Post Your Cases > Early lipid administration prevents deterioration to a pulseless arrhythmia
Brief summary: 82 y.o. essentially healthy female for total knee arthroplasty. Planned SAB for anesthesia and continuous femoral nerve block and single shot sciatic block for post-op analgesia. Femoral catheter placed uneventfully and dosed incrementally with 30 ml 0.5% ropiv + 1:200K epi. Labat approach sciatic block placed uneventfully with 30 ml of 0.5% bupiv + 1:200K epi. 30 seconds after needle removal she had a generalized tonic-clonic seizure that stopped with 3 mg midazolam. 60 seconds later she had a second seizure that quickly and spontaneously resolved. At this point she was in vent. tachycardia with a pulse, unresponsive but ventilating and oxygenating with a jaw thrust. 150 mg of amiodarone was bolused. 100 ml of 20% intralipid was given over 1 minute beginning approx. 3 min after onset of VT. At this point her femoral pulse began to diminish and a single 120 J synchronized countershock was administered and she converted to sinus rhythm. The remaining 400 ml of intralipid was infused over 15 minutes. She remained hemodynamically stable and gradually regained consciousness, returning to her normal mental status over the next 2 hours. We're convinced that early administration of intralipid not only facilitated conversion to sinus rhythm but prevented deterioration to a pulseless arrhythmia.
Thanks for the very interesting case. A few questions and comments: 1. did the patient have any cardiac history or ECG abnormalities? 2. did you begin a continuous infusion after the initial bolus? it is not uncommon in the animal expts to see a transient sag in blood pressure after the initial bolus. this is why we usually start a continuous infusion just after the bolus. however, my tech always insists i'm just not patient enough and that if we were to wait a short while longer then the BP does recover. Subsequent expts have shown he's right. But...I'm still impatient and prefer not waiting. 3. can you plot the time-course of hemodynamic recovery (BP or RPP vs time)? 4. note that it's very common for LA tox to present as progressive deterioration: e.g., sz to arrhythmias; bradycardia to asystole. but one important variant of this is recurrent arrhythmias or hypotension: eg, SVT resolves but then returns; sagging BP returns with pressor but soon drops again, often to a lower level. it seems to me (and i think you agree) this is what was happening to your patient. 5. perhaps you should consider a letter-to-the-editor. APSF newsletter, (see Baumgarten's letter in the last issue) or perhaps RAPM. if you have any ecg traces or that hemodynamic plot, it would support the submission. thanks again for a neat case, guy
1. This patient, although elderly, did not have any underlying cardiac co-morbidities with the exception of well-controlled hypertension and hyperlipidemia. Her pre-op EKG was normal.
2. It's interesting you all have noted hypotension with intralipid bolusing. She was in V Tach with good pulses and a non-invasive reading of 114/60. It was after the intralipid bolus that her BP dropped by palpation. We were having trouble to get the non-invasive cuff to read at the time and were unwilling to wait so we went ahead and cardioverted her. At this point we infused the remaining 400 cc over 15 minutes. Following conversion to NSR her BP remained stable.
3. The interesting thing is that she was never actually hypotensive except subjectively by a diminishing pulse a few seconds before the sync. cardioversion. Upon conversion to NSR her pulse again became strong and SBP was remained in the 120-150s.
4. I've never a case of LA tox. before but I've heard about the recurrent nature of the arrhythmias. I knew it was heading in that direction when we broke the first seizure with benzodiazepines and she immedietely seized again. We actually keep an "LA toxicity kit" in our our regional anesthesia area similar to your recommendations- it was less than 20 feet from the patient when this happened. Given this was our first use of intralipid I had a colleague discuss the situation with one of our CT surgeons and they went ahead and prepared a CPB circuit. I'm convinced it was the intralipid that kept the arrhythmias from recurring.
5. I've written it up already and we're trying to decide where to submit it. We have a rhythm strip that depicts the VT and conversion to NSR. We were thinking of submitting it to one of the critical care journals. I'll let you know how that goes.
1. ok. 2. interesting. that's me (VT, BP 120) while watching an intern intubate. to clarify, i should point out that our animals generally get a good BP response to lipid initially. the 'sag' usually occurs a few minutes later and is transient. not sure why lipid would cause a BP drop in the setting of VT in your patient. i'll have to give the PK/PD angle a little thought. 3. in light of a thready pulse, cardioversion was unquestionably the right thing to do. glad to hear the BP was solid after the electricity. THAT is what we want to see! 4. statistically, this is also likely to be the last episode you ever see. particularly since we can be confident the presence of lipid in the OR will ward off the remaining evil spirits. on the other hand, others in the dept might have an event, in which case, they'll contact the local expert.....you! 5. great. look forward to seeing it. guy
1. did the patient have any cardiac history or ECG abnormalities?
2. did you begin a continuous infusion after the initial bolus? it is not uncommon in the animal expts to see a transient sag in blood pressure after the initial bolus. this is why we usually start a continuous infusion just after the bolus. however, my tech always insists i'm just not patient enough and that if we were to wait a short while longer then the BP does recover. Subsequent expts have shown he's right. But...I'm still impatient and prefer not waiting.
3. can you plot the time-course of hemodynamic recovery (BP or RPP vs time)?
4. note that it's very common for LA tox to present as progressive deterioration: e.g., sz to arrhythmias; bradycardia to asystole. but one important variant of this is recurrent arrhythmias or hypotension: eg, SVT resolves but then returns; sagging BP returns with pressor but soon drops again, often to a lower level. it seems to me (and i think you agree) this is what was happening to your patient.
5. perhaps you should consider a letter-to-the-editor. APSF newsletter, (see Baumgarten's letter in the last issue) or perhaps RAPM. if you have any ecg traces or that hemodynamic plot, it would support the submission. thanks again for a neat case,
guy
2. It's interesting you all have noted hypotension with intralipid bolusing. She was in V Tach with good pulses and a non-invasive reading of 114/60. It was after the intralipid bolus that her BP dropped by palpation. We were having trouble to get the non-invasive cuff to read at the time and were unwilling to wait so we went ahead and cardioverted her. At this point we infused the remaining 400 cc over 15 minutes. Following conversion to NSR her BP remained stable.
3. The interesting thing is that she was never actually hypotensive except subjectively by a diminishing pulse a few seconds before the sync. cardioversion. Upon conversion to NSR her pulse again became strong and SBP was remained in the 120-150s.
4. I've never a case of LA tox. before but I've heard about the recurrent nature of the arrhythmias. I knew it was heading in that direction when we broke the first seizure with benzodiazepines and she immedietely seized again. We actually keep an "LA toxicity kit" in our our regional anesthesia area similar to your recommendations- it was less than 20 feet from the patient when this happened. Given this was our first use of intralipid I had a colleague discuss the situation with one of our CT surgeons and they went ahead and prepared a CPB circuit. I'm convinced it was the intralipid that kept the arrhythmias from recurring.
5. I've written it up already and we're trying to decide where to submit it. We have a rhythm strip that depicts the VT and conversion to NSR. We were thinking of submitting it to one of the critical care journals. I'll let you know how that goes.
Quinn
2. interesting. that's me (VT, BP 120) while watching an intern intubate. to clarify, i should point out that our animals generally get a good BP response to lipid initially. the 'sag' usually occurs a few minutes later and is transient. not sure why lipid would cause a BP drop in the setting of VT in your patient. i'll have to give the PK/PD angle a little thought.
3. in light of a thready pulse, cardioversion was unquestionably the right thing to do. glad to hear the BP was solid after the electricity. THAT is what we want to see!
4. statistically, this is also likely to be the last episode you ever see. particularly since we can be confident the presence of lipid in the OR will ward off the remaining evil spirits. on the other hand, others in the dept might have an event, in which case, they'll contact the local expert.....you!
5. great. look forward to seeing it.
guy