Propofol

This is a common misconception. Movement, asynchrony, and even tachycardia and hypertension are not specific signs of awareness or pain.

Whether the appropriate response is to give more sedation, or more analgesia, or do something else depends on several factors. But more fentanyl and more propofol isn't always the best route.

Edit: in the OP's situation, more sedation was (unfortunately, at only 40 mcg) not an option.

The propofol with addition of fentanyl statement was not meant to be a blanket statement. You're right. It may not be the best route and some patients may require a different strategy. In my experience however, treating the patient with adequate doses of fentanyl often allows for lower doses of propofol and together you achieve a comfortable and well sedated patient.

I've heard the argument from a few others that all patient's should be paralyzed for transport and I personally do not subscribe to that practice. If it's necessary to gain ventilator compliance or control of the patient because it is difficult to put the patient down with sedation/analgesia alone, than ok I see the indication.
 
I had a similar Pt one time I was fighting the Pt coming out of sedation and fighting hypotension. I followed my protocol for intubated Pt and gave 8mg Vecuronium 5mg of Versed and threw that Dipervan in the trash. When at the recieving facility the MD asked me where the Dipervan was I said in the trash where it belongs, he just laughed.
 
I had a similar Pt one time I was fighting the Pt coming out of sedation and fighting hypotension. I followed my protocol for intubated Pt and gave 8mg Vecuronium 5mg of Versed and threw that Dipervan in the trash. When at the recieving facility the MD asked me where the Dipervan was I said in the trash where it belongs, he just laughed.

I'm not sure I understand. Are you saying that the Propofol belonged in the trash for this patient because of their hypotension or that you feel Propofol is generally a poor agent for the sedation of intubated patients during transport? What indications does your airway / vent management protocol give for the use of NMB? Does it include options for analgesia?

In any event, I have found this discussion interesting. I use propofol often and am able to initiate , titrate and bolus it as we deem appropriate. Like others I view it as a useful agent and do not routinely paralyze patients. However I am certainly willing to if there is a need. I think the vast majority of providers fall in the middle of the two semi fictional extremes of "never paralyze a patient" and "always use paralytics".
 
I'm not sure I understand. Are you saying that the Propofol belonged in the trash for this patient because of their hypotension or that you feel Propofol is generally a poor agent for the sedation of intubated patients during transport? What indications does your airway / vent management protocol give for the use of NMB? Does it include options for analgesia?

In any event, I have found this discussion interesting. I use propofol often and am able to initiate , titrate and bolus it as we deem appropriate. Like others I view it as a useful agent and do not routinely paralyze patients. However I am certainly willing to if there is a need. I think the vast majority of providers fall in the middle of the two semi fictional extremes of "never paralyze a patient" and "always use paralytics".
I don't think it is not useful at all. I think it is less useful in the transport setting than in a stationary bed. For this patient it belonged in the trash because it was causing hypotension and was doing a poor job of sedating the patient. This was a wet CVA patient and the lack of paralysis and sedation probably caused spikes in ICP. I routinely paralize patients because that is how the protocol reads.
 
I agree that propofol is not an ideal agent for transport. Being pretty comfortable and familiar with most of these drugs, my ideal transport cocktail would be primarily based on hefty doses of opiates. Adjuncts available thereafter, though propofol would not be my first choice. CC medics need to have a constant vigilance over the patient's hemodynamics, as transport is a very high-risk time for deterioration in the setting of critical illness. And propofol, in a patient with inadequate analgesia, can become a dosing wrestling match. It can be a major distraction at a time when vigilance and monitoring are of utmost importance. I watch it happen in the ICU. I'm sure it is no better in the back of moving vanbulance.

I'm also believe paralysis for transport should not be routine. It should certainly be available when indicated for the patient's illness or when adequate sedation cannot be achieved in an agitated patient due to instability. Absent studies showing that routine paralysis for transport is superior, I think you are hard-pressed to justify it for transport in a calm, comfortable patient simply because you are transporting.
 
Ive had good results with propofol in the transport setting. Why does it matter if used stationary or while moving interfacility as suggested?

What was the dose of propofol? I'm curious to know if fentanyl was used to keep the propofol dose on the low side or if sedation was attenpted without analgesia. Also curious to know if a fluid bolus was tried to counter the hypotension.
 
Propofol works very well in transport. Perhaps it is a question of experience and training. The notion of not being able to titrate is crazy.

As for the idea of paralyzing anyone for transport - no dice. Perhaps I'm not getting the context of the transports as I work in a different system. There are many reasons not to paralyze anyone. It can interfere with ongoing care, mask issues, and cause HD stability. There are lots of times when it is indicated - but a blanket policy of paralytics 'for transport' is medieval.

I'm with 18G on that point - why does it matter if it's stationary or in transport? Paramedics can do themselves a disservice by throwing around 'transport environment' as a reason to depart from good critical care.
 
Ive had good results with propofol in the transport setting. Why does it matter if used stationary or while moving interfacility as suggested?

I'm with 18G on that point - why does it matter if it's stationary or in transport?

The difference between using propofol in the ICU vs. in transport is simply that there is much more stimulus in transport, so you need more sedative to maintain the same level of comfort.

Propofol always works......as long as you can use enough of it. The limiting factor in propofol dosing is its dose-dependent effects as a vasodilator and direct myocardial depressant. The more of it that you use, the less favorable the hemodynamic results.

When used alone in a stimulating environment, you can sometimes reach a point of diminishing returns with propofol at a surprisingly low dose range......where going up on the dose does more to drop the BP than it does to keep the patient still. I think this has more to do with patient-specific physiologic and pharmacologic factors than it does with the propofol itself, but it can be difficult to predict, especially if you don't know the patient and their history well, and even more so if you aren't experienced in these scenarios.

The problem of diminishing returns can usually be remedied or at least minimized by replacing some of the propofol with opioid.....my guess is that those among us who have never or rarely had bad experiences with propofol in transport can say that because they have protocols that call for healthy doses of opioid for these patients.
 
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There are many reasons not to paralyze anyone. It can interfere with ongoing care, mask issues, and cause HD stability.

Can you give examples of what type of ongoing care is interfered with by NMB, as well as how it can cause hemodynamic instability?
 
Granted the HD instability is rare, but NMBAs can cause hypotension through histamine release. As well, if a patient has some inherent pull on the vent (i.e. PSV) then paralyzing them could affect their HD status as you transition them to full vent support. (both admittedly minor issues and can be anticipated and compensated for).

My issue with the 'paralysis for everyone' approach is if this is employed without reference to the patient's condition. If a patient can do quite well on pressure support, why paralyze them and plop them onto whatever generic settings you use for transport? As well, while it can be good for dysynchrony, I believe paralytics should be used after attempts to troubleshoot the dysynchrony in the first place. A lot of cases of dysynchrony can be solved with a little medication titration and adjusting flows.

As for the propofol, I think it's obvious that there are downsides to it - it is certainly not for everyone. Like any other drug it has it's uses and dangers and should be used appropriately and titrated with reference to a patient's state and hemodynamics. I move people in planes, jets and helicopters (and the odd hovercraft), as well as by ground and propofol can be used effectively in the right patient. If one has propofol on the wrong patient however (i.e. cardiogenic shock), then I think you have a whole new set of issues to deal with.
 
Granted the HD instability is rare, but NMBAs can cause hypotension through histamine release. As well, if a patient has some inherent pull on the vent (i.e. PSV) then paralyzing them could affect their HD status as you transition them to full vent support. (both admittedly minor issues and can be anticipated and compensated for).

My issue with the 'paralysis for everyone' approach is if this is employed without reference to the patient's condition. If a patient can do quite well on pressure support, why paralyze them and plop them onto whatever generic settings you use for transport? As well, while it can be good for dysynchrony, I believe paralytics should be used after attempts to troubleshoot the dysynchrony in the first place. A lot of cases of dysynchrony can be solved with a little medication titration and adjusting flows.

As for the propofol, I think it's obvious that there are downsides to it - it is certainly not for everyone. Like any other drug it has it's uses and dangers and should be used appropriately and titrated with reference to a patient's state and hemodynamics. I move people in planes, jets and helicopters (and the odd hovercraft), as well as by ground and propofol can be used effectively in the right patient. If one has propofol on the wrong patient however (i.e. cardiogenic shock), then I think you have a whole new set of issues to deal with.


Hmmmmmm. Which drug are you using?
 
We use roc so don't have much issue. It was more of an info point on some of the other non-depolarizers. I have no idea what other services use. I'm sure the point is minor.
 
We use roc so don't have much issue. It was more of an info point on some of the other non-depolarizers. I have no idea what other services use. I'm sure the point is minor.

You're right, histamine release with most muscle relaxants is not clinically important.

The second issue you bring up is very relevant. And I think a lot of us medical folks think we understand what's going on when we don't fully.

I see it in very sick patients who had spontaneous ventilatory effort, assisted or unassisted, who following muscle relaxation (even with minimal or no induction agent) develop profound hypotension. And in my own experience it tends to be minimally responsive to fluid blouses, which I think is strange given that most of these patients are intravascularly volume depleted.

My best guess is the loss of negative intrathoracic pressure and transition to a positive pressure ventilation is impeding venous return. But, I'm unconvinced.

Nonetheless, it's another tick in my 'avoid relaxants if possible' box.

To add one more: a lot of medications are given in the operating room. A whole regimen of drugs for each case. And of all those drugs, the number one culprit for anaphylaxis in the OR : muscle relaxants.

Definitely things to add to your risk:benefit ratio before you pull out paralytics needlessly.
 
I see it in very sick patients who had spontaneous ventilatory effort, assisted or unassisted, who following muscle relaxation (even with minimal or no induction agent) develop profound hypotension. And in my own experience it tends to be minimally responsive to fluid blouses, which I think is strange given that most of these patients are intravascularly volume depleted.

My best guess is the loss of negative intrathoracic pressure and transition to a positive pressure ventilation is impeding venous return. But, I'm unconvinced.

This is the definitely current thinking, at least as I understand it. I've seen significant hypotension on intubation & initiation of PPV, but it's really not an issue of NMB vs. no NMB, is it? It's more an issue of the transition from spont. V or PSV to full PPV. If you can avoid PPV, then by all means do. But if you can't avoid PPV, then I don't see how choosing to use NMB is going to make the PPV-induced hypotension worse.

To add one more: a lot of medications are given in the operating room. A whole regimen of drugs for each case. And of all those drugs, the number one culprit for anaphylaxis in the OR : muscle relaxants.

Definitely things to add to your risk:benefit ratio before you pull out paralytics needlessly.

The anaphylaxis thing is interesting. I just came across a few things about this recently. Very broad estimates of incidence, I've seen anything from 1:1000 up to 1:100,000, with 1:10,000-1:20,000 being the most common range cited, with severe reactions of course being much less common than less severe ones. Also the most common offending agents vary, with some sources saying roc, some saying vec, but most blaming sux as most likely to cause a problem.

Yet, we still give the stuff out like candy in the OR....in my training I never once heard someone say "let's try to avoid the NMB so that we don't cause any increased risk of a reaction". Not that such nonchalance is evidence that we shouldn't consider it, of course, but the point is I think we generally accept the small risk of a severe reaction as much lower than the likely benefits of the drug. As we generally do with all the drugs we give routinely. If the drug is indicated, it's probably well worth the risk. If it isn't indicated, then it's not. With the NMB-in-transport issue, it all comes down to whether we consider them "indicated" or not.

There was an interesting article published in PEC a few years ago that retrospectively looked at HEMS transports of intubated patients in Ontario, CA. It was more of a descriptive article but they did some post-hoc analysis, too. Found a 17% incidence of "critical events" during transport, mostly hypotension that appeared to be mostly related sedative dosing. I think NMB was given in something like 20% of the transports.
 
Quick google search


http://www.ncbi.nlm.nih.gov/m/pubmed/18475086/


Though I thought it was common knowledge among anesthesia folk.
That article is 7 years old. Atracurium, which was the worst of the NMB offenders for allergic reactions, is rarely found in clinical use any more, if at all. Rocuronium just isn't a huge problem for anaphylaxis. The worst offenders are antibiotics and latex.
 
That article is 7 years old. Atracurium, which was the worst of the NMB offenders for allergic reactions, is rarely found in clinical use any more, if at all. Rocuronium just isn't a huge problem for anaphylaxis. The worst offenders are antibiotics and latex.

I guess somebody better call Ronald Miller and let him know that his textbook is wrong. Let him know it's page 1110.
 
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