Acid-base homeostasis: Difference between revisions

Jump to navigation Jump to search
No edit summary
Line 1: Line 1:
__NOTOC__
__NOTOC__
{{Acid-base homeostasis}}
{{Acids and bases}}
{{Acids and bases}}
{{SI}}
{{SI}}

Revision as of 19:45, 21 May 2018

Acid-base Homeostasis

Home

Overview

Mechanism

Blood Gas Analysis

Relationship between pH and H+

Compensation

Related Chapters

WikiDoc Resources for Acid-base homeostasis

Articles

Most recent articles on Acid-base homeostasis

Most cited articles on Acid-base homeostasis

Review articles on Acid-base homeostasis

Articles on Acid-base homeostasis in N Eng J Med, Lancet, BMJ

Media

Powerpoint slides on Acid-base homeostasis

Images of Acid-base homeostasis

Photos of Acid-base homeostasis

Podcasts & MP3s on Acid-base homeostasis

Videos on Acid-base homeostasis

Evidence Based Medicine

Cochrane Collaboration on Acid-base homeostasis

Bandolier on Acid-base homeostasis

TRIP on Acid-base homeostasis

Clinical Trials

Ongoing Trials on Acid-base homeostasis at Clinical Trials.gov

Trial results on Acid-base homeostasis

Clinical Trials on Acid-base homeostasis at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Acid-base homeostasis

NICE Guidance on Acid-base homeostasis

NHS PRODIGY Guidance

FDA on Acid-base homeostasis

CDC on Acid-base homeostasis

Books

Books on Acid-base homeostasis

News

Acid-base homeostasis in the news

Be alerted to news on Acid-base homeostasis

News trends on Acid-base homeostasis

Commentary

Blogs on Acid-base homeostasis

Definitions

Definitions of Acid-base homeostasis

Patient Resources / Community

Patient resources on Acid-base homeostasis

Discussion groups on Acid-base homeostasis

Patient Handouts on Acid-base homeostasis

Directions to Hospitals Treating Acid-base homeostasis

Risk calculators and risk factors for Acid-base homeostasis

Healthcare Provider Resources

Symptoms of Acid-base homeostasis

Causes & Risk Factors for Acid-base homeostasis

Diagnostic studies for Acid-base homeostasis

Treatment of Acid-base homeostasis

Continuing Medical Education (CME)

CME Programs on Acid-base homeostasis

International

Acid-base homeostasis en Espanol

Acid-base homeostasis en Francais

Business

Acid-base homeostasis in the Marketplace

Patents on Acid-base homeostasis

Experimental / Informatics

List of terms related to Acid-base homeostasis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Overview

Acid-base homeostasis is the part of human homeostasis concerning the proper balance between acids and bases, in other words the pH. The body is very sensitive to its pH level. Outside the range of pH that is compatible with life, proteins are denatured and digested, enzymes lose their ability to function, and the body is unable to sustain itself.

Mechanism

The kidneys maintain acid-base homeostasis by regulating the pH of the blood plasma. Gains and losses of acid and base must be balanced. The study of the acid-base reactions in the body is acid base physiology.

Buffering agents

Any substance that can reversibly bind hydrogen ions is called a buffering agent. They function to impede any change in pH. Hydrogen ions are buffered by extracellular (e.g., bicarbonate, ammonia) and intracellular buffering agents (including proteins and phosphate).

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

Approach to Acid–base Imbalance

 
 
 
 
 
 
 
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

Acid–base Imbalance

Imbalance has several possible causes. An excess of acid is called acidosis and an excess in bases is called alkalosis. Acidosis is much more common than alkalosis. The imbalance is compensated by negative feedback to restore normal values. There are various renal responses to acidosis and alkalosis.

Causes

Sources of acid gain:

  1. Carbon dioxide (since CO2 and OH-, hydroxide, form HCO3-, bicarbonate, and H+, a proton, in the presence of carbonic anhydrase)
  2. Production of nonvolatile acids from the metabolism of proteins and other organic molecules
  3. Loss of bicarbonate in faeces or urine
  4. Intake of acids or acid precursors

Sources of acid loss:

  1. Use of hydrogen ions in the metabolism of various organic anions
  2. Loss of acid in the vomitus or urine

Response

Responses to acidosis:

  1. Bicarbonate is added to the blood plasma by tubular cells.
    • Tubular cells reabsorb more bicarbonate from the tubular fluid.
    • Collecting duct cells secrete more hydrogen and generate more bicarbonate.
  2. Ammoniagenesis leads to increased buffer formation (in the form of NH3)

Responses to alkalosis:

  1. Excretion of bicarbonate in urine.
    • This is caused by lowered rate of hydrogen ion secretion from the tubular epithelial cells.
    • This is also caused by lowered rates of glutamine metabolism and ammonia excretion.

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

Mixed Acid−base Disorders

Disorder Key features Examples
Metabolic acidosis & respiratory alkalosis
Metabolic acidosis & respiratory acidosis
Metabolic alkalosis & respiratory alkalosis
  • PaCO2 does not increase as predicted
  • pH higher than expected
Metabolic alkalosis & respiratory acidosis
  • PaCO2 higher than predicted
  • pH normal
Metabolic acidosis & metabolic alkalosis
  • Only detectable with high−AG acidosis
  • AG >> ∆[[[Bicarbonate|HCO3]]]
Metabolic acidosis & metabolic acidosis
  • Mixed high−AG & normal−AG acidosis
  • ∆[[[Bicarbonate|HCO3]]] accounted for by combined change in ∆AG and ∆Cl

See also

  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.