Vasovagal reaction?

[amyl]

So not my case.... But confusing picture so I thought I'd pick everyone's brain. 40-50 year old pt history of anxiety and HTN on ace inhibitor, obesity. Has had syncope with IV placement before.
Case is lap converted to open colon resection for recital prolapse. Case uneventful. At end of case partner places spinal w 11mg bupi and 200 mcg duramorph. Shortly after pt Brady to low 40s hypotensive desat to mid 80s requiring significant pressor support. Hugely diaphoretic. Altered sensorium -- almost like post ictal. Resecure airway. Lines. B/l breath sounds no arrhythmia - Pt stabilizes and is extubated - sat'ing great on non rebreather aox3 but anxious with continued diaphoresis and low normal BPs wo support. Anaphylaxis? But prior morphine wo problems... Albeit not IT. PE? But sats return perfect. Just the worst vasovagal rxn ever?

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[GaseousClay]

Doesn't that seem like just a high spinal? Was this patient consented for an post op asleep spinal before the surgery? This was a laparoscopic case so I don't know if you routinely consent for spinal in the chance it goes open. I would probably have just gone with only the duramorph with maybe 0.5-1 ml of the bupi if anything esp if there was significant fluid shifts or blood loss.

 

[Planktonmd]

So not my case.... But confusing picture so I thought I'd pick everyone's brain. 40-50 year old pt history of anxiety and HTN on ace inhibitor, obesity. Has had syncope with IV placement before.
Case is lap converted to open colon resection for recital prolapse. Case uneventful. At end of case partner places spinal w 11mg bupi and 200 mcg duramorph. Shortly after pt Brady to low 40s hypotensive desat to mid 80s requiring significant pressor support. Hugely diaphoretic. Altered sensorium -- almost like post ictal. Resecure airway. Lines. B/l breath sounds no arrhythmia - Pt stabilizes and is extubated - sat'ing great on non rebreather aox3 but anxious with continued diaphoresis and low normal BPs wo support. Anaphylaxis? But prior morphine wo problems... Albeit not IT. PE? But sats return perfect. Just the worst vasovagal rxn ever?

Why did your partner do a spinal anesthetic at the end of the case?
It sounds to me that the problem is a simple hypotension and bradycardia caused by spinal anesthesia in a hypovolemic patient.
Similar to what you see in OB

 

[scudrunner]

Was the patient awake for the spinal? Did they get a level? Agree, sounds like a high spinal/sympathectomy causing profound hypotension. The post-ictal state could surely be accounted for with transient cerebral ischemia, especially in a chronic hypertensive.

Why not an epidural for postop pain rather than a spinal?

 

[vector2]

The Bezold–Jarisch reflex (also called the Jarisch-Bezold reflex) involves a variety of cardiovascular and neurological processes which cause hypopnea (overly shallow breathing or an abnormally low respiratory rate) and bradycardia (abnormally low resting heart rate).[1]

Physiology[edit]
Prolonged upright posture results in some degree of pooling of blood in the lower extremities that can lead to diminished intracardiac volume. This phenomenon is exacerbated if the individual is dehydrated. The resultant arterial hypotension is sensed in the carotid sinusbaroreceptors, and afferent nerve fibers from these receptors trigger autonomic signals that increase cardiac rate and contractility. However, pressure receptors in the wall and trabeculae of the underfilled left ventricle may then sense stimuli, activating high-pressure C-fiber afferent nerves from these receptors. They may respond by sending signals that trigger paradoxical bradycardia and decreased contractility, resulting in additional and relatively sudden arterial hypotension. The bradycardia reaction to acetic acid veratril in the cardiac pacemaker region was first described by von Bezold. Jarisch identified the reaction as chemoreceptor reflex via the vagus nerve, relayed in the nucleus tractus solitarii.

The Bezold–Jarisch reflex is responsible for the sinus bradycardia that commonly occurs within the first 60 minutes following an acute myocardial infarction,[2] and explains the occurrence of AV node block in the context of acute posterior or inferior myocardial infarction.[3]Bradycardia in this setting may be treated with atropine.

It usually occurs in nitrate therapy and use of serotonin agonists.[4] The Bezold–Jarisch reflex has been suggested as a possible cause of profound bradycardia and circulatory collapse after spinal anesthesia.[5] Also, it is one of the complications of interscalene brachial plexus block.[6] The reflex occurs with several biologically active chemicals, like nicotine and capsaicin,[7] when reaching sensitive areas.

 

[amyl]

Yea I thought high spinal too but he swore only 11mg... Not a small guy so that should've been an ok dose. Thanks vector for posting that - definitely sounds like what happened

 

[OB1🤙]

Could also be a subdural (rather than subarachnoid) dose. That causes all kinds of freakiness.

Doubt bezold-jarisch here, to be honest. Heart has to be pretty empty. Not impossible, but not likely.

 

[OB1🤙]

http://www.csen.com/subdural.pdf

 

[vector2]

Could also be a subdural (rather than subarachnoid) dose. That causes all kinds of freakiness.

Doubt bezold-jarisch here, to be honest. Heart has to be pretty empty. Not impossible, but not likely.

I think it's unlikely as well, but I'm also curious about how dry he was being run. Lap chole isn't gonna get a ton of fluid and perhaps they didn't catch up on losses when the belly was opened (not to mention the CRS guys crying about bowel edema and their precious anastomoses). This certainly would've been a nice opportunity to drop a TEE/slap on a TTE during the resuscitation and take a gander at the LV when your pressor requirement got way out of proportion to the spinal dose.

 

[vector2]

 

[vector2]

And for the CA-1's, here's a nice NYSORA algorithm for hypotension after spinals:

 

[Planktonmd]

A Bezold Jarisch reflex is not rare and it basically explains most of the cases of hypotension and bradycardia seen after spinal anesthesia and mistakenly thought to be a high spinal.
These cases can be differentiated from a true high spinal in that they improve with pressors and they are not associated with a high sensory block,

 

[Planktonmd]

A Bezold Jarisch reflex is not rare and it basically explains most of the cases of hypotension and bradycardia seen after spinal anesthesia and mistakenly thought to be a high spinal.
These cases can be differentiated from a true high spinal in that they improve with pressors and they are not associated with a high sensory block,

I am still unable to understand why any one would start a full spinal anesthetic at the conclusion of surgery?
I mean 11 mg Bupivacaine with Fentanyl will produce complete motor and sensory blockade, a real surgical block for 2-3 hours!

 

[WholeLottaGame7]

My first thought was Bezold-Jarisch, also. Especially if no high sensory level.

I'm also on Team That Was Weird Management. Why not a subcostal TAP or even a PVB?

 

[amyl]

I cannot say why he didn't short that dose. This was a lap converted to open colon resection - I'm not sure if fluid resuscitation was at all adequate prior to spinal although I would suspect not. This did respond to pressors which were only required for a few minutes... Supporting bezold jarisch. Pt was extremely diaphoretic.... I've never had a high spinal but I saw one once and they weren't diaphoretic....

 

[Scotty_G]

Amyl I see why you are leaving your group now lol. What kind of postop pain technique is this?!?!!?

 

[GaseousClay]

like i asked earlier, you sure there was consent for this post-op spinal?

 

[scudrunner]

I always thought the bezold jarisch reflex was more transient than the episode you described.

 

[amyl]

I'm sorry.... Not my case so I don't know if spinal was discussed

 

[fakin' the funk]

So not my case.... But confusing picture so I thought I'd pick everyone's brain. 40-50 year old pt history of anxiety and HTN on ace inhibitor, obesity. Has had syncope with IV placement before.
Case is lap converted to open colon resection for recital prolapse. Case uneventful. At end of case partner places spinal w 11mg bupi and 200 mcg duramorph. Shortly after pt Brady to low 40s hypotensive desat to mid 80s requiring significant pressor support. Hugely diaphoretic. Altered sensorium -- almost like post ictal. Resecure airway. Lines. B/l breath sounds no arrhythmia - Pt stabilizes and is extubated - sat'ing great on non rebreather aox3 but anxious with continued diaphoresis and low normal BPs wo support. Anaphylaxis? But prior morphine wo problems... Albeit not IT. PE? But sats return perfect. Just the worst vasovagal rxn ever?

Um...

WHAT THE F*CK??!!

- Why a spinal for postop analgesia?
- If so, why not just spinal duramorph?
- Was the pt consented for the spinal duramorph?
- Why a full surgical hyperbaric spinal dose of bupi?
- Why is the ddx not high spinal, B-Z, subdural?
- Why do ppl not know about bradycardia after spinal being A BIG DEAL?

 

[teeva]

I don't understand. Leaving the pt intubated and sedated for two weeks to allow for wound healing and disappearance of surgical pain would have been a better plan than postop asleep intubated spinal with complete block.

 

[Pooh & Annie]

In my group you'd have a meeting with the chief if you did a bupi spinal for post-op pain control. I'm not sure how you explain that.

 

[PainDrain]

In my group you'd have a meeting with the chief if you did a bupi spinal for post-op pain control. I'm not sure how you explain that.

I have heard of places where a spinal is placed for "post op pain control" purely to pad the billing. They choose to do this over an epidural because surgeons don't care for the epidural and the anesthesia staff would prefer not to manage an epidural. It sounds stupid but I guess every dollar counts to some, no matter the risk.

This case sounds like BJR and I recently read a paper on post spinal cardiac arrest and the view was that BJR was involved far more often than a high spinal.

 

[deleted162650]

I have heard of places where a spinal is placed for "post op pain control" purely to pad the billing.

A duramorph only spinal accomplishes the same thing and is not pants-on-head ******ed. You don't get paid extra for placing a spinal at the end of the case (unless you're gonna sit there and bill time until it wears off). You bill for the duramorph and the accompanying "post-op pain consult" on POD #1

 

[PainDrain]

A duramorph only spinal accomplishes the same thing and is not pants-on-head ******ed. You don't get paid extra for placing a spinal at the end of the case (unless you're gonna sit there and bill time until it wears off). You bill for the duramorph and the accompanying "post-op pain consult" on POD #1

I agree. Nothing about the placement of a bupi spinal in this case makes any sense. The instances in which I was referring were where a spinal was placed (largely in cases that didn't really need it) with Astromorph and they billed for the post op consult as you stated.

 

[narcusprince]

Possible me mechanism of increased risk of postop high spinal..... Fluid shift with interstitial edema in spinal cord resulting in cephlad displacement of csf with a decreased fluid present in spinal cord resulting in higher spread of local anesthetic? Almost like an EVE effect......

 

[pgg]

Possible me mechanism of increased risk of postop high spinal..... Fluid shift with interstitial edema in spinal cord resulting in cephlad displacement of csf with a decreased fluid present in spinal cord resulting in higher spread of local anesthetic? Almost like an EVE effect......

I don't think there's a need to conjure spinal cord edema to explain how a surgical dose of hyperbaric bupivacaine reached T1-4 in a horizontal patient.

This clown probably had him in Trendelenburg, too.

 

[fakin' the funk]

This case sounds like BJR and I recently read a paper on post spinal cardiac arrest and the view was that BJR was involved far more often than a high spinal.

Yep.

Spinal effect on thoracolumbar sympathetics --> low preload --> HR slows in low preload state (BJR or "reverse Bainbridge" as I think of it); BP lowers due to direct SVR effect --> low BP with low HR --> low BP with lowering HR --> zero BP with close to zero HR

Gotta break the cycle early with strong chronotropes/pressors like epinephrine if this spiral starts happening

 

[fakin' the funk]

Because of the nontrivial risk of bradycardia after spinal, if people have low or even low-normal HR, I often give 0.2-0.4mg glycopyrrolate before the spinal. It often keeps them more in the 70-90 bpm range, and the antisialagogue effect is beneficial if you're gonna do a MAC plus your spinal like for a TKA/THA

 

[deleted162650]

There's also that French study that showed pre-spinal Zofran attenuates the BJR. I've been giving pre-spinal zofran for the past 1.5 years and I think anecdotally it actually works. Please don't ask me why.

 

[Noyac]

This is the dumbest thing I may have ever seen.

 

[Noyac]

There's also that French study that showed pre-spinal Zofran attenuates the BJR. I've been giving pre-spinal zofran for the past 1.5 years and I think anecdotally it actually works. Please don't ask me why.

It also helps with the pruritis from the IT duramorph.

 

[BobBarker]

Yes, back when I did OB I read that study and did the zofran thing as well. I think it works.

 

[pgg]

Reminds me of this thread:

http://forums.studentdoctor.net/thr...seless-problem-based-learning-5-cases.850129/

 

[Arch Guillotti]

At end of case partner places spinal w 11mg bupi and 200 mcg duramorph.

 

[Arch Guillotti]

A Bezold Jarisch reflex is not rare and it basically explains most of the cases of hypotension and bradycardia seen after spinal anesthesia and mistakenly thought to be a high spinal.
These cases can be differentiated from a true high spinal in that they improve with pressors and they are not associated with a high sensory block,

How many times have you seen the Bezold Jarisch reflex? I think I have seen it once in the past 10 years.

I don't consider hypotension and bradycardia after a spinal to be a high spinal nor the Bezold Jarisch reflex. The high spinals that I have seen presented differently than some changes in blood pressure and heart rate.

 

[Planktonmd]

How many times have you seen the Bezold Jarisch reflex? I think I have seen it once in the past 10 years.

I don't consider hypotension and bradycardia after a spinal to be a high spinal nor the Bezold Jarisch reflex. The high spinals that I have seen presented differently than some changes in blood pressure and heart rate.

So how do you explain hypotension and bradycardia after a spinal if it's not high spinal(causing too much sympathetic blockade) and not a BJR?

 

[Arch Guillotti]

So how do you explain hypotension and bradycardia after a spinal if it's not high spinal(causing too much sympathetic blockade) and not a BJR?

Hypotension and bradycardia are common side effects of spinal anesthesia, and they represent normal physiologic responses to anesthetized spinal sympathetic nerve fibers.

(Hypotension and bradycardia during spinal anesthesia: Significance, prevention, and treatment
Neal, Joseph M.

1. Techniques in Regional Anesthesia & Pain Management , Volume 4 , Issue 4 , 148 - 154

The sympathetic cardiac accelerator fibers emerge from the T1 to T4 spinal segments, and blockade of these fibers is proposed as the cause of bradycardia.

The Bezold-Jarisch reflex (BJR) has been implicated as a cause of bradycardia, hypotension, and cardiovascular collapse after central neuraxial anesthesia, and in particular spinal anesthesia.[152,153] The

<http://www.nysora.com/index.php?news=3424>

We must have different definitions of high spinal. I consider it a high spinal if there is a very high sensory block that causes significant significant cardiopulmonary or neurological manifestations.

I don't think it's BJR unless there is actual or impending cardiopulmonary collapse.

 

[scudrunner]

High spinal is somewhat vague. In this situation I think we are referring to a T1-4 sympathetic blockade, allowing parasympathetic cardiovascular innervation to predominate, hence the brady/hypotension. Remember, there is differential blockade between nerve fibers with sensitivity being autonomic>sensory>motor. Autonomic blockade is assumed to be a couple levels above sensory. With a hyperbaric bupivicaine spinal in a supine position, a T6-4 sensory block is almost ubiquitous given the thoracic curvature. It is then easy to see how a sympathetic blockade (T1-4) occurs, and the situation in the original post could ensue. The refractory hypotension may also be explained by the fact the pt was on an ACEi. I feel like the BJR may be more implicated in an arrest situation, but not really just brady/hypotension.

 

[Planktonmd]

Hypotension and bradycardia are common side effects of spinal anesthesia, and they represent normal physiologic responses to anesthetized spinal sympathetic nerve fibers.

(Hypotension and bradycardia during spinal anesthesia: Significance, prevention, and treatment
Neal, Joseph M.

1. Techniques in Regional Anesthesia & Pain Management , Volume 4 , Issue 4 , 148 - 154

The sympathetic cardiac accelerator fibers emerge from the T1 to T4 spinal segments, and blockade of these fibers is proposed as the cause of bradycardia.

The Bezold-Jarisch reflex (BJR) has been implicated as a cause of bradycardia, hypotension, and cardiovascular collapse after central neuraxial anesthesia, and in particular spinal anesthesia.[152,153] The

<http://www.nysora.com/index.php?news=3424>

We must have different definitions of high spinal. I consider it a high spinal if there is a very high sensory block that causes significant significant cardiopulmonary or neurological manifestations.

I don't think it's BJR unless there is actual or impending cardiopulmonary collapse.

I am not sure I understand what you are trying to say here!
If the hypotension and bradycardia were due to a sympathetic blockade that reached T1-T4 then this is a high spinal isn't it? Now if the cause is high spinal blockade how do you explain the absence of a correlating sensory block? and how do you explain the recovery in 5-10 minutes after giving a pressor?
And if this is not high spinal nor BJR what is the physiological explanation of the bradycardia?
And how do you define an (impending) cardiovascular collapse?

 

[Planktonmd]

Someone is apparently teaching people that BJR is only seen in cardiac arrests!!!

 

[Planktonmd]

High spinal is somewhat vague. In this situation I think we are referring to a T1-4 sympathetic blockade, allowing parasympathetic cardiovascular innervation to predominate, hence the brady/hypotension. Remember, there is differential blockade between nerve fibers with sensitivity being autonomic>sensory>motor. Autonomic blockade is assumed to be a couple levels above sensory. With a hyperbaric bupivicaine spinal in a supine position, a T6-4 sensory block is almost ubiquitous given the thoracic curvature. It is then easy to see how a sympathetic blockade (T1-4) occurs, and the situation in the original post could ensue. The refractory hypotension may also be explained by the fact the pt was on an ACEi. I feel like the BJR may be more implicated in an arrest situation, but not really just brady/hypotension.

If the explanation of the bradycardia is simply a high sympathetic blockade then you would think the patient would need chrono/ ino tropes until that sympathetic blockade recedes, but as you probably know, these patients improve a few minutes after giving a pressor and remain stable after that.

 

[anbuitachi]

The Bezold–Jarisch reflex (also called the Jarisch-Bezold reflex) involves a variety of cardiovascular and neurological processes which cause hypopnea (overly shallow breathing or an abnormally low respiratory rate) and bradycardia (abnormally low resting heart rate).[1]

Physiology[edit]
Prolonged upright posture results in some degree of pooling of blood in the lower extremities that can lead to diminished intracardiac volume. This phenomenon is exacerbated if the individual is dehydrated. The resultant arterial hypotension is sensed in the carotid sinusbaroreceptors, and afferent nerve fibers from these receptors trigger autonomic signals that increase cardiac rate and contractility. However, pressure receptors in the wall and trabeculae of the underfilled left ventricle may then sense stimuli, activating high-pressure C-fiber afferent nerves from these receptors. They may respond by sending signals that trigger paradoxical bradycardia and decreased contractility, resulting in additional and relatively sudden arterial hypotension. The bradycardia reaction to acetic acid veratril in the cardiac pacemaker region was first described by von Bezold. Jarisch identified the reaction as chemoreceptor reflex via the vagus nerve, relayed in the nucleus tractus solitarii.

The Bezold–Jarisch reflex is responsible for the sinus bradycardia that commonly occurs within the first 60 minutes following an acute myocardial infarction,[2] and explains the occurrence of AV node block in the context of acute posterior or inferior myocardial infarction.[3]Bradycardia in this setting may be treated with atropine.

It usually occurs in nitrate therapy and use of serotonin agonists.[4] The Bezold–Jarisch reflex has been suggested as a possible cause of profound bradycardia and circulatory collapse after spinal anesthesia.[5] Also, it is one of the complications of interscalene brachial plexus block.[6] The reflex occurs with several biologically active chemicals, like nicotine and capsaicin,[7] when reaching sensitive areas.

Im confused by what this BJ reflex is based on this definition. First it says the carotid receptors send signals to increase HR, and contractility, then goes on to say left ventricle may sense "stimuli", causing hypotension, brady, decreased contractility.
What stimuli is it sensing???? it doesn't explain this at all. There is no connectivity between those 2 parts.

Ive been trying to google this as well, haven't found a good explanation to how BJ reflex works .. or what the purpose of this reflex is

 

[Planktonmd]

The stimulus is Ischemia at the level of the Sino-atrial Pacemaker or AV junction.

 

[scudrunner]

The stimulus is Ischemia at the level of the Sino-atrial Pacemaker or AV junction.

Where did you get ischemia from? The stimulus is trabeculae/myocardial over-contraction from an under-filled ventricle.

 

[Planktonmd]

Where did you get ischemia from? The stimulus is trabeculae/myocardial over-contraction from an under-filled ventricle.

What happens to the muscle blood supply when there is " over-contraction with an under-filled ventricle"?
It seems to me that this specialty is now plagued with residents who think they already know everything there is to know even before they start residency!

 

[scudrunner]

What happens to the muscle blood supply when there is " over-contraction with an under-filled ventricle"?
It seems to me that this specialty is now plagued with residents who think they already know everything there is to know even before they start residency!

Oh, gimme a break.

Can you post a reference to ischemia at the SA node as the cause of bradycardia in the BJR? Sure bradycardia can occur if the SA node is ischemic, but in BJR, the bradycardia is vagally mediated- at least that is what is stated in every resource I've read.

 

[scudrunner]

If the explanation of the bradycardia is simply a high sympathetic blockade then you would think the patient would need chrono/ ino tropes until that sympathetic blockade recedes, but as you probably know, these patients improve a few minutes after giving a pressor and remain stable after that.

Most bupivicaine spinals for c-section, which require a high thoracic level, need a phenylephrine infusion (+/- chronotropic support) for the duration of the case.

 

[Planktonmd]

Most bupivicaine spinals for c-section, which require a high thoracic level, need a phenylephrine infusion (+/- chronotropic support) for the duration of the case.

You start a phenylephrine infusion on most of the C sections? Really?

 

[scudrunner]

You start a phenylephrine infusion on most of the C sections? Really?

Yes, if they get a spinal. We shoot for T4 sensory blocks, so we start phenylephrine and open the fluids as soon the spinal is in.