ACID BASE BALANCE

- PHYSIOLOGY

DR. PREETHY DR.VIKAS

DR. VIDHYA DR.NITASHA

9th november, 2009

 HISTORY
Henderson coined the term ‘acid base balance’.
Refined by Hasselbach in 1916.
They described acid base balance in terms of hydration
equation for CO2.
Arrhenius in 1903 established the foundation for acid
base chemistry.
In 1981, stewart theory was proposed which was a
quantitative approach.
 BASIC DEFINITIONS

 pH is the the negative logarithm of H+

measured in moles per litre
 Normal pH of our body is 7.35-7.45
 Acidemia : pH< 7.35
 Alkalemia ph>7.45
 Changes in [H+ ] by a factor of 2 causes
pH change of 0.3
 Why ph imp….?

• Effect on small molecules: Intracellular

trapping of intermediary metabolites (ie

the Davis hypothesis)

 Effect on large molecules (proteins):
Maintaining optimal protein function both
intracellularly and extracellularly.
• Consequently, the body regulates pH very
tightly
 Types of Acids in the Body

• Volatile acids
– H2C03 (carbonic acid).

– Pco2 is most important factor in pH of body tissues.

• Fixed acids
– Sulphuric and phosphoric acids

– Cannot leave the solution

 HENDERSON HASSELBACH EQUATION

• Total co2 = p Co2*0.03 MMOL Co2 /L/mm Hg.

• pH= 6.1 + log { [ HCO 3 -]/Pco 2* 0.03}.

 Stewart model
• It is a quantitative approach to acid base balance.

• Used three parameters [SID-] , [A TOT] , P CO 2.

• Asserted that these parameters determine the only

path by which changes in pH arise.
 Strong ion difference

The major strong ions in our body are Na+, K+,Cl-,

SO4 2-,Mg 2+, Ca2+.
SID influences H+ concentration.

SID =[ Na+] + [K+] + [Ca2+] + [Mg2+] – { [Cl-]

+[A-]}.
SID = 40-44 mEq.
 Continued …..
[ A-] is the concentration of dissociated weak acids ;
mostly albumin and phosphate.
SIG = AG – [ A-].
AG = [Na+] + [K+] – [Cl-] – [HCO 3-].

SIG is normally equal to zero.

SIG is a better indicator of unmeasured anions than AG.

 WEAK ACID BUFFERS

 Stewart defined a second variable ‘A TOT’.

 A TOT = 5.72 ± 0.72[ albumin].
 Hydrogen Ion Regulation

concentration of hydrogen ion is regulated by

1. chemical buffer system.
2. respiratory system
3 renal mechanisms
 Production of hydrogen ions

Most of the acid formed as a result of CO 2

production from aerobic metabolism.
= 15000 mmol/ 24 hrs

Rest from oxidation of amino acids and

anerobic metabolism( 40- 80 mmol / 24 hrs)
 Chemical buffer

 One or two molecules that act to resist changes in

pH when strong acids are added to the body.
Three types :
1. bicarbonate
2. phosphate
3. protein.

May act either intracellularly or extracellularly.

 Bicarbonate buffer
System
 Most effective buffer system

It acts in blood and interstitial fluids but not

intracellularly
 pka of this system is 6.1

 H2CO 3 H+ + HCO3-.

Respiratory and renal system act on this system.

Bicarbonate Buffer System
 Protein Buffer System
• Plasma and intracellular proteins are the body’s most
plentiful and powerful buffers

• Some amino acids of proteins have:

– Free organic acid groups (weak acids)

– Groups that act as weak bases (e.g., amino groups)

• Amphoteric molecules are protein molecules that can

function as both a weak acid and a weak base
 Phosphate Buffer System
• This system is an effective buffer in urine and
intracellular fluid (ICF)

• Works much like the Bicarbonate System

• System involves:
– Sodium dihydrogen Phosphate (NaH2PO4-)
OH- + H2PO4-  H2O + HPO42-
– Sodium Monohydrogen Phosphate (Na2HPO42-)
H+ + HPO42-  H2PO4-
 RESPIRATORY SYSTEM

 2 nd line of defense
 Acts within mins ; maximal in 24 hrs.

 Since CO2 is lipid soluble, changes in ph occur rapidly.

 Regulated by two equations:

1.PaCO 2 = 0.863 * Vco 2 / V A

2. H+ = 24 * (PCO2 / HCO 3-).

 PHYSIOLOGICAL/ COMMENT
CONTROLLED ANATOMICAL
VARIABLE CORRELATE

VARIABLE ARTERIAL PCO2 Change in

arterial Pco2
alters ph
SENSORS CENTRAL AND Both respond.
PERIPHERAL
CHEMORECEPTORS
CENTRAL RESPIRATORY
INTEGRATOR CENTRE IN
MEDULLA
EFFECTO RESPIRATORY An increase in
RS MUSCLES minute
 Renal regulation

Role of kidneys:
 Excretion of fixed acids.
 Reabsorption of filtered bicarbonate.

These occur by two mechanisms:

1. reabsorption of bicarbonate

2. secretion of H+.
3. regeneration of new bicarbonate
 Urinary buffers
• Nephron cannot produce a urine pH < 4.5.
• In order to excrete more H+, the acid must be buffered.
• H+ secreted into the urine tubule and combines with
HPO4-2 or NH3.

• HPO4-2 + H+ H2PO4-
NH3 + H+ NH4+.
Acidification of Urine

Insert fig. 17.28

 Base excess approach

 Base excess is defined as no. of milliequivalents of acid or

base that are needed to titrate 1l of blood to Ph 7.4 at 37ο C.
 Buffer base increases in metabolic alkalosis and decreases in
metabolic acidosis.
 Base excess can have a negative value.
 Suppose pt is acidotic, BE = -8; 8 meq of base has to be
added.
 Anion gap approach

 Most widely used for investigating metabolic acidosis.

 Developed by Emmett and Narins.

 Based on the law of electrical neutrality.
 AG = ( [Na+] +[K+]) – ( [Cl –] +[HCO3-].

 NORMALLY IT IS 10- 12 MEQ/L.

 Limitation : AG is low in hypoalbuminaemia.
 Other parameters

 Delta ratio = (Increase in Anion Gap / Decrease in

bicarbonate)

 Urinary Anion Gap = ( UA - UC ) = [Na+]+ [K+] - [Cl-].

 Osmolarity = no. of osmoles/ litre
 Osmolality = no. of osmoles/ kg of solution
 Osmolar gap = osmolarity - osmolality