Physiology, Acidosis, Metabolic


Article Author:
MacKenzie Burger


Article Editor:
Derek Schaller


Editors In Chief:
Laurie Graham
Andrew Wilt
Mary Cataletto


Managing Editors:
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Benjamin Eovaldi
Radia Jamil
Sobhan Daneshfar
Pritesh Sheth
Hassam Zulfiqar
Steve Bhimji
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Hajira Basit
Phillip Hynes
Kavin Sugumar


Updated:
6/4/2019 6:07:07 PM

Introduction

Acid-base disorders, including metabolic acidosis, are disturbances in the homeostasis of plasma acidity. Any process that increases the serum hydrogen ion concentration is a distinct acidosis. The term acidemia is used to define the total acid-base status of the serum pH. For example, a patient can have multiple acidoses contributing to a net acidemia. Its origin classifies acidosis as either a respiratory acidosis which involves changes in carbon dioxide, or metabolic acidosis which is influenced by bicarbonate (HCO3).[1][2][3]

Metabolic acidosis is characterized by an increase in the hydrogen ion concentration in the systemic circulation resulting in a serum HCO3 less than 24 mEq/L. Metabolic acidosis is not a benign condition and signifies an underlying disorder that needs to be corrected to minimize morbidity and mortality. The many etiologies of metabolic acidosis are classified into 4 main mechanisms: increased production of acid, decreased excretion of acid, acid ingestion, and renal or gastrointestinal (GI) bicarbonate losses.[4][5][6]

Etiology

Determining the type of metabolic acidosis can help clinicians narrow down the cause of the disturbance. Acidemia refers to a pH less than the normal range of 7.35 to 7.45. In addition, metabolic acidosis requires a bicarbonate value less than 24 mEq/L. Further classification of metabolic acidosis is based on the presence or absence of an anion gap, or concentration of unmeasured serum anions. Plasma neutrality dictates that anions must balance cations to maintain a neutral charge. Therefore, sodium (Na), the primary plasma cation, is balanced by the sum of the anions bicarbonate and chloride in addition to the unmeasured anions, which represent the anion gap. Unmeasured anions include lactate and acetoacetate, and these are often some of the main contributors to metabolic acidosis.[7][8][9]

  • Anion gap (AG) = [Na] –([Cl] + [HCO3])

Anion gap metabolic acidosis is frequently due to anaerobic metabolism and lactic acid accumulation. While lactate is part of many mnemonics for metabolic acidosis, it is important to distinguish it is not a separate etiology, but rather a consequence of a condition.

Mnemonic for anion gap metabolic acidosis differential: CAT MUDPILES

  • C: Cyanide and carbon monoxide poisoning
  • A: Arsenic
  • T: Toluene
  • M: Methanol, Metformin
  • U: Uremia
  • D: DKA
  • P: Paraldehyde
  • I: Iron, INH
  • L: Lactate
  • E: Ethylene glycol
  • S: Salicylates

Non-gap metabolic acidosis is primarily due to the loss of bicarbonate, and the main causes of this condition are diarrhea and renal tubular acidosis. Additional and rarer etiologies include Addison’s disease, ureterosigmoid or pancreatic fistulas, acetazolamide use, and hyperalimentation through TPN initiation. GI and renal losses of bicarbonate can be distinguished via urine anion gap analysis:

  • Urine AG = Urine Na + Urine K – Urine Cl

A positive value is indicative of renal bicarbonate loss, such as renal tubular acidosis. Negative values are found with non-renal bicarbonate losses, such as diarrhea.

Epidemiology

Metabolic acidosis is a sign of underlying pathology, and while it is not uncommon, especially in acutely ill patients, the overall prevalence in the population is uncertain.

Pathophysiology

Hydrogen ion concentration is determined by acid ingestion, acid production, acid excretion, and renal and GI bicarbonate losses. Buffers such as bicarbonate minimize significant pH alterations.[10][11]

History and Physical

A focused history can elicit potential causes of acid-base disturbances such as vomiting, diarrhea, medications, possible overdoses and chronic conditions with a predisposition to acidosis including diabetes mellitus. 

The physical exam reveals signs unique to each cause such as dry mucous membranes in the patient with diabetic ketoacidosis. Hyperventilation may also be present as a compensatory respiratory alkalosis to assist with PCO2 elimination and correction of the acidemia. Compensatory reactions do not completely correct a disturbance to the normal pH range, however.

Evaluation

Interpretation Steps

Acid-base interpretation is crucial to identify and correct disturbances in acid-base equilibrium that have profound consequences on patient health. The following steps use lab values and equations to determine if a patient has metabolic acidosis and any additional acid-base disturbances.

Step 1: pH, determine if the acid-base status is acidemia or alkalemia

Blood pH is maintained within a narrow range for optimization of physiological functions. Acid-base equilibrium is achieved within a pH range of 7.35 to 7.45. Blood pH distinguishes between acidemia (pH less than 7.35) and alkalemia (pH greater than 7.45)

Step 2: CO2, determine if the disturbance is metabolic or respiratory

The pCO2 determines whether an acidosis is respiratory or metabolic in origin. For a respiratory acidosis, the pCO2 is greater than 40 to 45 due to decreased ventilation. Metabolic acidosis is due to alterations in bicarbonate, so the pCO2 is less than 40 since it is not the cause of the primary acid-base disturbance. In metabolic acidosis, the distinguishing lab value is a decreased bicarbonate (normal range 21 to 28 mEq/L).

Step 3: Determine if there is anion gap or non-anion gap metabolic acidosis

  • AG= Na – (Cl + HCO3)

The normal anion gap is 12. Therefore, values greater than 12 define an anion gap metabolic acidosis.

Step 4: CO2, assess if respiratory compensation is appropriate

Respiratory compensation is the physiologic mechanism to help normalize a metabolic acidosis, however, compensation never completely corrects an acidemia. It is important to determine if there is adequate respiratory compensation or if there is another underlying respiratory acid-base disturbance. Winter's formula is the equation used to determine the expected CO2 for adequate compensation.

  • Winter’s formula: Expected CO2 = (Bicarbonate x 1.5) + 8 +/- 2

If the patient’s pCO2 is within the predicted range, then there is no additional respiratory disturbance. If the pCO2 is greater than expected, this indicates an additional respiratory acidosis. If the pCO2 is less than expected, there is an additional respiratory alkalosis occurring.

Step 5: Evaluate for additional metabolic disturbances

A delta gap must be determined if an anion gap is present.

  • Delta gap = Delta AG – Delta HCO3 = (AG-12) – (24-bicarbonate)

If the gap is less than -6, then a NAGMA is present.

If the gap is greater than 6, then an underlying metabolic alkalosis is present.

If the gap is between -6 and 6 then only an anion gap acidosis exists.

Treatment / Management

The management of metabolic acidosis should address the cause of the underlying acid-base derangement. For example, adequate fluid resuscitation and correction of electrolyte abnormalities are necessary for sepsis and diabetic ketoacidosis. Other therapies to consider include antidotes for poisoning, dialysis, antibiotics, and bicarbonate administration in certain situations.

Refer to the specific conditions for a thorough explanation of the appropriate treatment.

Differential Diagnosis

The differential diagnosis depends on the cause of metabolic acidosis. Etiology of the derangement determines the characteristics that influence the differential diagnosis.

Prognosis

The prognosis of metabolic acidosis is dependent upon the etiology and the acid-base derangement. The prognosis is poor if derangements are large and vitals are unstable.

Pearls and Other Issues

Metabolic acidosis is a clinical disturbance defined by a pH less than 7.35 and a low HCO3 level.

The anion gap helps determine the cause of the metabolic acidosis. An elevated anion gap metabolic acidosis can be caused by salicylate toxicity, diabetic ketoacidosis, and uremia (MUDPILES). Non-Gap metabolic acidosis is due to GI loss of bicarbonate (diarrhea) or a failure of kidneys to excrete acid.

Lab tests that help evaluate metabolic acidosis are those that assess renal and lung function including electrolytes, venous or arterial blood gas, and toxin levels such as salicylate if an overdose is suspected.

Treatment of metabolic acidosis is case-dependent.

Enhancing Healthcare Team Outcomes

The management of metabolic acidosis should address the cause of the underlying acid-base derangement. Because there are many causes, the electrolyte disorder is best managed by a multidisciplinary teamt that also includes nurses and pharmacists. For example, adequate fluid resuscitation and correction of electrolyte abnormalities are necessary for sepsis and diabetic ketoacidosis. Other therapies to consider include antidotes for poisoning, dialysis, antibiotics, and bicarbonate administration in certain situations.

The outcomes depend on the cause, patient morbidity and response to treatment.


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Physiology, Acidosis, Metabolic - Questions

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Which condition does not cause anion gap acidosis?



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Which of the following does not cause a non-anion gap acidosis?



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Which of the following pairs is not correctly associated?



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A patient who fell from a two-story building is breathing spontaneously and has a room air blood gas of PO2 85, PCO2 30, and pH 7.18. What is the most likely cause of the abnormality?



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Which of the following acid base disorder is likely in a 38-year-old with renal tubular acidosis? (pH/HCO3/PO2/PCO2)



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A 17-year-old is brought to the emergency department due to nausea with vomiting for several days. On arrival his blood pressure is 140/70 mm Hg, pulse is 80/min., temperature is 38 C, and SaO2 is 97%. Prior to any medical treatment, which of the following blood lab results is most likely to be obtained?



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What type of metabolic acidosis is associated with diarrhea?



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Which of the following electrolyte abnormalities is associated with metabolic acidosis?



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Which of the following laboratory results is NOT consistent with a metabolic acidosis with respiratory compensation?



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Which of the following findings is NOT present in metabolic acidosis?



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A patient with pH=7.34, PCO2=31, HCO3=20 has what type of acid-base imbalance?



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Which of the following would explain an arterial blood gas with a pH of 7.36, PO2 of 105, PCO2 of 32 mm Hg, and bicarbonate of 17 mEq/L?



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A patient has the following laboratory values: sodium 135 meq/L, potassium 2.7 meq/L, HCO3 9 meq/L, chloride 116 meq/L, BUN 18 mg/dL, creatinine 1.0 mg/dL. The arterial blood gas shows PO2=80 mmHg, PCO2= 24 mmHg, pH=7.29. Select the correct description.



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A febrile patient presents to the emergency room with hypotension. Preliminary laboratory analysis reveals elevated lactic acid levels and evidence of metabolic acidosis. What is the major blood buffer which will help the patient counteract the acidosis?



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What metabolic derangement is associated with shock?



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Which chemical is increased in metabolic acidosis?



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What electrolyte abnormality is most likely to be found in a patient with severe diarrhea?



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Which is consistent with metabolic acidosis?



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A 17-year old known type 1 diabetic presents to the emergency department with labored respirations, polyuria, polydipsia and a fruity odor on her breath. She admits that she hasn’t been taking her insulin in order to lose weight. Labs are drawn. serum pH 7.29, PCO2 20, sodium (Na) 140 mmol/L, potassium (K) 5.0 mmol/L, chloride (Cl) 90 mmol/L, bicarbonate (HCO3) 20 mmol/L, and glucose 631 mg/dL. What is the acid-base status, and is her respiratory compensation appropriate?



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A homeless patient presents with nausea, vomiting, and blurry vision. Laboratory results are obtained. Labs show serum pH 7.30, sodium (Na) 145 mmol/L, chloride (Cl) 100 mmol/L, and bicarbonate (HCO3) 19 mmol/L. What is the most likely diagnosis?



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A 3-old male patient presents to the emergency department with nausea, vomiting and altered mental status. He is breathing rapidly and accompanied by a babysitter who witnessed him ingest “a handful of pills.” Labs show serum pH 7.51, PCO2 24 mmHg, sodium (Na) 145 mmol/L, potassium (K) 4.0 mmol/L, chloride (Cl) 105 mmol/L, and bicarbonate (HCO3) 15 mmol/L. What is his acid-base status?



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A 34-year old woman with nausea, vomiting, headache and altered mental status is rescued from a structure fire. Her nares are singed, and soot is present on her lips. Lab tests reveal an elevated carboxyhemoglobin level, elevated lactate, and cyanide poisoning. Which of the following patients may present with the same derangements?



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A patient presents with the following lab values: serum pH 7.28, PCO2 34, sodium (Na) 137 mmol/L, potassium (K) 3.5 mmol/L, chloride (Cl) 105 mmol/L, bicarbonate (HCO3) 20 mmol/L, urine Na 40 mmol/L, urine K 40 mmol/L, and urine Cl 50. What is the acid-base status?



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Physiology, Acidosis, Metabolic - References

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