This is Part V of the EMCrit Acid-Base Talks. If you haven’t listened to the initial series, you may be better off starting there:
- Part I lays out the background of the quantitative approach
- Part II puts it in mathematical terms to allow calculation of acid base status
- Part III takes you through some real world examples
- Part IV discusses the Acid-Base Effects of IV Fluids
Today’s topic comes from a debate I have been having with Steve Smith of the amazing EKG Blog. The main thrust of the debate started with this question…
Does Bicarb Fix pH if You Can’t Increase Minute Ventilation?
When you can adjust PaCO2 to maintain a certain value (i.e. you increase minute ventilation), bicarb will raise pH as evidenced by this animal study (Crit Care Med 1996; 24:827-834). However, if you can’t blow off the CO2 then the effects on pH will not be there (J Pediatr 1977;91(2):287).
In this study, NaBicarb did not correct the pH, while CarbiCarb did (Carbicarb: an effective substitute for NaHCO3 for the treatment of acidosis. (Surgery 102:835–839).
This review article recommends against bicarb for permissive hypercapnia (Intensive Care Med (2004) 30:347–356).
This study furthers the idea that NaBicarb is not all that great in closed systems (J Pediatr 1972;80(4):671) and then this discussion explores all of the biochemical reasons why administering bicarbonate as a rapid push in a closed system is a bad idea (J Pediatr. 1972 Apr;80(4):681-2.).
Here is a quote from another review article (Anesthesiology 1990;72(6):1064):
The key concept in the equation [above] is that pH is not related to the absolute value of either bicarbonate concentration nor PCo2, but rather to their ratio.
When exogenous bicarbonate is administered during acidemia, bicarbonate reacts with hydrogen ions to form carbonic acid. Physicochemical equilibrium is shifted, favoring dissociation of carbonic acid to C02 and water. C02 partial pressure increases. The degree of alkaliniza- tion resulting from increased [HC03“] is limited by the rise in Pco2* In (open) systems where increases in PCo2 are prevented (by ventilation) alkalination occurs. When CO2 cannot be eliminated, the pH of the system is only minimally changed. Ostrea and Odel demonstrated in vitro that when isotonic sodium bicarbonate was added to whole blood in a (closed) system where generated C02 could not escape, PCo2 increased and pH was unchanged. Only when C02 was eliminated was the system alkalinized. Similarly, Steichen and Kleinman noted in hypoxic acidotic dogs that administration of 2 mEq/kg of sodium bicarbonate over 3 min when ventilation was unchanged resulted in no net change in arterial pH, although PaCo2 rose from 46 to 61 mmHg. If C02 elimination cannot keep pace with increased C02 generation, administration of bicarbonate during acidemia produces hypercarbia (respiratory acidosis) with little net improvement in pH.
How about this quote from a strong-ion approach to the use of buffers (Crit Care 2004;8:259):
When ventilation is fixed, however, as commonly occurs in mechanically ventilated patients, the effect of sodium bicarbonate may be to lower arterial pH, as was seen in patients ventilated with a lung protective strategy [in this study-Am J Resp Crit Care Med 2000;161:1149].
Here is Table 4 from the Am J Resp Crit Care Article:
But don’t believe me, let’s get an expert…
I got to interview John Kellum, MD, master of all things acid-base in the critically ill. You’ll hear more from him in upcoming episodes; this time I asked him the following questions:
- Does giving NaBicarb actually do anything to the patient’s pH if the patient can’t increase their minute ventilation to blow off the generated PaCO2? (Closed System)
- Let’s say you can actually can increase pH with NaBicarb, Is there any clinical advantage to actually doing this in an Anion-Gap Acidosis?
- How about in a patient that received a ton of NS in the ED, should we switch them to a bicarb drip to get SID back in balance?
Even when you Fix the pH with Bicarb, have you done any good in patients with SIG Acidosis?
Advocates of NaBicarb discuss its salutary effects on hemodynamics. However based on the available evidence, there is no reason to think there is any additional effects above those you would see giving hypertonic saline.
Small head-to-head study of NaBicarb and NS showed deleterious effects of the Bicarb (Am J Med. 1989 Jul;87(1):7-14.)
One of the best reviews is by Forsythe and Schmidt in this article (Chest 2000; 117:260–267). Table 1 demonstrating the intracellular effects is particularly relevant.
The other is by Hindman et al. (Anesthesiology 1990;72(6):1064). Here is a passage from the article:
If you are going to use it, use it by slow infusion while increasing minute ventilation. Boyd et al. agree and say it better than I can (Curr Opin in Crit Care 2008;14:379).
Severe Acidosis in Trauma Patients
Not fantastic evidence, but in this recent trauma paper (J Trauma 2013;74:45) giving bicarb to severely acidotic patients was associated with increased mortality.
Comments and where they Go…
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Here is a bibliography of the Literature Reviewed for this Episode Arieff AI, Leach, W, Park, R, et al. Systemic effects of NaHCO3 in experimental lactic acidosis in dogs. The American journal of physiology. 1982;242: F586-591.  Bersin RM, Chatterjee, K, Arieff, AI. Metabolic and hemodynamic consequences of sodium bicarbonate administration in patients with heart disease. The American journal of medicine. 1989;87: 7-14.  Boyd JH, Walley, KR. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? Current opinion in critical care. 2008;14: 379-383.  Cuhaci B, Lee, J, Ahmed, Z. Sodium bicarbonate controversy in lactic acidosis. Chest. 2000;118: 882-884.  Dell RB. Acid-base effects of hypertonic sodium bicarbonate solutions: a commentary. The Journal of pediatrics. 1972;80: 681-682.  Forsythe SM, Schmidt, GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest. 2000;117: 260-267.  Gehlbach BK, Schmidt, GA. Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit – the role of buffers. Critical care. 2004;8: 259-265.  Hindman BJ. Sodium bicarbonate in the treatment of subtypes of acute lactic acidosis: physiologic considerations. Anesthesiology. 1990;72: 1064-1076.  Kallet RH, Jasmer, RM, Luce, JM, et al. The treatment of acidosis in acute lung injury with tris-hydroxymethyl aminomethane (THAM). American journal of respiratory and critical care medicine. 2000;161: 1149-1153.  Omron EM, Omron, RM. A physicochemical model of crystalloid infusion on acid-base status. Journal of intensive care medicine. 2010;25: 271-280.  Ostrea EM. The influence of bicarbonate administration on blood pH in a “closed system”: clinical implications. The Journal of pediatrics. 1972;80: 671-680.  Rhee KH, Toro, LO, McDonald, GG, et al. Carbicarb, sodium bicarbonate, and sodium chloride in hypoxic lactic acidosis. Effect on arterial blood gases, lactate concentrations, hemodynamic variables, and myocardial intracellular pH. Chest. 1993;104: 913-918.  Steichen JJ, Kleinman, LI. Studies in acid-base balance. I. Effect of alkali therapy in newborn dogs with mechanically fixed ventilation. The Journal of pediatrics. 1977;91: 287-291.  Wilson RF, Spencer, AR, Tyburski, JG, et al. Bicarbonate therapy in severely acidotic trauma patients increases mortality. The journal of trauma and acute care surgery. 2013;74: 45-50; discussion 50.
Now on to the podcast…
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