"Hemodynamically Benign" RSI

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sluggs

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Hi. IM/CCM here. I thought about posting this in CCM but wanted an anesthesiology opinion (or a few): called in the middle of the night to see a (strong/hearty) 82 y/o man with 1.5 liters of coffee ground liquid in his newly placed NG tube. HR 70s (but on Coreg), 80s/50s, mildly tachypneic, 7.34/48/62/17 with a lactate of 8. Bolus 1 liter of LR and 2 units prbc with BP to 122/70. He was struggling to I decided to intubate urgently in anticipation of EGD. RSI with 1 mg versed, 100 mg ketamine 100 mg roc (he was 78 kg).
Cycling cuff every 2 minutes. Tube and hyperventilate. Very quick with no drop in sats. Next bp 68/33.
I rescued with fluid and pressor. No further issues.
My question: I thought this should be a very hemodynamicaly benign cocktail? I also thought about etomidate, but I do take seriously the (albeit controversial) insult to the HPA axis.
Thoughts?
The paralytic should not drop the bp, nor "should" the ketamine, and the versed was a small dose.
Thanks in advance!
 
Med student here. Interested in hearing input. Rapid bolusing of ketamine should've supported his BP. My guess is this was a direct result of intubation/MV itself due to a drop in VR vs. the cocktail given.
 
The thing to realize is that this patient will get hypotensive with any kind of induction agent. BP is already low, catechols are likely maxed.

I use ketamine every day but this is one of those situations where its negative inotropic effect may show up, since he doesn't have any catechols left to squeeze out of his adrenals. I think what you did is mostly fine and certainly easily defensible, but probably overkill for this particular patient.

A sick 80 year old like this, I'd give a few mg of midazolam (2-3 maybe) and chase with sux, nothing more necessary. If I did give ketamine it'd be in the 20-50 mg range for this kind of patient. 100mg roc is fine as you did.

Even then I'd expect hypotension with initiation of positive pressure ventilation, and would chase the induction with a bump of phenylephrine or norepi.

Disclaimer: everything depends on the eyeball test in these scenarios. Hard to comment intelligently without seeing the patient.
 
A couple points. Firstly, ketamine itself is a myocardial depressant. In someone who still has a catecholamine reserve, you will likely see some degree of tachycardia and hypertension due to secondary catecholamine release. With a beta blocked patient in hypovolemic shock, his adrenergic tone has likely already been maxed out to maintain what little perfusion he has, and therefore it is still possible to tank his pressure if you give too much ketamine (try 50mg next time). Second, paralytics are known to decrease MAC/muscle tone and can contribute to hypotension. Finally, after the tube got placed, you probably did a couple more things to drop bp, one is hyperventilation, and the other is that we frequently use too much inspiratory pressure when using the ambu. Too much inspiratory pressure -> decreased venous return -> hypotension.

In this situation I would've done a couple things differently. If the airway was urgent, not emergent, take a couple minutes to pop in an a-line (especially if say he was on coreg because he has a history of CHF with hypertension). Have blood/albumin running wide open through large bore IVs before induction. Administer phenylephrine 100-200mcg before you push your drugs.
 
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I see you're a verified physician, so I'll assume this is a legitimate clinical scenario as opposed to "asking medical advice," or lawyers trolling for an opinion that supports their case...

Never underestimate the impact of positive pressure ventilation on hemodynamics, as HB said. I routinely intubate (altered, failing) patients in the ICU with topical anesthesia only, and they can still become hypotensive with PPV.

Your goals of the induction in a case like this are amnesia, rapid readiness for intubation, and avoidance of reflux and aspiration. Amnesia, as opposed to induction of unconsciousness, can be achieved with less drug than you'd expect, and a mg or two of midazolam is probably plenty.
 
sluggs said:
Hi. IM/CCM here. I thought about posting this in CCM but wanted an anesthesiology opinion (or a few): called in the middle of the night to see a (strong/hearty) 82 y/o man with 1.5 liters of coffee ground liquid in his newly placed NG tube. HR 70s (but on Coreg), 80s/50s, mildly tachypneic, 7.34/48/62/17 with a lactate of 8. Bolus 1 liter of LR and 2 units prbc with BP to 122/70. He was struggling to I decided to intubate urgently in anticipation of EGD. RSI with 1 mg versed, 100 mg ketamine 100 mg roc (he was 78 kg).
Cycling cuff every 2 minutes. Tube and hyperventilate. Very quick with no drop in sats. Next bp 68/33.
I rescued with fluid and pressor. No further issues.
My question: I thought this should be a very hemodynamicaly benign cocktail? I also thought about etomidate, but I do take seriously the (albeit controversial) insult to the HPA axis.
Thoughts?
The paralytic should not drop the bp, nor "should" the ketamine, and the versed was a small dose.
Thanks in advance!
Click to expand...

Your dosage of Ketamine is on the high side; as stated in another post, in a catecholamine depleted patient ketamine is cardiac depressant. That said, low dosages like 0.3-0.5 mg kg IV along with midazolam 1 mg IV is a better approach. Ketafol (Ketamine and propofol low dose) is another approach here. Remember, there is no free lunch so be prepared to treat the hypotension immediately post intubation (which is almost a guarantee with this patient). That means, arterial line placement and good IV access prior to the RSI (if time permits). The second thing is to have your pressor agents immediately on hand to give IV post induction or your patient may arrest before the nurse gets it for you. This means Noreip or Phenylephrine with a vial of vasopressin (better than Epi for post intubation refractory hypotension IMHO) ready to go as back-up just in case. Factors contribution to the hypotension during the RSI and immediately after include but are not limited to: Myocardial depressant activity of the drugs, decrease in SVR and a reduction in preload due to PPV.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4332295/#!po=27.7778

http://journal.publications.chestnet.org/article.aspx?articleid=1085562

Thanks for stopping by our forum.
 
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lots of ways to skin this cat

i give pressors just prior to my induction agent, rather than waiting for the hypotension to occur (lets face it - you know it will).

it doesn't actually matter that much which induction agent you choose, the dose is more important.
and then go easy on the positive pressure ventilation. lay off the peep, keep the mean airway pressure low, and accept the CO2 will go up for a bit.
a little head down can help too (once the tube is in).
 
JobsFan said:
lots of ways to skin this cat

i give pressors just prior to my induction agent, rather than waiting for the hypotension to occur (lets face it - you know it will).

it doesn't actually matter that much which induction agent you choose, the dose is more important.
and then go easy on the positive pressure ventilation. lay off the peep, keep the mean airway pressure low, and accept the CO2 will go up for a bit.
a little head down can help too (once the tube is in).
Click to expand...

Sure, that's fine but how do you know what the BP will settle in at 30 minutes post intubation? That's why an arterial line is valuable because you can titrate the pressors to a real time BP value.

I like Ketafol myself in low doses (maybe 30 mg propofol and 50 mg of ketamine in this patient) combined with 200 ug of phenylephrine upfront via the IV. Still, I'd rest easier with an arterial line in place during the entire process.
 
sluggs said:
I rescued with fluid and pressor. No further issues.
Click to expand...

Thanks for visiting the anesthesia forum. 🙂

One of the differences I see between inductions managed by anesthesiologists and those managed by IM / pulm-CC doctors is that the IM / pulm-CC doctors do not seem to use or have comfort with pushing vasopressors with a syringe.

If this is your practice, i.e. if your use of pressors is limited to infusions on pump, I would consider getting comfortable with giving a mL at a time of phenylephrine from a 100 mcg/mL syringe (or norepi 5 mcg/mL, or vasopressin 1 U/mL, something in that ballpark of concentration).

Starting and titrating an infusion is just too slow to handle abrupt and predictable drops with inductions.

The things I'd have done differently than you did were
1) put in an arterial line first - there was time
2) give 100 mcg of phenylephrine before anything else, mainly to gauge what kind of dose response you get
3) use a smaller induction dose and chase it with another dose of phenylephrine - the rocuronium will keep him still, and critically ill octogenarians don't need much for amnesia

Agree with previous comments about PPV, Trendelenburg, permissive hypercarbia.
 
BLADEMDA said:
Sure, that's fine but how do you know what the BP will settle in at 30 minutes post intubation? That's why an arterial line is valuable because you can titrate the pressors to a real time BP value.

I like Ketafol myself in low doses (maybe 30 mg propofol and 50 mg of ketamine in this patient) combined with 200 ug of phenylephrine upfront via the IV. Still, I'd rest easier with an arterial line in place during the entire process.
Click to expand...

Much of the trend in the ICU has been towards minimalism (no swans, fewer lines, fewer labs, eliminating daily CXR and TID ABGs on stable vented patients, pigtails instead of 30fr chest tubes etc), but in many units (mostly of the medical variety) I think the pendulum has swung too far. This is a guy who is currently in shock with a high volume GI bleed and questionable respiratory status, has a lactate of 8, and is almost certainly going to need frequent labs for the next 24-48 hrs. Put in the a-line and ask questions later.
 
As better stated above. Give a bump of neo with induction as insurance. There is no free lunch no matter how you massage the meds. +/- aline depending on trajectory. I like that you didn't mess around with the roc dose and get that airway first look!
 
BLADEMDA said:
Sure, that's fine but how do you know what the BP will settle in at 30 minutes post intubation? That's why an arterial line is valuable because you can titrate the pressors to a real time BP value.

I like Ketafol myself in low doses (maybe 30 mg propofol and 50 mg of ketamine in this patient) combined with 200 ug of phenylephrine upfront via the IV. Still, I'd rest easier with an arterial line in place during the entire process.
Click to expand...

I don't, and I agree with you - pre induction art line is helpful.
in the unstable patient, induction is often one of the biggest physiological changes the patient goes through - so art line before induction makes sense to me.

oh - and in the setting of anaesthesia (not the OPs question), I'd recommend slowly adding volatile and running the lightest you can (... advice for the newbies).
 
EM->CCM here.

Quick a-line for second to second feedback with NGT to suction. Call for blood. Bolus now and have IVF running during induction. Make sure you have great (not good) IV access.

There's an argument that can be made for either succs or roc. I don't think that matters.

The induction med also mostly doesn't matter much. This old guy is begging to be unconscious. What matters is giving the appropriate dose of whatever you choose, understanding (and monitoring for) the physiologic response and being ready to treat for that.

I forget if I heard this from an anesthesiologist at my residency or on a podcast, but I found a lot of wisdom in this:

When asked why he was using propofol for a sick patient. He said that he uses propofol for 99% of his inductions. He knows it inside and out, upside down. A critically ill patient isn't where you want to get fancy. He knows exactly how much propofol it was going to take to put the patient down, exactly how soon his BP was going to dip and go what extent. He preimptively gave a squirt of neo and the patient had a rock solid induction.

Agree with above, push dose pressors are your friend. It would be nice to have the entirely hemodynamically neutral induction agent (I usually go etomidate), but the patient above is going to drop his pressure with 25mcg of fentanyl. You're not going to regret increasing your dose of paralytic of decreasing your dose of sedative. If a critically ill patient ever remembers induction, fine. This isn't an 8yo with an appy or healthy 65yo getting a total knee. This is life or death. Him living is primary, amnesia is secondary.

There's not a "right way" to induce this patient, there are, however, many wrong ways.
 
Typically very sick, hemodynamically unstable patients don't remember much of their ICU stay anyway. Acute, critical illness is a great amnestic.
As I'm discharging patients from the ICU, I like to ask them if they remember much from their stay in the ICU, especially the parts where they were at their sickest. Most don't remember much at all.
If I'm inducing a sick patient like this, I typically use very low dose Ketamine (0.3-0.5 mg/kg) +/- Midazolam and paralytics. I usually push my own meds, and always give 1-2 cc of dilute Norepi (6.4 mcg/mL here), which typically works very well.
Lots of good wisdom in this thread that applies not only to the ICU, but also very sick trauma patients or emergent surgeries.
The mistake I see most fellows/medicine people make is not having pressors available (sticks, not just bags hanging) and not having fluids being bolused (not just running at 999 on the pump). Gotta have a line ready to bolus whatever you need.
 
Two excellent points of solid advice.

TimesNewRoman said:
.....I forget if I heard this from an anesthesiologist at my residency or on a podcast, but I found a lot of wisdom in this:

When asked why he was using propofol for a sick patient. He said that he uses propofol for 99% of his inductions. He knows it inside and out, upside down. A critically ill patient isn't where you want to get fancy. He knows exactly how much propofol it was going to take to put the patient down, exactly how soon his BP was going to dip and go what extent. He preimptively gave a squirt of neo and the patient had a rock solid induction.

.....If a critically ill patient ever remembers induction, fine. This isn't an 8yo with an appy or healthy 65yo getting a total knee. This is life or death. Him living is primary, amnesia is secondary.

There's not a "right way" to induce this patient, there are, however, many wrong ways.
Click to expand...
 
sluggs said:
Thanks for feedback. I almost always have a neo syringe... this hospital had none! Should have mixed my own!
Click to expand...

Mixing your own pressors is usually frowned upon for non-anesthesiologists. I've heard it's a med-mal risk, although I don't have days to back that up.
 
Midazolam is the most stable induction.

Actually, maybe scopalamine, then midazolam.

Anyway, I read an article years ago - can't find it again (bummer...) - but it compared induction agents in critically ill patients between etomidate, propofol, and just sux.

Interestingly, post induction hypotension was the same for all three. In other words, it is quit possible (and NEVER discussed) that the metal in the mouth is the problem when patients are on the ropes.

I found this article very profound - and it echoes many comments, that propofol, used correctly, may not necessarily blamed for hypotension - and that other agents (etomidate, ketamine) can just as easily cause problems.

Soon, it won't be an issue when we all start using alfaxone.
 
A lot of great answers here so I'm not going to add much regarding the induction strategy here other than say that there is a great learning point about Ketamine for a lot of people including training Anesthesia residents etc;

When you think about Ketamine everyone can and will tell you; hemodynamically stable and psychological effects. Most can tell you why these things are true ( increased sympathetic outflow and dissociative mechanism respectively).

But the fact that Ketamine itself is a myocardial depressant and relies on sympathetic reserve for its stable cardiovascular profile is definitely under appreciated and can lead to problems when people reach for it thinking it'll keep them safe in scenarios like this. Other notables; Ketamine is a great bronchodilator that doesn't depress ventilatory drive (as a single agent) but comes at the expense of increased airway/respiratory secretions.

Great topic/conversation. Thank you.
 
Interesting discussion! As a med student, i have a couple questions:

In an old sick guy with baseline HR 70, do you worry about reflex bradycardia from giving phenylephrine?

What kind of HR depression would you expect after giving this guy 100mcg? What is the lowest HR can someone like this can tolerate?

Why not use something like Epi instead? Even though he's maxed out his catecholamine production, he'll still respond to exogenous catecholamines or sympathomimetics, right? To what extent does the coreg block this action?
 
Phenylephrine 100mcg will likely not drop his heart rate too severely (probably just to the 60s, although I have seen dips from 70s down to 40s very rarely, mostly in young pts). Dilute epi (8-10mcgs) would be another choice, but often not a go-to, as it's not always right at hand. My pharmacy gives us 10mL syringes of 100mcg/mL phenylephrine with a long shelf life, so we often have a few tossed into the code bag.
 
teacher2md said:
Why not use something like Epi instead?
Click to expand...

Dilute epi is an option but be mindful of the tachycardia it can produce. The last thing this 82 year old heart needs is to be flogged up to 140 bpm.

10 mcg boluses are a good starting place.
 
pgg said:
Dilute epi is an option but be mindful of the tachycardia it can produce. The last thing this 82 year old heart needs is to be flogged up to 140 bpm.

10 mcg boluses are a good starting place.
Click to expand...

Epi is acceptable but Vasopressin 1-2 units IV is a better choice because there is no tachycardia related to the IV push of the drug; epi at low doses 5-10 ug typically doesn't produce much tachycardia but may exhibit a weak response in this patient. Vasopressin, on the other hand, almost always gets the job done.
 
BLADEMDA said:
Epi is acceptable but Vasopressin 1-2 units IV is a better choice because there is no tachycardia related to the IV push of the drug; epi at low doses 5-10 ug typically doesn't produce much tachycardia but may exhibit a weak response in this patient. Vasopressin, on the other hand, almost always gets the job done.
Click to expand...

I don't disagree, although vasopressin has become very expensive. Not quite nitroprusside extreme expensive, but still in the $100s. I think the best option here is a hit of phenylephrine pre-induction to gauge what kind of dose response you get. Vasopressin available as a backup. I would expect phenylephrine to work in this patient. This guy is a bit behind metabolically (lactate 8) but his pH is normal (7.34). Plain old phenylephrine will likely get the job done.
 
This stuff used to be dirt cheap. Here is the vial I used to get for just a few dollars.
debbies-cardiac-meds-presentation-final-nn-70-728.jpg
 
Vasopressin Prices
Another drug to jump in price is vasopressin, a blood-vessel constricting agent used in emergencies. Vasostrict, a branded version approved last year and owned by Endo International Plc, costs $116 per milliliter wholesale, more than 10 times the wholesale price of unapproved versions three years ago, according to DRX.

Such increases are causing problems for hospitals. Johns Hopkins has set up a task force to identify which established drugs could be next in line for the FDA program.

Tenet Healthcare Corp., the fourth-largest U.S. operator with almost 500 treatment centers, says it’s started refrigerating vasopressin because that can increase its shelf-life to two years from less than 12 months, so it doesn’t have to replace the drug as often.

Vasostrict was developed by Par Pharmaceutical Holdings Inc., which was bought by Endo last month. Keri Mattox, senior vice president at Endo, said in an e-mail that Par “invested significant time and resources to demonstrate the safety and efficacy of its reformulated product.” The company’s reformulation of the drug "corrected key overage and necessary refrigeration attributes of the old unapproved product," she said.
 
BLADEMDA said:
Vasopressin Prices
Another drug to jump in price is vasopressin, a blood-vessel constricting agent used in emergencies. Vasostrict, a branded version approved last year and owned by Endo International Plc, costs $116 per milliliter wholesale, more than 10 times the wholesale price of unapproved versions three years ago, according to DRX.

Such increases are causing problems for hospitals. Johns Hopkins has set up a task force to identify which established drugs could be next in line for the FDA program.

Tenet Healthcare Corp., the fourth-largest U.S. operator with almost 500 treatment centers, says it’s started refrigerating vasopressin because that can increase its shelf-life to two years from less than 12 months, so it doesn’t have to replace the drug as often.

Vasostrict was developed by Par Pharmaceutical Holdings Inc., which was bought by Endo last month. Keri Mattox, senior vice president at Endo, said in an e-mail that Par “invested significant time and resources to demonstrate the safety and efficacy of its reformulated product.” The company’s reformulation of the drug "corrected key overage and necessary refrigeration attributes of the old unapproved product," she said.
Click to expand...

tl;dr version - the old formulation worked but we renamed it and pushed a few slapdash studies so we could charge more. Plus we spent a lot of effort on the vial color scheme...


Sent from my iPhone using SDN mobile
 
BLADEMDA said:
This stuff used to be dirt cheap. Here is the vial I used to get for just a few dollars.
debbies-cardiac-meds-presentation-final-nn-70-728.jpg
Click to expand...

Last I heard at my hospital, that little puppy there is $120 a vial, if not more, when it used to be dirt cheap. And I like the idea of a 100mcg phenylephrine chaser, noticed recently several of my uppers do that.
 
0kazak1 said:
Last I heard at my hospital, that little puppy there is $120 a vial, if not more, when it used to be dirt cheap. And I like the idea of a 100mcg phenylephrine chaser, noticed recently several of my uppers do that.
Click to expand...


What's the 100mcg of phenylephrine for here? If 100mcg of neo will do anything why are you pushing Vaso?
 
teacher2md said:
Interesting discussion! As a med student, i have a couple questions:
...
Why not use something like Epi instead? Even though he's maxed out his catecholamine production, he'll still respond to exogenous catecholamines or sympathomimetics, right? To what extent does the coreg block this action?
Click to expand...

good questions
problems with adrenaline (epi) are 1. as previously described -- tachycardia, and 2. it has an extremely short half life, so bolus doses tend to cause wild swings in BP
 
8-10 mcg boluses of epi are pretty safe in the elderly critically ill. The downside is the short duration of action, but these types of boluses are only for buying time, not definitive resolution of hypotension. The fact that it's hard to find a patient like this not on a beta blocker aside, these patients don't have the horse power to mount wild swings in HR and MAP from such modest doses.
 
drmwvr said:
8-10 mcg boluses of epi are pretty safe in the elderly critically ill. The downside is the short duration of action, but these types of boluses are only for buying time, not definitive resolution of hypotension. The fact that it's hard to find a patient like this not on a beta blocker aside, these patients don't have the horse power to mount wild swings in HR and MAP from such modest doses.
Click to expand...

IMHO (which is extensive) these patients may not respond as well to low dose Epi vs low dose vasopressin IV push. The BP response is more predictable with 1-2 units IV push of vasopressin than 5-10 ug of IV epi. That said, there is nothing wrong with using phenylephrine or Noreip IV push along with some low dose Epi if needed. But, if I could have just one drug in my pocket which needed to work immediately and reliably in all "near death" situations it would be vasopressin.
 
BLADEMDA said:
IMHO (which is extensive) these patients may not respond as well to low dose Epi vs low dose vasopressin IV push. The BP response is more predictable with 1-2 units IV push of vasopressin than 5-10 ug of IV epi. That said, there is nothing wrong with using phenylephrine or Noreip IV push along with some low dose Epi if needed. But, if I could have just one drug in my pocket which needed to work immediately and reliably in all "near death" situations it would be vasopressin.
Click to expand...
Your opinion is well received here, Blade.
BUT, it has been my experience that vasopressin is just another phenyleprine in this situation.
I like epi. These pts are catacholamine depleted. I give them a catacholamine.

Vasopressin like phenylephrine is a direct stimulant, unlike ephedrine which is an indirect stimulant (that's for the med students). Ephedrine would probably has the least effect in this pt since the pt is depleted of endogenous catachols.

Vasopressin stimulate V1 & V2 receptors causing vasoconstriction.
Phenylephrine stimulates smooth muscle alpha receptors causing vasoconstriction.
Epinephrine stimulate alpha and beta receptors resulting in vasoconstriction and myocardial contraction.
 
Although vasopressin has similar pressor actions to the catecholamines, it also has unique actions in reversing some of the pathologic vasodilatory processes that occur in advanced shock (which may be refractory to catecholamine vasopressors).

In some patients with vasodilated septic shock the pressor response to catecholamines may be markedly reduced91,92 while the response to vasopressin is markedly enhanced.

Human experience
Vasopressin has been successfully used in two case reports of refractory hypotension due to haemorrhage.17 The first patient had prolonged severe hypotension (systolic arterial pressure (SAP) ~50mmHg for > 1 hour) from variceal bleeding that was refractory to volume replacement, high dose noradrenaline and dopamine infusion. After 10 minutes of vasopressin infusion at 4uU/kg/min, their SAP was 160mmHg and the catecholamines had been ceased. In the second case, prolonged severe hypotension occurred after a gastric bleed in young adult with end-stage renal failure. This persisted despite transfusion to a CVP of 17mmHg and noradrenaline infusion, however after 10 minutes of vasopressin infusion at 1uU/kg/min their SAP rose from 70 to 130mmHg.

http://www.anaesthesia.med.usyd.edu.au/resources/lectures/pforrest/Vasopressin and shock.htm
 
Noyac said:
Your opinion is well received here, Blade.
BUT, it has been my experience that vasopressin is just another phenyleprine in this situation.
I like epi. These pts are catacholamine depleted. I give them a catacholamine.

Vasopressin like phenylephrine is a direct stimulant, unlike ephedrine which is an indirect stimulant (that's for the med students). Ephedrine would probably has the least effect in this pt since the pt is depleted of endogenous catachols.

Vasopressin stimulate V1 & V2 receptors causing vasoconstriction.
Phenylephrine stimulates smooth muscle alpha receptors causing vasoconstriction.
Epinephrine stimulate alpha and beta receptors resulting in vasoconstriction and myocardial contraction.
Click to expand...

I disagree completely and please see my previous post.
 
Vasopressin is well known to be effective in vasoplegic states, which is why it's expensive again (new indication for post CPB vasoplegia), but I'm not sure that generalizes to Vasopressin being the drug of choice in all hypotension/hypovolemia refractory to neo.

With that said, I think vaso is a decent choice in a hypovolemic actively hemorrhaging GI bleed if only for the splancnic vasoconstriction which may in fact serve two purposes here.
 
Our hospital P&T committee took Vasopressin out of the code boxes, they are over $250 per vial here. Still readily accessible via Suremeds, I think it would be a great choice but Neo/Epi works wonderfully for the sick patients I have encountered.
 
Robotic Wis-Hipple said:
What's the 100mcg of phenylephrine for here? If 100mcg of neo will do anything why are you pushing Vaso?
Click to expand...

Missed a paragraph break and had a little wild train of thought, but I meant a phenylephrine chaser during induction, not after vaso. Sometimes by the time I have vaso in my hands (not in my backstand/ in OR Pyxis, have to ask a tech to go to the pharmacy and grab a stick), patient has gotten at least 1000mcg of phenylephrine and possibly some ephedrine.
 
BLADEMDA said:
Although vasopressin has similar pressor actions to the catecholamines, it also has unique actions in reversing some of the pathologic vasodilatory processes that occur in advanced shock (which may be refractory to catecholamine vasopressors).

In some patients with vasodilated septic shock the pressor response to catecholamines may be markedly reduced91,92 while the response to vasopressin is markedly enhanced.

Human experience
Vasopressin has been successfully used in two case reports of refractory hypotension due to haemorrhage.17 The first patient had prolonged severe hypotension (systolic arterial pressure (SAP) ~50mmHg for > 1 hour) from variceal bleeding that was refractory to volume replacement, high dose noradrenaline and dopamine infusion. After 10 minutes of vasopressin infusion at 4uU/kg/min, their SAP was 160mmHg and the catecholamines had been ceased. In the second case, prolonged severe hypotension occurred after a gastric bleed in young adult with end-stage renal failure. This persisted despite transfusion to a CVP of 17mmHg and noradrenaline infusion, however after 10 minutes of vasopressin infusion at 1uU/kg/min their SAP rose from 70 to 130mmHg.

http://www.anaesthesia.med.usyd.edu.au/resources/lectures/pforrest/Vasopressin and shock.htm
Click to expand...
So I now have had some time to look at your post. I will agree that vasopressin is a valuable tool in shock states. I hope I never gave you the impression that I thought it wasn't. But I believe we are discussing two different scenarios. One is the vasopressin infusion which your references are looking at in these cases. I am very familiar with this use of vasopressin and it is an impressive adjunct to the care of these pts. The other scenario however, is the one when we try to induce a hypovolemic hypotensive pt in the ICU. As quoted from your link, " However in vivo, vasopressin decreases cardiac output in patients with normal hearts or mild heart failure, presumably as a reflex response to an increase in SVR.41,42 High dose vasopressin decreases cardiac output by producing coronary vasoconstriction." So when we are pushing an induction agent (ketamine in this case) we are creating a situation of cardiac depression. My contention is that I believe epinephrine is a better choice in this situation. I would then start a vasopressin infusion to follow.
 
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