CPR in OR?

[waterbottle10]

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Recently had a couple cases where the BP cuff went from BP of ~110/60 to "prolonged measurement time" 3 minutes later. I re-cycle the cuff, making sure the surgeon isn't leaning on it, and it still doesn't generate a number. It's set on BP every 3 minutes. I feel for a radial pulse and do not feel one. I bolus 200 mcg of phenylephrine and still do not feel a radial pulse. Now when would you guys start CPR? Would you go feeling for a central pulse before starting CPR? In this case the head was not near me so I didn't go for carotid.

In this case the pulse ox on the same arm always had a good tracing and consistently showed 100% despite me not feeling a radial pulse. Now if we can't feel a pulse, but the pulse ox can pick up a pulse, doesn't that mean the patient never lost a pulse? Could it still be PEA if the pulse consistently had a good waveform despite us not able to palpate a pulse?

 

[Maverikk]

EKG?

 

[DrOwnage]

Lol... Why not feel the carotid, its ALCS standard and it's right there. Also 20-30 systolic more sensitive. EKG? telling surgeons to stop what they're doing so there's no artifact on the screen.

 

[waterbottle10]

The head was away so it wasn't right there for me. Would you start CPR in this case if you do not feel a carotid pulse? Even though there is a waveform on pulse ox?

EKG is unchanged, HR was also relatively unchanged. But without a pulse it can be PEA

 

[nimbus]

The head was away so it wasn't right there for me. Would you start CPR in this case if you do not feel a carotid pulse? Even though there is a waveform on pulse ox?

EKG is unchanged, HR was also relatively unchanged. But without a pulse it can be PEA

Assuming there was a good pulse ox waveform, I would give a small dose of epi, then a larger dose, then cpr. Simultaneously I would inform the team and start looking for a diagnosis.

 

[OB1🤙]

EtCO2, yo

 

[Twiggidy]

First, what was the surgery? Is there anything the surgeon can see to confirm there isn’t a heartbeat?

Next, you have a lot of monitors to evaluate before calling an arrest
-pulse ox
-EKG
-ETCO2 (did the wave dramatically decrease or disappear)
-faulty BP cuff

In reality, it may be a bit embarrassing but there isn’t really harm in pushing that code button early.

 

[pgg]

EKG?

PEA is a thing so I wouldn't hang my hat on the ECG, if I suspected an arrest. I mean, I'd look at it to see if the patient had some dysrhythmmia, but I wouldn't let NSR reassure me.

 

[urge]

Has anyone seen a pulse ox reading normally with a waveform when there is not even a patient in the room?

 

[dannyboy1]

Recently had a couple cases where the BP cuff went from BP of ~110/60 to "prolonged measurement time" 3 minutes later. I re-cycle the cuff, making sure the surgeon isn't leaning on it, and it still doesn't generate a number. It's set on BP every 3 minutes. I feel for a radial pulse and do not feel one. I bolus 200 mcg of phenylephrine and still do not feel a radial pulse. Now when would you guys start CPR? Would you go feeling for a central pulse before starting CPR? In this case the head was not near me so I didn't go for carotid.

In this case the pulse ox on the same arm always had a good tracing and consistently showed 100% despite me not feeling a radial pulse. Now if we can't feel a pulse, but the pulse ox can pick up a pulse, doesn't that mean the patient never lost a pulse? Could it still be PEA if the pulse consistently had a good waveform despite us not able to palpate a pulse?

You have unchanged etCO2 and a good pulse ox waveform with sat of 100%. Your patient is not in arrest. Also look at the head and mucous membranes. Pink is a good sign, ashen and pale not so much. If this happened suddenly and seemingly without cause check your BP cable. This exact scenario happened to me once, turned out someone was standing on the bp cable...

 

[Planktonmd]

If you really have a good SPO2 waveform and it's reading 100% as you said and you have good ETCO2 (I am assuming you are monitoring ETCO2), then it's not an arrest.

 

[btbam]

How did it take 5 responses for someone to say EtCO2?

 

[vector2]

Dont leave your NIBP at 3 min in this situation. With normal pulse ox waveform and EtCO2 >30 your cardiac output is fine and you're likely dealing with a low SVR situation. Give a huge slug of phenylephrine and/or ephedrine, open your fluids, check your field, vent, vaporizer, ekg, and start cycling q1m. Also, keep ACE/ARB hypotension in the back of your mind. Easy to forget if you haven't dealt with one of these in awhile.

 

[T-burglar]

I’d also add that you need to be 100% sure you’re looking at cardiac arrest before you start pounding and giving epinephrine. CPR and epi have the potential for major morbidity if you are wrong about the patient being in arrest.

 

[BobLoblaw78]

What was the Bis?


Lol. I would not start CPR. Check other pulses in addition to twiggidy's, etc input above. If I started compressions for every patient that had to repeat bp cycle and absent/poor radial pulse, I would have done unnecessary harm. If they are PEA, VT, etc every monitor should be "malfunctioning".

Anesthesia codes are usually worsened by people in denial that think all their monitors are messing up. So you want to make sure that you trust them all together and trust the patient.

 

[coffeebythelake]

That being said, if you have a pt utterly unresponsive to multiple escalating doses of pressers and inotropes u should be thinking cardiogenic shock or something. Obviously the patient comorbidities would suggest something like this. CPR might be appropriate if so refractory hypotensive, nonperfusing pressure.

 

[waterbottle10]

Sounds good. Pretty much what I did but curious what others would've done. All other vitals were pretty much unchanged so I initially suspected cuff malfunction. Gave 200mcg phenylephrine and switched to leg cuff, lowered anesthesia, and re cycled with still no BP. Bolused 400 phenylephrine then drew up stronger pressors while cycling cuff q1 min. Pressure then showed up as 60/30 after the 400. Was able to keep his pressure above sbp 85 during the case with 6 unit Vaso boluses every few minutes. I end up attributing it to his acei that he stopped day before.

 

[Twiggidy]

How did it take 5 responses for someone to say EtCO2?

Inexperienced

 

[nimbus]

Inexperienced

Dementia

 

[T-burglar]

Also keep in mind that even “apparent” PEA might have a pressure of 40 or 50 in the arteries , not actually truly pulseless,and without an arterial line you don’t know. if there is ANY cardiac output at all, that organized contraction will almost always provide more stroke volume than a chest compression. Even excellent CPR never does better than a pressure of 40 in the aorta if the patient has no native cardiac output.

So beating on the chest only helps if the rhythm isn’t causing any output. You can determine if there is output by viewing the opening of the aortic valve on echo.

If the organized rhythm is opening the aortic valve, then it’s not truly PEA because there is actually a pulse it just may be a very weak pulse. In these situations I don’t compress, I just give drugs and try to figure out what’s wrong. This small output is still better than compressions, and Studies have shown that people usually compress the LVOT and aortic root twice as often as they compress the ventricle because of bad hand placement. This either does nothing for full arrest, or actually HURTS in pseudo PEA. So I reserve chest compressions for truly no cardiac output.

 

[anbuitachi]

We are pretty spoiled with all these monitors. I wonder how often people code patients on the floor with no palpable pulse but with normal etco2 if they had etco2 monitor

 

[deleted547339]

We are pretty spoiled with all these monitors. I wonder how often people code patients on the floor with no palpable pulse but with normal etco2 if they had etco2 monitor

Er/icu doc here- responding to floor codes is a cluster....I’ve seen rosc by etco2 and no one notices or chest compressions and etco2 of damned near zero and no one notices that they’re not doing anything.

I would (probably) never start compressions on a radial pulse. Honestly, the only time I check radials is it I’m concerned about a vascular injury, just putting on a show or just getting a sense of the patient over all - never when something is going down.

Agree with above that I’ve seen a normal spo2 with no one hooked up, but the tracing is pretty reliable.

Since I don’t practice in the OR, I can’t be too insightful, but I would almost certainly wait the 10-20 seconds it takes to check a fem pulse, look at the rhythm, look at the etco2 tracing, the sp02 tracing and be sure.

 

[Arch Guillotti]

Also keep in mind that even “apparent” PEA might have a pressure of 40 or 50 in the arteries , not actually truly pulseless,and without an arterial line you don’t know. if there is ANY cardiac output at all, that organized contraction will almost always provide more stroke volume than a chest compression. Even excellent CPR never does better than a pressure of 40 in the aorta if the patient has no native cardiac output.

So beating on the chest only helps if the rhythm isn’t causing any output. You can determine if there is output by viewing the opening of the aortic valve on echo.

If the organized rhythm is opening the aortic valve, then it’s not truly PEA because there is actually a pulse it just may be a very weak pulse. In these situations I don’t compress, I just give drugs and try to figure out what’s wrong. This small output is still better than compressions, and Studies have shown that people usually compress the LVOT and aortic root twice as often as they compress the ventricle because of bad hand placement. This either does nothing for full arrest, or actually HURTS in pseudo PEA. So I reserve chest compressions for truly no cardiac output.

That all may be true but good chest compressions will demonstrably raise the BP on an arterial tracing.

Echo is not readily available for many of us.

 

[hankbb02]

Sounds good. Pretty much what I did but curious what others would've done. All other vitals were pretty much unchanged so I initially suspected cuff malfunction. Gave 200mcg phenylephrine and switched to leg cuff, lowered anesthesia, and re cycled with still no BP. Bolused 400 phenylephrine then drew up stronger pressors while cycling cuff q1 min. Pressure then showed up as 60/30 after the 400. Was able to keep his pressure above sbp 85 during the case with 6 unit Vaso boluses every few minutes. I end up attributing it to his acei that he stopped day before.

Think about adding epi early in these situations. Not code doses mind you but 5-10mcg boluses. If you find yourself bolusing a lot of SVR drugs consider other causes hypovolemia, acidosis, cardiomyopathy, anaphlyaxis. Also pay careful attention to what is going on in the case and whether they surgery could be contributing.

 

[Ronin786]

Sounds good. Pretty much what I did but curious what others would've done. All other vitals were pretty much unchanged so I initially suspected cuff malfunction. Gave 200mcg phenylephrine and switched to leg cuff, lowered anesthesia, and re cycled with still no BP. Bolused 400 phenylephrine then drew up stronger pressors while cycling cuff q1 min. Pressure then showed up as 60/30 after the 400. Was able to keep his pressure above sbp 85 during the case with 6 unit Vaso boluses every few minutes. I end up attributing it to his acei that he stopped day before.

That is a metric **** ton of vaso. As much as I love vasopressin, and its utility in RV failure and pHTN is paramount, the way most anesthesiologists use it in the OR is asinine. I've seen more than one anesthesiologist act impressed for maintaining BP after using the entire vial of vasopressin (20units) in a 3 hour case. Keep in mind that vasopressin infusions are considered "high" when they get to 0.1u/min and can cause myocardial and gastrointestinal ischemia. That's less than 6 units per hour!

 

[waterbottle10]

That is a metric **** ton of vaso. As much as I love vasopressin, and its utility in RV failure and pHTN is paramount, the way most anesthesiologists use it in the OR is asinine. I've seen more than one anesthesiologist act impressed for maintaining BP after using the entire vial of vasopressin (20units) in a 3 hour case. Keep in mind that vasopressin infusions are considered "high" when they get to 0.1u/min and can cause myocardial and gastrointestinal ischemia. That's less than 6 units per hour!

It was a short case, less than 1 hour long. Only used about 30 units, along with about a total of 3 mg bolus of phenylephrine

 

[anbuitachi]

That is a metric **** ton of vaso. As much as I love vasopressin, and its utility in RV failure and pHTN is paramount, the way most anesthesiologists use it in the OR is asinine. I've seen more than one anesthesiologist act impressed for maintaining BP after using the entire vial of vasopressin (20units) in a 3 hour case. Keep in mind that vasopressin infusions are considered "high" when they get to 0.1u/min and can cause myocardial and gastrointestinal ischemia. That's less than 6 units per hour!

i think you are thinking of ICU settings. OR is a different beast. You aren't going to see 100 mcg epi boluses in the ICU on top of infusions. The causes of hypotension is often different. Were the vasopressin studies done with isoflurane on? There's probably a difference between hypotension caused by septic shock in the ICU vs hypotension caused by anesthesia etc. Also a lot of vasopressin studies are conflicting and done in animals..

 

[Twiggidy]

It was a short case, less than 1 hour long. Only used about 30 units, along with about a total of 3 mg bolus of phenylephrine

Way too much. Re-evaluate that case from pre to post op because someone in that room was doing something wrong. Those numbers would get you trashed in an M&M

 

[vector2]

i think you are thinking of ICU settings. OR is a different beast. You aren't going to see 100 mcg epi boluses in the ICU on top of infusions. The causes of hypotension is often different. Were the vasopressin studies done with isoflurane on? There's probably a difference between hypotension caused by septic shock in the ICU vs hypotension caused by anesthesia etc. Also a lot of vasopressin studies are conflicting and done in animals..

We know for a fact that in both anesthetized + healthy and anesthetized + septic pig models that vasopressin increases mesenteric resistance and decreases mesenteric blood flow. After a string of cases where a likely vasoplegic pt didnt respond to 1-2 units of vaso but had a robust response to 8-16 mcg norepi, I'm much more apt to go this route anyway.

Regardless, I don't care if OP had 2 MAC of isoflurane on- something (beyond anesthetic vasodilation) is going pretty damn wrong if you're giving 30 units of vaso and 3mg of neo within 1 hr. OP didn't give much detail about the pt or the case, but when the hypotension is this profound I'm telling the surgeon to stop for a second and I'm gonna place an a-line, get a gas, and drop a TEE probe. Ace hypotension can indeed be profound (requiring epi and dozens of units of vaso), but I'd still want to be thinking about anaphylaxis or sepsis, and make sure the LV/RV/valves/PASP/pericardium look good and that I'm not missing some occult hypovolemia, hemorrhage, MI, PE, etc

 

[pgg]

It was a short case, less than 1 hour long. Only used about 30 units, along with about a total of 3 mg bolus of phenylephrine

Geez, I think you should recalibrate your definition of "only" ...

That's a lot of squeeze.

 

[AdmiralChz]

30 units is close to code dose Vaso. Yikes.

Did you have like 5% ISO with 50% N2O running?

 

[T-burglar]

These cases are a reminder of how hard it is for an anesthetist to kill most patients who aren’t really sick

 

[waterbottle10]

30 units is close to code dose Vaso. Yikes.

Did you have like 5% ISO with 50% N2O running?

Half a Mac of gas and .1 infusion of remifentanil. It was a esophageal stent and repair.

I did think about other potential causes. Checked for rashes with none found. No increased peak pressures or changes in other vitals including temperature. No bleeding. As soon as anesthesia was turned off at the end his pressure normalized.
Woke up well and was discharged from PACU a few hours later.

 

[Psai]

Half a Mac of gas and .1 infusion of remifentanil. It was a esophageal stent and repair.

I did think about other potential causes. Checked for rashes with none found. No increased peak pressures or changes in other vitals including temperature. No bleeding. As soon as anesthesia was turned off at the end his pressure normalized.
Woke up well and was discharged from PACU a few hours later.

Why remi

 

[waterbottle10]

Why remi

Quick on quick off. Lots of stimulation with the case since they did a suspension scope and goes to no stimulation right after scope is removed. Quick emergence and minimal pain post op so no need for long acting.

 

[osumd]

Have to wonder if the Remi was reconstituted correctly.


Would anyone be hesitant to send this guy home same day despite normal vitals in the pacu?

 

[Twiggidy]

I’m not that uptight about the remi. I use it all the time.

I wonder if some vaso-vagal action was occurring with the stent. Also, was it an old person with a sick heart?

Given the resuscitation I may have hesitated to send him on his way, especially if I’m concerned about something occult happening, but if this was done in a ASC then I would’ve had him as the last person to leave PACU if he was stable.

 

[jwk]

Half a Mac of gas and .1 infusion of remifentanil. It was a esophageal stent and repair.

I did think about other potential causes. Checked for rashes with none found. No increased peak pressures or changes in other vitals including temperature. No bleeding. As soon as anesthesia was turned off at the end his pressure normalized.
Woke up well and was discharged from PACU a few hours later.

I'm sorry - this all just screams "operator error". Too many things don't add up. Too few details to make any kind of real judgement on the patient or what happened, and comments like "only" 30 units of vasopressin make me think you really don't have much of a clue either.

 

[waterbottle10]

I’m not that uptight about the remi. I use it all the time.

I wonder if some vaso-vagal action was occurring with the stent. Also, was it an old person with a sick heart?

Given the resuscitation I may have hesitated to send him on his way, especially if I’m concerned about something occult happening, but if this was done in a ASC then I would’ve had him as the last person to leave PACU if he was stable.

I'm sorry - this all just screams "operator error". Too many things don't add up. Too few details to make any kind of real judgement on the patient or what happened, and comments like "only" 30 units of vasopressin make me think you really don't have much of a clue either.

He did not have any history of heart disease. Also thought of some vaso vagal or carotid action going on but no bradycardia. Still think the ACEI is most likely cause

 

[MoMoGesiologist]

It was a short case, less than 1 hour long. Only used about 30 units, along with about a total of 3 mg bolus of phenylephrine

You gotta pump those numbers up! Those are rookie numbers!

 

[midazzoler]

Reminds me of a pt a friend of mine had with an AICD/pacer. At the end of a colonoscopy (for anemia I think) the NIBP couldn't pick up anything. Pacer output never changed on EKG. Pt wasn't in Vtach so it didn't shock. EtCO2 on the nasal cannula seemed ok at first. Pulse ox eventually went down but I feel like it was a late sign. (I wasn't in the room so I can't really say.) ROSC achieved but only after a long code and still ended with poor outcome. When do you start compressions there? Should a patient like that get an a.line?

 

[drmwvr]

Sounds good. Pretty much what I did but curious what others would've done. All other vitals were pretty much unchanged so I initially suspected cuff malfunction. Gave 200mcg phenylephrine and switched to leg cuff, lowered anesthesia, and re cycled with still no BP. Bolused 400 phenylephrine then drew up stronger pressors while cycling cuff q1 min. Pressure then showed up as 60/30 after the 400. Was able to keep his pressure above sbp 85 during the case with 6 unit Vaso boluses every few minutes. I end up attributing it to his acei that he stopped day before.

Do people not give volume anymore?

 

[waterbottle10]

Do people not give volume anymore?

I had fluids wide open, managed to get in 1.5L from anesthesia start to finish

 

[vector2]

Do people not give volume anymore?

A fluid bolus is fine but volume is typically overrated for these kind of situations. For most ASA 1/2 outpatients coming for quick procedures, they are relatively euvolemic and hypotension post-induction is entirely attributable to vasodilation. It's possible in this case though (esophageal stent malposition) that the pt was significantly volume down before coming for surgery.

 

[T-burglar]

Reminds me of a pt a friend of mine had with an AICD/pacer. At the end of a colonoscopy (for anemia I think) the NIBP couldn't pick up anything. Pacer output never changed on EKG. Pt wasn't in Vtach so it didn't shock. EtCO2 on the nasal cannula seemed ok at first. Pulse ox eventually went down but I feel like it was a late sign. (I wasn't in the room so I can't really say.) ROSC achieved but only after a long code and still ended with poor outcome. When do you start compressions there? Should a patient like that get an a.line?

Hard to know what happened here. If they were very hypotensive for some time before PEA then not likely pacer dependency with lost capture. Lost capture is immediate arrest if 100% pacer dependent. A period of hypotension followed by true arrest or PEA screams rapid volume loss, compartment tension like tamponade or PTX, or anesthetic overdose, hypoxemia, or undiagnosed or under appreciated severe heart disease.

As an example, I’ve had to some TAVR patients on norepinephrine just to tolerate moderate sedation. That’s truly critical AS of course, however.

 

[CopaceticOne]

Esophageal stent & repair. You’re just mentioning this now? Ok, I’ll state the obvious: what is the PMHx of this patient? No co-morbidities have been mentioned other than the inferred HTN given the mention of ACEi.

Sorry, but this is a BS case discussion without all the info. Was this patient inpatient before the case and getting IVF? Were the outpatient and not eating? Do they have HFrEF and severe 4v CAD and AS? BMI 56? Starting Hct of 20? Previously documented allergy to the Roc you gave?

Yes, my questions above are sarcastic. But if the answer was yes to any one of them would totally change how people view this case, right?

 

[waterbottle10]

Esophageal stent & repair. You’re just mentioning this now? Ok, I’ll state the obvious: what is the PMHx of this patient? No co-morbidities have been mentioned other than the inferred HTN given the mention of ACEi.

Sorry, but this is a BS case discussion without all the info. Was this patient inpatient before the case and getting IVF? Were the outpatient and not eating? Do they have HFrEF and severe 4v CAD and AS? BMI 56? Starting Hct of 20? Previously documented allergy to the Roc you gave?

Yes, my questions above are sarcastic. But if the answer was yes to any one of them would totally change how people view this case, right?

I just reviewed the case again. The surgeon ended up doing laryngoscopy/esophagoscopy with balloon dilation of esophagus. Patient was 60s with HTN, poorly controlled DM, asthma, oropharyngeal cancer with radiation in the past now with some dysphagia.

No antibiotics or paralysis given

 

[wickedskillz]

AceI sounds likely imo, but that's a **** ton of pressor still. Glad he woke up ok

 

[coffeebythelake]

AceI sounds likely imo, but that's a **** ton of pressor still. Glad he woke up ok

Elective surgery using those doses of pressor? Would have cancelled the case.

 

[Ronin786]

As an aside, this case is an example as to why anesthesiologists need better training in TTE. This patient is in prime position for a subcostal view that would have eliminated a lot of differentials.