Acid-Base Balance : Basics

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- C.S.N.Vittal- C.S.N.Vittal- C.S.N.Vittal- C.S.N.Vittal

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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

VittalVittalAcid Base Balance

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

– 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

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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)

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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

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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-])

No Anion gapM acidosis

High Anion gapM acidosis

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ACID/BASE BALANCE AND THE BLOOD

Acidic Alkaline (Basic)

[OH -]

NeutralpH

Acidosis Alkalosis

Normal7.35-7.45

Venous Blood Arterial Blood

6.8 8.0

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

Respiratory

Buffer System

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Acid-Base Homeostasis

Kidneys

OutputOutput

Maintenance ofNormal [H+]

BuffersBuffers

Metabolism

InputInput

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CHEMICAL BUFFER SYSTEMS

Na+ Cl-

AddHCl

Na+ Cl-

H+ Cl-

Unbuffered Salt Solution All protons are free

H2CO3: HCO3- Buffer

AddHCl

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

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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

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Handerson Hasselbalch Equation

pH = 6.1 + logHCO3

PaCO2 X 0.0301

VittalVittalKassirer and Bleich Equation

(Handerson Equation)

H+ = 24 XpCO2

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

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

• Not so efficient (50%)• Less in preterm babies• Control of respiratory centre• A CO2 conc. of > 9% depresses centers and causes CO2 narcosis

Buffer System:• Act within seconds• Act at cellular level• ¾ of body’s buffering system from intracellular proteins and phosphates.

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)

Increased excretion of acid as phosphate buffer and as ammonia Na+ re-absorption during the formation of H+

VittalVittalProximal Convoluted Tube

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VittalVittalDistal Convoluted Tube

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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

VittalVittalResponse of body to increase in acid load

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

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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Acid-Base Balance : Basics

Health & Medicine