25. Acid–Base Balance

Question 1

Intro

Why important

What tryingto maintain as normal

How

Answer 1

A stable pH in body fluids is 
essential to maintain 
1 normal enzyme function, 
2 ion distribution and 
3 protein structure.

Homeostatic acid–base 
regulatory mechanisms aim 
to maintain a pH between 
7.35 and 7.45 
([H+] of 45–35 nmol/L) via:

> Buffers in tissue and blood

> Excretion of acids by kidneys
and
lungs

Normal acid–base balance relies on the following variables:

> pH ~ 7.40

> PCO2 ~ 5.3 kPa (40 mmHg)

> HCO3 – ~ 24 mmol/L

An acid–base disturbance occurs when at
least two of these three variables are abnormal.

The primary change determines whether a disturbance is respiratory (alteration of PCO2) or metabolic (alteration of the bicarbonate buffer system by means other than PCO2).

Question 2

Base

Answer 2

Proton acceptor,
or hydroxide (OH-) producer,
pH > 7.0

Question 3

Acid:

> Strong acid (e.g. HCl):

> Weak acid

Answer 3

Acid
proton donor, pH < 7.0
The strength of an acid is defined by its ability to give up protons:

Strong Acid
fully dissociates in solution

Weak Acid
(e.g. carbonic acid): 
does not fully dissociate, 
and together with its conjugate base, 
it acts as an acid–base 
buffer system to resist a
change in pH.

Question 4

pH:

Answer 4

measure of the acidity 
of a solution and 
is calculated as the 
negative logarithm to the 
base 10 of the 
hydrogen ion concentration.

Question 5

> Normal serum pH

Answer 5

> Normal serum pH

is 7.40 (range 7.36–7.44).

Question 6

Acidosis

Answer 6

Acidosis: a process
where there is acid accumulation
or alkali loss.

Question 7

Acidaemia

Answer 7

Acidaemia:
occurs when the arterial
pH < 7.35 or [H+] > 45 nmol/L.

Question 8

Alkalosis

Answer 8

Alkalosis:
a process where there
is acid loss or
alkali accumulation.

Question 9

Alkalaemia:

Answer 9

Alkalaemia:
occurs when the
arterial pH > 7.45 or [H+] < 35 nmol/L.

Question 10

Standard bicarbonate

define

what does it represent

Answer 10

Standard bicarbonate:

plasma concentration of bicarbonate 
when arterial PCO2 has been 
corrected to 5.3 kPa, 
haemoglobin is fully saturated 
and the body temperature is 37 °C. 

It represents what the actual bicarbonate
would be after eliminating
any respiratory component of
acid–base disturbance.

Question 11

Base excess (deficit):

What is it

when is positive and negative

What can be used to derive it

Answer 11

The amount of acid or base 
required to restore 1 litre of blood 
to normal pH at a 
PaCO2 of 5.3 kPa 
and at body temperature.

It is negative in acidosis 
and positive in alkalosis, 
and is a useful marker
of severity of the metabolic component 
of acid–base disturbances.

The Siggaard–Anderson nomogram can 
be used to derive the base
deficit and standard bicarbonate 
if the pH, 
PCO2 and 
haemoglobin are
know

Question 12

pKa

Answer 12

pKa:

the pH of an acid at
which it is 50% dissociated,
or in equilibrium with its conjugate base.

It is a measure of the strength
of an acid

(the lower the pKa, the stronger the acid)

and is calculated as the
negative logarithm to the
base 10 of the
dissociation constant of an acid.

Question 13

What compensatory mechanisms exist?

Why do the exist

What way doe they respond to primary change

Compensation

How long does each mechanism take

Answer 13

These aim to restore the pH
towards normal,

and are based on maintaining
the ratio PaCO2 /[HCO3–];

therefore, the variable in the compensatory

response always changes
in the same direction as the variable responsible
for the primary imbalance.

Correction occurs when
all three variables
(pH, HCO3– and PaCO2) are
restored to normal levels.

> Initial compensation is by

intracellular buffering
(carbonic acid– bicarbonate buffer system
and haemoglobin)

and occurs within 2 hours.

> Respiratory compensation reaches
its maximum by 24 hours and is by:

• Hyperventilation in the presence
of a metabolic acidosis.

• Hypoventilation in the presence
of a metabolic alkalosis.

> Renal compensation is by:

• Increased acid (H+) secretion
and HCO3 – retention
(reabsorption and
regeneration) in the

presence of a respiratory (and metabolic) acidosis.

• Decreased acid (H+) secretion
and HCO3 – retention

(reabsorption and regeneration)
in the presence of a respiratory
(and metabolic)
alkalosis.

The generation of bicarbonate, 
through urinary excretion of 
ammonium and phosphate, 
restores the depleted HCO3 – 
and buffer base 
reserves over 2–3 days.

Question 14

Table 25.1 Primary changes and compensatory mechanisms in acid–base
disorders

Answer 14

Table 25.1 Primary changes and compensatory mechanisms in acid–base
disorders

Question 15

Identify the abnormalities of
these arterial blood gases: pH 7.0;
PaCO2 7 kPa; PaO2 7 kPa.

Answer 15

Abnormality: Acidaemia (pH < 7.4)
Process: Acidosis (excess production of acid, in the form
of CO2)
Primary change:

Respiratory (↑PaCO2 and ↓PaO2, i.e. type 2
respiratory failure)

Acute v. chronic:
Likely acute as uncompensated
Base excess/deficit: Negative

Standard bicarbonate:
Low in acute setting, as slow renal
compensation is incomplete

Question 16

What would you expect the pH to
be in patients with a chronically
elevated PaCO2 at 7 kPa?

Answer 16

In chronic respiratory acidosis,
the renal compensatory mechanisms result in
a chronic elevation of plasma bicarbonate,
which in turn restores the pH to
within the normal range.

Typically, renal compensation is not complete, and
the normal level of pH 7.40 is never reached

Question 17

How does metabolic compensation take place?

Answer 17

The increased PaCO2 in the
renal tubular cells results
in an increased secretion of H+ ions.

Their secretion results in the following:

• Reabsorption of bicarbonate
by the dissociation of carbonic acid

• Regeneration of bicarbonate
by the excretion of H+ with
ammonia and phosphate in urine.

Metabolic compensation takes place over 2–3 days.

Question 18

Describe the physiological process accounting for the low pH.

Answer 18

Respiratory acidosis is a consequence

of hypoventilation or ventilation perfusion inequalities.

The resulting elevated PCO2
disrupts the ratio of HCO3− to PCO2
and causes a drop in pH.

Question 19

Comment on PaO2 of 7 with the above gas of pco2 7 ph 7

Answer 19

This is lower than normal, suggesting 
either a problem with 
ventilation,
diffusion, 
shunt or a 
ventilation–perfusion mismatch. 

Assuming the inspired concentration of
oxygen is known,

the alveolar partial pressure of oxygen
can be calculated using the
alveolar gas equation.

The A-a gradient can then be
worked out and type of
hypoxia can be assessed,
to help establish the cause.

Question 20

`Define anion gap and list causes

of an increased gap.

Answer 20

T he anion gap (AG) is the difference
between measured cations

(positively charged ions)

and measured anions

(negatively charged ions) in serum.

> This difference (gap) can be accounted
for by the presence of unmeasured anions,
such as albumin, lactic acid, ketones
(β-hydroxybutyrate and acetoacetate),
phosphates and sulphates.

Question 21

AG Eqn

Answer 21

> C lassically it has been calculated using the equation:
• AG = ([Na+] + [K+]) − ([Cl−] + [HCO3−])

• Normal range of 10–20 mmol/L
• [K+] may be excluded from the equation

(as its value is negligible compared
to the other measured ions)

giving a normal AG range of
8–16 mmol/L.

• Modern analysers now predict a
normal range of 3–11 mmol/L.

> In the presence of acidic 
unmeasured anions, 
there is a secondary loss 
of bicarbonate ions due to their 
buffering capacity, 

but chloride concentration remains
unchanged in order to maintain electroneutrality.

The AG, therefore, becomes elevated.