Base Excess/Deficit As Surrogate For Fluid Status

[wickedskillz]

How many of you use the Base Deficit/Excess as a surrogate for fluid status? If you do, what conditions do you use it in?

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[jdh71]

What's the rationale for its use in the first place?

 

[deleted171991]

How many of you use the Base Deficit/Excess as a surrogate for fluid status? If you do, what conditions do you use it in?

Old school surgical BS.

 

[wickedskillz]

I think the most likely rationale seems to be as a surrogate of lactic acidosis, as a surrogate for tissue perfusion. The thought is if they have a strong base deficit (say -6), then give fluid. The trauma people will also make sure the base deficit is "Clearing" or "normalizing" or "downtrending" when making decisions about adequate resuscitation. I remember as an intern my renal attendings used to hate it. Just seeing what the opinion is out there and if anyone uses it for anything, and why. I personally think the ABGs always have a Lactate level on them anyway, and I can use that as a direct measure of lactic acidosis, then work on figuring out the cause. I think if u use base deficit as a direct surrogate for tissue perfusion, you could be missing other causes of metabolic acidosis

 

[pulmoblast]

I never used base deficit for anything.


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[Hernandez]

If I'm in a SICU I'll eyeball it....and then place it next to the cvp numbers.....

 

[sluggs]

The short answer is "NO". You need to ask why the patient is acidotic-- it could be an RTA...? Most patients who are in hypovolemic shock or distributive shock will be acidotic with a base deficit, but not all acidotic patients are acidotic because of hypovolemia. You can develop hyperchloremic acidosis after a big NACL load.
You can calculate amps of bicarb a patient is short: weight in kilos x 2/3 x base deficit = MEQ of HCO3 short. However this does not mean that you replace the whole deficit (or even any of it).
Parse out the CAUSE of the deficit!

 

[engineeredout]

I've been trying to figure out for years what base deficit/excess provides that the rest of the abg/bmp doesn't. So far it's mostly been used to justify giving additional fluids to fluid overloaded patients without the bother of having to examine them or use any other index of resuscitation, but a few times so far I've been forced to use it to calculate bicarb deficit and administer said amounts of bicarb. I think the last time I had to do that I rolled my eyes so hard my retinas detached.

 

[deleted171991]

Old school surgical BS.

To be more precise: some old-school (trauma) prizewinners give fluids till the BD normalizes, because hypovolemia in acidosis lead to hypoperfusion, which leads to "lactic" acidosis, which creates a base deficit. But that is only in (some) trauma patients.

I wonder what the same geniuses would do with a patient in contraction alkalosis, as in having a base excess (after a few days of hypovolemia). Give diuretics? 😛

 

[AdmiralChz]

Interesting discussion. What about following BD as a trend over time rather than paying attention to the physical number?

 

[Hernandez]

No. Next question.

 

[wickedskillz]

makes sense. Thanks for your input guys.

 

[wickedskillz]

How about this: Is SVV as seen by changes in arterial waveform on the monitor a sensitive indicator of intravascular volume depletion? Assume you don't have access to echo or a non-invasive CO monitor such as a Lidco/Vigileo, and that the patient is mechanically ventilated with appropriate TVs and not overbreathing the vent, as well as NSR.

 

[Hernandez]

How about this: Is SVV as seen by changes in arterial waveform on the monitor a sensitive indicator of intravascular volume depletion? Assume you don't have access to echo or a non-invasive CO monitor such as a Lidco/Vigileo, and that the patient is mechanically ventilated with appropriate TVs and not overbreathing the vent, as well as NSR.

Data is far better with PPV than cvp. Note I said PPV not SVV, you will not be calculating SVV without a lidco/etc. and the data for PPV is better than SVV, as long as they aren't spontaneously breathing, aren't in afib, receiving large tidal volumes, etc. now you can get around some of the assumptions Michard makes to arrive at his protocol, which he did to improve specificity at the expense of sensitivity, if you understand the physiology that goes into the pull/pleura/cardio pressure gradients and how certain pathologies (like ards) can affect those numbers. And yes, you can you use PPV in someone on cpap, with some caveats. I'd argue that you also can use in other extremes, I.e. Non-intubated, or negative pressure ventilation, or APRV scenerio with a decease in specificity if you grasp some of the physiology.

 

[Dr.CCM]

Data is far better with PPV than cvp. Note I said PPV not SVV, you will not be calculating SVV without a lidco/etc. and the data for PPV is better than SVV, as long as they aren't spontaneously breathing, aren't in afib, receiving large tidal volumes, etc. now you can get around some of the assumptions Michard makes to arrive at his protocol, which he did to improve specificity at the expense of sensitivity, if you understand the physiology that goes into the pull/pleura/cardio pressure gradients and how certain pathologies (like ards) can affect those numbers. And yes, you can you use PPV in someone on cpap, with some caveats. I'd argue that you also can use in other extremes, I.e. Non-intubated, or negative pressure ventilation, or APRV scenerio with a decease in specificity if you grasp some of the physiology.

Any articles you got that discussed/explained this? I'd be interested.

 

[Hernandez]

I'll have to dig then out, and there are many other blurbs Michard makes in comments on others articles

 

[wickedskillz]

So if someone had no variation on his arterial line tracing and met all of the other conditions, would you pretty comfortable saying his hypotension is from a cause other than intravascular fluid depletion?

 

[Hernandez]

So if someone had no variation on his arterial line tracing and met all of the other conditions, would you pretty comfortable saying his hypotension is from a cause other than intravascular fluid depletion?

I would not, I'd be comfortable saying they'd likely respond to a fluid challenge, but other potential causes can come into play here, excessive peep for one, other causes of decreased venous return for another.

 

[Hernandez]

1 Michard F, Chemla D, Richard C, et al. Clinical Use of Respiratory Changes in Arterial Pulse Pressure to Monitor the Hemodynamic Effects of PEEP. Am. J. Respir. Crit. Care Med. 1999; 159:935-939
2 Michard F, Boussat S, Chemla D, et al. Relation between Respiratory Changes in Arterial Pulse Pressure and Fluid Responsiveness in Septic Patients with Acute Circulatory Failure. Am. J. Respir. Crit. Care Med. 2000; 162:134-138
3 Hofer CK, Senn A, Weibel L, et al. Assessment of stroke volume variation for prediction of fluid responsiveness using the modified FloTrac and PiCCOplus system. Critical Care (London, England) 2008; 12:R82
4 McGee WT. A Simple Physiologic Algorithm for Managing Hemodynamics Using Stroke Volume and Stroke Volume Variation: Physiologic Optimization Program. Journal of Intensive Care Medicine 2009; 24:352-360
5 Tavernier BMD, Makhotine OMD, Lebuffe GMD, et al. Systolic Pressure Variation as a Guide to Fluid Therapy in Patients with Sepsis-induced Hypotension. [Article]. Anesthesiology December 1998;89(6):1313-1321
6 Marik PE, Baram M, Vahid B. Does Central Venous Pressure Predict Fluid Responsiveness?*. Chest 2008; 134:172-178
7 Marik PE, Cavallazzi R, Vasu T, et al. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature. Critical Care Medicine 2009; 37:2642-2647
8 Putensen C, Wrigge H. Clinical review: Biphasic positive airway pressure and airway pressure release ventilation. Critical Care 2004; 8:492 - 497
9 Seymour CW, Frazer M, Reilly PM, et al. Airway Pressure Release and Biphasic Intermittent Positive Airway Pressure Ventilation: Are They Ready for Prime Time? The Journal of Trauma 2007; 62:1298-1309 1210.1097/TA.1290b1013e31803c31562f
10 Rathgeber J, Schorn B, Falk V, et al. The influence of controlled mandatory ventilation (CMV), intermittent mandatory ventilation (IMV) and biphasic intermittent positive airway pressure (BIPAP) on duration of intubation and consumption of analgesics and sedatives. A prospective analysis in 596 patients following adult cardiac surgery. European Journal of Anaesthesiology 1997; 14:576-582
11 Perner A, Faber T. Stroke volume variation does not predict fluid responsiveness in patients with septic shock on pressure support ventilation. Acta Anaesthesiologica Scandinavica 2006; 50:1068-1073


Some of these aren't relevant, I had a study going when I was a fellow to try and tease out just what I've said above, that ppv can be used in non-michard standard scenerios if you understand the physiology and limitations, sadly stats said I needed ~120 pts, and I got to 20 before I finished fellowship and then no one afterwards really understood the study.