI bleed after NSAID use. They wanted the pt intubated for the Upper scope. One 20g, no central access, no aline, eisenmengers from unreparied VSD. HCT had dropped from 60 to 45 over week. Pt had low platelets and mild PTT elevation. Parents did not want intubation for extended periods of time. Baseline Pox low 80's. Refused to do the case without medical mangemant being attempted as 6months ago when she bleed with NSAIDS she remitted spontaneoulsy.

 

[seinfeld]

Yes Ketamine.
I did one like this the other day but not a Down's pt. He was 5'10" 450lbs with an EF of 15% for "diagnostic" TEE. CPAP, PHTN all that ****.
I topicalized his throat well with viscous lido until his gag was gone (use whatever you want here but I like the viscous b/c they swallow it). I started a low dose propofol infusion. Don't remember the rate but it was around 75 mcg/kg/min, i think. They started to pop him with small doses of ketamine. It went great. Just be patient with the sedation and it will work.
I find that most Down's folks do well with sedation b/c they have had many things done to them and they are not so worked up. But if this isn't the case the ketamine dart is great. Then continue with above. Since they tried to sedate b/4 I'll bet she is sedatable (new word). We also have these face masks for O2 with a hole in them for scoping. Use this or cut out a hole big enough for the scope in a regular FM.

The airway is a problem especially with C1/2 instability, if present. Usually I find that once the probe is down it stents the airway open enough for the pt to breath. NOw if she has sev PHTN and her PCO2 is 60 now, then you don't want it to climb much. But for this short procedure you "should" be fine.
So if airway is god awful and cards gives you one hell of a reason to do this procedure then I don't know what to do. Glidescope or DL both work fine in Down's pts. I would screw with FOB unless first two fail. But I'm pretty much with Jet here, don't intubate unless necessary

Oh finally, do this in the OR where you have good help and space and tools etc.

Our plan if the bleeding did not stop was similar to what is described above, To the OR, Ketamine for sedation as well as to keep svr up and prevent further L to R shunt. Place aline for HCT and BP monitoring, get better IV Access.

 

[Noyac]

No need for intubation as well.

? does the pt have eisenmengers syndrome? I would guess that a vsd would have been diagnosed years ago but you never know so practically less of a concern about increasing Pulm HTN (hypoxia and hypercarbia) and increaseing shunt fraction.

I did have a case a year or so ago where i was called in the middle of the night by GI/Medical ICU fellow. 30 something year old Downs pt with eisenmengers and upper GI bleed after NSAID use. They wanted the pt intubated for the Upper scope. One 20g, no central access, no aline, eisenmengers from unreparied VSD. HCT had dropped from 60 to 45 over week. Pt had low platelets and mild PTT elevation. Parents did not want intubation for extended periods of time. Baseline Pox low 80's. Refused to do the case without medical mangemant being attempted as 6months ago when she bleed with NSAIDS she remitted spontaneoulsy.

GI bleed= intubation

 

[seinfeld]

Risk benefit. 50% chance of death on induction versus conservative management which worked last time, your choice as a clinician.... we chose to play it conservative

Also the family in this case really did not want intubation and was only pushed to say yes when the GI guys stated that he would be immediatly extubated afterwards which we could not promise to the family.

Gi bleed doesnt always = intubation. In that case in college a couple people i knew would have need intubation every saturday night for mallory weiss tears.

 

[huktonfonix]

The difference being, healthy 20 year old with minor esophageal bleeding and fairly active airway reflexes does not equal a patient with a high risk of aspiration and subsequent death from aspiration. Ketamine or anything used for induction will still have some inhibitory effect on the respiratory drive. Looking at SVR is only half of the equation. Increasing pCO2 and likely decreasing PO2 is gonna increase that right to left shunt too. I would rather have control of that patients ventilation. You can always argue about the SVR and positive pressure effects too, but the risk/benefit to me indicates intubation in that patient (not necessarily the one from the OP though). You could also argue that ketamine increases PVR too or that this patients PVR may already be fixed but that quickly becomes a big circle jerk. For me the bottom line is that this person one way or another is gonna have no airway reflexes, a stomach full of blood, and minimal pulmonary reserve that will benefit from a controlled airway if this procedure is absolutely necessary. If not I would do as you did and cancel pending medical management IF the patient is fairly stable.

 

[seinfeld]

If not I would do as you did and cancel pending medical management IF the patient is fairly stable.

That was the case here.

I too, as commented on in earlier post, was also concerned about hypoxia and hypercarbia.

thanks for the great discussion

 

[urge]

*C-spine film pending to evaluate atlanto-occipital joint instability*

Are people still asking for those? I thought that fad was gone. I know I don't, and I do a lot of down's people.



I might be tempted to intubate.

 

[Mman]

I think a down's patient for a TEE could definitely use some Ketamine. It would chill them out enough to get the probe in and it wouldn't compromise their ventilation.

And I would agree that if you are having too much trouble, cancel. The indication for this is what exactly? A technically poor TTE in a patient with cardiac issues? You aren't going to make the patient any better with the TEE and do place them at some risk.

 

[Noyac]

Are people still asking for those? I thought that fad was gone. I know I don't, and I do a lot of down's people.



I might be tempted to intubate.

I believe its just that we are getting more lazy b/c we can intubate a gravid fire ant without putting her in the sniffing position. I still believe there may be merit to the study rather than a fad.

 

[Noyac]

The difference being, healthy 20 year old with minor esophageal bleeding and fairly active airway reflexes does not equal a patient with a high risk of aspiration and subsequent death from aspiration. Ketamine or anything used for induction will still have some inhibitory effect on the respiratory drive. Looking at SVR is only half of the equation. Increasing pCO2 and likely decreasing PO2 is gonna increase that right to left shunt too. I would rather have control of that patients ventilation. You can always argue about the SVR and positive pressure effects too, but the risk/benefit to me indicates intubation in that patient (not necessarily the one from the OP though). You could also argue that ketamine increases PVR too or that this patients PVR may already be fixed but that quickly becomes a big circle jerk. For me the bottom line is that this person one way or another is gonna have no airway reflexes, a stomach full of blood, and minimal pulmonary reserve that will benefit from a controlled airway if this procedure is absolutely necessary. If not I would do as you did and cancel pending medical management IF the patient is fairly stable.

First of all, this pt doesn't have a belly full of blood. This is a TEE.
Secondly, this pt should be NPO so airway reflexes are of little concern. If he is not NPO then cancel of course.
Thirdly, you may feel better having control of the ventilation and I can't fault that but I have seen many with very little pulmonary reserve do just fine without intubation.

I think you may have confused the OP's case with seinfeld's friends.


BTW seinfeld, I'd tube your friends just as well if we were doing an EGD or anything like that. Are you saying you wouldn't?

 

[huktonfonix]

First of all, this pt doesn't have a belly full of blood. This is a TEE.
Secondly, this pt should be NPO so airway reflexes are of little concern. If he is not NPO then cancel of course.
Thirdly, you may feel better having control of the ventilation and I can't fault that but I have seen many with very little pulmonary reserve do just fine without intubation.

I think you may have confused the OP's case with seinfeld's friends.


BTW seinfeld, I'd tube your friends just as well if we were doing an EGD or anything like that. Are you saying you wouldn't?

No confusion, I very specifically was replying to Seinfelds post and case. If you'll notice I referenced the OPs patient mentioning that I wouldnt have intubated that one.

 

[Noyac]

No confusion, I very specifically was replying to Seinfelds post and case. If you'll notice I referenced the OPs patient mentioning that I wouldnt have intubated that one.

👍

 

[seinfeld]

BTW seinfeld, I'd tube your friends just as well if we were doing an EGD or anything like that. Are you saying you wouldn't?

No if the pt had an upper GI bleed bad enough to warrant scoping then tube for sure, i was mearly pointing out that a reflex mechanism (GI Bleed = tube)in every pt without assesing need for procedure and the possibilty of intact airway reflexs who has a GI bleed may not be appropriate and that each situation needs its own assessment.

 

[geogil]

Our plan if the bleeding did not stop was similar to what is described above, To the OR, Ketamine for sedation as well as to keep svr up and prevent further L to R shunt. Place aline for HCT and BP monitoring, get better IV Access.

Ignorant MS2 here: if you increase SVR, wouldn't that exacerbate Left to right shunting? and isn't a right to left shunt the problem in eisenmengers?

 

[seinfeld]

Youre right, i meant to prevent increased Right to left shunt, but for a more full description....

VSD creates a left to Right shunt as left side pressures are higher than right.

With time the increased volume changes the Right heart and increases pulmonary vascular resistance (PVR)

Those changes can cause shunt reversal with a Right to left shunt.

So now you have to think about fluid mechanics and decide what would cause fluid to move in which direction. If you decrease the SVR blood will flow more easily out of the left heart into the perpheral circulation. This then creates a "sink" on the left side where it is now easier for a portion of the right heart output to go into the left ventricle, especially now with increased PVR (flow follows the path of least resistance). This syndrome is often referred to as Eisenmengers syndrome.

AS less blood goes through the lungs the blood becomes more hypoxemic.. The more hypoxemic the blood becomes the less oxygen all organs recieve but as the heart recieves less oxygen the function decreases which makes it even harder the the right heart to pump blood through the lungs, then the potential to start on downward spiral exists.

This is why the treatment for hypoxemia in patients with Right to left shunts is to increase SVR, it prevents increasing the right to left shunt and forces blood through the lungs. IN peds hearts (given the R--> L shunt physiology) a decreasing pulse ox is treated with phenylephrine (a pure vasocontrictor).

hope that helps, hope i did not screw up the description of the pathology

 

[Noyac]

VSD creates a left to Right shunt as left side pressures are higher than right.

With time the increased volume changes the Right heart and increases pulmonary vascular resistance (PVR)

Those changes can cause shunt reversal with a Right to left shunt.

So now you have to think about fluid mechanics and decide what would cause fluid to move in which direction. If you decrease the SVR blood will flow more easily out of the left heart into the perpheral circulation. This then creates a "sink" on the left side where it is now easier for a portion of the right heart output to go into the left ventricle, especially now with increased PVR (flow follows the path of least resistance). This syndrome is often referred to as Eisenmengers syndrome.

AS less blood goes through the lungs the blood becomes more hypoxemic.. The more hypoxemic the blood becomes the less oxygen all organs recieve but as the heart recieves less oxygen the function decreases which makes it even harder the the right heart to pump blood through the lungs, then the potential to start on downward spiral exists.

This is why the treatment for hypoxemia in patients with Right to left shunts is to increase SVR, it prevents increasing the right to left shunt and forces blood through the lungs. IN peds hearts (given the R--> L shunt physiology) a decreasing pulse ox is treated with phenylephrine (a pure vasocontrictor).

hope that helps, hope i did not screw up the description of the pathology

Doing those funky pedi hearts is the best way to learn this.

 

[Arch Guillotti]

Youre right, i meant to prevent increased Right to left shunt, but for a more full description....

VSD creates a left to Right shunt as left side pressures are higher than right.

With time the increased volume changes the Right heart and increases pulmonary vascular resistance (PVR)

Those changes can cause shunt reversal with a Right to left shunt.

So now you have to think about fluid mechanics and decide what would cause fluid to move in which direction. If you decrease the SVR blood will flow more easily out of the left heart into the perpheral circulation. This then creates a "sink" on the left side where it is now easier for a portion of the right heart output to go into the left ventricle, especially now with increased PVR (flow follows the path of least resistance). This syndrome is often referred to as Eisenmengers syndrome.

AS less blood goes through the lungs the blood becomes more hypoxemic.. The more hypoxemic the blood becomes the less oxygen all organs recieve but as the heart recieves less oxygen the function decreases which makes it even harder the the right heart to pump blood through the lungs, then the potential to start on downward spiral exists.

This is why the treatment for hypoxemia in patients with Right to left shunts is to increase SVR, it prevents increasing the right to left shunt and forces blood through the lungs. IN peds hearts (given the R--> L shunt physiology) a decreasing pulse ox is treated with phenylephrine (a pure vasocontrictor).

hope that helps, hope i did not screw up the description of the pathology

That is a good simplified explanation of the physiology at work. However I did more than a few pedi hearts during residency and I never gave neo (although I always had the dilutions drawn up "just in case"). In theory neo is of course the correct drug to give but when I asked a pedi heart attending if he ever gave it he could only think of a couple of instances in all his years and that was for an uncorrected tet. I can't recall if I ever specifically had to treat this scenario but I would guess that epi would have been given rather than neo. Now this may be a regional/institutional thing so take it FWIW.

 

[excalibur]

Sorry for the late reply, as I've been coming home late from work...

Thanks for all the replies.

Well, my attending and I felt that doing this case without a secure airway was not an option. I've read all the replies, and there are plenty who mentioned they would not intubate, and some that said they would.

My attending also wanted a pre-induction A-line which we placed.

So the plan the night before, was to do an awake FOI with no sedation and see how well our pt cooperated after topicalization. Plan B was if the patient was not cooperating that we would induce with ketamine.

The next morning upon seeing the patient, my attending thought that her airway looked favorable and that we would induce and attempt intubation with glidescope, and have regular and fastrach LMA in the room along with the Fiberoptic. So, 0.5 mg midaz for A-line. Another 0.5 mg of midaz prior to induction along with 0.4 glycopyrrolate. PreO2 with good ETCO2. Induced with Ketamine 90 mg, able to assist ventilation easily. Sux 80 mg. Glidescope, visualize cords easily and intubate.

During TEE, we dealt with hypotension in the low 80's and high 70's systolic and pt required about 2000 mcg of phenylephrine. Emergence and extubation went smoothly and pt transferred back to PACU.

TEE revealed heart was essentially normal.

I know several members here would have approached this case very differently, and some may have approched it similarly with some modifications. Some may think this was overkill, and some may agree with parts of the approach, but that's the beauty of anesthesia.

Feel free to discuss now that you know what we did.

 

[Arch Guillotti]

Dude who cares if it was overkill. You got the pt. through a challenging case safely so props to you.

Personally I think an awake FOI on a Down's pt. is crazy unless they hand you a difficult airway letter or they have a trach scar on their neck.

 

[ncdoc1974]

I don't think starting with some propofol sedation/MAC is a bad idea...I would most likely start this way...however if the sedation was inadequate, I would NOT cancel the case, I would instead convert to GA and intubate the patient...so what if she has a bad airway? lots of folks do and we've got lots of tools to deal with a bad airway...we are the airway experts...Even with a bad airway I would not view the risk as "so high" that I would cancel the case...as for what was actually done in the case...I have to admit I personally would not have placed the A-line...seems like overkill...maybe a vasotrac instead?

 

[jetproppilot]

Sorry for the late reply, as I've been coming home late from work...

Thanks for all the replies.

Well, my attending and I felt that doing this case without a secure airway was not an option. I've read all the replies, and there are plenty who mentioned they would not intubate, and some that said they would.

My attending also wanted a pre-induction A-line which we placed.

So the plan the night before, was to do an awake FOI with no sedation and see how well our pt cooperated after topicalization. Plan B was if the patient was not cooperating that we would induce with ketamine.

The next morning upon seeing the patient, my attending thought that her airway looked favorable and that we would induce and attempt intubation with glidescope, and have regular and fastrach LMA in the room along with the Fiberoptic. So, 0.5 mg midaz for A-line. Another 0.5 mg of midaz prior to induction along with 0.4 glycopyrrolate. PreO2 with good ETCO2. Induced with Ketamine 90 mg, able to assist ventilation easily. Sux 80 mg. Glidescope, visualize cords easily and intubate.

During TEE, we dealt with hypotension in the low 80's and high 70's systolic and pt required about 2000 mcg of phenylephrine. Emergence and extubation went smoothly and pt transferred back to PACU.

TEE revealed heart was essentially normal.

I know several members here would have approached this case very differently, and some may have approched it similarly with some modifications. Some may think this was overkill, and some may agree with parts of the approach, but that's the beauty of anesthesia.

Feel free to discuss now that you know what we did.

HMMMMMMMMMMMM.......

YOUR ATTENDING (you're in training no-limit-holdem-stud-I-mean-Ex so its all good)

was OK with

1) an A-line........FOR A TEE?

2)Potentially subjecting this patient to a fiberoptic with all the potential sequelae, and then decides its OK to take a look, with all the potential sequelae, FOR A TEE?

3) Resultant intraoperative hypotension from general anesthesia, with all the potential sequelae, FOR A TEE?

This is a DIAGNOSTIC study.....(a study who's (mosta the) results could've been arrived at in a much less invasive fashion.)

Not a THERAPEUTIC intervention.

RISK VERSES BENEFIT.

Think about that for a minute.

What risk am I taking, and whats the benefit to the patient?

Then the TEE is NORMAL.

WOW.

Sorry, I'm not following the reasoning here for an invasive anesthetic for a DIAGNOSTIC study.

There is no reason for you to put you and the patient ON DA LINE for a DIAGNOSTIC study.

 

[geogil]

This is why the treatment for hypoxemia in patients with Right to left shunts is to increase SVR, it prevents increasing the right to left shunt and forces blood through the lungs. IN peds hearts (given the R--> L shunt physiology) a decreasing pulse ox is treated with phenylephrine (a pure vasocontrictor).

hope that helps, hope i did not screw up the description of the pathology

Thanks. we're doing cardio right now and I hadn't considered the sink phenomenon from decreasesing SVR.

 

[Noyac]

I'm sure you learned a lot from that case. Maybe even more than you realize.

Its easy to criticize after the fact so I won't.

Except to say an A-line? Why?