Cardiac Induction Case

[OB1🤙]

For the students and residents.

70 something y/o pt for CABG.

EF 30-35%, pretty bad CAD. ESRD, last HD last night. Inpatient. Pt is tiny, and anemic to boot. Hct high 20s. Looks frail. Edentulous. Has that aura of "I'm gonna give you trouble today."

To the room and baseline SBP 180s. Induce gently and the pressures hold in the 100s throughout line placement. Yay, we're out of the woods I thought.

I thought.

Then all of a sudden the pressure drops to the 60s, and the sats drop to the high 80s.

What are you thinking, and what do you do next?

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[CavGas]

I 'm just a lowly resident with no cardiac experience but I 'll give it a try..

First thoughts would be MI or PE due to sudden onset of lability. What do the rest of the vitals look like? Tachy, brady, arrhythmias? I would temporize with pressor, 100% FiO2, look at EKG for ST trouble, at ETCO2 for bigger drop than the one expected by the pressure dip, draw an ABG for gases/lytes then call attending to take a look with TEE.

 

[AdmiralChz]

Has that aura of "I'm gonna give you trouble today."

Ah the ol’ eye test. Hate that feeling!

 

[Katheudontas parateroumen]

Attempt to raise the pressure. Bolus NE and Epi. Make sure rhythm is stable. Check ventilator. Adequate ventilation, peak pressures etc. Could be PTX after lines? Call surgeons into room if not already there. Place TEE. Make sure heparin is drawn if crash bypass needed.

 

[Beeftenderloin]

Need more info. What do the rest of the vitals show? How are your airway pressures? What’s your ekg look like, ETCO2? DDX includes PTX from line placement or potentially over aggressive ventilation in a tiny frail old lady or main stem tube, did you wedge the swan and tear a PA? massive MI or PE, anaphylaxis, CO2 embolus from entrained air from line placement. New ESRD related effusion developed since initial work-up with tamponade physiology now that your on PPV. Arrhythmia.

Temporize with pressors. If R2 pads aren’t on yet, put em on. You have lots of resources in the heart room. Take the US you used for lines and check for lung sliding to rule out PTX. Drop your TEE and do a full exam. Send ABG/labs. Call your surgeon and tell him to start getting ready to cut, like now.

 

[pocafx]

Give some pressor. Fio2 100. Check breath sounds. TEE. US on chest for lung sliding. Thinking tension pneumo. MI PE

easy answer crash to bypass.

 

[JiPo]

To add on to what others have mentioned, perhaps patient couldn't tolerate an increase in pre-load from trendelenburg, and went into pulmonary edema, and RV crapped out? Anything came out of the ETT? Low on the list since she was dialyzed the day before and her EF isn't terrible.

 

[sevoflurane]

For the students and residents.

70 something y/o pt for CABG.

EF 30-35%, pretty bad CAD. ESRD, last HD last night. Inpatient. Pt is tiny, and anemic to boot. Hct high 20s. Looks frail. Edentulous. Has that aura of "I'm gonna give you trouble today."

To the room and baseline SBP 180s. Induce gently and the pressures hold in the 100s throughout line placement. Yay, we're out of the woods I thought.

I thought.

Then all of a sudden the pressure drops to the 60s, and the sats drop to the high 80s.

What are you thinking, and what do you do next?

Bro pull back the tube a few cm and slow down the vanco.

 

[Volatile]

Lower your a-line transducer and half your problem is fixed

Jk BTW, but I did have an attending that enjoyed secretly disconnecting parts of the anesthesia machine to make us residents sweat a little bit.... now I thoroughly enjoy doing it to my students

 

[GassYous]

Lower your a-line transducer and half your problem is fixed

Jk BTW, but I did have an attending that enjoyed secretly disconnecting parts of the anesthesia machine to make us residents sweat a little bit.... now I thoroughly enjoy doing it to my students

Haha I remember that happening to me as an early CA-1 and nearly crapped my pants as machine kept beeping at me. Now I know that the attending was standing right outside the door but man...

 

[deleted875186]

Agree, could be anything, listen to breath sounds and check airway pressures, check body for rash, sudden drop in sats worrisome for PTX or anaphylaxis, probably my top two at the moment. If you have a PA line in that would be helpful to know. Have epinephrine ready.

After that, ddx is hypovolemia, pump problem, or vasoplegia. Give pressors, get an Echo. Other hemodynamics could help narrow it down. Things like PE, tamponade or effusion, etc are possibly but probably less likely.

might add to ddx medication error. Vanco was mentioned above.

 

[deleted875186]

If it’s anaphylaxis, like said above, have to move quick, crashing on pump could be life saving.

 

[zizzer]

My approach would be:

Global assessment of everything else for clues, including: HR, peak pressure (mainstem ETT, PTX), EtCO2 level and waveform, anesthetic agent level, telemetry for ischemic changes or arrythmias

100% FiO2, temporize with some push dose NE or epi.

Given how sudden this sounds, my DDx from what I know would include acute myocardial ischemia, mainstem ETT, anaphylaxis to Abx (high peak pressures and rash?), VAE, PTX

How was his RV function preoperatively? Sudden changes in PAP and CVP might be informative, as would going ahead and inserting the TEE, which should be your next step about by now anyway if he didn't become unstable.

 

[FiO2@21]

For the students and residents.

70 something y/o pt for CABG.

EF 30-35%, pretty bad CAD. ESRD, last HD last night. Inpatient. Pt is tiny, and anemic to boot. Hct high 20s. Looks frail. Edentulous. Has that aura of "I'm gonna give you trouble today."

To the room and baseline SBP 180s. Induce gently and the pressures hold in the 100s throughout line placement. Yay, we're out of the woods I thought.

I thought.

Then all of a sudden the pressure drops to the 60s, and the sats drop to the high 80s.

What are you thinking, and what do you do next?

- buy yourself time to think, push some epi. Check your CVL make sure it’s dripping in properly while you’re at it.

- Do the 15 second standard scan of your setup. Look at vent waveform/peak pressures. Look at EtCO2, art line waveform. Look at the swan (if you placed one). If indicated look for lung sliding with linear probe.

- If still no answer throw in TEE, make global assessment.

Differential:

- vanc running in too fast
- your induction agent and gas finally caught up to you with the minimal stimulus
- PTX
- massive PE
- MI

 

[coffeebythelake]

bad CHF, loss of sympathetic tone can cause BP to tank even with a "cardiac stable" induction

 

[OB1🤙]

Good answers. Nothing looks terribly different on echo. EF 30%. No new RWMAs, global hypokinesis. RV looks normal- no sign of strain. There's no saddle in the PA. Quite underfilled. EKG has a LBBB that is not new.

A-line waveform is fine, but good thought there too. Always make sure the numbers you're basing decisions on are real.

We don't do vanc. Pt got ancef and has received it before.

Peak pressures are higher than I'd like. High 20s. No rash. Flat capnograph waveform- no upsloping.

I don't cause pneumos when doing neck lines. =) Someone mentioned t-berg and I don't put people in t-berg when doing lines under GA either.

 

[CodeBlu]

How much fluid they take off in dialysis? Probably too much.
Give some fluid and inotrope. Turn off the sevo. Bolus some midazolam.

 

[Twiggidy]

My approach would be:

Global assessment of everything else for clues, including: HR, peak pressure (mainstem ETT, PTX), EtCO2 level and waveform, anesthetic agent level, telemetry for ischemic changes or arrythmias

100% FiO2, temporize with some push dose NE or epi.

Given how sudden this sounds, my DDx from what I know would include acute myocardial ischemia, mainstem ETT, anaphylaxis to Abx (high peak pressures and rash?), VAE, PTX

How was his RV function preoperatively? Sudden changes in PAP and CVP might be informative, as would going ahead and inserting the TEE, which should be your next step about by now anyway if he didn't become unstable.

I like this answer because this is a very oral board question and this answer is nice and organized and sounds like a physician, which is what they’re looking for.

make sure you adequately oxygenated and ventilating. Check the HR and Rhythm. Then assess based on differential, ie, tube placement, pneumothorax, st elevation, arrhythmia, TEE exam, etc. and give a quick solution to each thought.

Nice answer

 

[vector2]

Good answers. Nothing looks terribly different on echo. EF 30%. No new RWMAs, global hypokinesis. RV looks normal- no sign of strain. There's no saddle in the PA. Quite underfilled. EKG has a LBBB that is not new.

A-line waveform is fine, but good thought there too. Always make sure the numbers you're basing decisions on are real.

We don't do vanc. Pt got ancef and has received it before.

Peak pressures are higher than I'd like. High 20s. No rash. Flat capnograph waveform- no upsloping.

I don't cause pneumos when doing neck lines. =) Someone mentioned t-berg and I don't put people in t-berg when doing lines under GA either.

Are you sure PPV didn't reveal any large shunts?

Also, what's the depth of the ET tube? How are the breath sounds? What kinda tidal volumes was this little lady getting before this happened? Bilat lung sliding on US?

 

[FiO2@21]

Good answers. Nothing looks terribly different on echo. EF 30%. No new RWMAs, global hypokinesis. RV looks normal- no sign of strain. There's no saddle in the PA. Quite underfilled. EKG has a LBBB that is not new.

A-line waveform is fine, but good thought there too. Always make sure the numbers you're basing decisions on are real.

We don't do vanc. Pt got ancef and has received it before.

Peak pressures are higher than I'd like. High 20s. No rash. Flat capnograph waveform- no upsloping.

I don't cause pneumos when doing neck lines. =) Someone mentioned t-berg and I don't put people in t-berg when doing lines under GA either.

Common things being common:

- Needs volume following dialysis, lack of sympathetic tone caught up with you
- probably too high on the tidal volumes given presumably short patient

Can’t miss: anaphylaxis

 

[Arch Guillotti]

We don't do vanc. Pt got ancef and has received it before.

Peak pressures are higher than I'd like. High 20s. No rash. Flat capnograph waveform- no upsloping.

Past performance is no predictor of future events.

 

[FiO2@21]

Past performance is no predictor of future events.

Was literally about to type that lol. In fact past exposure would make one more suspicious

 

[deleted875186]

Most likely now seems hypovolemia or vasodilation. But I’m still concerned about anaphylaxis if hypotension is not easily fixed with vasopressors.

 

[BloodySurgeon]

As with any situation i will evaluate rate, rhythm, preload, afterload and contractility

Hard to assess with limited information but will take a stab.

If happened after line placement then concern for pneumothorax vs ruptured pulmonary artery from line placement. 100% O2, check Peak and plateau pressure followed by TEE.

If happened after induction. Supply/demand mismatch (hopefully already on beta blocker)

Induction decreased LVEDP therefore reducing coronary perfusion pressure

Possible LCA vs LAD ischemia followed by MR or worsening ICM followed by decrease CO followed by CHF then pulmonary edema.

Unclear if preload was high or low after dialysis but lady is petite and not hard to become fluid overloaded state.

100% O2, start vasopressor followed by evaluating condition by looking at EKG followed by TEE prior to initiating an inotrope.

 

[OB1🤙]

So it has been alluded to- indeed, the tube was R mainstemmed. And the thing is- when taping the tube, I said out loud to the room- "man, this pt is so small that it would be easy to mainstem it." So I purposefully tried to leave it relatively shallow, but clearly not shallow enough. This is also where the edentulousness played a role- it's hard to get the tube to stay where you want it without that anchor.

So that's what made the sat go down and the peak pressures go up. But also absolutely had anaphylaxis on my radar. Fortunately, pulling the tube back even further fixed the sat and the PIPs.

What made the pressure low? Probably a combo of underfilling in the setting of recent dialysis (one thing about ESRD inpatients is that they're almost uniformly dry in my experience because everyone is terrified of volume in them) and ischemia, given how bad the coronaries were. A little levophed fixed it no problem.

So I bring this case up because common things are common. Unexpextedly low sats under anesthesia commonly means the tube is mainstemmed. Hypotension in a known CAD patient commonly means ischemia.

So multiple common problems happened simultaneously- which is uncommon! So in my mind, I had to sort through the differential of both entities- low sat and low BP- and think of single entities that could cause both at the same time (i.e. PE), but also whether separate processes could cause simultaneous unrelated clinical emergencies, which was indeed the case.

 

[dchz]

So multiple common problems happened simultaneously- which is uncommon! So in my mind, I had to sort through the differential of both entities- low sat and low BP- and think of single entities that could cause both at the same time (i.e. PE), but also whether separate processes could cause simultaneous unrelated clinical emergencies, which was indeed the case.

Common things being common, how often do you see a PE that develops that fast and cause hypotension AND hypoxia? Most people I take with significant disease for pulm embolectomy still sat 100% on room air because PE causes deadspace but not shunt.

 

[bigdan]

Common things being common, how often do you see a PE that develops that fast and cause hypotension AND hypoxia? Most people I take with significant disease for pulm embolectomy still sat 100% on room air because PE causes deadspace but not shunt.

What? Are you talking about CTEPH?

The acute massive PE I see causes hypotension, frequently with hypoxia. In fact, the massive PE is discovered because of the sudden onset of hypotenison and hypoxia...

 

[dchz]

What? Are you talking about CTEPH?

The acute massive PE I see causes hypotension, frequently with hypoxia. In fact, the massive PE is discovered because of the sudden onset of hypotenison and hypoxia...

nope, not CTEPH, Acute massive and sub massive PEs.

Edit: most of them are satting in the low 90, not 100% on room air, some of them in the mid to high 90s on facemask with oxygen. I was mistaken.

 

[Arch Guillotti]

Common things being common, how often do you see a PE that develops that fast and cause hypotension AND hypoxia?

Once. Very dramatic.

 

[chocomorsel]

What? Are you talking about CTEPH?

The acute massive PE I see causes hypotension, frequently with hypoxia. In fact, the massive PE is discovered because of the sudden onset of hypotenison and hypoxia...

What is CTEPH?

 

[GassYous]

What is CTEPH?

chronic thromboembolic pulm htn

 

[chocomorsel]

chronic thromboembolic pulm htn

Thanks. Some of y’all gotta realize that some of these abbreviations are not that commonly used.

 

[Beeftenderloin]

Thanks. Some of y’all gotta realize that some of these abbreviations are not that commonly used.

I feel like it’s starting to become more mainstream terminology. It’s literally group 4 from the WHO pulm HTN classification system.

 

[chocomorsel]

I feel like it’s starting to become more mainstream terminology. It’s literally group 4 from the WHO pulm HTN classification system.

Never heard of it. Just finished fellowship last year and even gave a lecture on it, but never heard of those abbreviations.

 

[GassYous]

First link on google for me

 

[Beeftenderloin]

Never heard of it. Just finished fellowship last year and even gave a lecture on it, but never heard of those abbreviations.

Emphasis on “starting to become”, clearly not all the way there yet.

 

[Hork Bajir]

Funny how regional these terms can be. Here in the NE most everyone uses the term CTEPH.

In fairness, while CTEPH is included in “group 4 pulmonary HTN”, aren’t other things as well? Rare cancers, other zebra diagnoses which can result in obstruction of the pulmonary arteriolar bed?

Group 4 Pulmonary Hypertension: Background, Pathophysiology, Risk Factors

emedicine.medscape.com

 

[deleted875186]

Funny how regional these terms can be. Here in the NE most everyone uses the term CTEPH.

In fairness, while CTEPH is included in “group 4 pulmonary HTN”, aren’t other things as well? Rare cancers, other zebra diagnoses which can result in obstruction of the pulmonary arteriolar bed?

Group 4 Pulmonary Hypertension: Background, Pathophysiology, Risk Factors

emedicine.medscape.com

Agreed, in New England I think most people are very familiar with the term. All the medicine people seem to like to use it.

 

[epidural man]

So it has been alluded to- indeed, the tube was R mainstemmed. And the thing is- when taping the tube, I said out loud to the room- "man, this pt is so small that it would be easy to mainstem it." So I purposefully tried to leave it relatively shallow, but clearly not shallow enough. This is also where the edentulousness played a role- it's hard to get the tube to stay where you want it without that anchor.

So that's what made the sat go down and the peak pressures go up. But also absolutely had anaphylaxis on my radar. Fortunately, pulling the tube back even further fixed the sat and the PIPs.

What made the pressure low? Probably a combo of underfilling in the setting of recent dialysis (one thing about ESRD inpatients is that they're almost uniformly dry in my experience because everyone is terrified of volume in them) and ischemia, given how bad the coronaries were. A little levophed fixed it no problem.

So I bring this case up because common things are common. Unexpextedly low sats under anesthesia commonly means the tube is mainstemmed. Hypotension in a known CAD patient commonly means ischemia.

So multiple common problems happened simultaneously- which is uncommon! So in my mind, I had to sort through the differential of both entities- low sat and low BP- and think of single entities that could cause both at the same time (i.e. PE), but also whether separate processes could cause simultaneous unrelated clinical emergencies, which was indeed the case.

Great case - and great discussion about your thoughts and misinterpretations.

I honestly didn't think of a main stem until someone mentioned it (and i just posted a case of it recently that happened to me!). It's a good lesson about going through the simple things, even with experienced hands, like yours.