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Metabolic Acidosis in Emergency Medicine

  • Author: Antonia Quinn, DO; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
 
Updated: Jun 20, 2016
 

Background

Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity. Metabolic acidosis should be considered a sign of an underlying disease process. Identification of this underlying condition is essential to initiate appropriate therapy.

This article discusses the differential diagnosis of metabolic acidosis and presents a scheme for identifying the underlying cause of acidosis by using laboratory tests that are available in the emergency department. Clinical strategies for treating metabolic acidosis are also reviewed.

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Pathophysiology

There are 3 approaches to understanding acid/base balance: A qualitative approach using the Henderson/Hasselbalch equation, a semiqualitative approach with base excess, and the Strong Ion Theory. The 3 theories are reviewed below.

Henderson-Hasselbalch approach to acid/base physiology

The Henderson-Hasselbalch equation describes the relationship between blood pH and the components of the H2 CO3 buffering system. This qualitative description of acid/base physiology allows the metabolic component to be separated from the respiratory components of acid/base balance.

pH = 6.1 + log (HCO3/ H2 CO3)

Bicarbonate (HCO3) is in equilibrium with the metabolic components.

  • Bicarbonate production in the kidney
  • Acid production from endogenous or exogenous sources

Carbonic acid (H2 CO3) is in equilibrium with the respiratory component, as shown by the below equation:

H2 CO3 = PCO2 (mm Hg) X 0.03

Metabolic acidosis can be caused by the following:

  • Increase in the generation of H + from endogenous (eg, lactate, ketones) or exogenous acids (eg, salicylate, ethylene glycol, methanol)
  • Inability of the kidneys to excrete the hydrogen from dietary protein intake (type I, IV renal tubular acidosis)
  • The loss of bicarbonate (HCO 3) due to wasting through the kidney (type II renal tubular acidosis) or the gastrointestinal tract (diarrhea)
  • The kidneys response to a respiratory alkalosis

Base excess approach to acid/base physiology

Unfortunately, the Henderson/Hasselbalch equation is not linear; pCO2 adjusts pH as part of the normal respiratory compensation for acid/base derangements. This nonlinearity of Henderson-Hasselbalch prevents this equation from quantifying the exact amount of bicarbonate deficit in a metabolic acidosis. This observation led to the development of a semiquantitative approach, base excess (BE).

BE = (HCO3 – 24.4 + [2.3 X Hgb + 7.7] X [pH – 7.4]) X (1 – 0.023 X Hgb)

Base excess attempts to give a quantitative amount of bicarbonate (mmol) that is required to be added or subtracted to restore 1 L of whole blood to a pH of 7.4 at a pCO2 of 40 mm Hg. To standardize BE for hemoglobin, the following formula was developed with improved in vivo accuracy, the standardized base excess (SBE):

SBE = 0.9287 X (HCO3 – 24.4 + 14.83 X [pH – 7.4])

Strong Ion approach to acid/base physiology

These classical descriptions of acid/base physiology often failed to account for acid/base findings in critically ill patients. An alkalosis was often noted in critically ill patients as their serum albumin level decreased, which could not be quantified by Henderson Hasselbalch or BE. Also, the "dilutional" acidosis frequently encountered after a large infusion of normal saline could not be explained by either of these 2 approaches to acid/base balance.

Both Henderson Hasselbalch and BE assume that the cations (Ca2+, Mg2+) and anions (Cl-, albumin, PO4-) in plasma remain unchanged in a patient with metabolic acidosis. Yet, in critically ill patients, these ions are known to be in dynamic flux. During the 1980s, Dr. Peter Stewart developed an acid/base theory (Strong Ion) using quantitative chemistry, which accounted for fluctuations of all the ions dissolved in plasma. Based on the requirements for electrical neutrality in any solution as any one of the concentrations of these ions changes, water must dissociate into H+ or OH- to balance the charge. The pH in this scheme is not a consequence of the ratio of acid to base in solution but determined by 3 independent variables:

  • Strong ion difference (SID) – Ions almost completely dissociated at physiologic pH.

SID = [Na+ + K+ + Ca2+ + Mg2+] – [Cl- + Lactate-]

(Ca2+ and Mg2+ are the concentrations of their ionized forms, Mg2+ X 0.7 = ionized Mg2+ concentration)

  • Total weak acid concentration (Atot) – Ions that can exist dissociated (A-) or associated (AH) at physiologic pH (buffers)

Atot = 0.325275 X [albumin] + 2 X [phosphate]

  • pCO 2 (mm Hg)

The Henderson Hasselbalch equation can be reformulated with variables from the Strong Ion Theory to give a more generalizeable solution to pH.

pH = pK1 ’ + log [SID] – Ka – [ATOT]/[Ka + 10–pH]

SPCO2

(K1’ is the equilibrium constant for the Henderson-Hasselbalch equation, Ka is the weak acid dissociation constant, and S is the solubility of CO2 in plasma.) See the image below.

Approach for evaluating metabolic acidosis. Approach for evaluating metabolic acidosis.

Once a metabolic acidosis is suspected by low bicarbonate concentration, an arterial blood gas analysis should be obtained. The low HCO3 level can be caused either by a primary metabolic acidosis or as the metabolic compensation for a respiratory alkalosis. The direction of the pH will separate metabolic acidosis (pH < 7.35) from a respiratory alkalosis (pH > 7.45).

The normal respiratory response (Kussmaul breathing) to a metabolic acidosis is a decrease in pCO2. This is given by the Winter’s equation:

PCO2 = 1.5 X (observed HCO3) + 8±2

(A quick rule of thumb: The PCO2 should approximate the last two digits of pH. For example, pH 7.25, PCO2 should be close to 25 mm Hg.)

Failure to have an appropriate respiratory response to metabolic acidosis represents a failure of airway and/or breathing, which must be addressed before any other workup commences.

Once an appropriate respiratory response for a metabolic acidosis has been established, the workup for the presence of unmeasured anions can progress by using the traditional anion gap, the delta-delta approach, or the strong ion gap. This allows the differential of metabolic acidosis to be narrowed and the appropriate therapy applied.

To differentiate between the causes of metabolic acidosis, one traditionally calculates the anion gap (AG), corresponding the presence of unmeasured anions.

AG = (Na+) - ([Cl-] + [HCO3-])

The anion gap allows for the differentiation of 2 groups of metabolic acidosis. Metabolic acidosis with a high AG is associated with the addition of endogenously or exogenously generated acids. Metabolic acidosis with a normal AG is associated with the loss of HCO3 from the kidney or GI tract, or the failure of the kidney to excrete H+.

The delta/delta concept allows for the partitioning of metabolic acidosis into an anion gap and a non-anion gap component, which can occur contemporaneously. The concept behind delta/delta is based on the assumption that for every increase in anion gap of 1 mmol/L above normal (12 mmol), serum HCO3- will drop by an equal amount.[1]

Δ anion gap = Δ HCO3

If the delta HCO3- is greater than the delta anion gap, then a concomitant non-anion gap acidosis must exist along side the anion gap acidosis. One example would be a patient with a congenital renal tubular acidosis in diabetic ketoacidosis (DKA).

Stewart provides a replacement for the standard anion gap and delta/delta, which allows one to directly measure the amount of unmeasured anions in solution corrected for changes from normal of Ca2+, Mg2+, albumin, and phosphate.[2] This is the Strong Ion Gap (SIG).

SIG = ([Na+ + K+ + Ca2+ + Mg2+] – [Cl- + lactate]) –

([2.46 x 10- X pCO2/10-pH] + [albumin{g/dL} X

{0.123 x pH – 0.631}] + [PO4 - {mmol/L} X {pH – 0.469}]

All the strong ions are expressed in mEq/L, and only the ionized portions of Mg2+ and Ca2+ are considered (to convert total to ionized Mg2+, multiply by 0.7). Because of the complexity of the above equation, several Internet resources are available to calculate the SIG. For example, The Stewart approach to acid-base is a good resource. The normal SIG is between 0 and 2. SIG has been shown to be better than blood lactate, pH, or injury severity scores in trauma patients and pediatric surgery patients as a predictor of mortality.

A report by Masevicius and Dubin stated, however, that the variables presumed to be independent in the Stewart approach are actually interdependent in various situations and that there is a lack of experimental evidence to show that water dissociates in response to SID changes. The report also contends that severe methodologic drawbacks exist in studies that have attempted to demonstrate that the Stewart approach is clinically superior to conventional methods for analyzing acid-base disorders, while the largest such study indicated that the Stewart approach can be used interchangeably with conventional techniques. Masevicius and Dubin concluded that the Stewart approach does not offer a significantly better method of understanding, diagnosing, and treating acid-base changes in critically ill individuals.[3]

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Prognosis

Because metabolic acidosis is a condition that occurs in response to a variety of disease states, the prognosis is directly related to the underlying etiology and the ability to treat or correct that particular disorder.

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Contributor Information and Disclosures
Author

Antonia Quinn, DO Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Assistant Residency Director, Attending Physician, Department of Emergency Medicine, Kings County Hospital Center, SUNY Downstate Medical Center

Antonia Quinn, DO is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Richard H Sinert, DO Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Vice-Chair in Charge of Research, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Karen L Stavile, MD, to the development and writing of this article.

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