Sedation after ROSC

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harold1981

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How do you feel about sedating a patient who is waking up post-CPR with 2,5 to 5mg Versed?

The rational behind this would be to reduce anxiety, reduce oxygen consumption, reduce awareness and prevent memories from the resuscitation setting.
I know that there are a few contraindications, eg hypotension, shock, brain injury, drugs/alcohol intox and muscular weakness.
I have had different medics disagree with the suggestion of sedating the awakening patient after ROSC, stating that I don´t want to knock down their respiratory drive. However, if respiratory depression or apnea reoccurs, we are there to resume ventilations with a BVM immediately (besided the patient is often still intubated).
Also, if need arises, the effect of the midazolam can be antagonized in the ED. And...we are giving a small dose, I believe they use 25mg in the OR as an anesthetic induction.

Please share your thoughts on this matter. Also, how do you feel about Midazolam in combination with IV fentanyl post-ROSC for the purpose of reducing the pain and discomfort of an AMI and chest compessions?
 
I do not think I would be giving a patient who just had cardiovascular collapse Versed. And I have never seen anyone induce anethesia with 25mg of Versed. There are better options like ketamine.
 
For a patient that had ROSC and is now agitated, not receiving a vasopressor and if you don't have Ketamine, a judicious use of Versed and Fentanyl seems entirely appropriate.

Hell, I'd like some sedation and analgesic on board if I was just resuscitated.
 
Uh... what??? 25mg?

And we do not give any med under the operating philosophy of "don't worry they can reverse that in the ED."

Determine the actual need to sedate. Just waking up after ROSC does not constitute a need and we do not blanket issue sedatives to prophylacticly reduce metabolic demand. We do in some circumstances.
 
harold1981 said:
How do you feel about sedating a patient who is waking up post-CPR with 2,5 to 5mg Versed?
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I feel like if it was me waking up I would want some sedation:).
harold1981 said:
I believe they use 2.5mg in the OR as an anesthetic induction...Also, how do you feel about Midazolam in combination with IV fentanyl post-ROSC for the purpose of reducing the pain and discomfort of an AMI and chest compessions?
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Perhaps you heard it wrong, or forgot the period. Us medical folk tend to be kinda stickler-ish about these sort of dosing errors, especially something such as 2.5 vs. 25 mg of Versed.

Anyhow, my service currently doesn't carry Ketamine, but like @Chase mentioned, assuming there's no cardiovascular collapse present, and the patient is hemodynamically stable, beginning to buck/ over breathe the ETT, tear, their HR spikes, etc., etc., etc., it seems inhumane not to provide proper/ adequate sedation and pain management.
 
If they're intubated you damn well better be sedating them.


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Handsome Robb said:
If they're intubated you damn well better be sedating them.


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I totally agree however with a post-arrest patient I would be extremely cautious. A little temporary discomfort may be preferable to another arrest. Post ROSC patients can be like those patients whom arrest immediately upon induction, they may be dependent on their sympathetic tone. I would choose the most cardiac stable agent I had available and Versed does not fit that role.
 
Chase said:
I totally agree however with a post-arrest patient I would be extremely cautious. A little temporary discomfort may be preferable to another arrest. Post ROSC patients can be like those patients whom arrest immediately upon induction, they may be dependent on their sympathetic tone. I would choose the most cardiac stable agent I had available and Versed does not fit that role.
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Agree with this. 2 days ago saw this exact thing. ROSC now starting to move around a bit with ET tube in... 2mg of versed and next thing you know we are pushing 0.5mg epi in the CT scanner and starting a levophed drip.

In this case the justification was the necessity for a good CT study (pt needed it).

Remember, we would like some assessment of the type of responsiveness if possible, particularly if they have purposeful movement. This drives the decision to cool the patient.

Plenty of intubated ROSC patients have very little agitation and wouldn't need sedation (and get cooled).

Some didn't get tube and wake up and don't need sedation.

And everything inbetween, some warran sedation.
 
Chase said:
I totally agree however with a post-arrest patient I would be extremely cautious. A little temporary discomfort may be preferable to another arrest. Post ROSC patients can be like those patients whom arrest immediately upon induction, they may be dependent on their sympathetic tone. I would choose the most cardiac stable agent I had available and Versed does not fit that role.
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I definitely agree with you there. I am not a fan of versed.

We actually have an SOC and people have had to use it for intra-arrest ketamine for awareness during resuscitation with the Lucas.


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I'm aware of the trend of using versed even intra-arrest in order to induce amnesia. There have been more than a few case studies of patients having distressing memories of their resuscitation, even while pulseless. I think it is a really bad idea, personally. I cannot see how it would not negatively affect the perfusion pressure your are trying to get the sick heart to generate and maintain in the coronaries and the brain, in at least some patients.

Post-arrest? I mean if they need it, sure. If they are tubed and hemodynamically stable and showing signs of awareness and agitation, treat them like any other sick, intubated patient. But like Summit explained above, you have to assess each patient's individual needs. You wouldn't go blindly giving every ICU patient that you transport the same exact sedation regimen, why would you do it in the immediate post-arrest setting?

Versed is actually very cardio stable - probably the most stable choice, in fact (ketamine is actually a direct myocardial depressant, and is not a reliable amnestic in small doses). The problem is that these patients are often so tenuous that even "stable" drugs can threaten their ability to maintain perfusion.

Go spend a day in the electrophysiology suite and watch how little sedation people get for cardioversions and pacemaker placements and battery changes. If you are there for a busy day you'll see at least one patient almost arrest (or actually do so) after 0.5mg of versed. You'll see lots of other patients squirming and moaning but have their BP drop dramatically from even very small doses of sedatives.
 
Also not to get off topic, but I felt like it was only fair to the OP to mention that 25mg of versed actually would be a reasonable induction dose. 0.2 - 0.3 mg/kg is the dose that you see in the books. That could easily work out to around 25mg, depending on the patient weight.

Bear in mind, no one uses versed for induction anymore, for numerous reasons. I don't even know if it was ever really common, but I think the setting it may have been used in at least occasionally was sick cardiac patients, precisely because it is so cardio stable.

So technically, the OP isn't wrong about that :)
 
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One more point here. Generally, hypothermia protocols have only been shown to benefit patients who suffer out-of-hospital cardiac arrest and subsequently remain comatose after resuscitation.

If you load a patient up on versed simply because you resuscitated them, you take away the ability of the physician to make the call about hypothermia.

If the patient needs it because they are obviously agitated or have discomfort, I would be supportive. If you are giving versed to a patient simply because you are worried about post-resuscitation recall, I think you may be interfering with future medical decision making.

And not the "don't give pain meds to abdominal pain and skew the exam" nonsense type of medical decision making.


This is something that could potentially matter.
 
Sort of still on topic, and perhaps @Nova1300 or somebody can elaborate, but this can also dictate one's decision to perform, or with hold an RSI in the field. If said patient is on the cusp of being able to protect their own airway, it may inhibit a proper neuro assessment on arrival at the ED.

Oftentimes we as providers, especially when newer, and/ or less experienced may not factor in the need for the receiving facility to perform such an assessment over the "sexiness" of performing an RSI in the field.

Now clearly, there are times when it's very much warranted, just keep in mind there are times when it can very much wait. I think this is worth mentioning, but again, boils down, and reflects a strong clinical assessment when to know with hold any procedure versus when not to.
 
Remi said:
Versed is actually very cardio stable - probably the most stable choice, in fact (ketamine is actually a direct myocardial depressant, and is not a reliable amnestic in small doses). The problem is that these patients are often so tenuous that even "stable" drugs can threaten their ability to maintain perfusion.
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Never have had to sedate someone since the only pt with ROSC I have had was already in the ER. So when it comes to sedation and K vs V, what would your (slightly expanded on the above quote) thoughts be? I carry both.
 
StCEMT said:
Never have had to sedate someone since the only pt with ROSC I have had was already in the ER. So when it comes to sedation and K vs V, what would your (slightly expanded on the above quote) thoughts be? I carry both.
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I think in the small doses that you'll probably be using in this setting, versed is probably a more reliable amnestic.
 
Remi said:
Versed is actually very cardio stable - probably the most stable choice, in fact (ketamine is actually a direct myocardial depressant, and is not a reliable amnestic in small doses).
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My understanding was that in general, that the opposite was in fact true: most of the time, it acted as a stimulant, causing tachycardia and hypertension, along with increased CO.

http://reference.medscape.com/drug/ketalar-ketamine-343099#4

Of course, in the spirit of medicine contradicting itself, another source seems to suggest that hypotension and bradycardia are COMMON side effects, along with hypertension and tachycardia:

https://online.epocrates.com/drugs/196905/ketamine/Adverse-Reactions

Do you have sources that discuss this more? Or that discuss the direct myocardial depressant properties? I had always been under the impression that ketamine didn't (generally) depress anything cardiovascularly.
 
medichopeful said:
My understanding was that in general, that the opposite was in fact true: most of the time, it acted as a stimulant, causing tachycardia and hypertension, along with increased CO.

http://reference.medscape.com/drug/ketalar-ketamine-343099#4

Of course, in the spirit of medicine contradicting itself, another source seems to suggest that hypotension and bradycardia are COMMON side effects, along with hypertension and tachycardia:

https://online.epocrates.com/drugs/196905/ketamine/Adverse-Reactions

Do you have sources that discuss this more? Or that discuss the direct myocardial depressant properties? I had always been under the impression that ketamine didn't (generally) depress anything cardiovascularly.
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Most of the time it does act as a stimulant. Ketamine acts directly on the myocardium to cause a negative inotropic effect. I don't recall the mechanism. It also acts as a central stimulant and reduces the re-uptake of norepi. This sympathetic stimulation usually has more of an effect than the myocardial depression, so the net result is usually the increase in HR and BP that we are all familiar with.

However, someone who is in shock may already be "maxed out" on the support that their endogenous catecholamine stores can provide. In this setting, the decreased re-uptake of norepi may not result in increased concentrations, and you get a crashing patient.

This is not a common result of ketamine administration, but in some populations it should definitely be a consideration. Anyone with severely depressed myocardial function or who has been critically ill for several days are the ones I would be hesitant to use a large dose of ketamine in.

I know this is covered in some detail in some anesthesia and anesthesia-oriented pharm texts. I just did a quick Google search and didn't see much that discusses this thoroughly.
 
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On our side of the pond Midazolam is widely used as an pre-induction agent in the OR. The dosis is 0,2 to 0,3 mg/kg. As it is a cardiopulmonary stable drug, it tends to be a good option in patients with pre-existing cardiopulmonary disease.
In the prehospital setting our protocols provide for 2,5 to 5mg of midazolam IV after ROSC in case of agitation, in combination with fentanyl if pain from mechanical compression is suspected. We don´t practice cookbook-medicine, so offcourse we will be looking at the heamodynamic stability and respiratory state of each patient vs the benefits of sedation and/or analgesics. However many medics are reluctant to sedate post-resus.
We also have a protocol for terminal asphyxia, where we give 25mg midazolam IV, for example in the case of massive lungbleed or carotid blow out syndrome, in the context of terminal sedation.
 
I have only seen one or two people completely regain consciousness after ROSC and they've had very short resuscitations.

If the patient fully wakes up and is in pain, agitated or restless then I don't see a problem with titrating 10-20 mcg of fentanyl with 1-2 mg of midazolam to settle them.

Patients who remain unconscious are generally intubated and will be given sedation and long acting neuromuscular blockade routinely if intubated with RSI, or if they begin to wake and haven't been intubated with RSI.
 
harold1981 said:
We also have a protocol for terminal asphyxia, where we give 25mg midazolam IV, for example in the case of massive lungbleed or carotid blow out syndrome, in the context of terminal sedation.
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Just curious how often are you seeing CBS that you actually need a protocol for it? I am very surprised you give terminal sedation. Who makes the decision what is "terminal"?
 
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