ACID BASE BALANCE

&
ELECTROLYTE BALANCE
BI 6.7
Describe the processes involved in maintenance of
normal pH, water & electrolyte balance of body
fluids and the derangements associated with
these.

BI6.8Discuss and interpret results of Arterial Blood

Gas (ABG) analysis in various disorders
• Define the terms acid, base, strong acid/base, weak
acid/base.
• Define the terms pH, pKa and buffer
• Describe Henderson Hasselbalch equation and it is
application
• Describe mechanism of action of buffer
• Enlist various acids and bases produced in the body
• Describe mechanism of regulation of blood pH by
blood buffer systems with respect to composition,
ratio, reaction to acid or base addition, advantages,
and disadvantages

• Explain the biochemical changes in the bicarbonate

buffer system in acidosis and alkalosis with the help of
Henderson Hasselbalch equation
1. Describe the role of respiratory system in regulation of blood pH with
respect to role of respiratory centre, isohydric transport of CO2 and
chloride shift.
2. Describe the renal mechanism in regulation of blood pH with respect to
H+ excretion, ammonium ion excretion, PO4 buffer, bicarbonate ratio,
reaction to acid or base reabsorption
3. Distinguish the acid-base disorders as acidosis and alkalosis with a note
on normal reference ranges of pH, pCO2, pO2 and bicarbonate.
• Describe anion gap, differentiate between high anion gap and
normal anion gap metabolic acidosis and their clinical
importance.
• Discuss the causes and clinical features of Respiratory
acidosis/alkalosis and Metabolic acidosis/alkalosis and the
compensatory mechanism
• List the important components (pH, pO2, pCo2, HCO3, SO2) of
an ABG report and state their reference range.
• Enlist other biochemical investigations to be done in the
diagnosis of various types of acidosis and alkalosis
• Analyse and interpret the ABG report for respiratory and
metabolic acidosis/alkalosis and briefly state the corrective
measures
• Acids , Bases,Buffers , Buffering capacity

• Production of acids & bases in the body

• Maintenance of blood pH
-Blood buffers
-Respiratory mechanism
- Renal Mechanism

• Disorders
 Normal pH= 7.35 – 7.45

Maintenance of blood pH is an important homeostatic

mechanism of the body.
pH of 7.0 – 7.6 [compatible to life]

Acid: Substance that yields H+(protons) when dissolved in

water. Proton Donors
HCl H+ + Cl-
Base: Proton acceptors
NH3 + H+ NH4+
Dissociation constant

HA H+ + A-

Ka = [ H+] [ A-]
[HA]

pKa : pH at which an acid is half ionized .

Strong acids have a low pK

Weak acids -----higher pK
Practical purposes H+is expressed as –ve
log [H+] & is designated as pH

pH = -log [H+] = log 1

[ H+]
pH is inversely proportional to acidity

Low pH -------- High acidity

High pH ---------Low acidity

pH Scale 0 – 14
pH of important biological fluids

Body fluid pH
Blood 7.35 – 7.45

CSF, tears interstitial fluid 7.2 --7.4

Human milk
Saliva 6.4 -- 7.0

ICF (cytosol) 6.5 - 6.9

Urine 5.0 – 7.5

Gastric juice 1.5 - 3.0
Biological Significance of pH

• Influences the ionized state of most of the biological

molecules and is responsible for structure & function

• Optimum pH essential for enzymatic activity

Henderson Hasselbach equqtion

Relation between pH, pKa, conc of acid & conjugate base (or salt) is
expressed by Henderson Hasselbach equation

[Base]
pH = pKa + log [Acid]

or
[Salt]
pH = pKa + log [Acid]

When [Base] = [Acid] then pH = pKa.

When acid is Half ionized pH= pKa
Application of Henderson Hasselbach equation

• Determination of pH on addition of known quantity of

acid or alkali
• By measuring the pH, ratio of of salt / acid can be
determined

• Clinical practice- Assess the acid base status &

predicting the limits of the compensation of body buffers.
Buffers: Solutions which tend to resist the changes in pH
when an acid or a alkali is added to it

Composition: Conjugate pairs

1) Weak acid/ conjugate base --- H2CO3 / HCO3-

2) Weak base / conjugate acid --- NH3 / NH4+

3) Weak acid / salt ---- CH3COOH / CH3COONa

4) Mixture of two salts of polybasic acid -Na2HPO4 / NaH2PO4

How do buffers act ?

Buffer + H+ H-Buffer

On addition of an acid

H+ + Buffer H-Buffer
[ Increase in H+ conc is minimized]

On addition of a Base

OH - + H- Buffer H+ + Buffer
[ Increase in OH - conc is minimized]
Mechanism of action

HCl CH3COOH + NaCl

CH3COOH / CH3COONa
NaOH CH3COONa + H2O
Effective range of a buffer

• 1 pH unit higher or lower than pKa

• Most effective when conc of salt and acid are equal

( pH= pKa )
Buffering capacity: Number of equivalents of acid or base to
be added to a litre of the buffer solution in order to change
its pH by I unit

Factors Affecting

1) pKa

2) Absolute concentration of salt & acid

Buffer Buffering pKa Conc
System capacity mmol/L

Bicarbonate 1 6.3 25

Phosphate 0.3 6.8 1.2

Protein 8 - -

Hemoglobin 40 7.2 53
Acid base balance can be studied under 3 headings

1) Production of acids

2) Transport

3) Removal /Disposal of acids

Transport
Production Disposal
[Tissues] Blood [Lungs, kidney]
SOURCES OF ACIDS AND BASES

Volatile - Carbonic acid -20000meq/day . Most predominant

[ formed fromCO2]

Nonvolatile: [Fixed acids] 60 - 80 meq /day

Lactate: Anaerobic glycolysis [muscles, RBC]

Sulphuric acid : Dietary Proteins , sulphur containing amino

acids (H2SO4- H+ + SO4 -2

Phosphoric acid : Organic phosphates, eg phospholipids

H3 PO4 H+ + H2PO4-
Uric acid ; Purine catabolism
SOURCES OF ACIDS AND BASES

Nonvolatile (Fixed acids) Volatile

Formed from metabolism of Formed from CO2

proteins & nucleic acids
Carbonic acid
[60 - 80 meq /day] [ 20000meq/day]

Lactate: Anaerobic glycolysis

Sulphuric acid : Sulphur containing amino acids

H2SO4- H+ + SO4 -2

Phosphoric acid : Organic phosphates,( phospholipids, nucleic acids)

H3 PO4 H+ + H2PO4-

Uric acid ; Purine catabolism

NON VEG DIET acid production

Reflected by excretion of acidic urine

VEG DIET Acid production

Reflected by excretion of neutral or slightly alkaline urine

Production of Bases: Negligible

Salts of organic acids - sodium lactate

Contribution of NH3 from amino acids is negligible

Vegetarian diet has a alkalizing effect on the body

II Transport of acids

 Role of buffers

 Transport of carbondioxide

Role of buffers:Transport the acid from site of production to the

site of removal without any change in pH.

Various buffer systems

-
Plasma – Bicarbonate buffer (HCO3 /H2CO3)
- Phosphate buffer (HPO42-/H2PO4-)
- Protein buffer ( Protein /H-Protein)

Erythrocytes : Hemoglobin buffer ( Hb/HHb)

Urine: Phosphate buffer

Ammonia buffer (NH3/NH4+)
Transport of CO2 by Hb

 75% of CO2 -- Bicarbonate ( HCO3- )

CA
CO2 + H2O H2CO3 HCO3- + H+

Plasma HHb

 15% of CO2 ----- Directly by Hb ; Carbamino hemoglobin

Hb –NH2+ CO2
-
Hb-NH-COO + H+

 10% ------ Dissolved form

Maintenance of blood pH

3 lines of defence to regulate blood pH

1) Buffer System

2) Respiratory mechanism

3) Renal mechanism
Buffer systems;

First line of defence against acid load.Temporarily act as

shock absorbents to reduce the free H+ ions.

Effective as long as the alkali reserve is no exhausted

BUFFER SYSTEMS

• Bicarbonate buffer (HCO3- / H2CO3)

•Hemoglobin buffer system (KHb / HHb & KHbO2 /

HHbO2 )

•Protein buffer system ( Na Protein- / H Protein)

•Phosphate buffer system (HPO4-- / H2PO4-)

 DISTRIBUTION OF BUFFERS

ECF ICF RBC Urine

NaHCO3- HPO42-
H2CO3 H2PO4 KHCO-3
H2CO3
Protein-
NaHPO2-4 H+Protein KHb HPO42-
H2PO4- - HHb H2PO4-

NaProtein- KHbO2
H+ Protein HHbO2

NH3
NH4+
Buffer Components Ratio pKa

Bicarbonate HCO3- / H2CO3 20 /1 6.1

(5.1 – 7.1)

Phosphate Na2HPO4 / NaH2PO4 4 /1 6.8

(5.8 – 7.8)

Ammonia NH3 / NH4+ 1 / 100 9.0

(8.0 – 10.0)

Hemoglobin Hb / HHb 6.0

(5.0 – 7.0)

Protein buffer Pr- / HPr 6.1

(6.1 – 7.1)
BICARBONATE BUFFER SYSTEM (pK= 6.1)

[HCO-3] Metabolic component

[H2CO3] Respiratory component

H2CO3 HCO3- + H+

• Most predominant buffer system

• Accounts for 65% of the buffering capacity in plasma

pH = pKa + log [Base]

[Acid ]
=pKa + log [HCO-3]
[H2CO3]
 HCO3- = 24 mmol l/L
7.4 = 6.1+ log [HCO3-]
[H2CO3 ] pCO2 = 40mmHg

1.3 = log [HCO3-] H2CO3 = 1.2 mmol/L

[ pCO2 x solubility constant]
H2CO3
40 X 0.03 = 1.2
20 = HCO3 -

1 H2CO3

Ratio of [HCO3-]/ [H2CO3 ]

at pH 7.4 = 20

Ensures maximum effectiveness

Bicarbonate buffer is the most imp buffer

i) Presence of bicarbonate in relatively high

concentrations
ii) Acid component is under respiratory conrol
Plasma HCO3- : Measure of the base that remains after all

the acids stronger than carbonic acid have been

neutralized. It represents the reserve of alkali available for

the neutralization of strong acids

Termed the ALKALI RESERVE

PHOSPHATE BUFFER SYSTEM : Na2HPO4- /NaH2PO4

pK = 6.8

Not imp as a blood buffer; 1% of total buffering capacity

7.4 = 6.8+ log [salt]

[acid]

7.4- 6.8 = log [salt]

[acid]

0.6 = log [salt]

[acid]
4 = [salt]
1 [acid]
Mechanism of action

HCl + Na2HPO4 NaH2PO4 + NaCl

NaOH + NaH2PO4 Na2HPO4 + H2O

Limitations - Low ratio of Base / Acid

• 1% of the total BC
• Has a pK of 6.8 ,close to normal pH of 7.4 & hence
exhibits maximum buffering power. But the Conc is very
low .Hence total buffering power is much less than that
of bicarbonate.

• Ratio of base to acid is 4 compared to 20 for

bicarbonate

• However it is imp in the tubular fluids of the kidneys

which has a lower pH & is closer to the pK of 6.8
PROTEIN BUFFER: Na+ Protein- / H Protein

Na+ Protein- + HCl H- Protein + NaCl

H2CO3 + Na+Protein- NaHCO3 + H- Protein

BC --- Depends on the pK of ionizable groups of

aminoacids

[His- pK 6.7]
Protein Buffer system (Na protein /H Protein)

• Accounts for 2% of the buffering capacity of the plasma

• BC is dependent on the pK of the ionizable group of

amino acids. Imidazole group of Histidine (pK= 6.7) is
the most effecive contributor of protein buffers.

• Hemoglobin buffer ( KHb /HHb &HbO2/ HHb)

Hb molecule contains 38 molecules of His. High conc &
appropriate pK makes Hb the efficient buffering agent of
blood at physiological pH.

• It buffers the carbonic acid & its anhydride CO2 from

the tissues
Buffering capacities of various buffers

Bicarbonate ------ 65%

Hb ------- 30%
Protein ------- 4%
Phosphate ------- 1%

•Buffers act quickly but not permanently. For the final

elimination of acids respiratory & renal regulations are very

essential.
Respiratory mechanism for pH Regulation

Second line of defence pH= pKa+ log [HCO3-] / [H2CO3-]

All the CO2 produced is transported to the lungs& eliminated from the
body in the expired air

H2CO3 carbonic CO2 + H2O

anhydrase

CO2 diffuses from the cells to the ECF & reaches the lungs through the
blood
 Role of Hemoglobin -- Isohydric transport

Tissue capillary Lung capillary

CO2
Expired Air
Catabolic
RNS
H2O + CO2 H2O + CO2 CO2

CA
CA
H2CO3
H2CO3
HbO2 HbO2

-
HCO3 + HHb + O2 -
HCO3 + HHb + O2
Cl-

HCO3- Inspired Air

Cl-

Chloride shift Haldane effect

 carbonic
H2CO3 CO2 (Expelled out)+ H2O
anhydrase

Production of CO2 is coordinated with its excretion through respiration

Rate of respiration is controlled by the chemoreceptors in the

respiratory centre - sensitive to changes in pH of blood

Decrease in pH ---- Hyperventilation

Increase in pH ---- Hypoventilation

Respiratory control is rapid but only a short term regulatory process

since hyperventilation cannot proceed for long’

 Responds to any change in pH immediately but does not proceed to

completion
.
Renal Regulation

Kidney regulates the blood pH by maintaining the alkali

reserve besides excreting or reabsorbing the acidic or
basic substances as the situation demands.

Urine pH is slightly acidic (pH-6.0) compared to plasma

pH of 7.4 indicating that acids are being excreted through
the kidney.

Carbonic anhydrase is of central importance in the renal

regulation of pH
Role of Kidney in Homeostasis

Occurs by the following mechanisms

1) Reabsorption of bicarbonate

2) Excretion of titrable acids

3) Excretion of ammonium ions

H+ excretion occurs in the proximal convoluted tubule & is
coupled with the regeneration of HCO3-.

About 80 – 90% of HCO3-. Is reabsorbed by the proximal

tubules

Effective mechanism to eliminate the acids from the body

With the simultaneous generation of bicarbonate.
 4000 mmol HCO3- /day
Reabsorption of Bicarbonate
Tubular lumen
Blood

Renal tubular cell

Na+ Na+ HCO3-

Na+ Na+

HCO3- + H+ H+
-
HCO3

HCO3_
H2CO3
H2CO3
CA
CA
CO2 + H2O Excreted
CO2 + H2O
HCO3- is added into the blood & serves to maintain the
alkali reserve

Also known as Reclaimmation of bicarbonate

This mechanism is responsible to conserve the blood

bicarbonate with the simultaneous excretion of H+.

Cyclical process with the net excretion of H+ ions

Distal tubules reabsorb the remaining 10- 20% of filtered

bicarbonate
 Excretion of titrable acid (fixed acids)
Tubular lumen

Na+ Na 2HPO428
Blood

Renal tubular cell

_
Na+ Na+ NaHPO42-

HCO3- + H+ H+
HCO3
NaH2PO4 -

CA
H2CO3 Excreted

CO2 + H2O
Excreted
Fixed acids generated during metabolism are
excreted as titrable acids

Protons generated trough the carbonic anhydrase

system are secreted into the lumen & combine with
HPO4 2- to form H2PO4- whih is excreted the urine

Active secretion of H+ acidifies the urine & changes

the pH from 7.4 to 6

Titrable acidity is a measure of the acid excreted into

the urine by the kidney.

Titrable acidity : of urine is the no of millilitres of 0.1N NaOH

required to titrate 1L of urine to pH of 7.4
 Excretion of Ammonium ions
Blood Tubular lumen

Renal tubular cell

Gln Glu + NH3 NH3
Na+
Na+ Na+

HCO3
HCO3- + H+
H+

H2CO3 NH4
_

CA

CO2 + H2O Excreted

 Glutaminase
Glutamine Glutamic acid
H2O
NH3

NH3+ H+ NH4+

Excretion of acid ammonium ion is associated with

increase in alkali reserve
• Another mechanism to buffer the H+ secreted into the tubular fluid.

• NH3 can readily cross the luminal membrane of the tubule

• Excretion of H+ ions in the form of NH4+ can be accomplished without

any loss of Na+ or K+

• About 2/3 of the acid load is buffered by this mechanism. Very

effective to excrete large quantities of acids produced in the body.
Mechanism becomes predominant in acidosis.

• Estimation of TA & NH3 is a measure of acid excreted from the body

.(Acid load)

• Maximum urine acidification is reached at pH 4.5

• Ammonia estimation: After addition of formaldehyde.

Cellular buffers :
CO2 – Central molecule of pH regulation

pH 7.4
Metabolism Lungs
( CO2 generated) CO2 (CO2 exhaled)
(H2CO3)

Erythrocytes HCO3- + H+ Kidneys

(CO2 transported,
HCO3- generated) (HCO3-generated,
H+ lost)
Disorders of acid base balance:
pH 7.0 - 7.6

Acidosis Alkalosis
(Decrease in blood pH ) ( Rise in blood pH )

i) Metabolic acidosis Metabolic alkalosis

ii) Respiratory acidosis Respiratory alkalosis

Metabolic ---- Alteration in bicarbonate conc

Respiratory ---- Alteration in carbonic acid level - pCO2

Acidemia ---- Decrease in pH in blood

Alkalemia ----- Increase in pH in blood

Disorders of acid base balance:

Acidosis ( pH )

 Metabolic acidosis [ HCO3-] Primary deficit of

bicarbonate

 Respiratory acidosis :[ H2CO3 ] Primary excess of carbonic

acid

Alkalosis ( pH H+, )

 Metabolic alkalosis [ HCO3- ]

 Respiratory alkalosis [ H2CO3 ]

Compensatory mechanisms of acid base disorders

Attempt is made to restore pH to normal

Secondary compensatory changes

 Buffering
 Respiratory compensation
 Renal Compensation

Sec compensatory change – in the counteracting variable

Eg : Primary change in HCO3- ---Involves

--- Alteration in pCO2

---- Change occurs in the same direction
---- Atempt is made to restore ratio to 20:1 & pH to 7.4
Buffering -

ECF: Involves consumption of bicarbonate, followed by

phosphate & finally proteins

ICF: Phosphate & protein buffers

Respiratory compensation to acidosis

 Hyperventilation ----- Decrease in pCO2 ---

hypocapnia /Hypocarbia

Respiratory compensation to alkalosis

 Hypoventilation --- Retention of CO2 ---

Hypercapnia/Hypercarbia
Takes several minutes to few hours
Renal compensation

Renal compensation to acidosis

•Excretion of H+ & regeneration of HCO3-
•Reabsorption of HCO3-
•Excretion of ammonium ions
•Excretion of titrable acids

Renal compensation to alkalosis

•Decreased secretion of H+
•Increased excretion of HCO3-
• Decreased excretion of ammonium ions

•Takes more time to set in. (3- 4 days)

• Uncompensated ; No compensatory response; pH
is beyond the normal range

• Partially compensated ; Compensatory response

present & pH is close to the normal value

• Fully compensated :compensatory response

present & pH is in the normal range
Compensation of acid base disorders

Attempt is made to restore pH to normal

Buffers ---- Neutralizes the change

HCO3--- Acts as alkali reserve

Respiratory mehcanism-- acts quickly but compensation

does not proceed to completion

Renal mechanism : Slow, achieves complete

compensation
Metabolic disorders Respiratory compensation

Respiratory disorders Renal compensation

Anion gap: Difference between the total concentration of measured
cations ( Na+ & K+ ) and the measured anions ( Cl- & HCO3-).

Commonly measured electrolytes

Na+ & K+ 95%

Cl- & HCO3- 80%

Remaining 20 % of anions are not normally measured . Includes

proteins, phosphate ,sulfate, urate & organic acids.

NV 12 - 18 mmol/L

Acid base disorders are associated with alteration in anion gap

Compensation is done by varying the other parameter of the
ratio in the same direction.

16/1 ---- 25/1

( 7.3 -- 7.5 )

Partial ( pH Close to normal limits)

Full ( pH Normal limits)

Uncompensated ( pH Outside normal limits)

Metabolic acidosis: in HCO3-
[Primary alkali deficit]

• Increased production
• Ingestion
• Loss of base
• Retention
Increased production:
Diabetic ketoacidosis Acetoacetate & B Hydroxy
Starvation (long term) butyrate anions

Lactic acidosis Lactate anions

Methanol poisoning Formate, glycolate & oxalate

anions
Aspirin poisoning Salicylate

Ingestion
Drugs Corticosteroids, nitrates
salicylic acid
Loss of base
Diarrhoea Loss of intestinal secretions,
Bicarbonate, sodium & Potassium

Retention
• Renal failure Excretion of H+ & generation of
• Renal tubular acidosis Bicarbonate are defective
• Terminal stages of nephritis
• Acetazolamide therapy
Decreased ammonium ion formation
Sulphuric, phosphoric & organic anions

Aminoacidurias Accumulation of acidic metabolic

intermediates due to block in the
normal metabolic pathway

Organic acidurias Accumulation of organic acids

Normal Anion gap Increased anion gap

Diarrhoea Renal failure

Acetazolamide therapy Diabetic ketoacidosis

Renal tubular acidosis Lactic acidosis

Drugs –Antacids
Anion gap: Difference between the total concentration of measured
cations ( Na+ & K+ ) and the measured anions ( Cl- & HCO3-).

Commonly measured electrolytes

Na+ & K+ 95%

Cl- & HCO3- 80%

Remaining 20 % of anions are not normally measured . Includes

proteins, phosphate ,sulfate, urate & organic acids.

NV 12 - 18 mmol/L

Acid base disorders are associated with alteration in anion gap

Compensation :

- Hyperventilation by the lungs.

- Results in increased elimination of CO2 from the body

( H2CO3)
Kussumal respiration

pCO2 falls & attempts to restore the ratio towards 20

Renal compensation:

Increased reabsorption of HCO3-

Increased excretion of NH4+ ions
Compensated metabolic acidosis :

Hyperventilation by the lungs (Kusumal respiration)

Fall in pCO2

HCO3-/H2CO3 restored towards 20:1 (Partial compensated)

Increased excretion of acid & conservation of

base (Renal compensation )

Ratio restored to 20:1 (Fully compensated )

Correction of cause ---- Normalacy restored

Metabolic acidosis is assoiated with hyperkalemia ??

Redistribution of K+&H+

pH < 7.2 dangerous

HCO3- --- <10mmol/L

Treatment :

Diabetic ketoacidosis- IV fluids, insulin & K+ replacement

Lactic acidosis - Oxygen administration

Bicarbonate administration
 Biochemical Findings

Uncompensated Compensated
pH

pCO2 N

HCO3-

Clinical Features
Kussmaul Respiration

Depressed myocardial
contractilty
Respiratory acidosis: ( H2CO3)
[ Primary CO2 excess)

Cause : HYPOVENTILATION

Obstruction of respiration Depression of

respiratory centre

- Pnuemonia - Toxic doses of morphine

- Emphysema
- Bronchitis
- Pulmonary &mediastinal tumors - Cerebral trauma
- Pulmonary fibrosis
-Poliomyelitis -Overdose of anaesthetics
Compensation

Renal mechanism:

- Activation of carbonic anhydrase

- Generation of more bicarbonate

- Excretion of NH4+
Biochemical Findings

Uncompensated Compensated
pH

pCO2

HCO3- N

Clinical Findings
Shortnesss of breath

Hypotension
Coma
Metabolic Alkalosis: ( HCO3 - )
[ Primary alkali Excess]

Causes

•Loss of Hcl -- Excessive vomitting, [ Pyloric stenosis]

•Alkali administration – Excess intake of HCO3 – for

therapeutic purpose ( control of gastric acidity)

•Administration of diuretics

•Cushings Syndrome ( retention of Na+, & losss of K+)

Metabolic Alkalosis: in HCO3-

[Primary alkali Excess]

• Addition of base
• Loss of acid
• Retention
• Loss of acid Excessive vomitting, (Pyloric
stenosis)
Gastric aspiration
• Addition of base Consumption of excess
antacids ( control of gastric
acidity)

Minerelocorticoid excess

Primary Aldosteronism Increased reabsorption of

Cushings syndrome sodium

Loss of H+ ions is associated

Use of diuretics with increased reabsorption of
HCO3-
Compensation

Respiratory mechanism: Hypoventilation to retain CO2

Renal mechanism : Excretion of HCO3 -

Retention of H+
K+ excretion from DCT

Hypokalemia is associated with Metabolic alkalosis

(Attempt to conserve H+ ions)

Biochemical Findings

Uncompensated Compensated
pH

pCO2 N

HCO3-

Clinical Findings

Hypoventilation

Increased neuromuscular activity

Tetany
Respiratory Alkalosis: ( H2CO3)
[ Primary CO2 deficit]

[HCO3-] / [H2CO3] -- >20/1

Causes

• Prolonged hyperventilation
–Hysteria,
Anxiety
- excessive artificial ventilation

• hypoxia

-raised intracranial pressure

- Early stage of salicylate poisoning- stimulate
respiratory centre
Compensation

Renal Mechanism - Excretion of HCO3 - in

urine
Biochemical Findings

Uncompensated Compensated
pH

pCO2

HCO3-
N

Clinical Findings
Hyperventilation

Muscle cramps
Paraesthesia
Paresthesia- ??

Alkaline pH favours bindin of caions to proteins resulting

in decreased ionized calcium

Arterial Blood Gas analysis: reference ranges

PARAMETER REFERENCE RANGE

pH 7.4 (7.35 - 7.45 )
H+ 40 (37- 45 ) nmol/L
HCO3- 24 (22- 28) mmol/ L
pCO2 40 (35 -- 45) mmHg
pO2 - 95 (85 -- 100)mmHg

ELECTROLYTE REFERENCE RANGE

Anion gap 15 (12- 18) mmol /L S (mmol/L)

Sodium (Na+) 136 -145

Potassium (K+) 3.5 - 5
Chloride (Cl-) 96 – 106

Bicarbonate 22 -28
(HCO3-)
Asessment of Acid base Parameters

• Blood gas analyzer

Arterial blood, heparinised

Blood should be analyzed within ½ an hour

Blood to be collected under paraffin

•pH, pCO2 & pO2 -- directly

HCO3- --- Indirectly by calculation

Management : Identification & treating the underlying
disorder

Metabolic acidosis - Admin of IV fluids; IV adminof

HCO3-

Metabolic alkalosis - Admin of IV fluids ( with water

& electrolytes )
Carbonic acid inhibitors

Respiratory acidosis- Improve alveolar ventilation

Respiratory alkalosis- Alleviating anxiety

Interpretation

 Look for pH : If deceased ---- Acidosis

If increased ---- Alkalosis

 Find out if the cause is Metabolic or Respiratory

Metabolic ; Alteration in metabolic component

Respiratory ; Alteration in respiratoty component

 Find out if compensated or uncompensated

Uncompensated; No alteration in the other component

Compensated ; Alteration in the other component
Interpret the acid base abnormality

pH pCO2 HCO3
-

7.20 70 27 Uncompensated respiratory acidosis

7.24 40 17
Uncompensated metabolic acidosis
7.5 46 35 Partially compensated metabolic alkalosis

7.38 24 14
Fully compensated metabolic acidosis

7.4 60 36
Fully compensated metabolic alkalosis
pH = pKa +log [HCO3-]
0.03xpCO2
Modified version of Henderson Equation

H+ [nmol/L ] = 24x pCO2

HCO3-

24x 40 24x45
18 42

= 53.3 = 25.71
Base excess is the quantity of base (HCO3-, in mEq/L) that is
above or below the normal range of buffer base in the body
(22 -28 mEq/L)

Base excess/deficit of +/- 2 mEq/L is normal.

A positive number is called a base excess and

indicates a metabolic alkalosis.

A negative number is called a base deficit and

indicates a metabolic acidosis.