#Case_14 Acute Abdomen and collapsed after induction.

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DrAmir0078

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Hi SDN Anesthesiologists,
I hope you are doing well. Bringing in this general forum, this case : 67 years old man with suspected Acute Abdomen - bilateral air under diaphragm. He was with - ve PMH and PSH, but noticeable moderate goiter (no treatment and no investigation). Mallampati 4. His vitals were Bp 240/140 mmgh and PR 126 bpm, SPO2 95%, RR > 20. Had 1 Lt crystaloid in the ER.

Then his BP rechecked again and it was 189/97. We agreed to RSI. Ketamine was given 30 mg, Propofol sleeping dose up to 80 mg and 100 mg scoline.

ETT was successful, first attempt with difficulty; while checking the breathing sounds, no air entry, it was by vision. Saturation dropped, and no Bp and no PR. Brought another two monitors and nothing.

ECG shows sinus tachycardia. Extermites were cold; immediate resuscitation started with Adrenaline 1 mg IV followed by 1 Lt NS. Then again 1 mg adrenaline. 16 mg dexamethasone and 200 mg Hydrocortisone. and again another 1 mg adrenaline and 0.5 Lt of Ringer. Blanket and another 1 Lt warm NS. We gave noreadrenaline infusion. No urine output. Surgery team Attending was there watching. Our Attending too working on the case. Patient got spontaneous breathing, switching to SIMV/PSV.
After 3 hours of resuscitation, patient last 30 minutes became better, urine output is okay, pluse lowered (it was reached 150s and slowed down to 130),still sinus. Muscle power regained, able to move his hands and can move his tongue. Spo2 went up and stayed 98%.

We gave it a try to extubate him and sent him to the ICU. Surgery refused to operate until the patient became stable claiming he can't tolerate the operation.... etc

What is your DDx?

What did we miss and better to add?

Remember : limited resources, no ABG, limited drugs.


Cheers.

P. S. This is my first time encounter such situation in using Adrenaline and was successful. My guess : his BP was reflecting intravascular dehydration and he had better to be managed in the ER with fluids. Other guess what happened is anaphylaxis due to scoline (his peak airway pressure was 14, but no air entry - how comes? But then after adrenaline was able to hear the breathing sounds); and I don't know if it was the effect of drugs administered like Ketamine and Propofol (catecholamines consumption - edge knife theory) as this patient with such goiter vs his hypovolemia or being fragile too and got his CVS collapsed. I can't think more!
 
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I think with anaphylaxis you should have warm extremities
I think the prop dose was too low. That's the dose I give for little old ladies
Hypertensive and tachy due to cathecholamines from hyperthyroid

I agree with above, low prop -> bronchospasm -> no air movement -> crash
hypoxia -> bradycardia -> hypotension

Probably was already volume depleted

Peak pressures probably just reflecting what you have on your bag as you're not moving any air and you're not seeing the real pressure in the airways or alveoli.
 
Thanks @anaesthetic and @GassYous

So, we immediately put him on PCV Pinsp 12 - vT was 480 and the Attending switch it to VCV and Ppeak 14 and couldn't hear the breathing sounds by usual manual squeezing the RB.

Propofol dose was a sleeping as we said (he was skinny senior guy like 60 kg), fasiculate from scoline and ETT in, prior ketamine 30 and I forgot 3 mg midazolam (my bad I forgot), we were trying to do balanced anesthesia. Thinking about propofol dose!

warm extremities are more with anaphylaxis - very interesting as it will be systemic vasodilation.

Sepsis is highly questionable too and he respond poorly at the beginning to fluids, but could have the support of noreadrenaline and aided him.

We were about to lose him, even my attentding thought of asystole and starts like 20 chest compressions, but it was shown sinus tachycardia on Defib monitor.

So, if time machine is handy, what should we do? Give more Propofol, prior check CVP and CV line inserted prior, load with fluid regardless of hypertension reading, get him rehydrated and then induce him deep and ETT him. What do you think?

Acute Abdomen - pre sepsis like and goiter both masked the presentation!

Thanks
 
Thanks @anaesthetic and @GassYous

So, we immediately put him on PCV Pinsp 12 - vT was 480 and the Attending switch it to VCV and Ppeak 14 and couldn't hear the breathing sounds by usual manual squeezing the RB.

Propofol dose was a sleeping as we said (he was skinny senior guy like 60 kg), fasiculate from scoline and ETT in, prior ketamine 30 and I forgot 3 mg midazolam (my bad I forgot), we were trying to do balanced anesthesia. Thinking about propofol dose!

warm extremities are more with anaphylaxis - very interesting as it will be systemic vasodilation.

Sepsis is highly questionable too and he respond poorly at the beginning to fluids, but could have the support of noreadrenaline and aided him.

We were about to lose him, even my attentding thought of asystole and starts like 20 chest compressions, but it was shown sinus tachycardia on Defib monitor.

So, if time machine is handy, what should we do? Give more Propofol, prior check CVP and CV line inserted prior, load with fluid regardless of hypertension reading, get him rehydrated and then induce him deep and ETT him. What do you think?

Acute Abdomen - pre sepsis like and goiter both masked the presentation!

Thanks
Did he have a pulse? He could have a rhythm but what you are describing sounds like PEA arrest. Check carotid.
In a septic patient I think the doses you gave were fine especially in the 60kg patient. May be a little much actually. Because the hyperthyroidism is masking the hypotension from sepsis like you are saying.
So hypotension and possibly bronchospasm only because you said you couldn’t hear any lung sounds. However severe hypotension on induction could do it alone. Did he look toxic?
 
Hypertension could be secondary to pain/sympathetic overdrive due to the acute abdomen presentation; doesn’t necessarily reflect volume status, especially given the tachycardia and response after induction.

Pre-induction art line, fluid load with colloid/crystalloid, RSI with norepi chaser, ETT. Deepen the anesthetic with sevo/prop for bronchospasm, epi if refractory. Although ketamine is a bronchodilator, in the setting of severe hypovolemia and likely catecholamine depletion, myocardial depression should be considered in this case as well.
 
No pluse was felt at all anywhere, even at ascultation, one resident said no, Attending grapped the stethoscope said hardly to hear, even a surgery resident said no. Defib showing as said sinus pretty P QRS T tachycardia; my question can such tachycardia called Pulsless Electrical Activity PEA??, and he was crashed and only 20 chest compressions and the 1 mg adrenaline prior and 1 mg after could bring him back and that means successful CPR. Wow!

Because all PEA I have seen before were bradycardia weaning off atropine, but not tachycardia!

The pulse returned strong, BP shot up again and we titrated the noreadrenaline until Off and got urine output!

Thanks
 
Hypertension could be secondary to pain/sympathetic overdrive due to the acute abdomen presentation; doesn’t necessarily reflect volume status, especially given the tachycardia and response after induction.

Pre-induction art line, fluid load with colloid/crystalloid, RSI with norepi chaser, ETT. Deepen the anesthetic with sevo/prop for bronchospasm, epi if refractory. Although ketamine is a bronchodilator, in the setting of severe hypovolemia and likely catecholamine depletion, myocardial depression should be considered in this case as well.
Sure, such tense abdomen will peak his BP reading, very possibly he couldn't tolerate (if not deep enough) intubation or under dosed induction agents, added more consumption of catecholamines.

Your approach to induce and to treat of bronchospasm and if refractory give Epi; shouldn't be the dose 10 mcg iv is enough to break up the spasm and can be repeated! We gave him 3 mg and now I am thinking of bronchospasm then crashed. Still thinking!

Thanks
 
No pluse was felt at all anywhere, even at ascultation, one resident said no, Attending grapped the stethoscope said hardly to hear, even a surgery resident said no. Defib showing as said sinus pretty P QRS T tachycardia; my question can such tachycardia called Pulsless Electrical Activity PEA??, and he was crashed and only 20 chest compressions and the 1 mg adrenaline prior and 1 mg after could bring him back and that means successful CPR. Wow!

Because all PEA I have seen before were bradycardia weaning off atropine, but not tachycardia!

The pulse returned strong, BP shot up again and we titrated the noreadrenaline until Off and got urine output!

Thanks
I mean if multiple people are confirming no pulse and you've got no bp and no spo2, then I'd say it's PEA no matter what the ecg said.
 
I mean if multiple people are confirming no pulse and you've got no bp and no spo2, then I'd say it's PEA no matter what the ecg said.
Yes, Dr. MirrorTodd, that is why the Attending was addressing giving Adrenalines and considered the case as Cardiac Arrest and run through ACLS, but gladly short term compressions.

Again, it is my first time seeing such PEAs with pretty normal shaped QRS in sinus tachy, and the Attending was the only who kept listening to his chest. What a case!
 
The ventilator is reporting low pressures, not high.
The bag feels like it's ventilating.
The patient is pulseless.
The ETCO2 is reading nothing. There is no ETCO2 being measured.
The patient was induced from an unstable state, with tachycardia and volume depletion pre-negative inotropic drugs, and IPPV was applied.

Sounds like an empty heart pushed into PEA by induction/IPPV.

Either the anaesthetic machine is lying about pressures or the boss was mistaken about not hearing breath sounds while doing a few chest compressions. I side with the machine given the stressful context.
 
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Belly sepsis can need a lot of fluid. The whole 30 ml/kg for general sepsis is a framework but the combination of massive inflammation with gram negatives + antibiotics causing LPS release they can easily need 5-8 liters or more. I agree with above, intravascular volume depletion + sudden change to PPV=no forward flow from the right side which means no flow from the left either. The epi bought enough time for the fluids you gave to actually get in there and work but ideally the patient would have been more completely resuscitated before surgery.
 
Sure, such tense abdomen will peak his BP reading, very possibly he couldn't tolerate (if not deep enough) intubation or under dosed induction agents, added more consumption of catecholamines.

Your approach to induce and to treat of bronchospasm and if refractory give Epi; shouldn't be the dose 10 mcg iv is enough to break up the spasm and can be repeated! We gave him 3 mg and now I am thinking of bronchospasm then crashed. Still thinking!

Thanks
No pulse, EKG is reading something it’s PEA. Basically the heart is kinda vibrating but not effectively squeezing.
PEA is PEA. No pulse, start ACLS. No matter what the monitor says.
This is a case of you turning off their brain and sympathetic drive in a patient who’s in extremis. The pre induction BP means nothing in this case other than his Goiter is in overdrive and he’s possibly in pain.
It was the drugs. Too much.
 
PEA arrest, air under diagphram means perforation, patient is septic, surgery should have proceeded after ROSC as the patient will not get better. Too high dose for induction, perhaps etomidate would have been a better choice in retrospect, or midazolam and fentanyl, or starting a norepi infusion before giving meds.
 
The ventilator is reporting low pressures, not high.
The bag feels like it's ventilating.
The patient is pulseless.
The ETCO2 is reading nothing. There is no ETCO2 being measured.
The patient was induced from an unstable state, with tachycardia and volume depletion pre-negative inotropic drugs, and IPPV was applied.

Sounds like an empty heart pushed into PEA by induction/IPPV.

Either the anaesthetic machine is lying about pressures or the boss was mistaken about not hearing breath sounds while doing a few chest compressions. I side with the machine given the stressful context.
Probably you were in a parallel world with us. Yes, few minutes after induction (after I checked no lung breathing sounds), the time where the Attending assessing the situation, and we were switching between manual and ventilation, the Ventilator machine bellow stopped, Attending thlnks a problem with the machine, we brought another one and once it arrives, the broken one works again.

I believe in physiology, and I admit, this induction was caused by underestimation of the complex physiology. I totally agree with you Dr.
 
Belly sepsis can need a lot of fluid. The whole 30 ml/kg for general sepsis is a framework but the combination of massive inflammation with gram negatives + antibiotics causing LPS release they can easily need 5-8 liters or more. I agree with above, intravascular volume depletion + sudden change to PPV=no forward flow from the right side which means no flow from the left either. The epi bought enough time for the fluids you gave to actually get in there and work but ideally the patient would have been more completely resuscitated before surgery.
It happens couple weeks ago, a patient died during induction and he was septic due to Mega colon obstruction, that night shift team tried to resuscitate prior with no benefit, just once induced, patient crashed!

So, one of our Attending said "once it is acute abdomen like SBO, immediate 1.5 Lt within 10 minutes and another 1.5 within 30 minutes prior to your second assessment and never to induce without reaching good rehydration"

We had almost weekly a case or two of perforated viscus vs BO during my first year of training at Baghdad Medical City, and we discuss those cases - post shift meetings!

But, I had many similar cases, but young and they tolerated the induction; this patient and although we think we tried balanced anesthesia, but again was like a turmoil!

We had learned what does sleeping dose of propofol - just once loose eyelash and corneal reflexes and fall asleep. Today I discussed with my PGY3 friend and he told me he had a case young female with 200 mg propofol he used in the induction and plus Sevoflurane for 3 minutes (he used Sux too) and he puts ETT, the patient develops bronchospasm, he couldn't manually giving her breath "rock like hardness the reservoir bag" and no breathing sounds, he was alone and told me "I was freaked out", but he is a smart guy and rapidly acted "another dose of Propofol + high sevoflurane + Hydrocortisone and aminophylline and also changed the tube to smaller size, then slowly brought her back".

The question is, since there are different cases, and without BIS and only reflexes, pain stimulus by jaw thrust, and not to ignore my patient physiology especially, how we could be more safe?

Thanks a lot!
 
I did say May be too much. Especially when he added he gave versed as well. I give Etomidate. Or very little propofol.
There is no rule to assume the dose of propofol in such cases. What alternatives?

One of the post shift meetings, presenting a case of BO and once the resident said "a touch dose of propofol", the meeting chairman said "what do you mean a touch dose? What even means sleeping dose"!

Other case was septic patient and the resident decides not to give propofol, he gave Ketamine and the patient passed.

This theory of "on the edge of knife" is not an easy phrase to incorporate in the practice, how far we can be conservatives in the setting of top Emergency case?
 
No pulse, EKG is reading something it’s PEA. Basically the heart is kinda vibrating but not effectively squeezing.
PEA is PEA. No pulse, start ACLS. No matter what the monitor says.
This is a case of you turning off their brain and sympathetic drive in a patient who’s in extremis. The pre induction BP means nothing in this case other than his Goiter is in overdrive and he’s possibly in pain.
It was the drugs. Too much.
I agree. Your physiology explanation hits the goal. Our induction drugs are too much, how if it was less much, would the patient falls asleep, do you think?
But, I would agree more, if he was resuscitated more and took extra hour of fluids and assessment, probably our drugs will be suitable as long as he maintains good volume status!!
 
There is no rule to assume the dose of propofol in such cases. What alternatives?

One of the post shift meetings, presenting a case of BO and once the resident said "a touch dose of propofol", the meeting chairman said "what do you mean a touch dose? What even means sleeping dose"!

Other case was septic patient and the resident decides not to give propofol, he gave Ketamine and the patient passed.

This theory of "on the edge of knife" is not an easy phrase to incorporate in the practice, how far we can be conservatives in the setting of top Emergency case?
Literally you can give1/4- 1/3 mg per kg of propofol and be fine. And they may still crash. And yes, septic patients and patients in extremis crash on ketamine. And versed. Have seen them crash on all the drugs except fentanyl. Preload them with a good liter if you can first.
And versed is unnecessary. Prop sux tube is fitting in this setting. I have gotten so out of the habit of using propofol I forget about induction doses sometimes.
Gotta refresh my memory when I get back to the OR.
 
PEA arrest, air under diagphram means perforation, patient is septic, surgery should have proceeded after ROSC as the patient will not get better. Too high dose for induction, perhaps etomidate would have been a better choice in retrospect, or midazolam and fentanyl, or starting a norepi infusion before giving meds.
I agree too Dr. DipriMan; the fear of norepinephrine support with such high BP I mentioned, I personally can't, it is very challenging, but I have learnt a lot from this post.
 
I agree. Your physiology explanation hits the goal. Our induction drugs are too much, how if it was less much, would the patient falls asleep, do you think?
But, I would agree more, if he was resuscitated more and took extra hour of fluids and assessment, probably our drugs will be suitable as long as he maintains good volume status!!
Yea they sleep. You can literally induce with 2mg of versed on these patients. Have done it.
 
I induce all my patients in the ICU with propofol. People don't die from propofol, they die from too much propofol (or from PPV throwing them over the edge). It only takes 20-40mg of propofol to knock someone out for a cardioversion when they're completely awake. In a very sick patient population you don't need a lot to get them under and rocuronium takes care of the rest. Phenylephrine pushes to keep the pressure up.

Since you have ketamine readily available, 30mg of ketamine and 30mg of propofol is a fairly stable induction regimen. This patient would have tanked regardless of induction meds given the combination of intravascular depletion and positive pressure ventilation.
 
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Patient was septic, hypovolemic, with very high sympathetic tone. Removal of sympathetic tone with induction, exacerbating ongoing hypovolemia, and reducing venous return from PPV are most likely the main culprits. The list for the differential diagnosis of PEA is not long with hypovolemia at the top in this case. Bronchospasm could also be from patient being aware during the resuscitation. Agree with the Epi and Norepi. Also agree surgery should have continued as the septic patient will continue with capillary leak and deteriorating physiologic profile.
 
Patient was septic, hypovolemic, with very high sympathetic tone. Removal of sympathetic tone with induction, exacerbating ongoing hypovolemia, and reducing venous return from PPV are most likely the main culprits. The list for the differential diagnosis of PEA is not long with hypovolemia at the top in this case. Bronchospasm could also be from patient being aware during the resuscitation. Agree with the Epi and Norepi. Also agree surgery should have continued as the septic patient will continue with capillary leak and deteriorating physiologic profile.
I agree with you too. We here lack lots of facilities, we only depend on the clinical examination. Even being cautious with pushing slowly the induction agents, but we had faced that bronchospasm earlier just after induction. I and the other residents couldn't hear the breathing sounds, so we suspect bronchospasm at the beginning, we resuscitate aggressively.
 
Agreed, the only induction drug that is absolutely necessary and should not be reduced is rocuronium or sux. Just give a small dose of some sort of hyponotic first.
Yes Dr. DipriMan, we anticipate difficult Intubation because of his airway examination, we faced high Blood pressure at the beginning prior to induction. He didn't sleep with easily pushing induction agents, he crashed later.
 
If someone was holding a gun to my head and said the induction needs to proceed within the next 30 seconds ... I'd probably induce this guy with pads on and 3mg of midazolam and 100mg of Rocuronium.

Otherwise I'd spend >30mins lining them up and grabbing a coffee while fluid pours in before giving a small dose of ketamine + 3mg midazolam + 100mg of Roc.

There's really sick people that aren't gonna change/will deteriorate with delays. Then there's sick people who will become less sick if you waste a bit of time optimising them
 
We will try to induce next time with 3 mg Midazolam or only 30 mg Ketamine + 30 mg Propofol + either Roc or Sux ! - we have plenty of incoming cases like these every week, and will give you my insight. Thanks ! Sepsis and Anesthesia is one of the challenging item to encounter. I believe in that.
 
OK, summarize your approach. First how to rule out Cardiogenic shock in such limited resources?
Septic Shock = wide pulse pressure, warm extremities (feel behind the knees)

Cardiogenic Shock = narrow pulse pressure, cool extremities

Very underrated part of the exam. No need to get fancy with CVP or trying to find a JVD or even random heart sounds.
 
Septic Shock = wide pulse pressure, warm extremities (feel behind the knees)

Cardiogenic Shock = narrow pulse pressure, cool extremities

Very underrated part of the exam. No need to get fancy with CVP or trying to find a JVD or even random heart sounds.
I myself have never had thought of the importance of pulse pressure variable until I listened to a podcast Em-Crit. Still it is ambiguous to me, how wide how narrow!

You brought up something cool to discuss.

My patient above had cold extremities even after resuscitation and even at the ICU.

From heart failure 360 map and my understanding wet and cold = cardiogenic shock isn't it?
 
Patient was septic and severely dehydrated but was hyperdynamic and compensating (high BP and High HR) which is common in young patients with healthy hearts., Then you took away his compensation with general anesthesia and positive pressure ventilation. So, he developed PEA. At that point you probably should have ruled out pneumothorax as another cause, but the fact that his pressure improved with fluids and pressors makes it less likely. Some initial optimization pre-op might have prevented this sudden hemodynamic collapse. A couple of liters of fluid may have been a good idea before induction. You said no ABG available but the chemistry and urine output could help you assess the volume status.
 
Septic Shock = wide pulse pressure, warm extremities (feel behind the knees)

Cardiogenic Shock = narrow pulse pressure, cool extremities

Very underrated part of the exam. No need to get fancy with CVP or trying to find a JVD or even random heart sounds.


It is also possible to have both.
 
Patient was septic and severely dehydrated but was hyperdynamic and compensating (high BP and High HR) which is common in young patients with healthy hearts., Then you took away his compensation with general anesthesia and positive pressure ventilation. So, he developed PEA. At that point you probably should have ruled out pneumothorax as another cause, but the fact that his pressure improved with fluids and pressors makes it less likely. Some initial optimization pre-op might have prevented this sudden hemodynamic collapse. A couple of liters of fluid may have been a good idea before induction. You said no ABG available but the chemistry and urine output could help you assess the volume status.
Thanks for the advice Dr. Planktonmd; pneumothorax was not suspected because of peak airway pressure, regardless of the no breathing sounds. So, let us say say to rule out pneumothorax; what shall we do "a decompression of the chest wall by inserting cannula at 2nd intercostal space, right?"; this would be disaster if it happened and not to mention the surgery team was requesting for the relative to come inside the OR room to see their guy alive; I was very curious as he asked twice. I would imagine if we punctured his chest and Inadvertently lead to pneumothorax? Honesty, I am glad to his Peak pressure wasn't elevated and ruled out pneumothorax and if even bronchospasm was treated. The lesson is that PPV would decrease both preload and afterload and to increase cardiac out in healthy individual, and this guy had an empty heart (the one thing I did which was unusual as I love it, I stopped the Peep respecting the physiology I have).

He was old guy, skinny and unknown goiter. We don't know his hypovolemia was for how long? We can't rule out his goiter and to be honest if this guy if he had SBO, I would go aggressively with fluids; it is not the first time to deal with DU acute abdomen, but not in the setting of sepsis to be honest, all were young with stable BP or upper border, not an old guy with 240/130 like on presentation and got a goiter; I am still blaming myself for that and thinking about how wild and tricky the presentation could be.

Thanks Dr. Planktonmd for your insight again.
 
Nice discussion and agree with everything said. However, whoever wants to give norepi on induction (small infusion maybe) in a patient who’s BP is 190/100… not to mention it was 240 systolic before. In hindsight maybe, but not a good practice with an already light induction IMO.
 
I think with anaphylaxis you should have warm extremities
I think the prop dose was too low. That's the dose I give for little old ladies
Hypertensive and tachy due to cathecholamines from hyperthyroid

I agree with above, low prop -> bronchospasm -> no air movement -> crash
hypoxia -> bradycardia -> hypotension

Probably was already volume depleted

Peak pressures probably just reflecting what you have on your bag as you're not moving any air and you're not seeing the real pressure in the airways or alveoli.
Uhhhhhh…. You think the prop dose was too low? I’m assuming you either didn’t read the case completely or you’re an assassin disguised as an anesthesiologist. This is a sick-as-**** 67 y/o patient who got 30mg of ketamine and 80mg of propofol. The propofol dose was what almost killed the patient. 80mg of prop is also too much for little old ladies. Lay off the milk bruh.

Also not bronchospasm. Pressures of 14 generating TV of 480? Highly unlikely.
 
Uhhhhhh…. You think the prop dose was too low? I’m assuming you either didn’t read the case completely or you’re an assassin disguised as an anesthesiologist. This is a sick-as-**** 67 y/o patient who got 30mg of ketamine and 80mg of propofol. The propofol dose was what almost killed the patient. 80mg of prop is also too much for little old ladies. Lay off the milk bruh.

Also not bronchospasm. Pressures of 14 generating TV of 480? Highly unlikely.

You're judging me by the 3rd post in the thread. A lot of the information you have now came afterwards. I did the best analysis with the data that I had and I thought that it was bronchospasm from the first post. I didn't know that they had a tv of 480. Initially he said that there was no air entry.

I take care of plenty of sick patients and acute abdomens. I trained at a level 1 trauma center. Many patients can handle a fair amount of propofol, even the little old ladies. This guy has a ton of sympathetic tone and when he lost it the cardiogenic shock/dehydration tipped him over the edge. l try to keep the prop below 1/kg or even 0.5/kg with phenylephrine in the same induction. I didn't think at the time that Iraqis are smaller than Americans. I didn't know that they got versed or whatever else wasn't mentioned in the first post. A lot of what I do depends on how the patient looks when I see them. If they look terrible then I'll do some etomidate or versed only as some people described above. I've also done the paralysis only intubations for patients that are on the verge of death.
 
You're judging me by the 3rd post in the thread. A lot of the information you have now came afterwards. I did the best analysis with the data that I had and I thought that it was bronchospasm from the first post. I didn't know that they had a tv of 480. Initially he said that there was no air entry.

I take care of plenty of sick patients and acute abdomens. I trained at a level 1 trauma center. Many patients can handle a fair amount of propofol, even the little old ladies. This guy has a ton of sympathetic tone and when he lost it the cardiogenic shock/dehydration tipped him over the edge. l try to keep the prop below 1/kg or even 0.5/kg with phenylephrine in the same induction. I didn't think at the time that Iraqis are smaller than Americans. I didn't know that they got versed or whatever else wasn't mentioned in the first post. A lot of what I do depends on how the patient looks when I see them. If they look terrible then I'll do some etomidate or versed only as some people described above. I've also done the paralysis only intubations for patients that are on the verge of death.
All good, fair points. My apologies… I was just yanking your chain. That came off more serious than I intended.
 
Uhhhhhh…. You think the prop dose was too low? I’m assuming you either didn’t read the case completely or you’re an assassin disguised as an anesthesiologist. This is a sick-as-**** 67 y/o patient who got 30mg of ketamine and 80mg of propofol. The propofol dose was what almost killed the patient. 80mg of prop is also too much for little old ladies. Lay off the milk bruh.

Also not bronchospasm. Pressures of 14 generating TV of 480? Highly unlikely.
No need to be an AH about it. Maybe he didn’t read properly. And besides his elaboration on the vent pressures was after this response.

What is in the milk? Crack? Never heard the saying.
 
You're judging me by the 3rd post in the thread. A lot of the information you have now came afterwards. I did the best analysis with the data that I had and I thought that it was bronchospasm from the first post. I didn't know that they had a tv of 480. Initially he said that there was no air entry.

I take care of plenty of sick patients and acute abdomens. I trained at a level 1 trauma center. Many patients can handle a fair amount of propofol, even the little old ladies. This guy has a ton of sympathetic tone and when he lost it the cardiogenic shock/dehydration tipped him over the edge. l try to keep the prop below 1/kg or even 0.5/kg with phenylephrine in the same induction. I didn't think at the time that Iraqis are smaller than Americans. I didn't know that they got versed or whatever else wasn't mentioned in the first post. A lot of what I do depends on how the patient looks when I see them. If they look terrible then I'll do some etomidate or versed only as some people described above. I've also done the paralysis only intubations for patients that are on the verge of death.
News Flash. EVERYONE is smaller than Americans. Except maybe Mexico. You can always tell when you board a plane headed here from Europe or wherever that “Yup, this plane is definitely heading to America” because of the size of the people.
I connect in Europe each time I go to the motherland.
 
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