2. Metabolism is the basis of life.
Metabolism is possible only because of
enzymes.
Enzyme activity is influenced by pH of the
surrounding medium.
So maintenance of acid base balance is
crucial for life.
3. Acid is a protein (H+) donor
Example HCl H+ + Cl
Base is a proton (H+) acceptor.
NaOH + HCl NaCl + H2O
Strong acids completely dissociate
into their constituent ions in
solution - HCl
Weak acids partially dissociate –
lactic acid, carbonic acid
8. It is a mixture of weak acid and its salt or
weak base and its salt, which resist pH
change on addition of a small amount of
strong acid or alkali.
Example : Bicarbonate buffer
Na+ HCO3
- / H2CO3
The buffering capacity depends on actual
concentrations of salt and acid, and its ratio.
Buffering capacity is maximum in the range
of 1 unit ± of its pK value.
11. 11
Includes hemoglobin, proteins in ICF
Carboxyl group gives up H+
Amino Group accepts H+
Some Side chains of amino acid
residues can buffer H+ - lysine,
arginine, histidine
12. Weak acids dissociate only partially in the
solution.
Conjugate base is the unprotonated form of
corresponding acid.
For example: Cl-
Weak acid H2CO3
, HCO3
-
H+
Proton
+ HCO3-
(conjugate
base)
Conjugate base of weak acid is strong.
Strong acid
HCl H+ + Cl- (conjugate base)
Conjugate base of strong acid is weak.
13. The dissociation of an acid is a freely
reversible reaction.
So at equilibrium, the ratio of
dissociated and undissociated
particles is constant. (Ka is the
dissociation constant)
Ka = H+ + A- dissociated / HA un
dissociated
H+ - proton A- - conjugatebase or
anion
14. It is the pH at which the acid is
half dissociated.
It is negative logarithm of acid
dissociation constant Ka to the
base 10.
At pK value, Salt : acid ratio is
1:1.
pKa = - log 10 Ka
15. pH = pKa + log 10 ( salt / acid)
Due to metabolism mainly acids are
produced. The acids are of two types.
1.Fixed acids or non volatile acids
Example phosphoric , sulfuric acids,
organic acids such as pyruvic , lactic,
ketoacids.
2.Volatile acid- carbonic acid
Carbonic acid is being volatile, it is
eliminated by lungs as CO2.
Fixed acids are excreted by kidneys.
16. pKa of carbonic acid is 6.1.
pH = 6.1 + log 10 (bicarbonate/ carbonic
acid – 0.03 x pa CO2 ) { paCO2- 40mm
of Hg} =6.1 + log 10 (24/1.2)
= 6.1 + 1.3 = 7.4
Arterial blood pH = 7.4
Bicarbonate represents alkali reserve and it
is twenty times more than carbonic acid to
ensure high buffering efficiency.
18. Histidine residue of hemoglobin can act as
acid or base.
Histidine amino acid has pKa value of 6.5 and
it is efficient buffer .
Deoxygnatered hemoglobin in tissues accepts
H+ ions to form HHb. (KHb / HHb buffer )
Oxygenated hemoglobin releases H+ ions in
lungs.
Amino groups of hemoglobin interact with
CO2 to form carbamino hemoglobin.
19. Action of hemoglobin buffer
In the tissues, CO2 diffuses into erythrocytes
and gets converted to carbonic acid by
carbonic anhydrase.
H2O + CO2 H2CO3
H2CO3 H+ + HCO3
-
KHb accepts H+ and releases K+ .
Bicarbonate diffuses into the plasma where
its concentration low.
To maintain electrical neutrality, Chloride
(Cl- ) enters the erythrocytes.
This is called chloride shift.
20.
21. In the lungs, oxygenation of
hemoglobin releases H+ which
combines with bicarbonate to form
carbonic acid by carbonic anhydrase.
Carbonic acid dissociates into water
and CO2.
CO2 is expired out by lungs.
Chloride comes out in exchange for
HCO3
- to maintain electrical
neutrality.
22.
23. pH = pKa + log {bicarbonate (metabolic
component)/ carbonic acid-paCO2
(Respiratory component)}
Respiratory component is maintained by
lungs and Metabolic component is
maintained by kidneys.
Carbonic acid is a volatile acid so it is
eliminated by lungs.
The rate of respiration is controlled by the
chemoreceptors in the respiratory centre
which are sensitive to pH change of blood.
24. Functions
Reabsorption of bicarbonate involves the
reabsorption of bicarbonate filtered without
excretion of H+ ions.
Excretion of H+ ions
Here there is net gain of bicarbonate for each
H+ excretion. As the H+ ion excretion
increases, the excretion of H+ against
concentration gradient becomes difficult.
So in the distal convoluted tubules, urinary
buffers buffer the free H+ ions.
25.
26.
27. Two important urinary buffers are
1. Phosphate buffer
2. Ammonia
The maximum limit of acidification of urine is
4.5.
Normally 70 meq acid is excreted daily. In
metabolic acidosis, this can raise to 400
meq/day.
28.
29.
30. Normal values -Arterial
pH = 7.35 –7.45
paO2 = 80-100 mm of Hg
paCO2 = 35-45 mm of Hg
HCO - = 23-27 mmol/L
+
3
Na = 135-145 mmol/L
K+ = 3.5-5 mmol/L
Cl- = 96-106 m/L
31. pH: 7.35 – 7.45
PCO2:
Males: 35 – 48 mm Hg
Females: 32 – 45 mm Hg
HCO3: 22 – 27 mEq/L
Base Excess:
Newborn (0 – 7 days): -10 to - 2 mmol/L
Infant (1 week – 1 year): - 7 to –1 mmol/L
Child (1 – 16 years): - 4 to +2 mmol/L
Adult (>16 years): - 3 to +3 m
32. Warm the area for 3-10 mins not > than
420C – arterialization - 0.2 ml
Lithium heparin – fill 2 capillary tubes without
air bubble –cap both ends
Within 15 mins – analyze
> 30 mins , clotted sample – discard
Critical values
pCO2: < 15 and > 70 mm Hg
pH: < 7.2 and > 7.6
33. Respiratory acidosis - failure of ventilation
depression of respiratory centre due to disease
or drug-induced respiratory depression, head injury.
Paralysis of muscles (eg, myasthenia gravis,
muscular dystrophy)
Airway obstruction- foreign body –trachea , asthma or
chronic obstructive pulmonary disease (COPD).
Obesity hypoventilation syndrome
The biochemical findings are:
pH < 7.35
paCO2 > 45 mm of Hg(Hypercapnia).
Renal compensation occurs in 3 - 5 days. This increase of
bicarbonate is called compensatory metabolic alkalosis.
34. It is caused by hyperventilation. The causes for
hyperventilation are: Anxiety, salicylate poisoning
, artificial ventilation and pulmonary embolism.
The biochemical findings are
pH is increased > 7.45
paCO2 is decreased < 35 mm of Hg
Bicarbonate is normal in uncompensated
condition.
In compensatory metabolic acidosis, bicarbonate
will be decreased. Kidney responds to decrease in
paCO2 and excretes more bicarbonate.
35. It can be due to 1.Increased acid production
2.Decreased removal of acids by kidneys (renal
failure)
3.loss of bicarbonate
Increased acid production: The causes are
lactic acidosis in shock, septicemia,
ketoacidosis in Von Gierkes’s disease, diabetes
mellitus and starvation.
Loss of bicarbonate due to diarrhoea
(gastroenteritis).
36. The sum of cations and anions in ECF are always equal.
Cations Na+ + K+ - 95% - anions Cl + HCO3
Account for only 86% among the measured electrolytes.
AG represents the plasma anions - not routinely measured
(albumin, phosphates, sulphates, organic anions).
So there is a difference among measured cations and anions.
The unmeasured anions constitute the anion gap.
Anion Gap = [Na+ + K+] – [Cl- +HCO3
-]
= [135 + 4] – [100 + 25]
= 139 – 125 = 14 meq/l. The anion gap ranges between 8-
16 meq/l.
37. Based on anion gap, Metabolic acidosis can be
grouped into : High anion gap metabolic acidosis
and normal anion gap metabolic acidosis.
High anion gap acidosis
It is caused by increased production of
unmeasured anions such as lactate, ketone
bodies.
Normal anion gap acidosis (Hyperchloremic
acidosis): when there is loss of both anion and
cations, normal anion gap acidosis will be there.
The causes are :
Diarrhea, intestinal fistula due to loss of
bicarbonate , Na+, K+.
Renal tubular acidosis
Carbonic anhydrase inhibitors: loss of HCO3-,
Na+, K+ occurs.
38. ketoacidosis
diabetic, alcoholic, starvation
lactic acidosis
acute renal failure
toxins
renal tubular acidosis
GIT loss of HCO3
diarrhoea
drainage of pancreatic or bile
juice
Cl-
HCO3
-
normal
anion gap
Na+ AG
Cl-
HCO3
-
physiologic
situation
Na+ AG
Cl-
HCO3
-
high
anion gap
Na+ AG
39. There will be deep and rapid respiration called Kussmaul
respiration.
Chest pain, headache, palpitation, altered mental status.
When pH<7.2 and bicarbonate <10 mmol/L , there will be
HCO3 is decreased- < 24 mmol/l
depressed myocardial contractility.
pH is decreased- < 7.35
paCO2 is normal or decreased during compensation.
Compensation by lungs
paCO2 will be reduced by 1 mm of Hg for every 1 mmol of
drop in bicarbonate.
Treatment
Treatment of the cause and administration of
Bicarbonate.
40. pH is increased due to rise in HCO3
-.
It is seen in vomiting (loss of H+ ions), intake
of antacids, in patients consuming more milk
(Milk-alkali syndrome).
Increased loss of acid by kidney:
hyperaldosteronism , Cushing’s syndrome.
Thiazide and loop diuretics
In vomiting, HCl is lost and so bicarbonate
accumulates. Plasma Cl-_ is decreased. This is
called hypochloremic alkalosis.
41. pH is increased > 7.45
HCO3
- > 27 mmol/L
paCO2 is normal if uncompensated and is
increased in case of compensatory respiratory
acidosis. So paCO2 will be increased by
hypoventilation.
In metabolic alkalosis
paCO2 is increased by 1 mm of Hg for every 1
mol/L rise in bicarbonate.
