Use of Bicarbonate in Lactic Acidosis

Five days post emergency colorectal surgery, an elderly woman, following a brief period of chest pain a few hours earlier, developed progressive hypotension and tachycardia on the ward. She had a background of hypertension, type 2 diabetes and a chronic left foot ulcer. On examination she was found to be clammy, mottled and peripherally vasoconstricted with a GCS of 15/15. Her abdomen was soft and non-tender. Her initial ECG had showed no ischaemic changes and subsequent ECGs showed only a sinus tachycardia.

Initial blood gas analysis showed a metabolic acidosis (pH 7.21 Lactate 2.8mmol/l, HCO3 11.1mmol/l with a pCO2 of 2.7kPa).  A starting differential diagnosis of a cardiac event, a pulmonary embolism, critical ischaemia or sepsis related to a hip or foot ulcer were made. Urgent orthopaedic and vascular review were obtained, and it was deemed that neither the hip, ulcer or vascular insufficiency were a likely source for the deterioration. Initially it was planned to transfer her for a CTPA, however she became progressively unstable, was no longer fluid responsive, and was intubated on the ward and transferred to the intensive care unit (ICU) for stabilisation.

On arrival on ICU she continued to deteriorate, and in addition to fluid resuscitation required a high dose noradrenaline infusion to maintain her blood pressure. Broad spectrum antibiotics were started, a bedside echocardiogram and blood tests performed and hydrocortisone started. Her metabolic acidosis continued to deteriorate, subsequent arterial blood gas showed a pH 6.91, Lactate of 13.7mmol/l, HCO3 7.7mmol/l, base excess -25mmol/l with a pCO2 of 5.4kPa. It was decided to correct this acidosis with a bicarbonate infusion and initially 200ml of 8.4% was given over an hour, based on correcting half the calculated bicarbonate deficit (bicarbonate deficit (mmol) = base deficit 0.3xbodyweight(kg)1).  The blood gas following this infusion showed improvement in the metabolic acidosis despite the increasing Lactate (pH 7.07, Lac 14.0mmol/l, HCO3 10mmol/l, BE -18.6mmol/l with a pCO2 of 4.85kPa). She continued to deteriorate and the results from her blood tests, troponin and bedside echo suggested a primary myocardial infarction to cause this decline. She was too unstable for primary coronary intervention and her condition continued to deteriorate. She died 6 hours post admission.

Tom Daubeny

The use of a base to treat lactic acidosis is controversial, and this was highlighted by the difference of opinion of the physicians involved in this case. A recent survey emphasising the different clinical practice found that only 67% of critical care physicians would use sodium bicarbonate for this indication, with 40% not treating until the pH was below 7.0. This compared to higher uptake by nephrologists, who would also use a higher pH at which they would treat2.

The advantages to bicarbonate administration lie in abating the adverse effects of acidaemia. It is well established that cardiac contractility is reduced3, response to catecholamines is diminished4, and arrhythmias are more likely5.

Despite these advantages, a clear benefit has not yet been shown. Two prospective, randomised, blinded cross over trials have failed to show any haemodynamic benefit to giving sodium bicarbonate compared to 0.9% sodium chloride. The first study included fourteen patients with base excess less than -10, with an increased mean lactate of 7.8mmol/litre with all patients ventilated, with pulmonary artery catheters in situ and thirteen were receiving catecholamines6. The second study had ten patients with lactate concentrations greater than 2.45mmol/litre who received randomised sequential treatment of 1mmol/kg sodium bicarbonate or an equal volume of sodium chloride7. No benefit was shown in haemodynamic variables or in tissue oxygen delivery, however, these trials were small and only included a few cases in which the pH was less than 7.16,7.

The adverse effects of sodium bicarbonate therapy include hypernatraemia, hyperosmality, hypokalaemia, ionized hypocalcaemia and a paradoxical increase in intracellular acidosis through the rapid diffusion of carbon dioxide into cells. Acidosis has also been shown to have a protective effect on cells, delaying apoptosis in anoxia 8. It may also reduce lactate production through decreased phosphofructokinase activity8 and reducing acidosis produces a left shift in the oxygen dissociation curve, inhibiting oxygen release to tissues. These concerns are emphasized by a recent single-centred retrospective analysis of with lactate acidosis which suggested sodium bicarbonate was independently associated with a higher mortality9.

Other agents that work similarly to bicarbonate but do not increase CO2 have recently been introduced and include THAM (tris-hydroxymethyl aminomethane, biologically inert amino alcohol, which buffers carbon dioxide) and CarbiCarb (a mixture of Na2CO3/NaHCO3 that buffers similarly to NaHCO3, but without net generation of CO2). These have been shown to be effective and have been recommended as an alternative to sodium bicarbonate10.

Current guidelines differ in their recommendations. The 2012 updated surviving sepsis guidelines recommend against sodium bicarbonate therapy for the purpose of improving haemodynamics or reducing vasopressor requirements in patients with hypoperfusion induced lactic acidemia with pH ≥7.15 11.  A 2014 review looking at the evidence concluded that 1-2mmol/kg boluses should be given in lactic acidosis if pH<7.1 and bicarbonate less than 6meq/L 12. However, many reviews conclude that there is not sufficient evidence for bicarbonate in lactate acidaemia and the resuscitation council only recommend bicarbonate in cardiac arrest in the setting of hyperkalaemia or tricyclic antidepressant overdose13.

The method of choosing the amount of bicarbonate for therapy is also controversial. Some papers recommend that the bicarbonate deficit should be calculated 11,14 and others recommend that a set dose should be given empirically (eg 1mmol/kg) and repeated according to targets and response 12.


Lessons Learnt

This case provided a useful insight into some of the controversies surrounding the treatment of profound lactic metabolic acidosis. A review of the evidence showed that there seems to be good evidence and consensus for not using bicarbonate therapy to treat acidosis with a pH more than 7.2, but below this opinion is divided. It illustrated the need to look at each case on its individual merits, some of the alternative therapies that may become available, and to continue to review emerging literature in what continues to be a controversial area.


References

  1. Busse MW, Maassen N, Böning D. The calculation of the osmotic volumes of distribution of hypertonic sodium bicarbonate and other hypertonic solutions: a theoretical approach. J Med. 1989; 20(2):143-61.
  2. Kraut JA, I Kurtz. Use of base in the treatment of severe organic acidosis and critical care physicians: Results of an online survey. Clin Exp Nephrol 2006 10 : 111–117
  3. Orchard CH, Kentish JC. Effects of changes of pH on the contractile function of cardiac muscle. Am J Physiol 1990; 258:C967.
  4. Marsh JD, Margolis TI, Kim D. Mechanism of diminished contractile response to catecholamines during acidosis. Am J Physiol 1988; 254:H20.
  5. Orchard CH, Cingolani HE. Acidosis and arrhythmias in cardiac muscle. Cardiovasc Res 1994; 28:1312.
  6. Cooper DJ, Walley KR, Wiggs BR, Russell JA. Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis. A prospective, controlled clinical study. Ann Intern Med 1990; 112:492.
  7. Mathieu D, Neviere R, Billard V, et al. Effects of bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic acidosis: a prospective, controlled clinical study. Crit Care Med 1991; 19:1352.
  8. Bing OH, Brooks WW, Messer JV: Heart muscle viability following hypoxia: Protective effect of acidosis. Science, 1973; 180 : 1297– 1298
  9. H. J. Kim, Y. K. Son, and W. S. An. Effect of sodium bicarbonate administration on mortality in patients with lactic acidosis: a retrospective analysis 2013; 65283.
  10. Luft F: Lactic acidosis update for critical care clinicians. J Am Soc Nephrol 2001, S15– S19
  11. R. Dellinger et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock. Crit. Care Med 2013; 41(2) 580-637.
  12. S. Sabatini and N. Kurtzman. Bicarbonate Therapy in Severe Metabolic Acidosis JASN April 2009 20: 692-695
  13. The Resuscitation Council. 2010 Resuscitation Guidelines. 2010; Ch.7 p.74.
  14. M. Wiederkehr, M. Emmett. Bicarbonate therapy in lactic acidosis. Uptodate 2014
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3 thoughts on “Use of Bicarbonate in Lactic Acidosis

  1. The evidence that acidosis on its own decreases cardiac contractility in humans in vivo is poor. The publications you site in this review are of bench studies of myocytes from chick embryos in a dish. The case is of a patient with another reason entirely for poor cardiac function. It doesn’t really make sense that acidosis should inhibit myocyte function: what would be the implications of this for exercise? The harder you exercise the worse your heart functions?

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  2. Nice review. A slightly off topic but relevant comment: In the acidemic patient with elevated ICP, there may be a role for sodium bicarb especially in the setting or acute kidney injury or if osmolar target is already reached. The evidence is small but physiologically makes sense albeit transient. http://www.ncbi.nlm.nih.gov/pubmed/21298358

    In practice, I tend to use bicarb in the triple acid- base disorder where there is disproportionate bicarb loss to level of anion GAP acidosis. On a more liver specific note, I am more cautious about doing this in cirrhotics who have a long standing low serum bicarb that is compensatory for the chronic respiratory alkalosis unless I don’t anticipate them coming off the vent for sometime or if I intend to bridge them on vent and vasopressors to transplantation. Is there evidence to support this? No…not that I know of and I don’t know if its justified from the strong ion perspective. A cirrhotic on too much vasopressors will look less appealing to the surgeons planning a liver transplant. Going into liver tranplantation with severe acidosis adds more work for the anesthesiologist trying to stabilize the patient prior to liver reperfusion and in the setting of uncontrolled hemorrhage. In Acute Liver Failure, we are often giving a ton of Bicarb anyway via CRRT but it is less conspicuous. I worry about the acidemia adding to the luxury brain perfusion and tend not to let pH get too low especially in established cerebral edema. Happy to hear any comments or criticism about my approach on this specific subpopulation from anyone.

    Thank you for the review! Forwarding to my fellows.

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