Cardiac Clinical Case

[sethco]

Thought this might be a good teaching case for residents/fellows. My twist on this is instead of talking about intraop management, we can talk about preop assessment/plans prior to that (kind of like oral boards). This is a private practice case where you are solo (i.e. No resident, CRNA. Just you and your trusty Anesthesia Tech). You do all your own lines, TEE interpretation, etc. Here we go...

71 y/o male previous living at home with significant other experiencing angina with progression over past couple months. Comes in to see PCP 2 months ago, TTE was done which showed EF 50% with Mod-Severe AS. PCP schedules patient for nuclear stress test also which was done 1 week ago. Pt experienced intermittent and transient hypotension with this and "was extremely fatigued after this" while at home. Test showed anterolateral wall motion abnormalities. Pt presented later to ED that day with chief complaint of fatigue and angina. EKG does not show any ST/T wave changes, but does show a new Left BBB and BNP is in the 3000 range and tropnins are positive. Pt taken to Cath lab and found to have 99% LM and 100% occluded RCA (non-dominant). LV Ventriculography shows EF 10-15% now. Decision made to place Intra-aortic Balloon Pump (IABP). Angina improves with this. In addition, ICU places an arterial line, double lumen CVC, and Cordis. ICU staff unable to place PA Catheter as if was curling in RV. Pt has Carotid duplex that shows bl Mod-Severe Carotid Stenosis with poor vertebral flows. TTE shows EF 10-15% with low flow Aortic Stenosis classified as severe, with Moderate AI. TTE also shows mod-severe MR and TR, thought to be functional. Decision made to perform Right CEA prior to planned CABG/AVR/MVR/TVR. This was done successfully without issue and pt was extubated post-procedure. Pt had a headache post-op, but this has resolved. He is now POD #2 from this surgery and has been very well diuresed (20% of total body weight!). MR and TR are now Mild-Moderate. You go see him this morning and ICU nurse tells you he started getting stridor about two hours ago and his right neck is really swollen. He is talking and conversing with you. ICU has him on 2L O2 and NTG/Precedex gtt (Heparin gtt off for past two hours). Labs show low platelet count and low H/H. Creatinine, which had spiked on admission to 1.7 is now 1.0. TEG with platelet mapping shows only mild AA/ADP inhibition. IABP is set to 1:1 and his BP is 150/55 with HR in high 50s on NTG drip.

Now, I know some people on this board have been doing this stuff for a while and know the answers (i.e. Sevo, Hawaiian Bruin, etc), but try to give the residents/fellows a chance...

1) What is low-flow Aortic Stenosis? How do we diagnose this and why is it a bad idea to perform this test in this particular patient? How do we classify severity of Aortic Stenosis on Cardiac Cath versus Echo? How does his poor EF affect the Aortic Valve area calculation?

2) (Cardiac Fellows question) What is functional MR? How do you classify the different types of MR?

3) What are the contraindications to placing a PAC? What risks exist in this patient for placement? More importantly, are you going to place one?

4) How does an Intra-aortic Balloon Pump work? What is the proper position for the distal tip? When should it not be used? Why not place an Impella in this patient?

5) As above, the patient is now experiencing acute stridor that is clearly audible, but patient is talking normally per family and does not appear SOB. What do you want to do for him prior to surgery? Any prep for the OR?

Lets stop here for now. We can talk later about Intraop management and I will tell you what we did for this pt.

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[sevoflurane]

Thought this might be a good teaching case for residents/fellows. My twist on this is instead of talking about intraop management, we can talk about preop assessment/plans prior to that (kind of like oral boards). This is a private practice case where you are solo (i.e. No resident, CRNA. Just you and your trusty Anesthesia Tech). You do all your own lines, TEE interpretation, etc. Here we go...

71 y/o male previous living at home with significant other experiencing angina with progression over past couple months. Comes in to see PCP 2 months ago, TTE was done which showed EF 50% with Mod-Severe AS. PCP schedules patient for nuclear stress test also which was done 1 week ago. Pt experienced intermittent and transient hypotension with this and "was extremely fatigued after this" while at home. Test showed anterolateral wall motion abnormalities. Pt presented later to ED that day with chief complaint of fatigue and angina. EKG does not show any ST/T wave changes, but does show a new Left BBB and BNP is in the 3000 range and tropnins are positive. Pt taken to Cath lab and found to have 99% LM and 100% occluded RCA (non-dominant). LV Ventriculography shows EF 10-15% now. Decision made to place Intra-aortic Balloon Pump (IABP). Angina improves with this. In addition, ICU places an arterial line, double lumen CVC, and Cordis. ICU staff unable to place PA Catheter as if was curling in RV. Pt has Carotid duplex that shows bl Mod-Severe Carotid Stenosis with poor vertebral flows. TTE shows EF 10-15% with low flow Aortic Stenosis classified as severe, with Moderate AI. TTE also shows mod-severe MR and TR, thought to be functional. Decision made to perform Right CEA prior to planned CABG/AVR/MVR/TVR. This was done successfully without issue and pt was extubated post-procedure. Pt had a headache post-op, but this has resolved. He is now POD #2 from this surgery and has been very well diuresed (20% of total body weight!). MR and TR are now Mild-Moderate. You go see him this morning and ICU nurse tells you he started getting stridor about two hours ago and his right neck is really swollen. He is talking and conversing with you. ICU has him on 2L O2 and NTG/Precedex gtt (Heparin gtt off for past two hours). Labs show low platelet count and low H/H. Creatinine, which had spiked on admission to 1.7 is now 1.0. TEG with platelet mapping shows only mild AA/ADP inhibition. IABP is set to 1:1 and his BP is 150/55 with HR in high 50s on NTG drip.

Now, I know some people on this board have been doing this stuff for a while and know the answers (i.e. Sevo, Hawaiian Bruin, etc), but try to give the residents/fellows a chance...

1) What is low-flow Aortic Stenosis? How do we diagnose this and why is it a bad idea to perform this test in this particular patient? How do we classify severity of Aortic Stenosis on Cardiac Cath versus Echo? How does his poor EF affect the Aortic Valve area calculation?

2) (Cardiac Fellows question) What is functional MR? How do you classify the different types of MR?

3) What are the contraindications to placing a PAC? What risks exist in this patient for placement? More importantly, are you going to place one?

4) How does an Intra-aortic Balloon Pump work? What is the proper position for the distal tip? When should it not be used? Why not place an Impella in this patient?

5) As above, the patient is now experiencing acute stridor that is clearly audible, but patient is talking normally per family and does not appear SOB. What do you want to do for him prior to surgery? Any prep for the OR?

Lets stop here for now. We can talk later about Intraop management and I will tell you what we did for this pt.

Waddup Sethco. 'bout time we got some good cardiac action on here.

Was thinking about one of your posts from a couple years back... had a very similar one.

But that is neither here or there... great post/case.

 

[LivetoTell]

First thing, secure airway. Have vascular surgeon and surgeon able to do trach at OR bedside ready to go.

 

[sethco]

Waddup Sethco. 'bout time we got some good cardiac action on here.

Was thinking about one of your posts from a couple years back... had a very similar one.

But that is neither here or there... great post/case.

Ha! I did one of these cases last week and got a nearly identical M-Mode tracing.

 

[pgg]

Thanks for posting a case.

 

[Shimmy8]

3.)

On a quick break so can't type much on my phone, but PAC relative contraindication with an already present LBBB to avoid complete block. And we'll make his TR a little worse for the time being.

And in this guy with a known crap EF and ischemic I certainly wouldn't put one in and don't think many of my attendings would at my program.

 

[OB1🤙]

 

[GhostTree]

Disclaimer: Im not a resident/fellow but I graduated residency one year ago and do cardiac at my current job. Probably should have done a cardiac fellowship because I really enjoy cardiac, but my job opportunity was too good to pass up. So I'm getting OJT and trying to learn via going to conferences and spending time with the cardiologists.

Thank you for posting the case, I'll take a shot.

I'm between cases now so my answers aren't fully fleshed out.

1. AVA is calculated by echo based on peak and mean gradient of the jet measured via TTE/TEE. This is flow dependent. In hearts with poor contractility, the heart cannot generate enough force to make the measured jet accelerate to the velocities we normally associate with stenotic valves in a normal heart. This may lead to an underestimation of AS. One can use the dimensionless index, a ratio of LVOT velocity to AV velocity, to attempt to get a better picture. One can also do a dobutamine challenge to see if the velocity increases or not. Not a great idea to give this pt dobutamine for many reasons. Cath lab gradients are based on peak to peak gradients acquired via catheter measurement, and may underestimate the peak gradient.

2. MR is classified typically by the carpentier classification. Broadly, type 1 has normal leaflet motion, type 2 has leaflet prolapse, and type 3 has leaflet restriction. MR post MI can be due to papillary muscle rupture, but more likely due to annular dilatation.

3. agree with shimmy 8. No need to cause complete heart block in this guy.

4. IABP should be below the left subclavian artery. works by expanding in diastole pushing blood forward decreasing afterload, and also augmenting diastolic coronary artery perfusion. Impella shouldn't be used with mod-severe AS, and it also requires anticoagulation AFAIK, which isn't ideal in a pt who may have a neck hematoma after CEA.

5. Hard question to answer without seeing the patient. The neck swelling doesn't quite fit with the clinical picture. Is there a drain in place?

I want lots of things for this pt. Without seeing him myself, it sounds like he has a hematoma from his CEA that may get worse soon, could also be RLN damage but his normal voice argues against that. Blood products, a surgeon to assess and possibly decompress the potential neck hematoma, difficult airway cart, are on the top of my list. Prep for femoral cannulation if need be. This will be a tough case. Fortunately he's lined up pretty well now.

Also, I'm thinking, what are we going to do in the OR? AVR/MVR/TVR CABG? that is going to be a lot for this pt. Just doing the AVR/CABG might be a better option.


Also, any hints on what is up with that m-mode picture? at least give me the TEE view it was taken from, I'll try to figure it out.

 

[GhostTree]

Just for kicks, what results do you get if you put this guys data in the sts risk calculator?

 

[Noyac]

Love it. Can't wait to contribute.
Been a while since I've done this kind of cardiac so I will be tuned in to the comments. I already saw one that I disagree with tho.

 

[TaoistDoc]

I'll give a stab at this even though im a freesh new attending. I also don't do any hearts, beenover a year since I did it as a ca 2.

1. Low flow AS probably refer to AS in a patient with LV systolic failure. Pump can't generate the force to produce high flow. So if all you're doing is measuring velocity through the AV to estimate the severity of AS, you will underestimate it due to the low flow state. If you use the continuity equation to estimate your AV, I think you should still be pretty accurate since flow through the LVOT would relatively be lower as well. Correct me if im wrong, but the dimentionless index and the continuity equation should be equally accurate as long as the LVOT is measured correctly. In reality, it may be difficult to get the real measurement of the LVOT due to the fact that its not a perfect cylinder so some people prefer the dimentionless index.

Aside from echo, the other test that can be performed to measure the gradient across the valve is a left heart cath. MIBI would be less accurate than echo I think. A left heart cath could kill this patient since you would have to stop the IABP.

2. This is a stab in the dark, but I guess functional MR is when MR occur due to a dilated LV during heart failure, which would improve when you get the contractility up to unload the excessive volume. I don't know the different types of MR

3. Would not place PAC. Reason is as posted above, and really no need for it with TEE

4. See above

5. main differential includes hematoma, recurrent laryngeal nerve injury, and airway edema. I donte care what family say, I would examine and talk to him myself. Hematoma would be obvious unless he has a giant neck. Recurrent laryngeal nerve injury would present with hoarseness. Otherwise, it is likely airway edema.

 

[sethco]

First thing, secure airway. Have vascular surgeon and surgeon able to do trach at OR bedside ready to go.

How and where are you going to secure the airway?

 

[sethco]

3.)

On a quick break so can't type much on my phone, but PAC relative contraindication with an already present LBBB to avoid complete block. And we'll make his TR a little worse for the time being.

And in this guy with a known crap EF and ischemic I certainly wouldn't put one in and don't think many of my attendings would at my program.

Good answer about the PAC. Having a preexisting LBBB is a relative contraindication. Does the risk outweigh the benefits? What patients do you place a PAC in if not this type of patient?

More questions to follow later...

 

[Scotty_G]

The impella device is a bad idea with this patient's AI and even with the significant AS if any of those calcium deposits get mobilized when the device is operating. However you could make case that moderate AI is a contraindication fro the balloon pump. Perhaps the AI became worse after placement of the balloon pump?

(Disclaimer non-cardiac fellow )

 

[BrandoNurse]

IABP will significantly increased Carotid mean pressures so watch out for hemotoma. Tranfuse platelets as they will be further damaged from IABP.

 

[Scotty_G]

Forgive me if I'm wrong but I thought you do not need systemic anticoagulation w/ an impella device.

 

[sethco]

Disclaimer: Im not a resident/fellow but I graduated residency one year ago and do cardiac at my current job. Probably should have done a cardiac fellowship because I really enjoy cardiac, but my job opportunity was too good to pass up. So I'm getting OJT and trying to learn via going to conferences and spending time with the cardiologists.

Thank you for posting the case, I'll take a shot.

I'm between cases now so my answers aren't fully fleshed out.

1. AVA is calculated by echo based on peak and mean gradient of the jet measured via TTE/TEE. This is flow dependent. In hearts with poor contractility, the heart cannot generate enough force to make the measured jet accelerate to the velocities we normally associate with stenotic valves in a normal heart. This may lead to an underestimation of AS. One can use the dimensionless index, a ratio of LVOT velocity to AV velocity, to attempt to get a better picture. One can also do a dobutamine challenge to see if the velocity increases or not. Not a great idea to give this pt dobutamine for many reasons. Cath lab gradients are based on peak to peak gradients acquired via catheter measurement, and may underestimate the peak gradient.

2. MR is classified typically by the carpentier classification. Broadly, type 1 has normal leaflet motion, type 2 has leaflet prolapse, and type 3 has leaflet restriction. MR post MI can be due to papillary muscle rupture, but more likely due to annular dilatation.

3. agree with shimmy 8. No need to cause complete heart block in this guy.

4. IABP should be below the left subclavian artery. works by expanding in diastole pushing blood forward decreasing afterload, and also augmenting diastolic coronary artery perfusion. Impella shouldn't be used with mod-severe AS, and it also requires anticoagulation AFAIK, which isn't ideal in a pt who may have a neck hematoma after CEA.

5. Hard question to answer without seeing the patient. The neck swelling doesn't quite fit with the clinical picture. Is there a drain in place?

I want lots of things for this pt. Without seeing him myself, it sounds like he has a hematoma from his CEA that may get worse soon, could also be RLN damage but his normal voice argues against that. Blood products, a surgeon to assess and possibly decompress the potential neck hematoma, difficult airway cart, are on the top of my list. Prep for femoral cannulation if need be. This will be a tough case. Fortunately he's lined up pretty well now.

Also, I'm thinking, what are we going to do in the OR? AVR/MVR/TVR CABG? that is going to be a lot for this pt. Just doing the AVR/CABG might be a better option.


Also, any hints on what is up with that m-mode picture? at least give me the TEE view it was taken from, I'll try to figure it out.

Some really great answers in this thread

Couple of points...

1) There are no great consensus numbers on determining severity of AS. ACC/AHA and Europe have different guidelines. For defining AS via Echo findings, I generally use values of maximum velocity across AV >4 m/s, Mean pressure gradient >40 mmHg, Dimensionless Valve Index (DVI) <0.25, and/or Valve Area <1 . However, during my intraop exam, I shy away from giving labels (i.e. Moderate versus Severe) and instead just focus on quantitative and qualitative data in my report. After a new valve is placed in a patient, I don't generally report valve areas, instead giving peak/mean pressure gradients, comment on perivalvular and transvalvular leaks, and DVI.
Valve Area is calculated based off the bernoulli equation and continuity principle.
Modified Bernoulli Equation: Pressure gradient = 4(Velocity Time Integral or VTI)Squared (Technically, the VTI of the LVOT should also be determined and subtracted from this, but it is generally negligible except where there are cases of LVOT obstruction)
Continuity Equation: (VTI of LVOT) X (Cross Sectional Area of LVOT) = (VTI of AV) X (Cross Sectional Area of AV), basically stating forward flow of blood (Velocity X Area) in one part of the heart is equal in another part of the heart. This can also be applied to the mitral valve.
Problem is there are sources of error in this equation. Biggest source of error is in calculating the Area of the LVOT. The diameter of the LVOT is measured then cut in half and then squared, so a small amount of error in measurement is compounded. Another problem is in cases of AI (which causes a high transvalvular velocity) and may overestimate the valve area. Versus in times of low cardiac output (low transvalvular velocity), may underestimate the valve area. Normally in this situation, we can do a Dobutamine Stress Echo and see if that increases the valve area size or if the valve area is fixed. In this patient adding Inotropes to a severely ischemic heart may cause acute decompensation. In this situation I am also lery about using DVI for determining severity, so if I can get a clean image I will use Planimetry (both 2D and 3D if available). In the Cath lab, they can measure aortic valve gradients also, but they use Peak to Peak velocities. This valvue is generally less than the peak instantaneous gradient that is derived from Echo.

2) Functional MR (Carpentier Class 3b) generally refers to when there is restricted leaflet motion of the mitral valve, but the valve itself it not diseased. That is because the valve is tethered from LV dysfunction. When a patient has MR from annular dilatation (Which could be the case in this patient with possible long standing AI), the motion of the mitral valve leaflets are generally normal (Class 1) and you would generally see a central regurgitant jet. If you have chordal rupture or flail leaflet, you will generally see excessive leaflet motion (Class 2) with an eccentric jet directed away from the disease leaflet

4) As above the IABP could certainly be contributing to the amount of AI present in this patient. Nobody really made mention of relative/absolute contraindications to IABP placement such as severe PAD, Severe aortic atheromatous disease, Severe AI, Infection at planned insertion site, dissection/aneurysm, aortic grafts/stents. In this patient with AI, a balloon pump may cause acute decompensation by worsening backward flow into the LV during balloon inflation during diastole. Unfortunately, in this patient the degree of AI was not known until the IABP was in place. Furthermore, and luckily, the patient appeared to benefit from the IABP as his angina became significantly improved. Although it is considered a ventricular assist device, it does not actually directly improve cardiac output, unlike an Impella or Heartmate device. When the IABP device inflates during diastole, it is increasing the diastolic blood pressure and thereby increasing coronary perfusion pressure. Then it deflates during systole to not add any increased afterload on the LV.
Regarding the Impella, it is contraindicated in patients with a Mechanical aortic valve or heart constrictive device, Severe AS or calcification, Mod-Severe AI, and Severe PVD.

5) This pt was POD #2 from a right CEA. Because of his unstable angina, he was kept on a Heparin gtt up to two hours prior to the planned CABG/AVR, with possible MVR/TVR. Unknown why a drain was not kept in place, knowing that this pt would remain on anticoagulation. I examined the patient myself. No hoarseness note or difficulty with phonating. Bilateral Breath sounds are present, so I know the patient is moving air. Had preop discussion with surgeon regarding timing of neck reexploration. Family is aware that he does not sound good right now. Pt has had this IABP in for almost a week and is now showing weak pulses in the same leg where the IABP is located.

Will get to more questions later...

BTW, the M Mode image above is in the mid esophageal position long axis. It is a classic image for this condition

The STS score for mortality was 13% if I remember correctly

Also, what is the benefit of staging this procedure? What are the downsides? What does that do to the STS score?

 

[sethco]

Forgive me if I'm wrong but I thought you do not need systemic anticoagulation w/ an impella device.

You need to be partially anticoagulated, similar to ECMO

 

[sethco]

IABP will significantly increased Carotid mean pressures so watch out for hemotoma.

I have never heard that before. Do you have a source for that?

 

[LivetoTell]

How and where are you going to secure the airway?

I would perform an airway exam,etc.. But my plan would be to intubate in the OR with trach surgeon at bedside ready to go. Since this is an emergency, I wouldn't bother with an awake intubation as time usage is critical with expanding hematoma. Inhalational induction, with some ketamine titrated in to maintain spontaneous ventilations.
Miller 2 is my preference, with fiberoptic, glidescope as my back-up. Retrograde wire, LMAs ready.

 

[itwasalladream]

Some good answers above. I'd give platelets and blood and prep for OR. He's moving air, so I'd take him to the OR for airway securing. Surgeon and usual toys around but not terribly worried based on info presented. If you're really concerned, can do a nasal fiberoptic peek under topical just to look at the glottis before committing to anything. I've actually seen a pretty big hematoma impinging on the cords that really wasn't apparent from the tightness of the neck. After asleep, right neck exploration and once hemostasis achieved then proceed with AVR/CABG. This may be aggressive, but you can do CEA/heart surgery at the same time, and you're on a bit of a time crunch with the IABP chewing up platelets, causing vascular insufficiency in the leg, and that 99% LM ticking away. Since diuresis improved his MR/TR, I agree with the thought that AVR/CABG might be a better approach.

I don't think I'd place a PAC. But it's not unreasonable to try, have pacing pads on, and bail if he gets unstable. Or try at the end of surgery once he's revascularized, with new valve(s). The more extensive the surgery, the more likely it is to help out in the ICU, IMHO.

 

[BrandoNurse]

I have never heard that before. Do you have a source for that?

I dont have a source but just as it significantly increases MAP in the aorta and coronary perfusion it will also increase cerebral perfusion. The tip of the balloon is not far from the carotid arteries.

 

[BLADEMDA]

For those that are unfamiliar with STS:


Home / Quality, Research & Patient Safety / STS Public Reporting Online / Explanation of Adult Cardiac Composite Measures / STS CABG Composite Score
STS CABG Composite Score
The STS CABG composite score is calculated using a combination of 11 measures of quality divided into four broad categories or domains. The first domain is risk-adjusted mortality, and the second domain is risk-adjusted major morbidity, which represents the percentage of patients who leave the hospital with none of the five most serious complications (often referred to as morbidities) of CABG—reoperation, stroke, kidney failure, infection of the chest wound, or prolonged need to be supported by a breathing machine, or ventilator. Overall, based on data from the STS National Database, about 85 percent of patients are discharged with no such complications. The third domain measures the percentage of CABG procedures that include the use of at least one of the arteries from the underside of the chest wall--the internal mammary (or internal thoracic) artery— for bypass grafting. This artery has been shown to function much longer than vein grafts, which can become blocked over time. The final domain measures how often all of the four medications believed to improve a patient’s immediate and long-term outcomes were prescribed. Those drugs include beta-blocking drugs prescribed pre-operatively, as well as aspirin (or similar drugs to prevent graft clotting), and additional beta-blockers and cholesterol-lowering medicines prescribed at discharge. Importantly, the 11 individual measures and the overall composite measure methodology are all endorsed by the National Quality Forum and have undergone careful scrutiny by quality measure experts.

STS Public Reporting Online lists participants’ scores for each of the four domains and the STS CABG overall composite score. Each of these numerical scores can be compared with the average scores for all participants in the Database. Participants also have a star rating. The star rating calculation begins by assuming all providers are average and then determines statistically if there is at least a 99 percent probability that the performance of any specific provider is lower than average (one star) or higher than average (three star). For the several years that STS has been calculating these scores, about 10-15 percent of all Adult Cardiac Surgery Database participants have been one-star, about 10-15 percent have been three-star, and the remainder have been two-star, or average programs.

Finally, it is important to understand that these scores compare the results of a hospital or surgical practice/group with those of an average hospital or practice participating in the Database and treating patients with the same mix of severity of illness. Even when the results are risk-adjusted, it is not necessarily appropriate to compare directly the scores of individual hospitals or surgical groups to each other, especially if they treat markedly different kinds of patients. In addition, a surgical group may practice at more than one hospital, and more than one surgical group may practice at a given hospital.

 

[Noyac]

I'll just address the airway for now.
What do you guys/gals think you will see when you try to DL this guy?
In my experience, it will be a narrow edematous airway that will be very difficult. Since it is on the right side this will make things worse.
There is a better way of managing this situation.

 

[OB1🤙]

And I'll just address the swan issue- I would swan this patient without a second thought once in the OR for cardiac surgery.

And I don't put in very many swans these days.

 

[sethco]

Alright, moving on...

1) The patient has a normal airway exam (aside from the audible stridor). MP 2 full neck flexion/extension, tmd > 5cm, no oral edema/tongue swelling appreciated. Pt is able to lie down flat. Previous anesthesia note states easy airway, induced with Midazolam 2 mg, Propofol 120, Fentanyl 100, and Rocuronium 40. Is this plan reasonable this time around? Why or why not?
2) Pt has had a right CEA, but still had moderate to high grade carotid stenosis on the left. What is your plan for neuroprotection during the operation?
3) His AKI has resolved but he still remains at increased risk. Any strategies you will employ? Is there any evidence for these?
4) Pt has been on Heparin for the past 5 days. Heparin assay and ACT shows heparin resistance. What is your plan for this? What is your ACT goal for CPB? What are you going to do if this patient is a Jehovah's Witness that refuses all blood products?

As an aside, like HB, I would definitely place a PAC. For me, not so much for intraop management, but more so for postop management. In these patients that appear high risk for compete heart block, I wait until the sternotomy is done before floating the swan. Maybe I am a little paranoid?

 

[urge]

From what I have read sounds like it will be a relatively easy dl intubation.

Do the case like usual. I would float pac once chest is open. Continue iabp post op. Assess hematoma at the end of the case to see if it needs to be explored. Hope he doesn't have a stroke in the process because that is about as much as you can do in that regard.

 

[GhostTree]

Is the TEE picture SAM? Would look for the dagger shaped CW of AoV velocity in deep TG

Getting back on track:

1. Just because his upper airway is not obstructed doesnt' mean that lower down at the cord level isn't edematous or obstructed by hematoma/venous congestion. consider awake glidescope look with topicalization. If looks good then titration of hypnotic then maybe some sux if it looks like you can get it in. I might be tempted to use some midazolam and ketamine to maintain spontaneous ventilation and then get them deep enough with mask sevo. Want to optimize first chance success. if not then either open the neck or awake intubation. Open the neck in the OR if you have to. Hard to say what to do without seeing the pt.

2. There is a lot of pharmocological methods that have been tried for neuroprotection. steroids, burst suppresion, Dilantin, packing the head with ice that are used on circ arrest. I'm not sure if any really have been demonstrated to benefit. Can use cerebral oximetry and keep up CPP. avoid hypergylcemia and hypocapnea. MAke sure his rt CEA is not obstructed after the surgeons take a look in the neck.

3. As before, lots of things have been tried. Dopamine, sodium bicarb, etc. Can use mannitol as a free radical scavenger. No clear benefit of help with any to my knowledge. The IABP could also cause some aki if the balloon is causing some blood flow obstruction.

4. heparin resistance is not uncommon after prolonged heparin infusion. IIRC its due to decreased antithrombin 3 levels. can give a higher dose to achieve the appropriate act. If this doesn't work the ffp transfusion or antithrombin 3 concentrate. Although I do believe commercial AT3 concentrate is taken from human blood so I don't know if the Jehovah's witness would accept that. If this is unacceptable you could consider direct thrombin inhibitors like bivalrudin or argatroban. Both are challenging to use in practice because of the specialized monitors required to maintain appropriate levels of anticoagulation for bypass and the lack of reversal agents.

 

[GhostTree]

benefits to staging: shorter pump run and potentially less myocardial dysfunction post.
downsides: another pump run with all that implies, repeated cannulation of recently cannulated great vessels and opening up a recently closed heart. redo sternotomy (provided the chest gets closed in the first place)

 

[Noyac]

Alright, moving on...

1) The patient has a normal airway exam (aside from the audible stridor). MP 2 full neck flexion/extension, tmd > 5cm, no oral edema/tongue swelling appreciated. Pt is able to lie down flat. Previous anesthesia note states easy airway, induced with Midazolam 2 mg, Propofol 120, Fentanyl 100, and Rocuronium 40. Is this plan reasonable this time around? Why or why not?

I say No it is not.
I have seen and done a handful of these airways and they always seem to fool the anesthesiologist if they haven't seen it before. I've even seen this occur with an ant cervical fusion pt.
My plan would be, go to the OR prep and drape the neck for wound exploration and clot evacuation. As soon as clot is evacuated the surgeon must stop working while you intubated the pt. There are a couple reasons for this. This pt has stridor so we know there is edema of the airway. The clot is adding pressure to the airway. Any manipulation of the wound will induce greater edema quickly. Your best shot at this airway is early but after some pressure has been removed. Attack the airway in your preferred method, DL or glidescope would be my approach.

 

[sevoflurane]

Is the TEE picture SAM? Would look for the dagger shaped CW of AoV velocity in deep TG

Nice...
you mean something like this....?

 

[GhostTree]

Nice...
you mean something like this....?

Exactly.

 

[Robokor]

I say No it is not.
I have seen and done a handful of these airways and they always seem to fool the anesthesiologist if they haven't seen it before. I've even seen this occur with an ant cervical fusion pt.
My plan would be, go to the OR prep and drape the neck for wound exploration and clot evacuation. As soon as clot is evacuated the surgeon must stop working while you intubated the pt. There are a couple reasons for this. This pt has stridor so we know there is edema of the airway. The clot is adding pressure to the airway. Any manipulation of the wound will induce greater edema quickly. Your best shot at this airway is early but after some pressure has been removed. Attack the airway in your preferred method, DL or glidescope would be my approach.

in my shop: drape chest. If 1xDL fails - CRASH ON PUMP, should take an experienced surgeon less than 3 minutes on a chest that has not been opened before, but that's in Europe. F...ing around with his trachea and the desat associated with it will kill him....

 

[Noyac]

in my shop: drape chest. If 1xDL fails - CRASH ON PUMP, should take an experienced surgeon less than 3 minutes on a chest that has not been opened before, but that's in Europe. F...ing around with his trachea and the desat associated with it will kill him....

Personally I think this is a bad plan.
You need to canulate while the pt is still breathing. Counting on a surgeon to crack the chest and go on bypass as your backup is just plain crazy.

 

[dutchmaster]

in my shop: drape chest. If 1xDL fails - CRASH ON PUMP, should take an experienced surgeon less than 3 minutes on a chest that has not been opened before, but that's in Europe. F...ing around with his trachea and the desat associated with it will kill him....

If crashing on pump is your backup plan for securing this airway, i would recommend sheaths in the groins for emergent femoral CBP rather than cracking the chest. During my cardiac fellowship in a case with a bad mediastinal mass we were actually prepared to use this as a backup if an awake intubation failed.

I agree with Noyac though. I think securing the airway after clot evacuation is a better idea. Alternatively, a well conducted awake intubation could be employed here.

 

[sethco]

Sorry I am just getting back to this now.

Lots of good comments. Here is how it went down...

CT surgeon saw pt in the morning. We both noted stridor audible and saw growing hematoma on right side of neck. ICU nurse says this has been a new development in the past 1-2 hours. CT surgeon and I discuss and agree that it is this patients best interest to not delay this case. We agree that we will also do a hematoma evacuation either before or after the bypass run. CT surgeon also notes that TEE was done during the CEA by one of my colleagues and the MR/TR is now mild-moderate. Probably much improved due to vigorous diuresis. Despite that, CT surgeon has discussed this with colleagues and they all agree that patient with get a mitral valve repair and watch after the bypass run to see if anything needs to be done with the tricuspid. Surgeon also agrees to be by bedside for induction. I think this is a reasonable plan given that, despite the stridor, the patient is still moving air with audible breath sounds and maintaining good O2 sats on nasal cannula. Pt is already lined up, as my colleague was successful in floating a PA Cath from the Left IJ. So, we get down to OR, monitors all hooked up ready to go. I induce with Midazolam, low dose Fentanyl, even lower dose Propofol/Sevo, and Sux. I find now that I cant ventilate despite two person assist. I take a look with DL and see epiglottis with my MAC 3, lift it up and see the worst airway edema I have ever seen. I see enough of a tiny opening to fit a 6.5 ETT through with moderate resistance. Get ETCO2 and know I get extremely lucky.

Looking back on it, this was probably the first case I have done since finishing training where I know that if I had to do it again, I would have done it differently. I would probably shy away from an awake look with a Glidescope or FOB as this could possibly of made the swelling worse and cause complete airway obstruction. I think I would of done like Noyac said and have the surgeon prep the neck and drain the hematoma before anything, then done an awake look knowing that the suregon could do an awake Trach if needed.

Definitely agree that crashing on pump is not a great idea at all. If that is a possibility, I would have discussed with the surgeon need for femoral cannulation prior to induction

 

[Noyac]

I told you so!!!!


Just kidding, you know I had to say that.

My first ever case like this was a post-op carotid hematoma that we evacuated with the pt awake. I was a new grad and was supervising crnas at the time as well as doing my own cases. I had a fairly decent crna in the case and I stayed in the room for the evacuation. It went well and we all thought we were out of the woods. The surgeon closed the incision and I left the room with the pt still awake and maintaining his airway. I wasn't 20' down the hall when the circulator yelled for me to come back. The guy had completely lost his ability to move any air. Crna attempted the intubated unsuccessfully and the pt was blue. Real blue. I grabbed the laryngoscope and knew I had one shot at it. I saw exactly what Sethco described, tremendous amount of edema and a tiny little hole that I assumed to lead to his airway. I forced the tube through it and we got ETCO2. I swore never to do it that way again.

Great case.

 

[Arch Guillotti]

in my shop: drape chest. If 1xDL fails - CRASH ON PUMP

 

[Laryngophed]

Isn't the board answer to evac the hematoma first and then awake FOI? Given the stridor, you could argue (and I'm pretty the squeaking with respiration makes the argument for you) that you already have airway compromise. So prep for awake FOI in your manner, knife to hematoma with evac, precedex or ketamine and tube 'em?