Author: Dr Sanjay Sharma BSc (Hons), FRCP (UK), MD (Lond)

Senior Lecturer for Medipass Intensive MRCP II Courses

Table Of Contents

ACIDOSIS ......................................................................................................................................................................... 3
ALKALOSIS...................................................................................................................................................................... 5
SELF ASSESSMENT....................................................................................................................................................... 6
ANSWERS ........................................................................................................................................................................ 7

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

Find more revision resources at www.medibyte.com

Page 2
 Author: Dr Sanjay Sharma BSc (Hons), FRCP (UK), MD (Lond)
Senior Lecturer for Medipass Intensive MRCP II Courses

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 HCO3- may result in an acidosis.

+
CO2 + H2O <--> H2CO3 <--> H + HCO3-

Three 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.

Find more revision resources at www.medibyte.com

Page 3
 Author: Dr Sanjay Sharma BSc (Hons), FRCP (UK), MD (Lond)
Senior Lecturer for Medipass Intensive MRCP II Courses

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.

Find more revision resources at www.medibyte.com

Page 4
 Author: Dr Sanjay Sharma BSc (Hons), FRCP (UK), MD (Lond)
Senior Lecturer for Medipass Intensive MRCP II Courses

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 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)

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

Find more revision resources at www.medibyte.com

Page 5
 Author: Dr Sanjay Sharma BSc (Hons), FRCP (UK), MD (Lond)
Senior Lecturer for Medipass Intensive MRCP II Courses

Self Assessment

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 pH 7.33

gases 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.

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 131 mmol/l

Potassium 7.2 mmol/l1
Urea 3 mmol/l
Creatinine 121mmol/l
Bicarbonate 8 mmol/l
Chloride 96 mmol/l

Abdominal X-ray Normal

Urinalysis Glucose +++

1. What is the acid base disturbance?

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

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

Find more revision resources at www.medibyte.com

Page 6
 Author: Dr Sanjay Sharma BSc (Hons), FRCP (UK), MD (Lond)
Senior Lecturer for Medipass Intensive MRCP II Courses

Answers

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 factor causing 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.

Find more revision resources at www.medibyte.com

Page 7