Hypothetical question

[Noyac]

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lets say we are doing a shoulder in the beach chair position and our pt has essential HTN. We want to keep his BP up in a safe range, usually not more than 20% below baseline. If you we were to place an LMA so that the pt were breathing spontaneously would we be better able to determine how low we could safely drop the BP? In other words, would a spontanteously breathing pt start to reveal derangements in their breathing pattern if they were starting to hypoperfuse the brain?

 

[Wiscoblue]

I wouldn't count on respiratory changes to indicate cerebral hypoperfusion. Ask your Ortho to consider doing shoulders in lateral position for the older sicker patients.

 

[norwood]

In other words, would a spontanteously breathing pt start to reveal derangements in their breathing pattern if they were starting to hypoperfuse the brain?

Not reliably, I'd say. The average pt with a mild-moderate CVA doesn't present with particularly abnormal breathing...

 

[pgg]

Possibly. The mechanism of respiratory distress in a high spinal is brainstem ischemia.

I sure wouldn't count on it as a warning sign though. 🙂

 

[deleted162650]

The respiratory center is deep in the brainstem and is among the most primitive and most resilient parts of the CNS. It requires profound hypoxia/damage before the respiratory centers go down. Think about how close someone is to death before agonal breathing kicks in. If breathing is affected 2/2 to hyoperfusion during your anesthetic it means you've already lost.

And there's no reason to ask your orthopod to change his technique, just run a little pressor, A-line with transducer at the head if your really worried.

 

[deleted171991]

I wouldn't count on respiratory changes to indicate cerebral hypoperfusion. Ask your Ortho to consider doing shoulders in lateral position for the older sicker patients.

^^^This. Doing shoulders in beach chair is like doing cataracts with retrobulbar blocks. Both belong to the last century.

 

[deleted171991]

And there's no reason to ask your orthopod to change his technique, just run a little pressor, A-line with transducer at the head if your really worried.

I thought we were the no.1 patient advocates, not just some surgical valets. Of course the surgeon should alter his/her technique based on the patient's health. If we learn how to skin a cat in many ways, so should they. Not for our comfort, but for the patient's safety.

 

[Ignatius J]

I thought we were the no.1 patient advocates, not just some surgical valets. Of course the surgeon should alter his/her technique based on the patient's health. If we learn how to skin a cat in many ways, so should they. Not for our comfort, but for the patient's safety.

Global malperfusion, yes. But patients with atherosclerosis of cerebral vessels that are pressure dependent as they are maximally dilated, no. I would say in a young, healthy lad- absolutely and good point. Wouldn't do it in someone with risk factors for cerebrovascular disease though.

 

[deleted162650]

I thought we were the no.1 patient advocates, not just some surgical valets. Of course the surgeon should alter his/her technique based on the patient's health. If we learn how to skin a cat in many ways, so should they. Not for our comfort, but for the patient's safety.

I never advocated being a surgical valet or doormat.

Please explain how the pt is at increased risk of cerebral ischemia if the BP is closely monitored and kept at the pts baseline. I'm pretty sure that pts with cerebrovascular Dz do occasionally sit upright and even stand once in a while. Now if the Orthopod says he wants the BP down due to bleeding or whatever then you step-up and explain why that's not gonna happen.

 

[deleted171991]

I never advocated being a surgical valet or doormat.

Please explain how the pt is at increased risk of cerebral ischemia if the BP is closely monitored and kept at the pts baseline. I'm pretty sure that pts with cerebrovascular Dz do occasionally sit upright and even stand once in a while. Now if the Orthopod says he wants the BP down due to bleeding or whatever then you step-up and explain why that's not gonna happen.

http://forums.studentdoctor.net/threads/tough-case-beach-chair-position.917317/
http://www.apsf.org/newsletters/html/2013/spring/05_beachchairimpact.htm

http://www.aaos.org/news/aaosnow/jan13/managing7.asp

http://ppmrrg.com/FileUploads/Issue33.pdf

Of course it can be done, but why assume unnecessary risks, especially in an ASA 3+ patient?

 

[deleted171991]

The respiratory center is deep in the brainstem and is among the most primitive and most resilient parts of the CNS. It requires profound hypoxia/damage before the respiratory centers go down. Think about how close someone is to death before agonal breathing kicks in. If breathing is affected 2/2 to hyoperfusion during your anesthetic it means you've already lost.

^^^ This. Remember that breathing in persistent vegetative states is usually normal. Breathing is a function of the brainstem, not the cortex.

If you want better monitors for cerebral ischemia, see CNS monitoring for carotid surgery under GA.

 

[BLADEMDA]

lets say we are doing a shoulder in the beach chair position and our pt has essential HTN. We want to keep his BP up in a safe range, usually not more than 20% below baseline. If you we were to place an LMA so that the pt were breathing spontaneously would we be better able to determine how low we could safely drop the BP? In other words, would a spontanteously breathing pt start to reveal derangements in their breathing pattern if they were starting to hypoperfuse the brain?

Noy,

I don't get it. We have discussed this in detail. I wold maintain the patient's BP at a mean of 90 if only using a cuff on the arm especially with essential HTN. In addition, you could place a Cerebral Oximeter on the head ,as I do this routinely, for additional reassurance of adequate cerebral perfusion. FYI, I have seen the Cerebral Oximetry drop off by 10-15 points in these patients when the MEAN BP by cuff fell to 60 and go right back up to 75 when the MEAN BP was restored to above 80.

 

[BLADEMDA]

Regional Anesthesia & Pain Medicine:
January/February 2012 - Volume 37 - Issue 1 - p 120
doi: 10.1097/AAP.0b013e31823a9934
Letters to the Editor
The Beach-Chair Position and General Anesthesia
Weiner, Menachem M. MD; Fischer, Gregory W. MD; Rosenblatt, Meg A. MD


1 which reviewed more than 4000 ambulatory shoulder surgeries performed in the beach-chair position and reported a zero incidence of stroke despite the use of intraoperative hypotension to reduce surgical bleeding. It is only through continued interest and research in this topic that patient safety will improve and we will be able to prevent the devastating complication of perioperative stroke in the beach-chair surgical population. However, we believe that the more crucial study to conduct is on patients undergoing surgery in the beach-chair position who are under general anesthesia with mechanical ventilation.

As the authors correctly acknowledge, there are no published case reports of patients with permanent neurologic deficit following shoulder surgery performed with regional anesthesia with spontaneous ventilation. All 4 patients in the case series of cerebral ischemia during shoulder surgery, reported by Pohl and Cullen,2 had received general anesthesia with mechanical ventilation. The same is true for other case reports of this catastrophic complication, including one of visual loss.3

Although no similar large-scale studies have been conducted on patients under general anesthesia, 2 smaller studies deserve mention. No strokes occurred in either study, but both studies used cerebral oxygen saturation as determined using near-infrared spectroscopy as a surrogate marker of cerebral blood flow. Murphy et al4 compared the beach-chair position to the lateral decubitus position in patients undergoing shoulder surgery under general anesthesia and found significant reductions in cerebral oxygenation in patients in the beach-chair position as opposed to the lateral decubitus position. At our institution, we performed a small study, with institutional review board approval, comparing mechanical ventilation to spontaneous ventilation (both general anesthesia and sedation) that we presented at the annual meeting of the American Society of Anesthesiologists in 2010. Unfortunately, because of surgical preference, we were able to enroll only 8 patients in the mechanical ventilation group as compared with 74 in the spontaneous ventilation one. We found that the mechanical ventilation group showed a dependency between cerebral oximetry values and systemic perfusion pressure. In other words, cerebral blood flow was no longer pressure independent within a physiologic blood pressure range as would be predicted by cerebral autoregulation, but it correlated directly with systemic perfusion pressure. In contrast, the spontaneous ventilation group showed cerebral oximetry values that were independent of systemic blood pressure.

Further large studies are needed to prove whether mechanically ventilated patients are at greater risk for stroke while in the beach-chair position. In the interim, it may be prudent to monitor this subgroup of patients with cerebral oximetry.

Menachem M. Weiner, MD

Gregory W. Fischer, MD

Meg A. Rosenblatt, MD

Department of Anesthesiology

Mount Sinai School of Medicine

 

[BLADEMDA]

lets say we are doing a shoulder in the beach chair position and our pt has essential HTN. We want to keep his BP up in a safe range, usually not more than 20% below baseline. If you we were to place an LMA so that the pt were breathing spontaneously would we be better able to determine how low we could safely drop the BP? In other words, would a spontanteously breathing pt start to reveal derangements in their breathing pattern if they were starting to hypoperfuse the brain?

I guess you could place Cerebral Oximetry while awake for a baseline and then after positioning the patient post LMA monitor the BP drop until there is 5-10% change in the Cerebral Oximetry. If the patient is spontaneously breathing a lower BP may be tolerated without Cerebral Desaturation compared to Mechanically Ventilated patients. That said, I wouldn't be comfortable at this point with that strategy but one could certainly argue it is safe provided you maintain a Mean BP above 70 on the cuff with no cerebral desaturation. Again, that technique isn't my choice but it is likely safe in ASA 1 and 2 patients.

 

[Noyac]

I was under the same impression that the majority of you are under, that the brainstem would have to take the hit in order to cause a change in respiratory patterns. But this may not be the reality. It appears that the cerebral hemisphere is where this respiratory changes occur. Central periodic breathing, ie: cheyne-stokes breathing, is more common in acute cerebral hemisphere strokes, not brainstem strokes. Also, the anterior circulatory system may be more likely involved in these strokes. One theory is that these larger insults may release humoral agents that enter the CSF and blood stream which may effect the respiratory centers.

I'm not trying to debate the seated vs the lateral approach. I'm just wanting to discuss something that I thought of today for some reason. So my question is, could/would we start to see a resp pattern change in a pt if they were spontaneously breathing and beginning to have a CVA? I'm sure we "could" but would it be too late? Probably. I wonder if any of the cases that have occured had a spontaneously breathing pt and if they saw a change in resp pattern. They almost all claim that the pt just didn't wake up at the end of the case.

 

[pgg]

The respiratory center is deep in the brainstem and is among the most primitive and most resilient parts of the CNS. It requires profound hypoxia/damage before the respiratory centers go down. Think about how close someone is to death before agonal breathing kicks in. If breathing is affected 2/2 to hyoperfusion during your anesthetic it means you've already lost.

Old and recurrent written board question. Can't remember if I saw it on an ITE or the written, or it might've been in Hall.

NYSORA mentions it here but don't offer a citation:

High spinal anesthesia can result in profound respiratory embarrassment, most likely due to brainstem ischemia.

The best quote I can find at the moment is from Cousins and Bridenbaugh's book (p227) which says

The most likely cause of transient respiratory arrest during high spinal anesthesia is ischemia of medullary respiratory neurons secondary to decreases in blood pressure and cardiac output severe enough to impair cerebral blood flow. Medullary ischemia as the cause of apnea during high spinal anesthesia is evidenced by the fact that respiratory arrest rarely occurs in the absence of hypotension severe enough to be associated with impending loss of consciousness. Further, restoration of blood pressure and cardiac output in cases of respiratory arrest during spinal anesthesia, if done promptly, is associated with immediate return of spontaneous respiration.

(So this is actual hypoperfusion-related ischemia, not direct local anesthetic effects on the brainstem.)


I do believe that during a sitting shoulder case, depression of spontaneous respiration WOULD be early-ish evidence of inadequate brain perfusion. More of a hypothetical curiosity? Sure, I wouldn't count on it as a warning sign. But if I did see it ... I would be inclined to double check the BP and reconsider if it's where I really want it to be. Which I think is where Noyac was going with this.

 

[BLADEMDA]

Anesth Analg. 2012 Jun;114(6):1301-4. Epub 2011 Nov 3.
Case report: focal cerebral ischemia after surgery in the "beach chair" position: the role of a congenital variation of circle of willis anatomy.

Drummond JC, Lee RR, Howell JP Jr.
Source

FRCPC, VA Medical Center-125, 3350 La Jolla Village Dr., San Diego, CA 92161. [email protected].

Abstract

A 50-year-old man underwent shoulder surgery in the beach chair position. His mean arterial blood pressure at arm level was approximately65 mm Hg. Postoperatively, there was delayed awakening and a right hemiparesis. Radiologic evaluation revealed a congenital asymmetry of the circle of Willis that resulted in limited collateral flow to the left anterior and middle cerebral artery distributions. Similar anatomical variations are relatively common in the general population and may render some patients relatively and unpredictably more vulnerable to hypotension.

 

[Noyac]

"We found that the mechanical ventilation group showed a dependency between cerebral oximetry values and systemic perfusion pressure. In other words, cerebral blood flow was no longer pressure independent within a physiologic blood pressure range as would be predicted by cerebral autoregulation, but it correlated directly with systemic perfusion pressure. In contrast, the spontaneous ventilation group showed cerebral oximetry values that were independent of systemic blood"

So is this saying that the spontaneously breathing pts were able to tolerate lower systemic blood pressure? That's what I understand.

 

[BLADEMDA]

Clin Sci (Lond). 2013 Jul;125(1):37-44.
Cerebral hypoperfusion modifies the respiratory chemoreflex during orthostatic stress.
Ogoh S1, Nakahara H, Okazaki K, Bailey DM, Miyamoto T.
Author information

Abstract
The respiratory chemoreflex is known to be modified during orthostatic stress although the underlying mechanisms remain to be established. To determine the potential role of cerebral hypoperfusion, we examined the relationship between changes in MCA V(mean) (middle cerebral artery mean blood velocity) and ˙VE (pulmonary minute ventilation) from supine control to LBNP (lower body negative pressure; −45mmHg) at different CO(2) levels (0, 3.5 and 5% CO(2)). The regression line of the linear relationship between ˙V(E) and PETCO(2) (end-tidal CO(2)) shifted leftwards during orthostatic stress without any change in sensitivity (1.36+− 0.27 l/min per mmHg at supine to 1.06+− 0.21 l/min per mmHg during LBNP; P=0.087). In contrast, the relationship between MCA V(mean) and PETCO(2) was not shifted by LBNP-induced changes in PETCO2. However, changes in ˙V(E) from rest to LBNP were more related to changes in MCA V(mean) than changes in PETCO(2). These findings demonstrate for the first time that postural reductions in CBF (cerebral blood flow) modified the central respiratory chemoreflex by moving its operating point. An orthostatically induced decrease in CBF probably attenuated the ‘washout’ of CO(2) from the brain causing hyperpnoea following activation of the central chemoreflex.

 

[BLADEMDA]

"We found that the mechanical ventilation group showed a dependency between cerebral oximetry values and systemic perfusion pressure. In other words, cerebral blood flow was no longer pressure independent within a physiologic blood pressure range as would be predicted by cerebral autoregulation, but it correlated directly with systemic perfusion pressure. In contrast, the spontaneous ventilation group showed cerebral oximetry values that were independent of systemic blood"

So is this saying that the spontaneously breathing pts were able to tolerate lower systemic blood pressure? That's what I understand.

Yes. The hypercarbia/hypercapnia appears to be protective against CVA probably due to preservation of CBF while under GA with Vapor.

 

[deleted171991]

"We found that the mechanical ventilation group showed a dependency between cerebral oximetry values and systemic perfusion pressure. In other words, cerebral blood flow was no longer pressure independent within a physiologic blood pressure range as would be predicted by cerebral autoregulation, but it correlated directly with systemic perfusion pressure. In contrast, the spontaneous ventilation group showed cerebral oximetry values that were independent of systemic blood"

So is this saying that the spontaneously breathing pts were able to tolerate lower systemic blood pressure? That's what I understand.

Wouldn't be surprised at all. Correlates with my subjective observation during residency that healthy patients breathing spontaneously autoregulate their BP better than the same patients while mechanically ventilated. Might be related to CO2.

 

[Noyac]

Wouldn't be surprised at all. Correlates with my subjective observation during residency that healthy patients breathing spontaneously regulate their BP better than mechanically ventilated ones.

Absolutely!!!
When a pt is spontaneously breathing we all know that they usually maintain their BP better. Contrary to this, pts with controlled ventilation tend to require more cardiovascular support. This requires meds like phenylephrine which squeeze all vessels. Therefore, we may be further decreasing blood flow to the Mellon.

 

[deleted171991]

Absolutely!!!
When a pt is spontaneously breathing we all know that they usually maintain their BP better. Contrary to this, pts with controlled ventilation tend to require more cardiovascular support. This requires meds like phenylephrine which squeeze all vessels. Therefore, we may be further decreasing blood flow to the Mellon.

Phenylephrine should not produce cerebral vasoconstriction.

http://journals.lww.com/anesthesia-...al_Blood_Flow_and_the_Alpha_1_Agonist.37.aspx
http://aa2day.org/2014/04/phenylephrine/

Except, apparently, if the patient is hypocapnic (or even normocapnic):
https://www.ics.uci.edu/~zhaoxia/publications/paper23_Yuzx_BritishJAnaesth2012.pdf

Hypercapnia seems to protect the cerebral circulation from phenylephrine. Bingo!

 

[Noyac]

Phenylephrine should not produce cerebral vasoconstriction.

http://journals.lww.com/anesthesia-...al_Blood_Flow_and_the_Alpha_1_Agonist.37.aspx

Except, apparently, if the patient is hypocapnic:
https://www.ics.uci.edu/~zhaoxia/publications/paper23_Yuzx_BritishJAnaesth2012.pdf

Bingo!

Yes but it needs to be used as an infusion for this to be the case. How many of use use an infusion routinely in these cases?

 

[BLADEMDA]

With poor brain
perfusion, the central chemoreceptor will sense a relatively
higher [H] for a given change of PaCO2 and will correspondingly
trigger a more vigorous ventilatory response. However,
when CBF was further reduced to 50%, which nearly abolished
CBF-CO2 reactivity, there was a marked blunting of the minute
ventilation (V˙ E)-PaCO2 response, possibly as a consequence of
hypoxic depression of the respiratory neurons (36). Thus, on
the basis of these animal experiments, there seems to be a
threshold at which changes in CBF and cerebrovascular CO2
reactivity may lead to differential alterations in the ventilatory
responsiveness to CO2.

http://ajpregu.physiology.org/content/ajpregu/296/5/R1473.full.pdf

 

[BLADEMDA]

In summary, the finding in goats that, at 50% CBF, the
ventilatory response to CO2 was reduced is broadly analogous
to the finding that ventilatory responsiveness to CO2 is depressed
in patients with severe cerebrovascular disease (136,
163, 215). Such changes likely reflect impairment of metabolism
of respiratory neurons, as reflected in a marked decline in
whole brain O2 consumption in patients with severe brain
ischemia (104). Collectively, on the basis of animal and human
pathological studies, there seems to be a threshold at which
changes in CBF and cerebrovascular CO2 reactivity may lead
to differential alterations in the ventilatory responsiveness
to CO2.
A number of related experiments utilizing TCD have speculated
that a reduction of CBF-CO2 reactivity may lead to
subsequent alterations in ventilatory reactivity to CO2 (7, 8, 14,
43, 63, 144, 156, 221). Specifically, these studies indicated that
a reduced CBF-CO2 reactivity results in an enhanced ventilatory
sensitivity to CO2 (measured using steady-state methods)
via a CBF-related attenuation of brain [H] washout and
greater stimulus at the central chemoreceptors. Three important
considerations arise. 1) Is there direct evidence for a role of
cerebrovascular CO2 reactivity in the ventilatory response to
PaCO2
? 2) Does a change in ventilatory response to CO2 affect
cerebrovascular CO2 reactivity? 3) Does the commonly used
TCD-measured blood flow velocity in the MCA reflect blood
flow in the vicinity of the central chemoreceptors?
Is there direct evidence of a role for cerebrovascular CO2
reactivity in the ventilatory response to PaCO2
? Recent elegant
studies have utilized powerful pharmacological manipulation
of CBF-CO2 reactivity to determine the influence of CBF
reactivity per se on steady-state ventilatory responsiveness.
The pharmacological intervention used in these studies was
indomethacin, a potent reversible cyclooxygenase inhibitor
that effectively decreases CBF and attenuates the cerebrovascular
sensitivity to hypercapnia and hypocapnia (49, 61, 116,
193, 210, 214, 219, 222) without concomitant changes in
metabolic rate (222) or plasma catecholamines (31, 61, 116,
193). Such acute reductions in CBF-CO2 sensitivity result in an
elevation in V˙ E-CO2 sensitivity under steady-state testing conditions
(221).

 

[BLADEMDA]

lets say we are doing a shoulder in the beach chair position and our pt has essential HTN. We want to keep his BP up in a safe range, usually not more than 20% below baseline. If you we were to place an LMA so that the pt were breathing spontaneously would we be better able to determine how low we could safely drop the BP? In other words, would a spontanteously breathing pt start to reveal derangements in their breathing pattern if they were starting to hypoperfuse the brain?

Based on the available evidence the answer to your question is "no." As the CBF gradually drops below the critical threshold for brain perfusion the typical physiological response is increased respiratory rate or minute ventilation. But, as the CBF becomes more and more reduced (50% more than baseline?) the respiratory rate drops off significantly. IMHO, this means you would see an increase in respiratory rate in your scenario describe above if the CBF decreased below the critical threshold for brain perfusion.

Your response to the increased respiratory rate would likely be to increase the depth of the anesthetic or give additional narcotics both of which only exacerbate the problem. But, The Cerebral Oximeter would likely show you that Brain Saturation/perfusion was dropping prior to any change in resp. rate.

If you wait until Resp. Rate drops off Significantly in the scenario described above above the likelihood of a postop Cerebral event, e.g., CVA, is quite high. You would need to make an intervention PRIOR to significant decrease in Resp. rate.

 

[Noyac]

Based on the available evidence the answer to your question is "no." As the CBF gradually drops below the critical threshold for brain perfusion the typical physiological response is increased respiratory rate or minute ventilation. But, as the CBF becomes more and more reduced (50% more than baseline?) the respiratory rate drops off significantly. IMHO, this means you would see an increase in respiratory rate in your scenario describe above if the CBF decreased below the critical threshold for brain perfusion.

Your response to the increased respiratory rate would likely be to increase the depth of the anesthetic or give additional narcotics both of which only exaggerate the problem. But, The Cerebral Oximeter would likely show you that Brain Saturation/perfusion was dropping prior to any change in resp. rate.

So as I see it, then "yes" it would. I'm not asking if our response would be appropriate. I'm asking if we could see respiratory derangements in the light of cerebral perfusion deficits.

 

[Noyac]

Also, if BP Is low and resp patten is increasing I would consider something odd may be going on. Usually, if it is pain related increasing resp rate the BP will also increase.

 

[BLADEMDA]

Also, if BP Is low and resp patten is increasing I would consider something odd may be going on. Usually, if it is pain related increasing resp rate the BP will also increase.

Okay. Yes, you could see an increase in Resp. Rate as the CBF/Cerebral Saturation decreases below the Critical threshold. That said, I wouldn't want my anesthetic technique to be based on this physiological occurrence. Instead, If you INSIST on relative hypotension (mean of 60-65 by cuff) while in the Beach Chair Position please consider the use of Cerebral Oximetry along with Spontaneous Respirations. If, by chance, Mechanical Ventilation must be instituted during the case I would abandon the technique altogether and maintain a higher mean BP.

At this time the safest course of action is to maintain a mean BP of 65-70 at the level of the tragus (circle of Willis) along with Spontaneous respirations. That said, Perhaps all you need is a mean of 50-55 at the level of the tragus with spontaneous respirations?

 

[BLADEMDA]

If I wanted to make the surgeon "happy" in your scenario: place an arterial line with transducer at the level of the tragus, utilize cerebral oximetry and maintain spontaneous respirations.

This way when the surgeon sees 80/50 on the screen he won't complain. I have NEVER had a surgeon complain when I state the BP is 80/50 so I would never see the need to go lower than that BP especially for a patient with essential Hypertension.

 

[deleted162650]

http://forums.studentdoctor.net/threads/tough-case-beach-chair-position.917317/
http://www.apsf.org/newsletters/html/2013/spring/05_beachchairimpact.htm

http://www.aaos.org/news/aaosnow/jan13/managing7.asp

http://ppmrrg.com/FileUploads/Issue33.pdf

Of course it can be done, but why assume unnecessary risks, especially in an ASA 3+ patient?

Still, from these references CVA's from beach chair positioning is a concern in the setting of hypotension. I think that as long as BP is maintained appropriately, beach chair does not pose additonal risk. Sure it requires some extra effort and vigilance. I'll agree that cerebral oximetry monitoring may add some additional margin of safety. I'll also agree that that spont vent and relative hypercarbia help preserve hemodynamics and cerebral bloodflow. Unless contraindicated I run pretty all my cases w/ etCO2 in the mid to high 40's to provide increased cerebral bloodflow and encourage O2 offloading from Hgb (can't really say whether this has any meaningful clinical effects, but it makes me feel better).

 

[deleted126335]

Didn't read the article, but I would be very hesitant to do an open shoulder in beach chair with spontaneous ventilation. Worried about VAE. Not sure if the study was limited to shoulder scopes.

 

[deleted171991]

I think that as long as BP is maintained appropriately, beach chair does not pose additonal risk.

VAE. I even saw one in a spinal surgery, so shoulder- should be downright ripe for it.

 

[deleted171991]

Didn't read the article, but I would be very hesitant to do an open shoulder in beach chair with spontaneous ventilation. Worried about VAE. Not sure if the study was limited to shoulder scopes.

Same time, same thought. Funny. 🙂

 

[Noyac]

Ok, we all agree that the lateral approach is safer in shoulders and that the mean pressure should be kept at a reasonable number. I'm not arguing this well known issue. I just used the shoulder case as an example. Let's forget the shoulder case.

Can we observe respiratory changes in spontaneously breathing pts that would clue us into cerebral hypoperfusion? Another question would be, is it too late once these respiratory changes occur?

I don't have cerebral oximetry at my facilities. I'm sure many others here are in my boat. So can we use something else? I don't need a CVP or a Swan to tell me my pt is hypovolemic.

 

[Noyac]

VAE. I even saw one in a spinal surgery, so shoulder- should be downright ripe for it.

Why?
Why would spontaneous ventilation be more ripe than mechanical?

 

[deleted171991]

Why?
Why would spontaneous ventilation be more ripe than mechanical?

For VAE? Negative thoracic pressure during inspiration.

Plus, in shoulder surgery, the surgical site is much higher than the heart, than in spinal surgery. Which was my actual point.

 

[Noyac]

For VAE? Negative thoracic pressure during inspiration.

Plus, in shoulder surgery, the surgical site is much higher than the heart, than in spinal surgery. Which was my actual point.

Yes I understand this. Just wanted to be clear that we are talking about the same thing. I have seen my fair share of VAE. Mostly in residency. None of them were ever in spontaneously breathing pts. All mechanically breathing. I have even seen one devastating one in a shoulder case. But this was because the surgeon decided to inject air into the surgical field under the scope in order to see better. I had never heard of this but one of my partners had heard of this technique. It was a clean kill!
So I find the risk is greater with low BP more than the mode of ventilation. The negative pressure generated when spontaneously breathing is low and not transmitted throughout the body even when that part of the body is bovie the heart somewhat. The vessels will collapse before drawing in that much air and if they didnt we would see large variations in filling volumes of the heart and lungs in this scenario. Now, if one were to close the glottis then we may see this occur but not in a typical breath.

 

[deleted162650]

Not too long ago I looked up VAE in shoulder surgeries after one of our more persnickety Neurosurgeons poked his head into my shoulder room (why I have no idea), and then casually gave me crap for not using a precordial doppler (this particular neurosurgeon still does a fair number of sitting posterior fossa crani's and is well acquainted with VAE). There have been a number of fatal/near fatal VAE's during sitting shoulder operations but every one I found was in the setting of arhthroscopy using air instead of fluid like Noy's case.

 

[Noyac]

The difference in neurosurgical cases (crani's) vs shoulders is that the cranial sinuses are not collapsible like the rest of the venous system.

 

[Noyac]

Not too long ago I looked up VAE in shoulder surgeries after one of our more persnickety Neurosurgeons poked his head into my shoulder room (why I have no idea), and then casually gave me crap for not using a precordial doppler (this particular neurosurgeon still does a fair number of sitting posterior fossa crani's and is well acquainted with VAE). There have been a number of fatal/near fatal VAE's during sitting shoulder operations but every one I found was in the setting of arhthroscopy using air instead of fluid like Noy's case.

That's awesome. So your neurosurgeon thought he would show you how smart he was but in the end he showed how dumb he is. I would,d think any average or even below average neurosurgeon would understand this issue. I have been proven wrong.

 

[deleted162650]

Ya not sure what his deal is. The guy is actually very smart, and he's even a very good surgeon but I think he stopped maturing sometime around age 3. It's really like working with a spoiled toddler. You hit the nail on the head with the dural sinuses being the real culprit in crani's. The only other scenario where I could it being a possibility with shoulder cases (aside from air insufflation 😵) is with TSA's where you have raw freshly cut bone that could (maybe ?) entrain some air??

 

[Noyac]

Ya not sure what his deal is. The guy is actually very smart, and he's even a very good surgeon but I think he stopped maturing sometime around age 3. It's really like working with a spoiled toddler. You hit the nail on the head with the dural sinuses being the real culprit in crani's. The only other scenario where I could it being a possibility with shoulder cases (aside from air insufflation 😵) is with TSA's where you have raw freshly cut bone that could (maybe ?) entrain some air??

Well we don't see it in total knees or hips. The shoulder is only slightly above the heart which isn't very different from the lateral hip or raised knee. And the tourniquet wouldn't prevent VAE in a TKA because it can't collapse the bone.

 

[Planktonmd]

Back to the initial question: Do respiratory changes in a spontaneously breathing patient predict cerebral hypoperfusion?
The answer: No one knows but probably not!
Now to the rest of the discussion: Do we know if anything we do could protect the patient from having a CVA during shoulder surgery (or any other surgery)?
The answer is unfortunately no!
All the other stuff is just mental masturbation.

 

[Noyac]

This article starts to address what might cause respiratory changes in PTS with strokes

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2117643/

 

[Planktonmd]

This article starts to address what might cause respiratory changes in PTS with strokes

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2117643/

This is Cheyne-Stokes breathing that is seen in brain injuries and massive CVAs, but it's also seen under the influence of CNS depressants, so we don't know if this change of breathing pattern will still happen if anesthetics or opiates are on board, or if it has any significance under anesthesia.
I guess the only way to study that would be in an animal study but I don't think any one has done that yet.

 

[BLADEMDA]

Back to the initial question: Do respiratory changes in a spontaneously breathing patient predict cerebral hypoperfusion?
The answer: No one knows but probably not!
Now to the rest of the discussion: Do we know if anything we do could protect the patient from having a CVA during shoulder surgery (or any other surgery)?
The answer is unfortunately no!
All the other stuff is just mental masturbation.

I don't agree unless you state "maintaining BP for adequate cerebral perfusion is essential for patients under GA in the Beach chair perfusion."

http://www.smh.com.au/nsw/man-died-...lder-surgery-inquest-told-20130422-2i9md.html

 

[Planktonmd]

I don't agree unless you state "maintaining BP for adequate cerebral perfusion is essential for patients under GA in the Beach chair perfusion."

http://www.smh.com.au/nsw/man-died-...lder-surgery-inquest-told-20130422-2i9md.html

Maintaining blood pressure for adequate perfusion of the brain is essential in every surgery, in any position.
There is simply no evidence that any technique or monitoring device lowers the risk of CVA in shoulder surgery.
Even the news paper story from Australia that you posted, we really don't know what actually happened.
And although I hate the cut and paste style this large retrospective study actually concludes that In relation to orthopedic procedures performed in the supine position, beach chair positioning does not appear to increase the risk of intraoperative cerebrovascular event.

http://www.healio.com/orthopedics/s...ry-and------association-with-patient-position

 

[BLADEMDA]

There are case reports of postop CVAs after surgery. Cerebral Oximetry has been shown to have a good positive and negative predictive value. While I agree the technology is fairly new it may be the addition of this monitor will help prevent postop CVAs.


http://icvts.oxfordjournals.org/content/12/3/454.full


http://www.anesthesiologynews.com/download/CerebralOximetry_ANSE12_WM.pdf