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Case #47 The Medical Train Wreck


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#21 fiznat

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Posted 25 February 2009 - 04:55 PM

It occurred to me that I've never been in this situation before, but where exactly is the intersection between intubation and CPAP? All of the (non vent) CPAP devices I've seen fit over the mouth and nose together and have no attachment for an ET tube. If we intubate this guy and he needs continuous positive pressure, what is our solution? BVM with PEEP? Is that a good compromise?
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#22 JLP

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Posted 25 February 2009 - 05:32 PM

Sorry if this makes me look like a moron, but what's "bronch"? Thanks for all the pointers. This forum and of all you guys are an amazing resource!


you'll have to get in line behind me if you want to join the "look like a moron" club compared to this crowd.

By bronch I meant bronchoscope.

By the way, I meant to say that I probably would not use SUX unless I had a lot more info. I just remember an OR that shall not be named that RSI'd a late teen Duchenne muscular dystrophy survivor whose K was normal, gave SUX, patient shortly had hyperkalemic arrest . Unused muscles saving up K for years and overexpression of ACh receptors.
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#23 Speed

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Posted 25 February 2009 - 05:48 PM

where exactly is the intersection between intubation and CPAP?


Usually drive, WOB, LOC. those kinda things.

All of the (non vent) CPAP devices I've seen fit over the mouth and nose together and have no attachment for an ET tube. If we intubate this guy and he needs continuous positive pressure, what is our solution? BVM with PEEP? Is that a good compromise?


Your ventilator. If I think that's what your asking? A BVM with PEEP would work, but you would have a vent, right?
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Mike Williams CCEMT-P/FP-C

#24 MSDeltaFlt

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Posted 25 February 2009 - 08:08 PM

Before we get the cart before the horse and "assuming" it's CHF, can we confirm it with CXR? You can have audible rales with pulmonary infiltrates from pneumonia as well. I want to know if any and to what degree this poor soul has regarding CHF, pneumonia, pleural effusion, and/or atelectasis. CPAP just might not cut it here.
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Mike Hester, RRT/NRP/FP-C
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#25 jobrien

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Posted 25 February 2009 - 10:30 PM

Sorry if this makes me look like a moron, but what's "bronch"? Thanks for all the pointers. This forum and of all you guys are an amazing resource!

A "bronch" is referring to a bronchoscope that gives visual assistance in looking into a person's airways and suctioning, and/or lung tissue samples can be obtained. I agree with the above-mentioned treatment but probably would not want to intubate unless absolutely necessary (i.e. don't think you can make it to the referring facility) because I have seen bad situations made worse with RSI in CPMR- patient is difficult to reposition and almost impossible to BVM. Sometimes all you need is a nasal trumpet and suctioning and non-invasive ventilation can also be successful.
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#26 Mike MacKinnon

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Posted 25 February 2009 - 11:27 PM

Ok to answer some of the questions:

viking563: Welcome, keep getting involved it only helps you learn more. I believe my colleagues answered some of your questions as good (better) than I could :)

"How is his baseline mental status?"

Baseline is generally non-verbal but aware per parents.

ST RN/PM:

excellent responses.

Airway assessment:

Pt does not really help you here. His mouth opening you cannot really tell, everything else looks normal.

You pegged HCTS.

Attempt CPAP does not seem to work, he will not keep his face still with mask on.

12 lead shows II III AVF ST Depression

NTG drip up, lopressor given BP drops to 90/50 HR to 66 (quickly!) ST changes deepen Why did this happen?

Speed:

[quote]What kind of "contractures" are these? I see the RA, but I'd expect to see more deformity if it's bad enough to fix the joints in a contracture.[/quote]

Very true, that pic is just an example. Assume its mostly CP causing that. Also, just ignore the papules in the pic (i didnt even see em till you picked em out!)

[quote]The high iron, low clearance kinda points to why his skin is dark[/quote]

Exactly.

[quote]what's his output been, what does it look like[/quote]

Per mom he 'pees fine'. Thats all she can say

How would you intubate?

LWT:

[quote]besides the breathing, is there anything else she sees different about her son, such as his arm positioning qnd his skin color always the way it is presenting and if not how long ago did it get like that? How has his urine output been(does he have a foley)? What is his temperature?[/quote]

Mom says everything else seems the same as before. Temp is normal

EMT I2RN:

Welcome :)

Everything is latex free

semi-fowler does not work, why?

Lasix given, 80 mg... will that help anytime soon with his resp. distress?

nitro drip, 5mcg/min ius a bit low. If we are thinking MI then (as you know) its 400 mcg X 3 (sl nitro). If we are thinking fluid shifts probably best to start at 10 but good idea!

What is the concern with giving this guy versed? What can it do?

Would suxx be dangerous in the patient? Or not really?

MSdelta:

[quote]First off, is this his normal mentation?[/quote]

Mom says he seems a bit distressed but yes.

Not a DNR.

[quote]Onset of symptoms (suddenly, hours, days)[/quote]

Last 2 days.

[quote]When was the hemochromatosis diagnosed? Treated and how often/last treatment (last phlebotomy, if ever)? Known extent of damage to liver? Renal failure?[/quote]

hemochro was diagnosed 2 years ago, just Oral treatment 1st phlebotomy one week ago. (excellent question). Why do they do this?

Liver and kidney extent unknown by mom.

No fever no ports

last cardiac eval was months ago.. mom does not remember anything new, no MIs and does not know EF

No choaking no swallowing issues.

RR is fast TV is not good.

Blood glucose 375

Ht ~6 ft wt ~155 nothing else odd.

Medic09:

[quote]Why is he on a beta blocker? Lasix?[/quote]

HTN and CHF :)

[quote]Are the contractures new?[/quote]

nope not at all.

[quote]Does he normally have some level of respiratory compromise?[/quote]

He has had multiple resp. infections per mom, but never like this.

:"How's his WOB? Is there reasonable chest expansion?"

working hard expansion seems minimal.

JVD is obvious... but is it the WOB and terror or past HX? hard to say..
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Mike MacKinnon MSN CRNA
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#27 viking563

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Posted 25 February 2009 - 11:57 PM

NTG drip up, lopressor given BP drops to 90/50 HR to 66 (quickly!) ST changes deepen Why did this happen?

Inferior ischemia already, NTG and Lopressor caused him to become hypovolemic increasing the poor perfusion and in turn made the ischemia worse. I'd slow the NTG until his pressure came back up. As far as airway control try a nasal intubation with maybe a little versed, if that doesn't work try an awake intubation with sedation and topical anesthetic. If that doesn't work plan C would be back to basics with a NP airway and some good suctioning. Do the heart sounds sound distant and are the lung sounds equal and present? Checking in the off chance that this may be a slow developing tension pneumo or even tamponade.
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#28 MedicNurse

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Posted 26 February 2009 - 06:57 AM

Hemochromatosis is a metabolic disorder (common cause hereditary) that causes iron absorption to be increased, impaired iron cycling at the cell level and causes excessive iron deposits in various organs. When excess iron builds in the myocardium (other organs, too!) - they fail to function properly - CHF/Pulmonary edema, AMI, diabetes and endocrine disorders are all expected in advanced disease.

The disease cannot be "cured" just managed via chelation by deferoxamine or therapeutic phelobotomy as the standard treatment. Approx 1 unit of blood is removed periodically (every 10 days or so) until iron marker levels near normal. Therapeutic phelebotomy remains a standard practice and if the disease is caught early this therapy will prevent end organ damage with few to any side-effects.

As blood is extracted, bone marrow is stimulated to make new red blood cells (RBCs).
Iron is transported from body stores to make hemoglobin, an integral part of the RBC. RBC production further increases to replace blood removed through phlebotomy.
Phlebotomy allows donations that will deplete iron strores and in turn increase RBC production and the patient's iron level is reduced to a safe and healthy level.

So a blood letting may be called for - not that I'd know how to MacGyver this one.

Sure there are EKG changes (seems to be a straight forward inferior MI) and the standard treatment has unexpectedly bottomed the pressure - the overriding EKG changes may be "masking" others or hell - who knows - this man is sick.

I think this patient is highly suspect for a PE. Coagulopathies can exist in hepatic disease. If this is a PE - the best treatment is support oxygenation/ventilation and CO - and fly like the wind to interventional CT and maybe they can remove the PE and place a filter???


I maintain controlling the airway and maximizing oxygen delivery MUST occur in this patient.

I'm not too worried about Ducheenes or other MD etiologys - I'd think that CP, DD/MR and the other medical challenges are enough. So, as for succs - if I need it - I'd proceed and be prepared to immediately intervene if hyperkalemia becomes apparent. Others note that versed might be bad - well, that drug is metabolized in the liver - but, the need had to be better than the consequences. He already takes daily longer acting benzos - so I'd be cautious.

So - Nasal ETT would be my first choice and commit to RSI if not able to secure quickly.

Give succs and versed (judiciously) if you need to and proceed.

The dudes HR dropped because he was given the "standard" IV doses of Lopressor cause he was already taking a beta blocker.

Well, the "standard" treatment for the abnormal EKG is not working too well. Still think that some judicious IVF may assist.

I know that emergent phelobotomy might be necessary-I'm not sure where/how to start that one.


Waiting to hear other fine opinions.


Fly SAFE!!
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#29 EMT-I2RN

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Posted 26 February 2009 - 03:08 PM

Ok to answer some of the questions:

viking563: Welcome, keep getting involved it only helps you learn more. I believe my colleagues answered some of your questions as good (better) than I could :)

"How is his baseline mental status?"

Baseline is generally non-verbal but aware per parents.

ST RN/PM:

excellent responses.

Airway assessment:

Pt does not really help you here. His mouth opening you cannot really tell, everything else looks normal.

You pegged HCTS.

Attempt CPAP does not seem to work, he will not keep his face still with mask on.

12 lead shows II III AVF ST Depression

NTG drip up, lopressor given BP drops to 90/50 HR to 66 (quickly!) ST changes deepen Why did this happen?

Speed:
Very true, that pic is just an example. Assume its mostly CP causing that. Also, just ignore the papules in the pic (i didnt even see em till you picked em out!)
Exactly.
Per mom he 'pees fine'. Thats all she can say

How would you intubate?

LWT:
Mom says everything else seems the same as before. Temp is normal

EMT I2RN:

Welcome :)

Everything is latex free

semi-fowler does not work, why?

Lasix given, 80 mg... will that help anytime soon with his resp. distress?

nitro drip, 5mcg/min ius a bit low. If we are thinking MI then (as you know) its 400 mcg X 3 (sl nitro). If we are thinking fluid shifts probably best to start at 10 but good idea!

What is the concern with giving this guy versed? What can it do?

Would suxx be dangerous in the patient? Or not really?

MSdelta:
Mom says he seems a bit distressed but yes.

Not a DNR.
Last 2 days.
hemochro was diagnosed 2 years ago, just Oral treatment 1st phlebotomy one week ago. (excellent question). Why do they do this?

Liver and kidney extent unknown by mom.

No fever no ports

last cardiac eval was months ago.. mom does not remember anything new, no MIs and does not know EF

No choaking no swallowing issues.

RR is fast TV is not good.

Blood glucose 375

Ht ~6 ft wt ~155 nothing else odd.

Medic09:
HTN and CHF :)
nope not at all.
He has had multiple resp. infections per mom, but never like this.

:"How's his WOB? Is there reasonable chest expansion?"

working hard expansion seems minimal.

JVD is obvious... but is it the WOB and terror or past HX? hard to say..


Thanks for the warm welcome Mike and others. Semi-fowlers not working? Perhaps him being contracted has something to do with it. I'm not entirely sure how long it takes Lasix to work, but I'm pretty confident once it does, the respiratory distress would improve. And, I don't think it would hurt to have it on board. Thanks for the tip on the NTG gtt. To tell you the truth, I'm not sure the effects Versed would have on a patient with CP. I tried using my go to guy, Mr. Google, but he doesn't have much info about it either. To answer the question about Suxx, I will have to quote JLP, who said, "By the way, I meant to say that I probably would not use SUX unless I had a lot more info. I just remember an OR that shall not be named that RSI'd a late teen Duchenne muscular dystrophy survivor whose K was normal, gave SUX, patient shortly had hyperkalemic arrest . Unused muscles saving up K for years and overexpression of ACh receptors". I definitely would not give Suxx to this patient. But then again Mike, this is one of your case studies so popular for their zebra populations, he might just arrest anyway ;). Thanks for all the tips and tricks guys!
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#30 fiznat

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Posted 26 February 2009 - 06:13 PM

Your ventilator. If I think that's what your asking? A BVM with PEEP would work, but you would have a vent, right?


Nope. Most ground services don't as far as I know. I understand this website is for flight EMS though, who probably all carry vents. Carry on!
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#31 Joe Percer

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Posted 27 February 2009 - 12:59 AM

Nope. Most ground services don't as far as I know. I understand this website is for flight EMS though, who probably all carry vents. Carry on!


Not to sound snobby, but any ground service that seriously undertakes any sort of Critical Care transport should carry a vent. (Preferably something more than the autovent, capable of A/CMV, SIMV, PSV, and CPAP/BIPAP)

Also: I'm not sure about the emergency phlebotomy, the only thing I could think of to do is to empty out a 1L bag of NS and attach it to the biggest IV catheter you can get on the patient, and hang the bag lower... Would be interesting to see if this would be indicated.

This is an interesting case!
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#32 jwalshfan

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Posted 27 February 2009 - 11:56 AM

Chasing for your zebra here, Mike. Does your patient have a history of Botox injections? Sounds silly, but I remember reading an article about the off-label use of Botox in treating CP and that there were some deaths reported as a result of pneumonia & strokes that were attributed to the Botox injections in CP patients.

Warren, RN/LP
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#33 MSDeltaFlt

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Posted 27 February 2009 - 05:28 PM

Ok to answer some of the questions:

viking563: Welcome, keep getting involved it only helps you learn more. I believe my colleagues answered some of your questions as good (better) than I could :)

"How is his baseline mental status?"

Baseline is generally non-verbal but aware per parents.

ST RN/PM:

excellent responses.

Airway assessment:

Pt does not really help you here. His mouth opening you cannot really tell, everything else looks normal.

You pegged HCTS.

Attempt CPAP does not seem to work, he will not keep his face still with mask on.

12 lead shows II III AVF ST Depression

NTG drip up, lopressor given BP drops to 90/50 HR to 66 (quickly!) ST changes deepen Why did this happen?

Speed:
Very true, that pic is just an example. Assume its mostly CP causing that. Also, just ignore the papules in the pic (i didnt even see em till you picked em out!)
Exactly.
Per mom he 'pees fine'. Thats all she can say

How would you intubate?

LWT:
Mom says everything else seems the same as before. Temp is normal

EMT I2RN:

Welcome :)

Everything is latex free

semi-fowler does not work, why?

Lasix given, 80 mg... will that help anytime soon with his resp. distress?

nitro drip, 5mcg/min ius a bit low. If we are thinking MI then (as you know) its 400 mcg X 3 (sl nitro). If we are thinking fluid shifts probably best to start at 10 but good idea!

What is the concern with giving this guy versed? What can it do?

Would suxx be dangerous in the patient? Or not really?

MSdelta:
Mom says he seems a bit distressed but yes.

Not a DNR.
Last 2 days.
hemochro was diagnosed 2 years ago, just Oral treatment 1st phlebotomy one week ago. (excellent question). Why do they do this?

Liver and kidney extent unknown by mom.

No fever no ports

last cardiac eval was months ago.. mom does not remember anything new, no MIs and does not know EF

No choaking no swallowing issues.

RR is fast TV is not good.

Blood glucose 375

Ht ~6 ft wt ~155 nothing else odd.

Medic09:
HTN and CHF :)
nope not at all.
He has had multiple resp. infections per mom, but never like this.

:"How's his WOB? Is there reasonable chest expansion?"

working hard expansion seems minimal.

JVD is obvious... but is it the WOB and terror or past HX? hard to say..


He's already on a beta blocker and it precipitated the Lopressor which is also making me think his inferior heart is fed by RCA, so that's a no go. Stick with the NTG drip. This can also make Versed a bit tricky. I'd want to see his temp and his K level before we give succs. We might need to use something else.

He's got a lot of stuff going on cardiac wise with his HCTS, but let's not forget "B". Granted they are related, but "B" still comes before "C".
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Mike Hester, RRT/NRP/FP-C
Courage is resistance to fear, mastery of fear - not absence of fear -- Mark Twain

#34 Speed

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Posted 01 March 2009 - 03:13 PM

[quote]Attempt CPAP does not seem to work, he will not keep his face still with mask on.

12 lead shows II III AVF ST Depression

NTG drip up, lopressor given BP drops to 90/50 HR to 66 (quickly!) ST changes deepen Why did this happen?[/quote]

I would not be giving any more meds on top of each other that have a negative effect on BP, and not without titrating up to your dosage goals using broken up boluses. He's got a BP and it's 28 minutes to the destination. He could have an accumulative or exaggerated reaction from the addition of beta-blockers but usually you'd expect to see tolerance, more of a drop with BB's and Ca channel blockers together. I'd expect pt's with AS who drop like that after nitro and beta-blockers to have some pretty good obstruction going on. So, I'd be very conservative with agents that drop BP or speed up the rate, increase demand for O2, etc..


[quote]Assume its mostly CP causing that. Also, just ignore the papules in the pic (i didnt even see em till you picked em out!)


How would you intubate?[/quote]

Contractures are from pain response to the CP? In that case I'd just follow the DAI/RSI protocol with caution on the hemodynamic effects, and if a suspected deterioration arises from K, treat it.



[quote]Lasix given, 80 mg... will that help anytime soon with his resp. distress?

What is the concern with giving this guy versed? What can it do?

Would suxx be dangerous in the patient? Or not really?[/quote]

It's in and will start, but of course you wouldn't expect results immediately, versed can drop his BP and again with AS big drops can be very dangerous. If you are saying his "contractures" are from pain and not so much pathological then I thinks it's a non-issue. Even if he had them for a long time I'd still consider using suxx, just depends. If his chest and diaphragm "restriction" were the main reason for distress I'd be leery of starting the procedure with a long-acting paralytic.




[quote]RR is fast TV is not good.

He has had multiple resp. infections per mom, but never like this.

working hard expansion seems minimal.

JVD is obvious[/quote]

This still sounds like he has some limitations on chest wall expansion that he's trying to keep up with demand while limited by volume like chest wall splinting or the like, similar to being tachypneaic and auot-peeping with exacerbations of COPD or reactive airway diseases with they've lost volume or alveoli surface area, but this sounds more like a mechanical affect outside of the lungs with probably near fulminate pulmonary edema on top of that. I'm still not clear how active or ambulatory this person usually is and if not so much I'm sure he could always have a little bronchiolitis/pneumonia that lingers, so the deep suctioning would be good for that and the edema as well. The JVD would normally have me looking or watching for pericardial/pleural effusions in such a wet person, but I'm not seeing the hemodynamic changes yet with one that would trigger me to have to do something about it. But, look for it briefly anyway...
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#35 Speed

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Posted 01 March 2009 - 03:20 PM

Did we give any ASA? And analgesia might help as well in limited doses, not creating a poly-med pile up....space it all out for safety and diagnostic reasons.
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Mike Williams CCEMT-P/FP-C

#36 MSDeltaFlt

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Posted 01 March 2009 - 04:23 PM

Speed's mention of the word "mechanical" got me to thinking. What are the odds of this guy also having a pleural effusion? I doubt it, but if he does have one and it's sufficient enough, it might need tapping.
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#37 rfdsdoc

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Posted 01 March 2009 - 09:42 PM

Hey folks

Happy 2009 to all you northern hemisphere colleagues!

Once again Mike has given us quite a conundrum! We had a case like this about 2 weeks ago and despite IABP support, dobutamine, lasix, fluid boluses, he still deteriorated and the RSI/intubation almost killed him during the procedure.

Point is this patient in the case is having a big inf/right ventricular MI that has caused the hypotension when nitrates were given. The fact he is also in left ventricular failure is a sign the infarct has extended and compromised and already weakened left ventricle affected by his pre-existing HCTS and AS.

Drugs and intubation are not going to achieve much unless you can lyse this infarct, which looks like it does not meet the criteria currently.

ASA as speed says is a good idea but a bit academic given it takes about 12-24hrs to have a noticeable antiplatelet effect. You have to keep him alive for the 28 min flight!

he is in desperate need of respiratory and cardiac support. CPAP has not worked. Intubation with drugs may well kill him. I'd start up some dopamine or noradrenaline at this point in preparing for possible RS/intubation.

emergency phlebotomy was used in days past prior to lasix . It works and in a perverse way may be indicated in this man with HCTS. It is nothing fancy. take a IV fluid bag, empty it and put a large bore IV in , connect to giving set and put bag on floor. Venesect about 300-500mls then stop. In principle though I would not do it as this man is not fluid overloaded his problem is a failing heart, he needs all the oxygen carrying capacity he can get and his RV needs adequate preload not a reduction of preload.

I would actually be leaning towards starting inotropes, putting him on a NRBM, sitting him up, then either trying a blind nasal under IV fentanyl or ketamine, or a surgical cricothyroidotomy under LA +/- ketamine/fentanyl.

ketamine is theoretically contraindicated in acute coronary syndrome due to its propensity for tachycardia and hypertension. Personally I consider that in this setting where inotropes do exactly the same thing I believe ketamine use to be reasonable if it allows us to secure an airway for assisted mechanical ventilation.
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#38 Mike MacKinnon

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Posted 04 March 2009 - 12:26 AM

No botox ;)

Chasing for your zebra here, Mike. Does your patient have a history of Botox injections? Sounds silly, but I remember reading an article about the off-label use of Botox in treating CP and that there were some deaths reported as a result of pneumonia & strokes that were attributed to the Botox injections in CP patients.

Warren, RN/LP


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Mike MacKinnon MSN CRNA
WWW.NURSE-ANESTHESIA.ORG

"What gets us into trouble is not what we don't know
It's what we know for sure that just ain't so" - Mark Twain

#39 Mike MacKinnon

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Posted 04 March 2009 - 12:32 AM

Some additions:

I'd expect pt's with AS who drop like that after nitro and beta-blockers to have some pretty good obstruction going on. So, I'd be very conservative with agents that drop BP or speed up the rate, increase demand for O2, etc..


YES!

AS requires high perfusion pressures to get CO through the stenosis. But why then are we seeing ischemia on the EKG? (explain the physiology of why this happened related to the AS)



With Suxx what are some "relative" contraindications in a non-emergency intubation (where seconds count)?

Does this patient meet any of those risks? If so what would you use instead, if not why?
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Mike MacKinnon MSN CRNA
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"What gets us into trouble is not what we don't know
It's what we know for sure that just ain't so" - Mark Twain

#40 Mike MacKinnon

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Posted 04 March 2009 - 12:37 AM

Minh yer all over it buddy!

Lemme add some here:


[quote]Point is this patient in the case is having a big inf/right ventricular MI that has caused the hypotension when nitrates were given. The fact he is also in left ventricular failure is a sign the infarct has extended and compromised and already weakened left ventricle affected by his pre-existing HCTS and AS.[/quote]

Well not an inferior MI JUST yer but most certainly headed there with severe ST depression and ischemia. BUT, what is it from? Was the ischemia before or after tx, is it r/t disease or tx? What did we do (related to the other coexisting issues) that may have precipitated this?


[quote]emergency phlebotomy was used in days past prior to lasix . It works and in a perverse way may be indicated in this man with HCTS. It is nothing fancy. take a IV fluid bag, empty it and put a large bore IV in , connect to giving set and put bag on floor. Venesect about 300-500mls then stop. In principle though I would not do it as this man is not fluid overloaded his problem is a failing heart, he needs all the oxygen carrying capacity he can get and his RV needs adequate preload not a reduction of preload.[/quote]

agreed ;) tho still done apparently at times, its not a great idea in extremis :)

[quote]I would actually be leaning towards starting inotropes, putting him on a NRBM, sitting him up, then either trying a blind nasal under IV fentanyl or ketamine, or a surgical cricothyroidotomy under LA +/- ketamine/fentanyl.

ketamine is theoretically contraindicated in acute coronary syndrome due to its propensity for tachycardia and hypertension. Personally I consider that in this setting where inotropes do exactly the same thing I believe ketamine use to be reasonable if it allows us to secure an airway for assisted mechanical ventilation.[/quote]

Hmm ;)
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Mike MacKinnon MSN CRNA
WWW.NURSE-ANESTHESIA.ORG

"What gets us into trouble is not what we don't know
It's what we know for sure that just ain't so" - Mark Twain