Hydrogen ion homoeostasis and

blood gases
Dr. Inas Almazari
 Acid-base balance

Data about patient’s acid-base balance & blood gas

homeostasis are used to assess patients in life-
threatening situations
Normal [H+] in ECF ranges from 36-44 nmol/L (pH
7.34-7.44)
Any H+ values outside this range will affect many
metabolic processes of the body
A pH below 7.34 is referred to as acidosis, whereas a
pH above 7.44 is referred to as alkalosis.
Lungs & kidneys play important roles in regulating
blood pH.
Values greater than 120 nmoI/L or less than 20 nmol/L
are usually incompatible with life
 H+ production

H+ are produced in the body as a result of metabolism, (from

oxidation of the sulfur containing amino acids of protein ingested as
food); but all H+ produced are efficiently excreted in urine

Large amounts of CO2 are produced by cellular activity each day

→Under normal circumstances all of this CO2 is excreted via the
lungs, having been transported in the blood. Only when respiratory
function is impaired do problems occur.
 Buffering
A buffer is a solution of a weak acid & its salt (or a weak base and its
salt) that is able to bind H+ & therefore resist changes in pH.
Buffering is only a short-term solution to the problem of excess H+.
Ultimately, the body must get rid of the H+ by renal excretion.
The body contains a number of buffers to correct sudden changes in
H+ production.
Ex: Proteins & the haemoglobin.
 In the ECF, bicarbonate buffer is the most important. Bicarbonate
(HCO3-( combines with H+ to form carbonic acid (H2CO3), which
dissociate to H2O & CO2 .
 H+ excretion in the kidney
 The mechanisms for HCO3- recovery
& its regeneration are very similar &
are sometimes confused
 H+ excretion in the kidney
 The excreted H+ must be buffered in urine or [H+] would rise to very
high levels. Phosphate acts as one such buffer, while ammonia is
another
 Assessing status

 H2CO3 component is proportional to the dissolved CO2,

which is proportional to the partial pressure of CO2

 Because the body’s cellular and metabolic activities are pH

dependent, the body tries to restore acid-base homeostasis
whenever an imbalance occurs (Compensation)
 Assessing status

 The [H+] in blood varies as [HCO3-] & pCO2 change. If everything

else remains constant:
• Adding H, removing HCO3- or increasing pCO2 will all  [H+]
• Removing H+, adding HCO3- or ↓ pCO2 will all cause [H+] to ↓

 An indication of the acid-base status of the patient can be obtained

by measuring the components of the HCO3- buffer system.
 Assessing status
 Blood [H+] is controlled by our normal pattern of
respiration and the functioning of our kidneys.
 the body accomplishes this by altering the factor not
primarily affected by the pathologic process. e.g. if the
imbalance is of non-respiratory origin, the body
compensates by altering ventilation (fast response).
 For disturbances of the respiratory component, the
kidneys compensate by selectively excreting or
reabsorbing anions and cations. The kidneys are slower to
respond (2-4 days)
 Normal ranges

Lactate 0.7–1.8 mmol/L, Chloride 95–108 mmol/L

 Terminology in acid-base disorders

Metabolic acidosis.
– The primary disorder is a decrease in bicarbonate concentration.

Metabolic alkalosis.
– The primary disorder is an increased bicarbonate.

Respiratory acidosis.
– The primary disorder is an increased PCO2.

Respiratory alkalosis.
– The primary disorder is a decreased PCO2.
 Causes of metabolic acidosis
 Metabolic acidosis with an elevated anion gap occurs in:
 Renal disease. H+ are retained along with anions (sulphate & phosphate).
 Diabetic ketoacidosis. Altered metabolism of fatty acids, as a
consequence of the lack of insulin, causes endogenous production of
acetoacetic & β–hydroxybutyric acids
 lactic acidosis. In acute hypoxic states (respiratory failure or cardiac
arrest) . It can be caused by liver disease. The presence of a lactic
acidosis can be confirmed by measurement of plasma [lactate].
 Certain cases of overdosage or poisoning. As in salicylate overdose
where build-up of lactate occurs, or methanol poisoning when
formate accumulates, or ethylene glycol poisoning where oxalate is
formed.
 Causes of metabolic acidosis
 Metabolic acidosis with a normal anion gap is s/t referred to as a
hyperchloraemic acidosis because a ↓ed [HCO3-] is balanced by
ed [Cl-]. It is seen in :
 Chronic diarrhoea or intestinal fistula. Fluids containing
bicarbonate are lost from the body
 Renal tubular acidosis. Renal tubular cells are unable to excrete
H+ efficiently & bicarbonate is lost in the urine
 Clinical effects of acidosis
 The compensatory response to metabolic acidosis is
hyperventilation. since the increased [H+] acts as a powerful
stimulant of the respiratory centre.
 The deep rapid and gasping respiratory pattern is known as
Kussmaul breathing.
 Hyperventilation is the appropriate physiological response to
acidosis and it occurs rapidly
 A raised [H+] leads to increased neuromuscular irritability. There is a
hazard of arrhythmias progressing to cardiac arrest, & this is made
more likely by the presence of hyperkalemia, which will accompany
the acidosis.
 Depression of consciousness can progress to coma and death.
 Metabolic alkalosis
The causes of a metabolic alkalosis may be due to:
 Loss of H+ in gastric fluid during vomiting. This especially seen
when there is pyloric stenosis preventing parallel loss of bicarbonate-
rich secretions from the duodenum
 Ingestion of absorbable alkali e.g. sodium bicarbonate. Very large
doses are required to cause a metabolic alkalosis unless there is renal
impairment
 Potassium deficiency. In severe K+ depletion (as a consequence of
diuretic therapy), H+ are retained inside cells to replace the missing
K+. In the renal tubule more H+, rather than K+, are exchanged for
reabsorbed Na+. So, despite alkalosis, the patient passes acidic urine.
 Clinical effects of alkalosis
 Hypoventilation
 Confusion and eventually coma
 Muscle cramps, tetany & paraesthesia, a consequence of a decrease in
unbound plasma [Ca], which is a consequence of the alkalosis.
 Respiratory acidosis
Respiratory acidosis may be acute or chronic.
In acute RA: Renal compensation has no time to develop (HCO3-
reabsorption takes 48–72 hrs to become fully effective).
If airflow is completely or partially reduced, the PCO2 in the blood
will rise immediately and the [H+] will rise quickly.
A resulting low PO2 and high PCO2 causes coma. If this is not
relieved rapidly, death results.
Examples of acute (uncompensated) respiratory acidosis are:
choking
bronchopneumonia
acute exacerbation of asthma/COAD (chronic obstructive
airways disease)
 Respiratory acidosis
 Chronic respiratory acidosis usually results from COAD &
accompanied by maximal renal compensation
 In a chronic respiratory acidosis the primary problem is impaired
alveolar ventilation, but renal compensation contributes markedly to
the acid–base picture.

 The kidney  H+
excretion & ECF
HCO3 levels . Blood
[H+] tends back
towards normal
 Respiratory acidosis
In chronic respiratory conditions, extensive renal compensation will
keep blood [H+] near normal. In stable chronic bronchitis [H+] may
be within reference interval despite a very high PCO2. This is
achieved only by maintaining a plasma [HCO3] twice that of
normal. The PO2 is usually depressed, & becomes more so as lung
damage  with time.
Examples of chronic respiratory disorders are:
chronic bronchitis
emphysema.
 Causes of respiratory acidosis
 lung diseases: in which CO2 is not effectively removed from the
blood. In certain patients with chronic obstructive pulmonary
disease (COPD), where CO2 is retained in the blood, causing
chronic hypercarbia (elevated pCO2).
 In bronchopneumonia, gas exchange is impaired because of the
secretions, white blood cells, bacteria, and fibrin in the alveoli.
 Hypoventilation caused by drugs such as barbiturates, morphine,
or alcohol will increase blood pCO2 levels
 Mechanical obstruction or asphyxiation (strangulation or aspiration).
 Decreased cardiac output, such as in CHF, also will result in less
blood to the lungs for gas exchange and an elevated PCO2
 Respiratory alkalosis
Respiratory alkalosis can occur when respiration is stimulated or is no
longer subject to feedback control.
Usually these are acute conditions, & there is no renal compensation.
The treatment is to inhibit or remove the cause of the hyperventilation,
& the acid–base balance should return to normal.
Examples are:
 hysterical overbreathing
 mechanical over-ventilation in an intensive care patient
 raised intracranial pressure, or hypoxia, both of which may
stimulate the respiratory center.
 Causes of respiratory alkalosis
 Hypoxemia
 Chemical stimulation of the respiratory center by drugs, such as
salicylates
 An increase in the environmental temperature; fever; hysteria
(hyperventilation); pulmonary emboli; and pulmonary fibrosis.

 The kidneys compensate by excreting HCO3- in the urine and

reclaiming H+ to the blood.
 The popular treatment for hysterical hyperventilation, breathing into
a paper bag, is self-explanatory.
 Mixed acid–base disorders
It is not uncommon for patients to have more than
one acid–base disorder.
A patient may have both a metabolic and
respiratory acidosis, such as the chronic bronchitic
patient who develops renal impairment.
In such a patient with a raised [H+], the PCO2 will
be increased and the bicarbonate concentration will
be low, both expected findings in primary
respiratory and primary metabolic acidosis.
 Mixed acid–base disorders
Where the two acid–base conditions are
antagonistic in the way they affect the [H+],
one of the disorders may mimic the
compensatory response.

A patient may present with a metabolic

acidosis and a coexistent respiratory alkalosis.
The respiratory disorder may appear, at first
sight, to be simply the compensatory response.
 Mixed acid–base disorders
Other examples of mixed acid–base disorders commonly
encountered are:
1. Apatient with chronic obstructive airways disease, causing a
respiratory acidosis, with thiazide-induced potassium depletion
and consequent metabolic alkalosis.
2. Hyperventilation causing a respiratory alkalosis, with prolonged
nasogastric suction that causes a metabolic alkalosis.
3. Salicylate poisoning in which respiratory alkalosis occurs due to
stimulation of the respiratory centre, together with metabolic
acidosis due to the effects of the drug on metabolism.
 Specimens for blood gas analysis

[H+] and PCO2 are measured directly in an

arterial blood sample. This is usually taken
from the brachial or radial arteries into a
syringe that contains a small volume of
heparin as an anticoagulant.

There is no need to measure the third

variable, the bicarbonate.
Interpreting results
 The steps in classifying the acid–
base disorder are:
 Look first at the [H+]. Decide if an acidosis or an alkalosis
is present.
 If the [H+] is elevated, decide what is the primary cause of
the acidosis. Look at the PCO2. If this is elevated, then
there is a respiratory acidosis. Look at the bicarbonate. If
this is decreased, there is a metabolic acidosis.
 If the [H+] is decreased, decide what is the primary cause
of the alkalosis. Look at the PCO2. If low, then there is a
respiratory alkalosis. Look at the bicarbonate. If this is
high, then there is a metabolic alkalosis.
 The steps in classifying the acid–
base disorder are:
 Having decided on the primary acid–base disorder, look to see if
there is compensation. If there is, there will be a change in the
other component (the one which was not used to determine the
primary disorder), in the direction which ‘compensates’ for the
primary disorder, i.e. returns the ratio, and hence the [H+],
towards normal. If there is not, the acid–base disorder may be
uncompensated. If the change is in the opposite direction then a
second acid–base disorder may be present. Even if there is
compensation consider the possibility that there is a second
acid–base problem that mimics the compensatory response.
 If there is compensation, decide if the disorder is fully
compensated or partially compensated. If fully compensated,
the resulting [H+] will be within the reference limits.
 Referance levels
Lactate 0.7–1.8 mmol/L, Chloride 95–108 mmol/L,
H+ 35 and 45 nmol/L
 Cases:

A patient with chronic bronchitis. Blood gas

results are: [H+] = 44 nmol/L; PCO2 = 9.5
kPa; [HCO3–] = 39 mmol/L.

A compensated respiratory acidosis is

present.
 Management of acid–base disorders
Many acid–base disorders are secondary to some other
disorder. In most cases the management of an acid–base
disorder is to treat the underlying illness.
This may involve:
1. Fluid therapy and insulin in diabetic ketoacidosis
2. Artificial ventilation by intermittent positive pressure
ventilation (IPPV) in acute status asthmaticus.
3. Improvement of GFR by restoring blood volume in a
patient with acute blood loss.
 Management of acid–base
disorders
In cases where there is a life threatening acidosis
(e.g. [H+] >100 nmol/L), the infusion of sodium
bicarbonate may be considered. The circumstances
when this might be appropriate include severe
diabetic ketoacidosis.

Sodium bicarbonate must always be used with

caution. Careful monitoring of the patient by
repeatedly measuring the blood gases may be
necessary.