Acid-Base Balance : Basics
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Transcript of Acid-Base Balance : Basics
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ACIDS, BASES AND SALTS
• CHEMICAL COMPOUNDS CAN BE PROTON DONORS OR ACCEPTORS
• PROTON DONORS ARE ACIDS
• PROTON ACCEPTORS ARE BASES
• ACIDS AND BASES REACT TO NEUTRALIZE EACH OTHER FORMING SALTS
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H+ ion & pH SCALE
• H+ ion conc. of plasma:0.000 000 04 mol/L
or 40 nmol/L
• pH is the negative logarithm of hydrogen ion conc.
Normal : 7.35 – 7.45
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Introduction
Metabolic processes continually produce acid and, to a lesser degree, base.
H+ : can attach to negatively charged
proteins &
in high concentrations, alter their overall charge, configuration, and function.
VittalVittal Acid Base BalanceIntroduction
To maintain cellular function, the body has elaborate mechanisms that maintain blood H+ concentration within a narrow range—
typically : 37 to 43 nmol/L
(pH 7.35 to 7.45), &
ideally : 40 nmol/L (pH = 7.4)
Disturbances of these mechanisms can have serious clinical consequences.
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Volatile acid – Can leave solution and enter the atmosphere (e.g. carbonic
acid)
– Produced by aerobic metabolism
Fixed acids– Acids that do not leave solution (e.g. sulfuric and phosphoric
acids)
– Generated during catabolism of amino acids
Organic acids– Participants in or by-products of aerobic and anaerobic
metabolism
– Metabolic byproducts such as lactic acid, ketone bodies
Types of acids in the body
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Acid-Base Physiology Acid-Base Physiology Most acid comes from carbohydrate and fat Most acid comes from carbohydrate and fat
metabolism (15,000 to 20,000 mmol of COmetabolism (15,000 to 20,000 mmol of CO22 daily)daily)
COCO22 combines with water (H combines with water (H22O) in the blood O) in the blood to create carbonic acid (Hto create carbonic acid (H22COCO33), which in the ), which in the presence of the enzyme carbonic anhydrase presence of the enzyme carbonic anhydrase dissociates into Hdissociates into H++ and HCO and HCO33
−−. . The HThe H++ binds with Hb in the blood and is binds with Hb in the blood and is
released with oxygenation in the alveoli, the released with oxygenation in the alveoli, the above reaction is reversed, creating Habove reaction is reversed, creating H22O and O and COCO22, which is exhaled, which is exhaled
Very little metabolic acid is produced - Very little metabolic acid is produced - which is eliminated by kidney and liver.which is eliminated by kidney and liver.
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Acid-Base Physiology Acid-Base Physiology
Most base comes from metabolism Most base comes from metabolism of anionic amino acids (glutamate of anionic amino acids (glutamate and aspartate) and and aspartate) and
from oxidation and consumption of from oxidation and consumption of organic anions such as lactate and organic anions such as lactate and citrate, which produce HCOcitrate, which produce HCO33
−−
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pH : the negative logarithm of the hydrogen ion concentration
o a "decrease" in pH means an "increase" in acidity.
Standard pH: (Hasselbalch, 1916)
the pH under standard conditions: o PCO2=40 mmHg, and 37oC, and saturated with oxygen
Arterial pH = 7.4
Venous pH = 7.36
pH
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PaCO2 :
the partial pressure of carbon dioxide. The normal value in arterial blood is 40 mm Hg (or 5.33 kPa)
PaCO2 ∝ CO2 production + inspired CO2
Low PaCO2 reflects the rate of CO2 elimination
Principal physiological cause of hypocapnia is hyperventilation Intentional, incidental (HFV, ECMO)
PaCO2
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HCO3- : concentration (in mEq/L) of the
bicarbonate ion is not measured, it is calculated from the PCO2 and pH
Standard Bicarbonate : (Jorgensen and Astrup, 1957)
bicarbonate concentration under standard conditions: PCO2=40 mmHg, and 37oC, and saturated with oxygen. an excellent measurement of the metabolic
component.= 21-27 mmol/l
Bicarbonate
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a better method of measuring the metabolic component.
In essence the method calculated the quantity of Acid or Alkali required to return the plasma in-vitro to a normal pH under standard conditions.
Base Escess(Astrup and Siggard-Andersen, 1958)
VittalVittalBase Excess & Base Deficit
(Astrup and Siggard-Andersen, 1958)
Amount of strong acid or base that has to be added to a sample of blood to produce a pH of 7.4 under the specified conditions fro standard bicarbonate.
a more accurate in assessing metabolic component of acid-base status.
Normal Buffer Base = 48mMol/L(41.8 + 0.4 X Hb in g/dL)
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Base Excess & Base Deficit
Base excess – 3 mmol/l : means 3 mmol of strong acid had to be added to each litre of original sample to get a pH of 7.4 while kept at 370C and a PaCO2 of 40 mm Hg.
Base deficit – 3 mmol/l : means 3 mmol of strong base had to be added to each litre of original sample to get a pH of 7.4 while kept at 370C and a PaCO2 of 40 mm Hg.
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Base Excess & Base Deficit
A base excess below -2.0 mmol/l : Metabolic acidosis
A base excess above +2.0 mmol/l : Metabolic alkalosis
Normal
Range
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the difference between major plasma cations and major plasma anions.
Anion gap = ([Na+] +[K+]) - ([Cl--] +[HCO3-])
Gap = Na+ + K+ - Cl- - HCO3- [ 15 = 140 + 5 - 105 - 25 mMol/L]
Anion Gap
Normal Anion Gap Children : 9mo. 19 yrs = 8 + 2 mMol /LAdults : 12 + 2 mMol /L
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Metabolic Acidosis: Types “Normal Anion Gap”, “ Anion Gap”
[Na+] - ([Cl-] + [HCO3-])
Na+
Cl-
HCO3-
Alb-
Na+
Cl-
HCO3-
Alb-
A-
Na+
Cl-
HCO3-
Alb-
No Anion gapM acidosis
High Anion gapM acidosis
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ACID/BASE BALANCE AND THE BLOOD
Acidic Alkaline (Basic)
[OH -]
[H+]
NeutralpH
0 147
Acidosis Alkalosis
Normal7.35-7.45
Venous Blood Arterial Blood
6.8 8.0
7.4
VittalVittal Abnormal acid-base Abnormal acid-base balancebalance
Acid-base imbalances can be defined Acid-base imbalances can be defined
as as acidosisacidosis or or alkalosis.alkalosis. AcidosisAcidosis is a state of excess H is a state of excess H++
AcidemiaAcidemia results when the blood pH is < 7.35 results when the blood pH is < 7.35 AlkalosisAlkalosis is a state of excess HCO is a state of excess HCO3-3-
AlkalemiaAlkalemia results when the blood pH is > 7.45 results when the blood pH is > 7.45
You can have acidosis without acidemia butYou can not have acidemia without an acidosis!
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Regulation of arterial pH
Respiratory
Buffer System
Renal
Respiratory
Buffer System
Renal
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Acid-Base Homeostasis
Kidneys
OutputOutput
Lungs
Maintenance ofNormal [H+]
BuffersBuffers
Metabolism
InputInput
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CHEMICAL BUFFER SYSTEMS
H2CO3
HCO3-
H+
Na+ Cl-
AddHCl
Na+ Cl-
H+ Cl-
Unbuffered Salt Solution All protons are free
H2CO3: HCO3- Buffer
AddHCl
H2CO3
HCO3- + H+
Protons taken up as Carbonic Acid
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Buffer
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Weak acid/salt systems act as a “sponge” for protons
As acidity tends to increase they take protons up
As acidity tends to decrease they release protons
CHEMICAL BUFFER SYSTEMS
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Extracellular Buffers : Carbonic acid/Bicarbonate: Primary buffer
against non-carbonic acid changes
Serum Proteins (albumin) Ammonia ( in renal tubules)
Intracellular Buffers : Hemoglobin Intracellular proteins Phosphates
CHEMICAL BUFFER SYSTEMS
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Handerson Hasselbalch Equation
pH = 6.1 + logHCO3
-
PaCO2 X 0.0301
pK
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(Handerson Equation)
H+ = 24 XpCO2
HCO3-
With this formula, any 2 values (usually H+ and Pco2) can be used to calculate the other (usually HCO3 −).
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Saturation of
carbonic acid – bicarbonate
buffer does not occur because
carbonic acid
is continuously
breaking down into
carbon dioxide
and
water.
VittalVittal Regulation of arterial pH
Respiratory Control:•The power of the lungs to excrete large quantities of carbon dioxide enables them to compensate rapidly, i.e. metabolic acidosis and metabolic alkalosis normally elicit characteristic partial respiratory compensation almost immediately.
• Respiratory • Buffer System• Renal
• Respiratory • Buffer System• Renal
• Not so efficient (50%)• Less in preterm babies• Control of respiratory centre• A CO2 conc. of > 9% depresses centers and causes CO2 narcosis
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Buffer System:• Act within seconds• Act at cellular level• ¾ of body’s buffering system from intracellular proteins and phosphates.
• Respiratory • Buffer System• Renal
• Respiratory • Buffer System• Renal
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Renal Control: HCO3
- Reclamation of almost (80%) all the filtered HCO3
- (5000 mEq)
Substantial task: 180 L x 24 mmol/L = 4320 mmol bicarbonate filtered/day
Generation of new HCO3- with net secretion of H+
(energy dependant) (1 - 1.5 mmol/kg/day)
H+
Increased excretion of acid as phosphate buffer and as ammonia Na+ re-absorption during the formation of H+
• Respiratory • Buffer System• Renal
• Respiratory • Buffer System• Renal
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Acid-Base in the G-I Tract
CO2 H+ + HCO3-
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Dominant site of lactate metabolism Only site of urea synthesis
Acid-base and the Liver
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Severe Liver Failure
NH4+ + oxo-glutarate ---X--> glutamine
NH4+ + CO2 --X--> Urea + H+
• metabolic alkalosis
• NH4+ toxicity
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Overview
1. Induces extra-cellular buffering by HCO3-
2. Within minutes Respiratory Compensation
with decrease in pCO2 and H2CO3 [to
maintain a ratio of HCO3- : H2CO3 ] of 20 : 1
3. Intracellular buffering – in 1 to 4 hours
4. Renal acid excretion and production of new
HCO3- formation : in hours to days
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Acid-base disturbance
Disorder typeDisorder type
Primary change in HCO3 - → Metabolic disorder
Primary change in blood pCO2 → Respiratory disorder
• Simple
• Mixed
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Acid-base imbalance
Plasma pH Primary disturbance
Compensation
Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis-
Metabolic alkalosis-
Abnormal acid-base balances
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Acid-base imbalance
Plasma pH Primary disturbance
Compensation
Respiratory acidosis Low Increased pCO2Increased renal net acid excretion with resulting increase in serum bicarbonate
Respiratory alkalosis High Decreased pCO2Decreased renal net acid excretion with resulting decrease in serum bicarbonate
Metabolic acidosis- LowDecreased HCO3- Hyperventilation with
resulting low pCO2
Metabolic alkalosis- HighIncreased HCO3- Hypoventilation with
resulting increase in
pCO2
Abnormal acid-base balances
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Conclusions
Acid Base Homeostasis is a Dynamic Process
Buffers form the first line of Defence
Bicarbonate buffers are by far the most important
Lungs, Kidneys and Liver play important role in Acid Base Homeostasis
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