Acid-Base Disturbance for the MRCP II Examination

Acidosis

The main source of acid (H+ ions) in the body is tissue respiration. Carbon dioxide produced
by cellular respiration is converted to carbonic acid, which dissociates to generate H+ (acid)
and HCO3- ions (buffering base). The retention of CO2, increase in H+ or reduction in HCO3may result in an acidosis.
CO2 + H2O <--> H2CO3 <--> H+ + HCO3Three types of acidosis are recognized:

Respiratory acidosis.
Metabolic acidosis with a high anion gap.
Metabolic acidosis with a normal anion gap.

Respiratory acidosis is characterised by a fall in arterial pH (<7.35) due to CO2 retention.

Metabolic acidosis may result from the retention of fixed or organic acids causing a
reduction in the bicarbonate level (which is the main buffering agent for H+ in the blood)
without any change in the chloride situation. In these situations, it is termed metabolic
acidosis with a high anion gap. Alternatively, metabolic acidosis may occur as a consequence
of bicarbonate loss from the gastrointestinal tract or the kidneys. In these situations,
chloride is retained as the bicarbonate, resulting in a hyperchloraemic acidosis or a
metabolic acidosis with a normal anion gap. The anion gap is calculated by subtracting the
sum of the sodium and potassium concentrations from the sum of the chloride and
bicarbonate concentrations. The normal anion gap is between 10-18 mmol/l. The hallmark
of metabolic acidosis of either type is a low arterial pH and a low bicarbonate level.
Regulation of arterial pH is controlled by the kidneys and the lungs. Acidosis can be
compensated either by removing CO2 from the body (lungs) or by retaining bicarbonate ions
(kidneys). Respiratory acidosis is compensated by the kidneys, which retain bicarbonate
ions. In compensated respiratory acidosis the pH is normal, or almost normal, and the
bicarbonate level is high. In compensated metabolic acidosis the arterial pH is normal, or
almost normal, and the pCO2 is low. Respiratory acidosis is compensated by the respiratory
system through a centrally mediated mechanism which results in hyperventilation and a
consequent reduction in the pCO2. Causes of respiratory and metabolic acidosis are
tabulated below.

Reproduced from A Rapid Review of Clinical Medicine by Sanjay Sharma, with kind
permission from Manson publishing.

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Alkalosis
Alkalosis may be respiratory or metabolic in origin. In respiratory alkalosis, there is a high pH
due to hyperventilation, causing a low pCO2. Metabolic alkalosis is usually due to increased
loss of H+ from the kidney or gastrointestinal tract, or to increased ingestion of alkaline
agents. It is characterised by a high bicarbonate and a high pH. Respiratory alkalosis is rare
and is usually acute. Chronic cases, usually due to chronic hyperventilation, are
compensated by increasing bicarbonate excretion by the kidneys. Metabolic alkalosis - which
is much more common than respiratory alkalosis - is compensated by respiratory
hypoventilation, which results in an increase in pCO2 and hence an increase in H+.

Causes of respiratory and metabolic acidosis

Respiratory acidosis
Hypoventilation from any cause, e.g. obesity, thoracic cage deformities and
neuromuscular disorders
Obstructive airways disease
Acute asthma
Metabolic acidosis (high anion gap)
Diabetic ketoacidosis
Uraemic acidosis
Salicylate poisoning
Lactic acidosis:
shock
liver failure
metformin therapy
glucose-6-phosphate dehydrogenase deficiency
leukaemia
Methylene poisoning
Ethylene glycol poisoning
Metabolic acidosis (normal anionic gap)
Severe diarrhoea
Pancreatic fistula
Ureterosigmoidostomy
Renal tubular acidosis
Acetazolamide therapy

Reproduced from A Rapid Review of Clinical Medicine by Sanjay Sharma, with kind
permission from Manson publishing.

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Causes of respiratory and metabolic alkalosis

Respiratory alkalosis
Hyperventilation
Hysteria
Encephalitis
Brainstem lesions
Aspirin toxicity
Metabolic alkalosis
Vomiting
Diuretics
Antacids
Hypokalaemic states (these increase renal loss of H+ by the distal convoluted tubule)

SELF-ASSESEMENT

Question 1*
A 75 year old man was seen by his general practitioner with a five day history of wheeze and
ankle swelling. He was prescribed some medication but continued to deteriorate and was
admitted to hospital. Investigations were as follows:
Arterial blood gases pH 7.33
pO2 7kPa
pCO2 6.5kpa
Bicarbonate 20mmmol/l
Biochemistry
Sodium 133mmol/l
Potassium 5mmol/l
Urea 28mmol/l
Creatinine 200mmol/l
What is the most likely cause of her presentation?
1. What is the acid base disturbance?
2. Suggest two possible causes for this metabolic picture.

Reproduced from A Rapid Review of Clinical Medicine by Sanjay Sharma, with kind
permission from Manson publishing.

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Question 2*
A 13 year old girl is admitted under the surgeons with acute abdominal pain. The blood
pressure was 100/60 mm. Hg.
Investigations are as follows:
Biochemistry

Sodium
Potassium
Urea
Creatinine
Bicarbonate
Chloride

Abdominal X-ray

Normal

Urinalysis

Glucose +++

131 mmol/l
7.2 mmol/l1
3 mmol/l
121mmol/l
8 mmol/l
96 mmol/l

1. What is the acid base disturbance?

2. What is the most likely cause for the abnormality?
3. List three therapeutic management steps.

*Answers can be viewed on the next page

Reproduced from A Rapid Review of Clinical Medicine by Sanjay Sharma, with kind
permission from Manson publishing.

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Answer to Question 1
1. Combined respiratory and metabolic acidosis.
2. Acute cardiac failure. Severe exacerbation of obstructive airways disease and pre renal
failure from diuretics.
The patient has a respiratory acidosis, which is characterised by a pCO2 of 6.5kPa or more
and a pH below 7.35 and is hypoxic. In the acute situation respiratory acidosis is not
compensated by the kidney but after 3-5 days the kidneys retain HCO3 ions to compensate
which results in normalisation of the pH at the expense of a relative metabolic alkalosis. In
this patient the HCO3 is slightly low suggesting a metabolic acidosis. This may be due to
coexistent renal disease which prevents adequate compensation or due to another
factorcausing metabolic acidosis. The serum urea and creatinine are elevated but there is a
relatively larger increase in the serum urea suggesting dehydration in this case. It is possible
that he was prescribed a diuretic for symptoms of chronic obstructive airways disease which
have precipitated renal failure by causing dehydration.
An alternative suggestion is that he has developed severe cardiac failure leading to
pulmonary oedema causing hypoxia and respiratory acidosis and hypo-perfusion of the
kidneys causing metabolic acidosis from renal failure.
Other causes of combined respiratory and metabolic acidosis include:

Aspirin poisoning.
Severe pneumonia with renal failure due to septicaemia or interstitial nephritis
(Legionnaire's disease).
Septicaemia from any cause complicated by ARDS.
Malaria complicated by pneumonia.
Acute renal failure and fluid overload.
Renal pulmonary syndromes: Anti GBM disease, Wegener;s granulomatosis,
microscopic polyarteritis nodosa.
Acute massive pulmonary embolism.
Cardiac arrest (before ventilation).

Answer to Question 2
1. Metabolic acidosis with a high anion gap.
2. Diabetic ketoacidosis.
3. a) Intravenous calcium gluconate to prevent hyperkalaemic cardiac arrest
b) Intravenous insulin infusion to halt further ketoacidosis
c) Intravenous saline to rehydrate patient and correct acidosis.

Reproduced from A Rapid Review of Clinical Medicine by Sanjay Sharma, with kind
permission from Manson publishing.

www.medibyteacademy.com 0208 297 9100

info@medibyteacademy.com