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Revision as of 14:01, 15 May 2018

Acid Base Disorders

Blood Gas Analysis

Blood gas analysis Vessel Range Interpretation
Oxygen Partial Pressure (pO2) Arterial 80 to 100 mmHg Normal
<80  mmHg Hypoxia
Venous 35 to 40 mmHg Normal
Oxygen Saturation (SO2) Arterial >95% Normal
<95% Hypoxia
Venous 70 to 75% Normal
pH Arterial <7.35 Acidemia
7.35 to 7.45 Normal
>7.45 Alkalemia
Venous 7.26 to 7.46 Normal
Carbon Dioxide Partial Pressure (pCO2) Arterial <35 mmHg Low
35 to 45 mmHg Normal
>45 mmHg High
Venous 40 to 45 mmHg Normal
Bicarbonate (HCO3−) Arterial <22 mmol/L Low
22 to 26 mmol/L Normal
>26 mmol/L High
Venous 19 to 28 mmol/L Normal
Base Excess (BE) Arterial <−3.4 Acidemia
−3.4 to +2.3 mmol/L Normal
>2.3 Alkalemia
Venous −2 to −5 mmol/L Normal
Osmolar gap = Osmolality – Osmolarity >10 Abnormal
Anion gap = [Na+] – {[Cl−]+[HCO3−]}

Corrected AG = (measured serum AG) + (2.5 x [4.5 − Alb])

<8 Low
8 to 16 Normal
>16 High

Compensation

  • There are compensation mechanisms in the body in order to normalizing the pH inside the blood.[1]
  • The amount of compensation depends on proper functioning of renal and respiratory systems. However, it is uncommon to compensate completely. Compensatory mechanisms might correct only 50–75% of pH to normal.
  • Acute respiratory compensation usually occurs within first day. However, chronic respiratory compensation takes 1 to 4 days to occur.
  • Renal compensation might occur slower than respiratory compensation.
Primary disorder pH PaCO2 [HCO3−] Compensation Compensation formula
Metabolic acidosis ↓ ↓ ↓ Respiratory
  • Expected paCO2 = 1.5 x serum HCO3− + 8 ± 2 (Winters' formula)
  • Expected paCO2 = Serum HCO3− + 15
Metabolic alkalosis ↑ ↑ ↑ Respiratory
  • Expected paCO2 = 0.5 − 1 increase/ every 1 unit increase in serum HCO3− from 24
Respiratory acidosis ↓ ↑ ↑ Renal
  • Acute: HCO3− increases by 1mEq/L for every 10 mmHg increase in paCO2 above 40
  • Chronic: HCO3− increases by 3.5mEq/L for every 10 mmHg increase in paCO2 above 40
Respiratory alkalosis ↑ ↓ ↓ Renal
  • Acute: HCO3− decreases by 2mEq/L for every 10 mmHg derease in paCO2 above 40
  • Chronic: HCO3− decreases by 5mEq/L for every 10 mmHg decrease in paCO2 above 40

Approach to acid–base disorders

 
 
 
 
 
 
 
Check pH on ABG
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
pH < 7.35= Acidosis
 
 
 
 
 
 
 
pH > 7.45= Alkalosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Check PaCO2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
PaCO2 > 45mm Hg =
Respiratory acidosis
 
PaCO2 Normal or < 35mm Hg =
Metabolic acidosis
 
 
 
 
 
Check PaCO2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
PaCO2 > 45mm Hg =
Metabolic alkalosis
 
PaCO2 < 35mm Hg =
Respiratory alkalosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
[HCO3-] > 29
 
 
Check [HCO3-]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Normal or slight decrease =
Acute respiratory alkalosis
 
 
 
Decreased < 24 =
Chronic respiratory alkalosis

Management of Acidosis

 
 
 
 
 
 
 
 
pH < 7.35
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Acidosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Determine the primary disorder
Metabolic or respiratory?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Check [HCO3-] and PaCO2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Low [HCO3-]
and
Low to normal PaCO2
 
 
 
 
 
 
 
 
 
 
 
High PaCO2
and
High to normal [HCO3-]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Metabolic acidosis
 
 
 
 
 
 
 
 
 
 
 
Respiratory acidosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Check for respiratory compensation

Calculate expected PCO2
 
 
 
 
 
 
 
 
 
 
 
Check for renal compensation

Calculate expected [HCO3-]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Decrease in PaCO2=1.25 x (24- measured HCO3-)?
 
 
 
 
 
 
 
Acute acidosis?

Increase [HCO3-]=0.1 x (measure PaCO2-40)?
 
 
 
 
 
Chronic acidosis?

Increase [HCO3-]=0.1 x (measure PaCO2-40)?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
PaCO2 too low?

Mixed metabolic acidosis with respiratory alkalosis
 
 
PaCO2 too high?

Mixed metabolic acidosis with respiratory acidosis
 
 
 
[HCO3-] too low?

Mixed respiratory acidosis with metabolic acidosis
 
 
[HCO3-] too high?

Mixed respiratory acidosis with metabolic alkalosis
 
[HCO3-] too low?

Mixed respiratory acidosis with metabolic acidosis
 
 
E04=[HCO3-] too high?

Mixed respiratory acidosis with metabolic alkalosis
 
 
 
Measured PaCO2 is equal to expected value?

Compensated metabolic acidosis
 
 
 
 
 
 
 
 
 
Measured [HCO3-] is equal to expected value?

Compensated respiratory acidosis
 
 
 
 
 
 
 
Measured [HCO3-] is equal to expected value?

Compensated respiratory acidosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Click here for the management of metabolic acidosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Click here for the management of respiratory acidosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

Metabolic Acidosis

Differential diagnosis of metabolic acidosis is as follow:[2][3][4][5]

Category Disease Mechanism Clinical Paraclinical Gold standard diagnosis Other findings
Symptoms Signs Lab data
ABG CBC Chemistry Renal U/A
↑ acid
production 		Loss of
bicarbonate 		↓ renal acid
excretion 		Fever N/V Diarrhea Dyspnea Toxic/ill BP Dehydration LOC HCO3− paCO2 O2 WBC Hb BS Cl− K+ Na+ Ketones Lactic acid Serum AG[6] Osmolar gap[7] Bun Cr Urine pH Urine AG Urine ketone
Toxin/Medication[8] Alcohol[9][10]
  • Methanol
  • Ethylene glycol
  • Propylene glycol
 + − − − + − − + ↓ ↑ + ↓ ↓ ↓ ↓ Nl Nl ↑ ↑ ↑ Nl + ↑ ↑ ↑ Nl or ↑ Nl or ↑ ↓ + + Clinical
  • Positive oxalate crystals in urine
  • Isopropyl alcohol[11]
 + − − − + − − + ↓ + ↓ ↓ ↓ ↓ Nl Nl Nl ↑ ↑ Nl + ↑ Nl ↑ Nl Nl or ↑ ↓ + + Clinical
Toluene[12] + − + − + − − + ↓ − ↓ ↓↓ ↓ Nl Nl Nl Nl Nl ↓ Nl − ↑ Nl or ↑ Nl ↑ ↑ ↓ − + Clinical
  • Most widely abused inhaled drugs
Salicylates[13] + − − − + − + + ↓ + ↓ ↓ ↓↓ ↓ Nl Nl Nl to ↓ Nl ↓ Nl − ↑ ↑ ↑ ↑ ↑ ↓ − − Clinical and elevated serum salicylate
  • Paradoxical alkalosis
  • Elevated serum salicylate
Metformin[14] + − − − + − − + ↓ ± Agitated ↓ ↓ Nl Nl to ↑ ↓ ↓ Nl Nl Nl Nl ↑ ↑ ↑ Nl or ↑ Nl ↓ − − Clinical
  • Liver failure
Isoniazid[15] + − − − + − − + ↑ + Agitated ↓ ↓ Nl Nl ↓ Nl Nl Nl Nl Nl ↑ ↑ Nl Nl or ↑ Nl ↓ − − Clinical
  • Seizure
  • Ataxia
Acetazolamide[16] - + - - - - - - ↓ + Nl ↓ ↓ Nl to ↓ Nl Nl Nl Nl Nl Nl Nl Nl Nl Nl Nl or ↑ Nl ↓ − − Clinical
Amphotericin B[17] - - + - + + - + ↓ + ↓ ↓ ↓ Nl to ↓ Nl Nl Nl Nl Nl Nl Nl Nl Nl Nl ↑ ↑ ↓ - - Clinical
CO[18] + - + - ± - - + Nl - ↓↓ ↓ ↓ Nl to ↓ Nl Nl Nl Nl Nl Nl Nl ↑ ↑ Nl Nl Nl ↓ − − Clinical
Cyanide[19] + − − - + − − + ↓ ± ↓↓ ↓ ↓ ↓ Nl to ↑ ↓ Nl Nl Nl Nl Nl ↑ ↑ Nl Nl or ↑ Nl ↓ − − Blood cyanide concentration
Category Disease ↑ acid
production 		Loss of
bicarbonate 		↓ renal acid
excretion 		Fever N/V Diarrhea Dyspnea Toxic/ill BP Dehydration LOC HCO3− paCO2 O2 WBC Hb BS Cl− K+ Na+ Ketones Lactic acid Serum AG Osmolar gap Bun Cr Urine pH Urine AG Urine ketone Gold standard diagnosis Other findings
Ketoacidosis Diabetic[20] + − − + + + + + ↓ + ↓ ↓ ↓ Nl to ↓ ↑ Nl to ↑ ↑↑ Nl ↓ ↓ ↑ ↑ ↑ ↑ Nl to ↑ Nl ↓ + + Clinical + hyperglycemia + ketosis
Starvation[21] + − − − + − − + ↓ + ↓ ↓ ↓ Nl Nl Nl Nl to ↓ Nl ↓ ↓ ↑ Nl ↑ Nl Nl Nl Nl + − Clinical
Alcoholic (Ethanol)[22] + − − − + ± − + ↓ ↑ + Agitated ↓ ↓ ↓ Nl to ↑ Nl to ↑ ↓ Nl ↑ Nl ↓ ↓ ↑↑ ↑ ↑ ↑↑ ↑ Nl ↓ + + Clinical + ketosis
  • Chronic alcohol abuse
  • Zero or low alcohol level
Systemic Sepsis[23] + − − + + − + + ↓ ↑ + ↓ ↓ ↓ Nl to ↓ ↑ Nl Nl Nl ↑ ↓ Nl Nl to ↑ Nl Nl ↑ ↑ Nl − − Clinical and lab finding
Ischemia[24] + − − − + − + + ↓ + − ↓ ↓ ↑ Nl to ↓ Nl to ↑ Nl Nl Nl ↑ ↓ Nl Nl to ↑ Nl Nl Nl to ↑ Nl to ↑ Nl − − Clinical and lab finding
Lactic acidosis[25] + − − ± + − − + ↓ ↑ ± Agitated ↓ ↓ ↓ Nl to ↑ ↓ Nl Nl Nl Nl Nl ↑ ↑ ↑ Nl or ↑ Nl ↓ − − Clinical and lab finding
Renal Uremia[26] − − + + + − − + ↓ ↑ ± ↓ ↓ ↓ Nl to ↓ ↑ ↓ Nl Nl ↑ ↑ Nl ↑ ↑ ↑ ↑ ↓ + − Clinical and lab finding
Ureteral diversion + Nl Nl
Renal failure[27] − − + − + − − + ↓ + ↓ ↓ ↓ Nl to ↓ ↑ ↑ ↑
Renal tubular acidosis[28] Type I[29] − − + ± ± − − − ↓ ↑ − − ↓ ↓ Nl Nl Nl Nl ↑ ↓ ↓ Nl Nl Nl Nl ↑ ↑ ↑ + − Clinical and lab finding
  • Associated with autoimmune diseases
  • Growth retardation in children
Type II − + − ± ± − − − ↓ ↑ − − ↓ ↓ Nl Nl Nl Nl ↑ ↓ Nl Nl Nl Nl Nl Nl Nl Nl − − Clinical and lab finding
Type IV − − + ± ± ± − − ↓ − − ↓ ↓ Nl Nl Nl Nl ↑ ↑ Nl Nl Nl Nl Nl Nl Nl Nl + − Clinical and lab finding
  • Hypoaldosteronism
Category Disease ↑ acid
production 		Loss of
bicarbonate 		↓ renal acid
excretion 		Fever N/V Diarrhea Dyspnea Toxic/ill BP Dehydration LOC HCO3− paCO2 O2 WBC Hb BS Cl− K+ Na+ Ketones Lactic acid Serum AG Osmolar gap Bun Cr Urine pH Urine AG Urine ketone Gold standard diagnosis Other findings
Heart Heart failure[30] + + − − ± − + + ↓ ↑ + − ↓ ↓ ↑ ↓ Nl Nl Nl Nl ↓ ↓ Nl Nl Nl Nl Nl to ↑ Nl to ↑ Nl − − Clinical and echocardiogram
  • Hypoalbuminemia
  • Elevated serum natriuretic peptide
MI[31] + − − − + − + + ↓ ↑ − ↓ ↓ ↓ ↑ Nl to ↓ Nl to ↑ Nl Nl Nl ↑ ↓ Nl ↑ Nl Nl Nl to ↑ Nl to ↑ Nl − − Clinical and ECG
GI Diarrhea − + − ± + + − + ↓ + − ↓ ↓ Nl Nl ↓ ↓ ↑ ↑ Nl Nl Nl Nl Nl ↑ Nl Nl − −
Hyperalimentation + + − − − + − − Nl − − ↓ ↓ Nl Nl ↓ ↓ ↑ ↑ ↑ Nl Nl Nl Nl Nl Nl Nl Nl − − Clinical
Liver failure Nl Nl
Endocrine Hyperparathyroidism + Nl Nl
Addison's disease Nl Nl
Category Disease ↑ acid
production 		Loss of
bicarbonate 		↓ renal acid
excretion 		Fever N/V Diarrhea Dyspnea Toxic/ill BP Dehydration LOC HCO3− paCO2 O2 WBC Hb BS Cl− K+ Na+ Ketones Lactic acid Serum AG Osmolar gap Bun Cr Urine pH Urine AG Urine ketone Gold standard diagnosis Other findings

Metabolic Alkalosis

Differential diagnosis of metabolic alkalosis is as follow:

Category Disease Mechanism Clinical Paraclinical Gold standard diagnosis Other findings
Symptoms Signs Lab data Imaging
ABG U/A Electrolytes Renin
↑ acid
production 		Loss of
bicarbonate 		↓ renal acid
excretion 		Fever Dyspnea Edema Toxic/ill BP Dehydration pH Serum AG Urine Cl− Cl− K+ Na+ US CT scan
Exogenous HCO3− loads Acute alkali administration
Milk−alkali syndrome
Gastrointestinal origin Vomiting + ↓
Nasogastric tube suction + ↓
Gastric aspiration
Congenital chloridorrhea
Villous adenoma
Renal origin Diuretics + ↓
Posthypercapnic state
Hypercalcemia/hypoparathyroidism
Recovery from lactic acidosis or ketoacidosis
Nonreabsorbable anions including penicillin, carbenicillin
Hypomagnesemia − Nl
Hypokalemia − Nl
Bartter's syndrome − Nl
Gitelman’s syndrome
Renal artery stenosis ↑ Nl ↑
Endocrine Cushing's syndrome ↑ Nl ↓
Hyperaldosteronism ↑ Nl ↓
Other Licorice ingestion − Nl ↓

Mixed Acid−Base Disorders

Disorder Key features Examples
Metabolic acidosis & respiratory alkalosis
  • High− or normal−AG metabolic acidosis
  • Prevailing PaCO2 below predicted value  
  • Lactic acidosis
  • Sepsis in ICU
Metabolic acidosis & respiratory acidosis
  • High− or normal−AG metabolic acidosis
  • Prevailing PaCO2 above predicted value 
  • Severe pneumonia
  • Pulmonary edema  
Metabolic alkalosis & respiratory alkalosis
  • PaCO2 does not increase as predicted
  • pH higher than expected
  • Liver disease
  • Diuretics
Metabolic alkalosis & respiratory acidosis
  • PaCO2 higher than predicted
  • pH normal
  • COPD on diuretics
Metabolic acidosis & metabolic alkalosis
  • Only detectable with high−AG acidosis
  • ∆AG >> ∆[HCO3−]
  • Uremia with vomiting
Metabolic acidosis & metabolic acidosis
  • Mixed high−AG & normal−AG acidosis
  • ∆[HCO3−] accounted for by combined change in ∆AG and ∆Cl−
  • Diarrhea and lactic acidosis
  • Toluene toxicity
  • Treatment of diabetic ketoacidosis

Related Chapters

  1. ↑ Sood P, Paul G, Puri S (April 2010). "Interpretation of arterial blood gas". Indian J Crit Care Med. 14 (2): 57–64. doi:10.4103/0972-5229.68215. PMC 2936733. PMID 20859488.
  2. ↑ Lim S (2007). "Metabolic acidosis". Acta Med Indones. 39 (3): 145–50. PMID 17936961.
  3. ↑ Morris, C. G.; Low, J. (2008). "Metabolic acidosis in the critically ill: Part 1. Classification and pathophysiology". Anaesthesia. 63 (3): 294–301. doi:10.1111/j.1365-2044.2007.05370.x. ISSN 0003-2409.
  4. ↑ Morris CG, Low J (April 2008). "Metabolic acidosis in the critically ill: part 2. Causes and treatment". Anaesthesia. 63 (4): 396–411. doi:10.1111/j.1365-2044.2007.05371.x. PMID 18336491.
  5. ↑ Casaletto, Jennifer J. (2005). "Differential Diagnosis of Metabolic Acidosis". Emergency Medicine Clinics of North America. 23 (3): 771–787. doi:10.1016/j.emc.2005.03.007. ISSN 0733-8627.
  6. ↑ Brubaker RH, Meseeha M. High Anion Gap Metabolic Acidosis. [Updated 2017 Oct 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448090/
  7. ↑ Kraut JA, Xing SX (September 2011). "Approach to the evaluation of a patient with an increased serum osmolal gap and high-anion-gap metabolic acidosis". Am. J. Kidney Dis. 58 (3): 480–4. doi:10.1053/j.ajkd.2011.05.018. PMID 21794966.
  8. ↑ Pham, Amy Quynh Trang; Xu, Li Hao Richie; Moe, Orson W. (2015). "Drug-Induced Metabolic Acidosis". F1000Research. doi:10.12688/f1000research.7006.1. ISSN 2046-1402.
  9. ↑ Zehtabchi S, Sinert R, Baron BJ, Paladino L, Yadav K (2005). "Does ethanol explain the acidosis commonly seen in ethanol-intoxicated patients?". Clin Toxicol (Phila). 43 (3): 161–6. PMID 15902789.
  10. ↑ Roberts, Darren M.; Yates, Christopher; Megarbane, Bruno; Winchester, James F.; Maclaren, Robert; Gosselin, Sophie; Nolin, Thomas D.; Lavergne, Valéry; Hoffman, Robert S.; Ghannoum, Marc (2015). "Recommendations for the Role of Extracorporeal Treatments in the Management of Acute Methanol Poisoning". Critical Care Medicine. 43 (2): 461–472. doi:10.1097/CCM.0000000000000708. ISSN 0090-3493.
  11. ↑ Ashurst JV, Nappe TM. Toxicity, Isopropanol. [Updated 2018 Mar 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK493181/
  12. ↑ Camara-Lemarroy, Carlos Rodrigo; Rodríguez-Gutiérrez, René; Monreal-Robles, Roberto; González-González, José Gerardo (2015). "Acute toluene intoxication–clinical presentation, management and prognosis: a prospective observational study". BMC Emergency Medicine. 15 (1). doi:10.1186/s12873-015-0039-0. ISSN 1471-227X.
  13. ↑ Wright, Dallas; Sop, Jessica (2015). "Normal anion gap salicylate poisoning". The American Journal of Emergency Medicine. 33 (11): 1714.e3–1714.e4. doi:10.1016/j.ajem.2015.03.042. ISSN 0735-6757.
  14. ↑ Galiero, Francesca; Consani, Giovanni; Biancofiore, Gianni; Ruschi, Stefano; Forfori, Francesco (2018). "Metformin intoxication: Vasopressin's key role in the management of severe lactic acidosis". The American Journal of Emergency Medicine. 36 (2): 341.e5–341.e6. doi:10.1016/j.ajem.2017.10.057. ISSN 0735-6757.
  15. ↑ Watkins RC, Hambrick EL, Benjamin G, Chavda SN (January 1990). "Isoniazid toxicity presenting as seizures and metabolic acidosis". J Natl Med Assoc. 82 (1): 57, 62, 64. PMC 2625939. PMID 2304098.
  16. ↑ Teppema, Luc J.; Balanos, George M.; Steinback, Craig D.; Brown, Allison D.; Foster, Glen E.; Duff, Henry J.; Leigh, Richard; Poulin, Marc J. (2007). "Effects of Acetazolamide on Ventilatory, Cerebrovascular, and Pulmonary Vascular Responses to Hypoxia". American Journal of Respiratory and Critical Care Medicine. 175 (3): 277–281. doi:10.1164/rccm.200608-1199OC. ISSN 1073-449X.
  17. ↑ Bates, D. W.; Su, L.; Yu, D. T.; Chertow, G. M.; Seger, D. L.; Gomes, D. R. J.; Dasbach, E. J.; Platt, R. (2001). "Mortality and Costs of Acute Renal Failure Associated with Amphotericin B Therapy". Clinical Infectious Diseases. 32 (5): 686–693. doi:10.1086/319211. ISSN 1058-4838.
  18. ↑ Piantadosi CA (June 1999). "Diagnosis and treatment of carbon monoxide poisoning". Respir Care Clin N Am. 5 (2): 183–202. PMID 10333448.
  19. ↑ Baud FJ, Borron SW, Mégarbane B, Trout H, Lapostolle F, Vicaut E, Debray M, Bismuth C (September 2002). "Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning". Crit. Care Med. 30 (9): 2044–50. doi:10.1097/01.CCM.0000026325.65944.7D. PMID 12352039.
  20. ↑ Wolfsdorf, Joseph I; Allgrove, Jeremy; Craig, Maria E; Edge, Julie; Glaser, Nicole; Jain, Vandana; Lee, Warren WR; Mungai, Lucy NW; Rosenbloom, Arlan L; Sperling, Mark A; Hanas, Ragnar (2014). "Diabetic ketoacidosis and hyperglycemic hyperosmolar state". Pediatric Diabetes. 15 (S20): 154–179. doi:10.1111/pedi.12165. ISSN 1399-543X.
  21. ↑ Mostert M, Bonavia A (October 2016). "Starvation Ketoacidosis as a Cause of Unexplained Metabolic Acidosis in the Perioperative Period". Am J Case Rep. 17: 755–758. PMC 5070574. PMID 27752032.
  22. ↑ Howard RD, Bokhari S. PMID 28613672. Vancouver style error: initials (help); Missing or empty |title= (help)
  23. ↑ Ganesh K, Sharma RN, Varghese J, Pillai MG (2016). "A profile of metabolic acidosis in patients with sepsis in an Intensive Care Unit setting". Int J Crit Illn Inj Sci. 6 (4): 178–181. doi:10.4103/2229-5151.195417. PMC 5225760. PMID 28149822.
  24. ↑ Kimmoun, Antoine; Novy, Emmanuel; Auchet, Thomas; Ducrocq, Nicolas; Levy, Bruno (2015). "Hemodynamic consequences of severe lactic acidosis in shock states: from bench to bedside". Critical Care. 19 (1). doi:10.1186/s13054-015-0896-7. ISSN 1364-8535.
  25. ↑ Kraut, Jeffrey A.; Ingelfinger, Julie R.; Madias, Nicolaos E. (2014). "Lactic Acidosis". New England Journal of Medicine. 371 (24): 2309–2319. doi:10.1056/NEJMra1309483. ISSN 0028-4793.
  26. ↑ Brown, Denver; Melamed, Michal L. (2018). "New Frontiers in Treating Uremic Metabolic Acidosis". Clinical Journal of the American Society of Nephrology. 13 (1): 4–5. doi:10.2215/CJN.11771017. ISSN 1555-9041.
  27. ↑ Kraut, Jeffrey A.; Madias, Nicolaos E. (2016). "Metabolic Acidosis of CKD: An Update". American Journal of Kidney Diseases. 67 (2): 307–317. doi:10.1053/j.ajkd.2015.08.028. ISSN 0272-6386.
  28. ↑ Gil-Peña, Helena; Mejía, Natalia; Santos, Fernando (2014). "Renal Tubular Acidosis". The Journal of Pediatrics. 164 (4): 691–698.e1. doi:10.1016/j.jpeds.2013.10.085. ISSN 0022-3476.
  29. ↑ Hemstreet, Brian A (2004). "Antimicrobial-Associated Renal Tubular Acidosis". Annals of Pharmacotherapy. 38 (6): 1031–1038. doi:10.1345/aph.1D573. ISSN 1060-0280.
  30. ↑ Park, Jin Joo; Choi, Dong-Ju; Yoon, Chang-Hwan; Oh, Il-Young; Lee, Ju Hyun; Ahn, Soyeon; Yoo, Byung-Su; Kang, Seok-Min; Kim, Jae-Joong; Baek, Sang-Hong; Cho, Myeong-Chan; Jeon, Eun-Seok; Chae, Shung Chull; Ryu, Kyu-Hyung; Oh, Byung-Hee (2015). "The prognostic value of arterial blood gas analysis in high-risk acute heart failure patients: an analysis of the Korean Heart Failure (KorHF) registry". European Journal of Heart Failure. 17 (6): 601–611. doi:10.1002/ejhf.276. ISSN 1388-9842.
  31. ↑ Mann, Sarah; Bajulaiye, Akinyemi; Sturgeon, Kathleen; Sabri, Abdelkarim; Muthukumaran, Geetha; Libonati, Joseph R. (2014). "Effects of acute angiotensin II on ischemia reperfusion injury following myocardial infarction". Journal of the Renin-Angiotensin-Aldosterone System. 16 (1): 13–22. doi:10.1177/1470320314554963. ISSN 1470-3203.
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