So for anyone who has been reading any of my stuff, you know that I believe we best serve our patients by using the information in good evidence and blending it with bedside assessment (ultrasound being an integral part of physical examination) and physiology to come up with the best therapeutic approach to the one patient we are treating. Contrast that to the blinded and naive belief that one protocol from one study is the best thing for all patients suffering from disease X.
So I am constantly looking for a way to fine tune resuscitation to the individual patient, given his/her particular cardiovascular function, volume tolerance (not just volume responsiveness), vasopressor tolerance (blue fingers probably mean blue livers and kidneys to some degree) and metabolic reactions.
One of my friends and mentors is Dr. Andre Denault. Absolutely incredible guy who is a complete triple threat of academia (internist/intensivist/anaesthetist massively published), experience and raw neuronal power. Throw in open-mindedness and humility (he actually once picked my brain about abdominal compartment syndrome pressure monitoring) and you have a lethal package. So after killing off the filed of intraoperative/critical care TEE (yes the leading textbook is his), he’s plunged into NIRS spectroscopy and is now dragging it from the OR to the ICU, and so in the last few years he’s put me on this trail with anecdotes and his (unpublished yet but coming) findings.
So a quick few words about NIRS (Near InfraRed Spectroscopy). The technology looks at hemoglobin saturation, and does so in a predominantly venous way. Hence this behaves similarly to a central or mixed venous gas, except at the local tissue level. A gross normal is >70% but this has to be interpreted in clinical context, along with the knowledge of simultaneous arterial saturation. Hence lower values (assuming normal arterial sats) will mean one of two things: increased demand or decreased supply. The demand issue is a clinical one. What we are looking for using this type of monitoring is decreased supply, e.g. cardiac output that is inadequate for current demands.
The information gleaned from our discussions was enough to make me get some loaner time with some devices, and that was enough to have a few clinical cases pique my interest.
Here is one:
In the ICU at Scarborough General in Toronto, I admit a lady with urosepsis on a stone-obstructed hydronephrosis. We get urology to slip in a double J, but she is still very norepinephrine-dependant. She isn’t intubated, lactate about 5 and on high doses of norepi to maintain MAP 60-65. Extremities are cold and mottled and there is mottling up to the thighs. She is awake and communicating. Over the next hour or so lactate rises to 5.5. I’m not liking this.
I put on the NIRS monitor with a cerebral lead and one on the thigh. They both read in the 50’s, somewhat suboptimal.
Bedside US reveals a good sized IVC with little variation. She’s well filled. Her LVEF is 50-60%, her RV is dynamic and with a normal RV/LV ratio. The hydronephrosis is improved on the affected side.
So I have a patient who’s adequately preloaded, without obstructive or systolic failure, who is on very high doses of norepinephrine with a rising lactate, despite source control and antibiotics. However, she doesn’t “look” that bad aside from the cold and blueish extremities…
So I decrease the norepinephrine. Systolic BP drops to 80…but…cerebral NIRS and tissue NIRS rise…now in the high 50’s. Patient remains awake and communicating. Drop norepinephrine some more. Systolic 75. Cerebral NIRS 62%, tissue 61%. Systolic 70. Cerebral 59%, tissue 57%. Back up to 75%. NIRS back up. I finally settle on 75-80 systolic. NIRS settles in low 60’s. An hour later, lactate is 4, two hours later 2.5, then normalizes. Over that time span, the mottling gradually resolves and the urine output picks up. By the next morning she is off norepinephrine, and her BP sits around systolic 85-90 on its own. Turns out her usual BP is in the low 100’s.
I’m not sure how long – without the reassurance of improved tissue saturation – I would have been able to tolerate systolic BPs in the 70’s. Remember that lactate takes time to clear and urine takes time to make.
So this case reinforced my belief that not every patient’s needs are best met by an MAP of 65, and that targeting this may be harmful. It isn’t hard to imagine a scenario (which I may very well have pursued at a more junior stage) where further fluid resuscitation, coupled with insistence on a BP value may have resulted in iatrogenic fluid overload or Paul Marik’s “salt water drowning” (more commonly thought of as “ARDS”) and tissue ischemia/organ dysfunction (partly related to over-vasoconstriction) and who knows what outcome could have transpired… And very possibly, a bad outcome may have been blamed on severity of illness… Food for thought.
So one definitely possible use for NIRS is to find the “sweet spot” for the BP/vasopressor relationship.
More on NIRS in Part 2 in the next week or so.
thinking critical care 
Very very interesting. I have never used / seen this device but it seems promising. This is a huge problem – sepsis and fluid resuscitation in sepsis. We DO give too much fluids, we DO give too much noradrenaline. In your case : reducing noradrenaline until a systolic of 80 => salutary, interesting, took a lot of guts, and probably a lot of explaining to the nurses (ok, you had the device and you could show them something scientifically based). Try to do this without it. And not only the nurses, there are so many doctors who have to be convinced. Who have to be convinced that mottled skin = mottled internal organs and that generalized edema – what we see from outside, happens inside of the body as well. And the more it accumulates in the interstitium, the more complicated is for oxygen to find the cells.
Great post !
Greetings from Hamburg, Germany
Thanks!
Indeed, very difficult to do without some real-time reassuring data. One could also use ScVO2 but knowing the brain isn’t desaturating is comforting enough to allow holding the course. I now have a device full time, so am accumulating cases and experience. More to come.
We have to learn to guide the physiology back to normal, not try to catapult it. There isn’t a shred of evidence to support pressure-bag bolusing. It is from our own traditions and from a well-intentioned place, but not necessarily a scientifically sound one.
cheers!
P
Actually this is one of the biggest problem, that a lot of critical care physician forget the normal physiology. We are sometimes treating the monitor values and our own panic (giving Lasix or NaHCO3 and then everything looks better :)) ). We give fluids until even the tightest junctions become so loose, that everything goes in the interstitium. I think the whole fluid therapy and concepts should be rewritten. I wonder if apart from our “balanced IV solutions”, one should also apply simple and pure water through the NGT.
I don’t know about ScvO2 – I have seen so many ill patients with normal ScvO2. I think we have to go deeper into the problem – with a NIRS monitor. I will be following your posts.
Cheers ! Alex
Philippe
Thanks for the comments. I have not seen such a case so far but there are a few hypothesis. First there is very poor correlations between cerebral NIRS and systolic blood pressure. There are many reasons and one of the most common I see in the OR and ICU is the poor reliability of the radial blood pressure. This is why in the approach to the hemodynamically unstable we wrote in the Canadian J Anesth last year we mention to always confirm that the hypotension is really true. There is a coming paper in A&A coming up in the next 6 months regarding thsi fundamental issue. Therefore we have seen patients with radial artery pressure below 100 but the femoral was more than 150 mmHg. Second, some vasoactive drugs can worsen cerebral NIRS. This has been shown with neosynephrine or any alpha agents particularly if there is any occult LV dysfunction is present. If this occurs you will increase afterload and make the CO worse. In septic shock it is very common and often if you repeat the US exam, you will seen new onset of LV dysfunction once you start such drugs. Using a new modality, like LV strain, we will probably be able to pick that up earlier. The third point is that NIRS never lie. At the MHI we have used it for more than 6000 cases since 2002 and a low value is always abnormal. The problem is to find why but there is no doubt in the literature that low values (particularly those who become low or start higher) will be associated with poor outcome. I just reviewed a paper from a pediatric cardiac center showing that post op NIRS was the best outcome predictor and abnormal values will appear before lactate level. Therefore the association you saw between the two is not surprising. NIRS is also appearing to us as an early predictor of RV dysfunction and venous congestion. In both situations NIRS will be reduced because venous congestion will increase NIRS photon absorptions. This is what you see in SVC and IVC syndrome. Mjor drop in NIRS values or the head or the legs. Did you look at her hepatic and portal vein? How much fluid did she received? These elements could point toward a potential etiology. However, my first bet is that the blood pressure was measured with a radial artery, subclinical LF dysfunciton was present and removal of noradrenaline was the best treatment.
Thanks for the invitation to reply
Amitiés
André Denault
[…] Finding the “Sweet Spot” – I think (hope) that anyone reading this with professional interest understands that pressure does not necessarily equal perfusion. With that in mind, adjusting vasopressors to a pressure makes little sense, and represents at best a guesstimate of perfusion, which is what we really are after. We can all agree, however, that a certain minimum pressure is required, but whether that is 65, 55 or 45 MAP no one can say for sure. So the way I like to use it is to establish a baseline and watch the direction of the tissue saturation with vasopressor therapy. If the saturation begins to drop off, we may have reached a point at which excessive vasoconstriction is worsening tissue perfusion, and that inflexion point may represent the upper beneficial limit of the vasopressor – this may happen to be under 60 or 65 of MAP. However, it is key to understand that this inflexion point is reflective of the current state of hemodynamics, such that a change in volume status or cardiac output, in one direction or the other, would likely change the position of this physiological point. For example, a volume depleted patient may reach a decreasing tissue saturation point at 55 MAP, but, once volume replete, may reach a higher MAP of 65 or above before a drop in saturation is seen. Conversely, a patient whose best tissue saturations were around 65 MAP who suffers an MI and sudden drop in cardiac output may now see his perfusion compromised at that same MAP, which would now be achieved with a greater vasoconstriction, less cardiac output and consequently, poorer flow… I posted a case discussion which illustrates this. […]
[…] Finding the “Sweet Spot” – I think (hope) that anyone reading this with professional interest understands that pressure does not necessarily equal perfusion. With that in mind, adjusting vasopressors to a pressure makes little sense, and represents at best a guesstimate of perfusion, which is what we really are after. We can all agree, however, that a certain minimum pressure is required, but whether that is 65, 55 or 45 MAP no one can say for sure. So the way I like to use it is to establish a baseline and watch the direction of the tissue saturation with vasopressor therapy. If the saturation begins to drop off, we may have reached a point at which excessive vasoconstriction is worsening tissue perfusion, and that inflexion point may represent the upper beneficial limit of the vasopressor – this may happen to be under 60 or 65 of MAP. However, it is key to understand that this inflexion point is reflective of the current state of hemodynamics, such that a change in volume status or cardiac output, in one direction or the other, would likely change the position of this physiological point. For example, a volume depleted patient may reach a decreasing tissue saturation point at 55 MAP, but, once volume replete, may reach a higher MAP of 65 or above before a drop in saturation is seen. Conversely, a patient whose best tissue saturations were around 65 MAP who suffers an MI and sudden drop in cardiac output may now see his perfusion compromised at that same MAP, which would now be achieved with a greater vasoconstriction, less cardiac output and consequently, poorer flow… I posted a case discussion which illustrates this. […]