Moments from call

[G-Man82]

The combination of norepi + milrinone actually works really well and is my usual go-to in known cardiac cripples. I'll usually start norepi first. If an echo then shows that their LV (and definitely RV) needs some assistance I'll usually go with milrinone next if the BP is ok or consider epi or dobutamine next. Lactate, urine output, venous pH and oxygen saturation, and if you have it you could also do tissue oximetry (Sto2 - assess micro circulation). It's not always about the numbers, but about the whole clinical situation.

If I had to choose one drug in the world for anesthesia or CCM to take with me to a deserted island .... Norepinephrine it is.


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[deleted171991]

This applies to Dobutamine more than Milrinone, but yes adding a medication that causes peripheral vascular constriction could help decrease the reflex tachycardia caused by the vasodilation of Milrinone.
But wouldn't you want to do both simultaneously? a positive inotrope and a vasoconstrictor?

You are right; I would. I would try to keep the balance, in order not to overwhelm the heart.

What I want to point out is that, in intensive hemodynamic care, there are few golden solutions. It's mostly trial and error, with periodic (re)evaluation. I love that they have the Evaluate-Identify-Intervene cycle in PALS, because that's exactly what somebody should do continuously in a critical situation. And it's exactly what many physicians are not trained to do. They try one thing, then they walk away for hours, then maybe come back to bedside when the patient crashes or the nurse calls, but by then the harm is already done.

 

[deleted171991]

On of my favorite call cases this year was a sweet fragile 90 year-old who had a leg cellulitis. She had a history of significant CHF, especially right-sided (if I remember well).

They initially fluid-overloaded her nicely on the floor then, when her heart failed (cold extremities, midly hypoxemic on room air, SBP of 70, and of course the lactate went up from systemic hypoperfusion), the cardiac fellow declared that she must be septic. I admitted her to the ICU for the "this patient needs a real doctor" reason. All she got from us was lasix and like 5-10 mcg/min of phenylephrine (aiming for her home BP), on top of the same antibiotics. Turned around overnight, but was kept her longer for the same reason. It was just textbook bad judgment and knee-jerk medicine before us.

 

[deleted171991]

The question is: if an inotrope does not cause tachycardia or if the tachycardia is somehow suppressed does it really improve the cardiac output in a clinically meaningful way?
I mean is the whole class of inotropes useless?

I would say that an inotrope helps, as long as it's judiciously titrated. That applies to most cardiovascular ICU medications, by the way, and that's the reason we like to combine stuff pretty early, to take advantage of the fewer side effects at low-dose for each medication, while achieving a better outcome.

 

[Planktonmd]

You are right; I would. I would try to keep the balance, in order not to overwhelm the heart.

What I want to point out is that, in intensive hemodynamic care, there are few golden solutions. It's mostly trial and error, with periodic (re)evaluation. I love that they have the Evaluate-Identify-Intervene cycle in PALS, because that's exactly what somebody should do continuously in a critical situation. And it's exactly what many physicians are not trained to do. They try one thing, then they walk away for hours, then maybe come back to bedside when the patient crashes or the nurse calls, but by then the harm is already done.

Evaluate - identify - intervene is the essence of the practice of medicine, regardless of specialty, but unfortunately here in the good old U.S. it's not taught, and people are instead told to try to fit the patient into a prefabricated scenario so the prefabricated protocol would apply, people are trained to be more robots and less physicians with critical thinking!

 

[Planktonmd]

I would say that an inotrope helps, as long as it's judiciously titrated. That applies to most cardiovascular ICU medications, by the way, and that's the reason we like to combine stuff pretty early, to take advantage of the fewer side effects at low-dose for each medication, while achieving a better outcome.

My question is: Can an inotrope be an inotrope if no increase of the heart rate is triggered?

 

[deleted171991]

Evaluate - identify - intervene is the essence of the practice of medicine, regardless of specialty, but unfortunately here in the good old U.S. it's not taught, and people are instead told to try to fit the patient into a prefabricated scenario so the prefabricated protocol would apply, people are trained to be more robots and less physicians with critical thinking!

The problem is that many specialties are used to one, maybe two cycles per day, when they round, while ICU patients might need even multiple cycles per hour, occasionally. And that's something few people (are trained to) do.

 

[deleted171991]

My question is: Can an inotrope be an inotrope if no increase of the heart rate is triggered?

If you mean milrinone/dobutamine, I don't know. But I don't care if the heart rate goes up a bit, as long as it stays under 100. Obviously, the lower the better.

If the heart rate goes up a lot, probably much of the increase in cardiac output is coming from the increased HR (chronotropy), not the SV (inotropy), which means that the inotropic medication should be dialed down, because we are shooting ourselves in the leg. And that's exactly what pisses me off when I see it.

 

[Planktonmd]

If you mean milrinone/dobutamine, I don't know. But I don't care if the heart rate goes up a bit, as long as it stays under 100. Obviously, the lower the better.

If the heart rate goes up a lot, probably much of the increase in cardiac output is coming from the increased HR (chronotropy), not the SV (inotropy), which means that the inotropic medication should be dialed down, because we are shooting ourselves in the leg. And that's exactly what pisses me off when I see it.

That's my point... if we take away chronotropy do these intropes continue to be inotropes?

 

[deleted171991]

That's my point... if we take away chronotropy do these intropes continue to be inotropes?

Most of them are both positive inotropes AND chronotropes, not just chronotropes. Meaning that the increase in cardiac output is not due only to the increase in heart rate, but also to an increase in contractility, i.e. stroke volume.

 

[Planktonmd]

Most of them are both positive inotropes AND chronotropes, not just chronotropes. Meaning that the increase in cardiac output is not due only to the increase in heart rate, but also to an increase in contractility, i.e. stroke volume.

That's what we are told but is that clinically relevant?

 

[deleted171991]

That's what we are told but is that clinically relevant?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC423546/pdf/jcinvest00119-0335.pdf

I would say that getting a 30% increase in stroke volume index (21 to 27) with barely any increase in heart rate (92 to 94) is clinically relevant.

 

[deleted171991]

2016 ESC (European) Guidelines for the diagnosis and treatment of acute and chronic heart failure

This is in the early phase:

And this is about cardiogenic shock:

"12.3.4 Management of patients with cardiogenic shock
Cardiogenic shock is defined as hypotension (SBP <90 mmHg) despite adequate filling status with signs of hypoperfusion (Table 12.2). The pathogenetic scenarios of cardiogenic shock range from low-output advanced end-stage chronic HF to acute-onset de novo cardiogenic shock most often caused by STEMI, but also by various aetiologies other than ACS. A patient in cardiogenic shock should undergo immediate comprehensive assessment. ECG and echocardiography are required immediately in all patients with suspected cardiogenic shock. In patients with cardiogenic shock complicating ACS, an immediate coronary angiography is recommended (within 2 h from hospital admission) with an intent to perform coronary revascularization.114,535 Invasive monitoring with an arterial line should be also considered.

There is no agreement on the optimal method of haemodynamic monitoring in assessing and treating patients in cardiogenic shock, including pulmonary artery catheterization.

Pharmacologic therapy aims to improve organ perfusion by increasing cardiac output and blood pressure. After fluid challenge, pharmacologic management consists of an inotropic agent and a vasopressor as needed. Treatment is guided by the continuous monitoring of organ perfusion and haemodynamics. Pulmonary artery catheterization may be considered. As a vasopressor, norepinephrine is recommended when mean arterial pressure needs pharmacologic support. Dobutamine is the most commonly used adrenergic inotrope. Levosimendan may also be used in combination with a vasopressor.582,583 Levosimendan infusion in cardiogenic shock following AMI on top of dobutamine and norepinephrine improved cardiovascular haemodynamics without leading to hypotension.582,583 PDE3 inhibitors may be another option, especially in non-ischaemic patients.561,584

However, rather than combining several inotropes, device therapy has to be considered when there is an inadequate response. Recently the IABP-SHOCK II trial showed that the use of an IABP did not improve outcomes in patients suffering from AMI and cardiogenic shock.585,586 Therefore, routine use of an IABP cannot be recommended."

 

[vector2]

I like the wording... an arterial line "should be also considered" ...I wonder if that's why an a-line is considered optional on the CCU for pts in decompensated cardiogenic shock.

 

[pgg]

My question is: Can an inotrope be an inotrope if no increase of the heart rate is triggered?

Calcium? (Obviously not as an infusion.)

 

[ranvier]

I learned alot titrating in real time (tte in the icu) tee in the OR.

 

[IkeBoy18]

On of my favorite call cases this year was a sweet fragile 90 year-old who had a leg cellulitis. She had a history of significant CHF, especially right-sided (if I remember well).

They initially fluid-overloaded her nicely on the floor then, when her heart failed (cold extremities, midly hypoxemic on room air, SBP of 70, and of course the lactate went up from systemic hypoperfusion), the cardiac fellow declared that she must be septic. I admitted her to the ICU for the "this patient needs a real doctor" reason. All she got from us was lasix and like 5-10 mcg/min of phenylephrine (aiming for her home BP), on top of the same antibiotics. Turned around overnight, but was kept her longer for the same reason. It was just textbook bad judgment and knee-jerk medicine before us.

Since this woman is 90, and there's always a chance it couldve been sepsis, if she didnt turn around overnight would there have been a good reason to not start abx since at that point getting ahead of the sepsis 12-24 hours later would be that much more difficult in an old lady?

Im not questioning mgmt at all, this is asked with all due respect, just a pgy1 trying to learn here.

 

[G-Man82]

I think not starting antibiotics in a 90 year-old lady with cellulitis and hypotension would be pretty ballsy. The issue in this case is not so much the initiation of broad spectrum antibiotics and the usual sepsis care, but that a lot of people (non-intensivists mostly) still equate sepsis with "give a lot of fluid." Older intensivists still think like this, too. I had a Pulmonologist in fellowship tell me that in sepsis you give "enough fluid that it comes up the ETT." The push these days aside from early recognition is to actually limit fluids somewhat and initiate vasopressors sooner rather than later. Norepinephrine would have been good in her case because it would increase MAP and also squeeze (assist) the RV (and LV). Now sepsis and septic shock would still be more common in her (given a source of infection) than cardiogenic shock. But you can tip someone her age over the edge very easily. Septic and cardiogenic shock don't do well together.


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[IkeBoy18]

I think not starting antibiotics in a 90 year-old lady with cellulitis and hypotension would be pretty ballsy. The issue in this case is not so much the initiation of broad spectrum antibiotics and the usual sepsis care, but that a lot of people (non-intensivists mostly) still equate sepsis with "give a lot of fluid." Older intensivists still think like this, too. I had a Pulmonologist in fellowship tell me that in sepsis you give "enough fluid that it comes up the ETT." The push these days aside from early recognition is to actually limit fluids somewhat and initiate vasopressors sooner rather than later. Norepinephrine would have been good in her case because it would increase MAP and also squeeze (assist) the RV (and LV). Now sepsis and septic shock would still be more common in her (given a source of infection) than cardiogenic shock. But you can tip someone her age over the edge very easily. Septic and cardiogenic shock don't do well together.


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Thanks for the reply. Actually, after going back and rereading the original post, FFP says "on top of the same antibiotics." The first time I read it, I missed that part, and thought they just gave pressors and she turned around.

 

[fakin' the funk]

... periodic (re)evaluation. I love that they have the Evaluate-Identify-Intervene cycle in PALS, because that's exactly what somebody should do continuously in a critical situation. And it's exactly what many physicians are not trained to do. They try one thing, then they walk away for hours, then maybe come back to bedside when the patient crashes or the nurse calls

Agree with you big time here. Most non-anesthesiology trainees on ICU rotations (MICU, SICU, CVICU) aren't doing constant reevaluation and changing of their interventions. Especially medicine residents, who seem to think that medical care itself consists of computer order entry with q4hr (max) reevaluation. They don't get the fact that in an ICU you are almost always constantly rounding and re-rounding. In a CT surgery ICU this is particularly pertinent.

One of my attendings liked to say, being in the ICU is like being a shark -- never stop swimming.

 

[deleted171991]

Since this woman is 90, and there's always a chance it couldve been sepsis, if she didnt turn around overnight would there have been a good reason to not start abx since at that point getting ahead of the sepsis 12-24 hours later would be that much more difficult in an old lady?

Im not questioning mgmt at all, this is asked with all due respect, just a pgy1 trying to learn here.

She was already on antibiotics for cellulitis, and they were working. AFAIR, we did not feel the need to broaden them, because she just did not look septic to us. Tachycardia and hypotension, and even SIRS (which is now obsolete for sepsis purposes) don't necessarily mean sepsis or septic shock. (Many times I am called to some dehydrated patient in "SIRS".)

You are perfectly right. This is the kind of patient where you go in with your guns blazing, covering every single possibility at first. Except that I was so convinced it was fluid overload leading to CHF exacerbation that I didn't risk a C Diff in her. (First do no harm.) I must have put an echo probe on her heart and lungs.

Btw, I did not just order this stuff and walked away. We basically round on our (possibly) sick patients frequently, until we get convinced they are stable. So we watched her the first night, and it was clear after a few hours that all she needed was diuresis and tender loving care. She had excellent mentation throughout, so she was our best indicator that things were going the right way (or not). Also, her home baseline SBP was around 90, so 70 wasn't that impressive to me. Plus the fact that she maintained 90 with only 5-10 mcg/min of phenylephrine virtually excluded septic shock. (I gave pressor because I wanted her SBP to be close to her usual, given the significant RV failure, plus I was diuresing her.)

 

[Cytarabine]

You might, but you start with the pressor, and keep in mind that the inotrope (while fixing the numbers) will squeeze your heart like a diuretic the kidney. We don't give diuretics in AKI, do we? So we should watch the inotrope and the heart like a hawk.

The idea is that the inotrope should be an adjunct, not the first line. I want to optimize that Starling curve, not overwhelm the heart. As with most stuff in critical care, it ends up with a little bit of this and a little bit of that; using medications at doses where one takes advantage of their therapeutical effects with minimal side effects.

It just drives me crazy to see patients on milrinone-only with heart rates of 130-150 for days.

Not to derail the discussion I'm enjoying reading, but with regard to the bolded, on nephro we slammed monster doses of loops in AKI all the time both for prognostication and fluid management. You avoid an acei obviously in a renovascular etiology, but could you elaborate on the bolded?

 

[PainDrain]

Not to derail the discussion I'm enjoying reading, but with regard to the bolded, on nephro we slammed monster doses of loops in AKI all the time both for prognostication and fluid management. You avoid an acei obviously in a renovascular etiology, but could you elaborate on the bolded?

What decade was this in? 1970s???

 

[GravelRider]

Not to derail the discussion I'm enjoying reading, but with regard to the bolded, on nephro we slammed monster doses of loops in AKI all the time both for prognostication and fluid management. You avoid an acei obviously in a renovascular etiology, but could you elaborate on the bolded?

The thinking was that it converts oliguric renal failure to non-oliguric and that it helped to decompress the nephron to improve blood flow and this improve renal tissue oxygen supply and demand. I don't think there has been any study to show an improvement in morbidity and mortality with using loop diuretics, but it may decrease the need for or time on renal replacement therapy. If used, a lasix drip is better than huge boluses.

 

[Planktonmd]

The thinking was that it converts oliguric renal failure to non-oliguric and that it helped to decompress the nephron to improve blood flow and this improve renal tissue oxygen supply and demand. I don't think there has been any study to show an improvement in morbidity and mortality with using loop diuretics, but it may decrease the need for or time on renal replacement therapy. If used, a lasix drip is better than huge boluses.

When the kidneys are close to the end of the road due to chronic kidney disease, adding high doses of loop diuretics will buy you some time before dialysis.
It does not change the inevitable need for kidney replacement therapy it just delays it a little.
Actually there is some evidence that Diuretics could be helpful in patients on dialysis who still have some residual renal function:
http://www.ncbi.nlm.nih.gov/pubmed/17336704
This is not true when the renal failure is acute and secondary to other reversible etiology like in the case of renal failure secondary to heart failure or hypo perfusion in general.

 

[deleted171991]

What decade was this in? 1970s???

That would have been my question, too,

AFAIK, there is no proof that non-oliguric AKI is better than oliguric, as in that diuretics help. This is why the "renal dose" of dopamine has fallen out of favor. Everywhere where I trained, people stop using diuretics when the creatinine starts going up.

This is what Uptodate says:

"Diuretics, particularly high doses of loop diuretics, are frequently administered to patients with AKI. This is done in part in an attempt to convert oliguric to nonoliguric AKI.

Among patients with established renal failure, a variety of studies, including two randomized trials, have found that diuretics augment urine output, but do not have an effect upon renal and patient survival [65,219-222].

The best-designed and largest study found that high-dose furosemide maintained urine output, but had no effect upon renal and patient survival [219]. In this trial, 388 patients with established AKI requiring dialysis were randomly assigned to furosemide or placebo. Furosemide was administered at a dose of 25 mg/kg per day intravenously (IV; maximum of 2 g/day, given over four to six hours) or 35 mg/kg per day orally (maximum of 2.5 g/day). The use of furosemide was significantly associated with a decreased time to a 2 L/day diuresis (5.7 versus 7.8 days), as well as an increased likelihood of obtaining such a diuresis (57 versus 33 percent). Despite the increase in urine output, there were no differences between the two groups in terms of patient survival, renal recovery rates, number of dialysis sessions required, and time on dialysis.

A similar lack of benefit on these hard endpoints with furosemide in established ATN was noted in an earlier trial, in which high-dose diuretic therapy (3 g/day) led, in a few patients, to hearing loss that can be permanent [220].

The dissociation between increasing the urine output and not affecting the course of ATN with diuretic therapy in these trials probably reflects the ability of the diuretic to enhance the urine output in those few nephrons that are still functioning. However, since there is little recruitment of previously nonfunctioning nephrons, there is no effect on the course of the renal failure.

Summary — We agree with the 2012 Kidney Disease: Improving Global Outcomes (KDIGO) guidelines that suggest that diuretics not be used to treat AKI, except in the management of volume overload [140]. They can be given for a short length of time for volume control, but such use should not postpone the initiation of dialysis (if required) [223]. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Recovery of renal function and effect of hemodialysis membrane", section on 'Supportive management' and "Renal replacement therapy (dialysis) in acute kidney injury in adults: Indications, timing, and dialysis dose", section on 'Indications for and timing of initiation of dialysis'.)"

 

[PainDrain]

I was always taught that a rising Cr meant to stop the diuretic. I still have had old school surgeons ask for lasix due to "poor urine output" but this just helps them sleep at night and is actually detrimental to the patient. If it's a matter of volume overload in AKI then start CVVH/HD; don't kill the remaining nephrons with diuretics.

 

[GravelRider]

I was always taught that a rising Cr meant to stop the diuretic. I still have had old school surgeons ask for lasix due to "poor urine output" but this just helps them sleep at night and is actually detrimental to the patient. If it's a matter of volume overload in AKI then start CVVH/HD; don't kill the remaining nephrons with diuretics.

Post-op oliguria is most likely hypovolemia. Lasix + hypovolemia = bad. However, there would be certain situations where a rising creatinine MAY call for Lasix...low output heart failure, for instance. Giving Lasix in renal failure is a pretty nuanced decision that should be done under the guidance of a good nephrologist.

 

[deleted171991]

Post-op oliguria is most likely hypovolemia. Lasix + hypovolemia = bad. However, there would be certain situations where a rising creatinine MAY call for Lasix...low output heart failure, for instance. Giving Lasix in renal failure is a pretty nuanced decision that should be done under the guidance of a good nephrologist.

To quote Marik, Lasix (in the ICU) is the devil's medicine. I tend to agree, most of the time.

 

[Cytarabine]

This was certainly not in the 70s, and was with different big name nephrologists

Summary — We agree with the 2012 Kidney Disease: Improving Global Outcomes (KDIGO) guidelines that suggest that diuretics not be used to treat AKI, except in the management of volume overload [140]. They can be given for a short length of time for volume control, but such use should not postpone the initiation of dialysis (if required) [223]. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Recovery of renal function and effect of hemodialysis membrane", section on 'Supportive management' and "Renal replacement therapy (dialysis) in acute kidney injury in adults: Indications, timing, and dialysis dose", section on 'Indications for and timing of initiation of dialysis'.)"

Snipped away a lot of your post, if you feel it's relevant feel free to redirect me to it, but the bit I quoted is the crux of what we did. I'm not seeing where anything posted says to avoid diuretics in aki, merely that they don't alter the course of aki (true). Kdigo specifically offers diuretics as treatment for volume overload in aki. While the evidence hasn't shown them to alter outcomes, physiologically it makes sense that if you have a patient on the brink of needing renal replacement for volume overload but they're still diuretic-responsive, you've bought the kidneys more time on their path to self recovery and potentially avoided RRT.

As far as prognostically - http://www.ncbi.nlm.nih.gov/pubmed/25655065

 

[deleted171991]

Except as a hail Mary for volume overload in AKI, there is no indication for diuretics. Especially since they can give deafness.

"While the evidence hasn't shown them to alter outcomes, physiologically it makes sense that if you have a patient on the brink of needing renal replacement for volume overload but they're still diuretic-responsive, you've bought the kidneys more time on their path to self recovery and potentially avoided RRT."

Those are old theories (that led to the renal dose of dopamine), never proven. It simply doesn't work that way. You are opening up some channels in the remaining healthy tubules, but you are not really buying that much time. Especially because you are not excreting enough physiologic waste (hence the rise in creatinine). That's why there is no change in outcome. Also I don't see how I am helping the recovery of an organ by overworking the remaining healthy parts.

http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO AKI Guideline.pdf , Chapter 3.4 and Summary:

"Epidemiologic data have suggested that the use of loop diuretics may increase mortality in patients with critical illness and AKI, along with conflicting data that suggest no harm in AKI. Finally, furosemide therapy was also ineffective and possibly harmful when used to treat AKI."

"RESEARCH RECOMMENDATION - Given the potential to mitigate fluid overload but also to worsen renal function and possibly cause kidney injury, further study is required to clarify the safety of loop diuretics in the management of patients with AKI."

"3.4.1: We recommend not using diuretics to prevent AKI. (1B)
3.4.2: We suggest not using diuretics to treat AKI, except in the management of volume overload. (2C)
3.5.1: We recommend not using low-dose dopamine to prevent or treat AKI. (1A)"

 

[Cytarabine]

Except as a hail Mary for volume overload in AKI, there is no indication for diuretics. Especially since they can give deafness.


Those are old theories (that led to the renal dose of dopamine), never proven. It simply doesn't work that way. You are opening up some channels in the remaining healthy tubules, but you are not really buying that much time. Especially because you are not excreting enough physiologic waste (hence the rise in creatinine). That's why there is no change in outcome.

Also I don't see how I am helping the recovery of an organ by overworking the remaining healthy parts.

I'm aware of the old theory on diuretics in aki, and that's not what I'm getting at. My argument wasn't "use diuretics in aki", it's that there isn't a reason not to use them in diuretic-responsive aki when concerned about fluid overload. I've seen that misconstrued into "avoid diuretics in aki". All you're doing with diuresis is improving your volume status. With volume overload being an indication for RRT and with aki being a self limited condition (barring progression to esrd and the nuance of other chronic damage to the kidney), if you put off RRT by whatever means you've theoretically put yourself a day further toward renal recovery. As far as a hail Mary, well, yea, it is to the extent in that you're throwing it to avoid dropping a line, which has its own issues and is particularly meaningful in ckd patients on the road to esrd where lines can mess up future access (though the risk of an IJ is fairly low). With regard to "stressing functioning nephrons" with a loop, I'm not sure how inhibiting a transporter is supposed to do so physiologically and I'm not aware of evidence they do so

 

[Consigliere]

Man you guys got a lot of free time on your hands.

 

[G-Man82]

It's great! It's like critical care rounds with an interested party. I think anesthesiologists are great in the ICU, but tell that to my residents. They have a countdown to when they're done with this rotation. Most of them just have no interest and would rather be in the OR. I don't blame them; the ICU is more work and being a resident in the unit is so vastly different from being and attending or fellow in critical care.


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[ranvier]

These discussions are like shooting the breeze with your favorite smart attending.

 

[Planktonmd]

Man you guys got a lot of free time on your hands.

Now some CRNA is going to see this post and quote it saying: See... those rich bastards have plenty of free time and they hardly ever do anything!

 

[Consigliere]

Now some CRNA is going to see this post and quote it saying: See... those rich bastards have plenty of free time and they hardly ever do anything!

 

[polar403]

Pt rushed to OR for worsening shock on multiple pressors. I remove the clonidine patch on his shoulder. He did well after three liters of blood removed from his abdomen. "It was a home medication."

Permissive hypotension? Imagine the blood loss with rebound hypertension... The horror!

 

[ranvier]

It was actually arterial bleeding and he did well with fluids and a map of 50. Once the map goal went to 70 he likely popped the clot and bled more needing more pressors and round and round that went all night until OR in am.

Maybe the clonidine offered some decrease in sympathetic tone.

Sometimes intensive care just isn't that intense!

 

[Laryngophed]

My question is: Can an inotrope be an inotrope if no increase of the heart rate is triggered?

Yeah, it just isn't a chronotrope.

 

[Laryngophed]

Calcium? (Obviously not as an infusion.)

Digoxin?

 

[rakotomazoto]

It would be funny if it weren't sad: http://journal.publications.chestnet.org/data/Journals/CHEST/21722/1129.pdf

This was a great read, thanks for sharing.

 

[ranvier]

I do think that a whiff of lasix during a long robotic/laparoscopic case is reasonable as I believe mild siadh can occur. This isn't a hypovolemic situation and I'm talking 2.5 mg or so. Big boluses in ARF, not good.

 

[confusingleaf]

related to the inotrope conversation...on wednesday did 3V cabg on a sick lady (but only 62)....had arrested out of hospital and shocked multiple times before getting to ER, shocked in ER, cooling protocol, intubated a couple weeks, pneumonia, etc etc etc. At any rate, the got extubated and they deemed her healthy enough for surgery. Starts surgery at EF of roughtly 30%, valves OK. my sphincter was tight but we ended up coming off pump on only milrinone and epi along with a pacer (though the function was still about 30--no real noticeable difference immediately after revascularization). fast forward to thursday, she's extubated, they wean her epi off and she has a couple hypotensive episodes (80s-90s systolic)....so someone puts her on levophed. she is off and on the levophed, low dose (4 or so) for a few hours. UOP remains low, , intermittent hypotension, i think nobody recognizes that she's teetering on the edge. overnight coverage (SICU resident covers our CTICU at night) gets called about low UOP and fluid challenges her twice, once with 250 and once with 500 albumin, no response. Then in the middle of the night she dumps and the levophed goes up to 20. When the surgical team gets there in the morning she is basically circling the drain. They intubate, she arrests with the meds, they crack the chest and she dies.

i just heard about all this after the fact as i was in OR with an ascending aortic aneurysm repair. one of those cases where i wonder when and how much the attending was notified and secures my belief that CTICU really needs dedicated overnight coverage, not cross coverage from a SICU resident that isn't skilled at dealing with cardiac patients or titrating pressors/inotropes.

 

[ranvier]

related to the inotrope conversation...on wednesday did 3V cabg on a sick lady (but only 62)....had arrested out of hospital and shocked multiple times before getting to ER, shocked in ER, cooling protocol, intubated a couple weeks, pneumonia, etc etc etc. At any rate, the got extubated and they deemed her healthy enough for surgery. Starts surgery at EF of roughtly 30%, valves OK. my sphincter was tight but we ended up coming off pump on only milrinone and epi along with a pacer (though the function was still about 30--no real noticeable difference immediately after revascularization). fast forward to thursday, she's extubated, they wean her epi off and she has a couple hypotensive episodes (80s-90s systolic)....so someone puts her on levophed. she is off and on the levophed, low dose (4 or so) for a few hours. UOP remains low, , intermittent hypotension, i think nobody recognizes that she's teetering on the edge. overnight coverage (SICU resident covers our CTICU at night) gets called about low UOP and fluid challenges her twice, once with 250 and once with 500 albumin, no response. Then in the middle of the night she dumps and the levophed goes up to 20. When the surgical team gets there in the morning she is basically circling the drain. They intubate, she arrests with the meds, they crack the chest and she dies.

i just heard about all this after the fact as i was in OR with an ascending aortic aneurysm repair. one of those cases where i wonder when and how much the attending was notified and secures my belief that CTICU really needs dedicated overnight coverage, not cross coverage from a SICU resident that isn't skilled at dealing with cardiac patients or titrating pressors/inotropes.

I'm sorry. Sometimes it's too easy to second guess in the morning but I wonder if anybody put a TTE on her at any point and what they used to intubate/induce.

You got her through a big surgery and 62 is not that old.

Why not put her back on the last gtt that helped her...epi!

 

[Hoya11]

related to the inotrope conversation...on wednesday did 3V cabg on a sick lady (but only 62)....had arrested out of hospital and shocked multiple times before getting to ER, shocked in ER, cooling protocol, intubated a couple weeks, pneumonia, etc etc etc. At any rate, the got extubated and they deemed her healthy enough for surgery. Starts surgery at EF of roughtly 30%, valves OK. my sphincter was tight but we ended up coming off pump on only milrinone and epi along with a pacer (though the function was still about 30--no real noticeable difference immediately after revascularization). fast forward to thursday, she's extubated, they wean her epi off and she has a couple hypotensive episodes (80s-90s systolic)....so someone puts her on levophed. she is off and on the levophed, low dose (4 or so) for a few hours. UOP remains low, , intermittent hypotension, i think nobody recognizes that she's teetering on the edge. overnight coverage (SICU resident covers our CTICU at night) gets called about low UOP and fluid challenges her twice, once with 250 and once with 500 albumin, no response. Then in the middle of the night she dumps and the levophed goes up to 20. When the surgical team gets there in the morning she is basically circling the drain. They intubate, she arrests with the meds, they crack the chest and she dies.

i just heard about all this after the fact as i was in OR with an ascending aortic aneurysm repair. one of those cases where i wonder when and how much the attending was notified and secures my belief that CTICU really needs dedicated overnight coverage, not cross coverage from a SICU resident that isn't skilled at dealing with cardiac patients or titrating pressors/inotropes.

I dont think it was the albumin or the change in pressors. Some people crump. Bad outcomes hurt. But they still may not have been prevented on even the most well managed unit with the most senior staff on 24/7. This lady was teetering ever since being uncooled. She couldnt get through the case. She died then instead of 2 week, 2 months from then... If your body is THAT sensitive that 750ml of albumin and a change from epi to norepi kills you, you are not going to make it.

 

[BLADEMDA]

http://www.surgicalcriticalcare.net/Guidelines/Vasopressors and Inotropes in Shock.pdf

I see this stuff all the time in my practice (unfortunately). My patient population is older and sicker than most in the USA.

 

[BLADEMDA]

I am posting a link to an excellent review article on Cardiogenic shock and its treatment. I enjoyed reading it.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4495097/


In analogy to septic shock, the target mean arterial pressure should be titrated to 65–70 mmHg, as a higher blood pressure is not associated with beneficial outcome with the exception of previously hypertensive patients.

• 2-
  Norepinephrine should be used to restore perfusion pressure during cardiogenic shock (strong agreement).

The only randomized study comparing two types of vasopressors—norepinephrine and epinephrine—showed that, for the same hemodynamic efficacy, epinephrine was associated with a higher heart rate, more arrhythmia, and lactic acidosis [11]. In a cohort study, De Backer et al. reported a reduction in mortality with norepinephrine when compared with dopamine [12]. Lastly, norepinephrine-induced increase in blood pressure in patients with post-MI CS is associated with an increase in cardiac index without an increase in heart rate and with increased SvO2 and reduced blood lactate [13].

• 3-
  Epinephrine can be a therapeutic alternative to the combination of dobutamine and norepinephrine, but is associated with a greater risk of arrhythmia, tachycardia, and hyperlactatemia (weak agreement).

In terms of hemodynamic effect, epinephrine clearly increases cardiac output, essentially by a heart rate effect, but is associated with severe hyperlactatemia of metabolic origin that hampers interpretation of lactate as a marker of the adequacy of tissue perfusion [14].

• 4-
  Dobutamine should be used to treat low cardiac output in cardiogenic shock (strong agreement).

 

[BLADEMDA]

The combination of norepi + milrinone actually works really well and is my usual go-to in known cardiac cripples. I'll usually start norepi first. If an echo then shows that their LV (and definitely RV) needs some assistance I'll usually go with milrinone next if the BP is ok or consider epi or dobutamine next. Lactate, urine output, venous pH and oxygen saturation, and if you have it you could also do tissue oximetry (Sto2 - assess micro circulation). It's not always about the numbers, but about the whole clinical situation.

If I had to choose one drug in the world for anesthesia or CCM to take with me to a deserted island .... Norepinephrine it is.


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Nice post. I agree with you about Norepi as the first choice but perhaps Try Dobutamine as the second pressor of choice in cardiac cripples. Yes, HR and oxygen demand will go up so I can see how Milrinone would be reasonable if the BP and SVR are in the acceptable ranges.

• Phosphodiesterase inhibitors or levosimendan should not be used first-line (strong agreement).

However, these drug classes, and in particular levosimendan, can improve the hemodynamics of patients with cardiogenic shock refractory to catecholamines. There is a pharmacological rationale for the use of this strategy in patients on chronic beta-blocker treatment (weak agreement).

 

[BLADEMDA]

I do think that a whiff of lasix during a long robotic/laparoscopic case is reasonable as I believe mild siadh can occur. This isn't a hypovolemic situation and I'm talking 2.5 mg or so. Big boluses in ARF, not good.

I had an attending who told me in the 70's it was common to give a touch of diuretic in the O.R. on big cases where large amounts of crystalloid was used; the theory was that the inhalational vapor/stress of the operation did induce a bit of SIADH in the O.R. and the lasix helped to correct it. The dosage he quoted me was in the 5-10 mg IV x 1 range as larger amounts didn't improve the situation. To this day I still use 0.1 mg/kg IV of lasix in the O.R. when I am convinced the fluid replacement is more than adequate but urine output is low/reduced. Yes, I realize that C.I./C.O. and host of other factors could be the underlying mechanism but many times the small dose of lasix induces the necessary diuresis.

Glad to read someone else has this "theory" as well in 2016 and that dosages as low as 2.5 mg IV are adequate.