Question 9 of 192

A patient has an arterial blood gas sample taken and the following result is obtained:
pH 7.48

pO2 10.1

Bicarbonate 30

pCO2 4.5

Chloride 10meq

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What is the most likely cause?

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Respiratory alkalosis

Metabolic alkalosis
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Type 1 respiratory failure

Metabolic acidosis with normal anion gap

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Metabolic acidosis with increased anion gap

This would be a typical result of prolonged vomiting.

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Disorders of acid - base balance

Disorders of acid- base balance are often covered in the MRCS part A.

The acid-base normogram below shows how the various disorders may be categorised
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Image sourced from Wikipedia

Metabolic acidosis

• This is the most common surgical acid - base disorder.

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• Reduction in plasma bicarbonate levels.
• Two mechanisms:

1. Gain of strong acid (e.g. diabetic ketoacidosis)

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2. Loss of base (e.g. from bowel in diarrhoea)

- Classified according to the anion gap, this can be calculated by:
(Na+ + K+) - (Cl- + HCO3-).
- If a question supplies the chloride level then this is often a clue that the anion gap should be
calculated. The normal range = 10-18 mmol/L
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Normal anion gap ( = hyperchloraemic metabolic acidosis)

• Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula

• Renal tubular acidosis
• Drugs: e.g. acetazolamide
• Ammonium chloride injection
• Addison's disease

Raised anion gap

 • Lactate: shock, hypoxia
• Ketones: diabetic ketoacidosis, alcohol
• Urate: renal failure
• Acid poisoning: salicylates, methanol

Metabolic acidosis secondary to high lactate levels may be subdivided into two types:

• Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)

• Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

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Metabolic alkalosis

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• Usually caused by a rise in plasma bicarbonate levels.
• Rise of bicarbonate above 24 mmol/L will typically result in renal excretion of excess
bicarbonate.
• Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly to problems of
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the kidney or gastrointestinal tract

Causes

• Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis, nasogastric suction)
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• Diuretics
• Liquorice, carbenoxolone
• Hypokalaemia
• Primary hyperaldosteronism
• Cushing's syndrome
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• Bartter's syndrome
• Congenital adrenal hyperplasia
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Mechanism of metabolic alkalosis

• Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor

• Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule
• ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised
aldosterone levels
• In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to
maintain neutrality
Respiratory acidosis

• Rise in carbon dioxide levels usually as a result of alveolar hypoventilation

• Renal compensation may occur leading to Compensated respiratory acidosis

Causes

• COPD
•

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Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary
oedema
• Sedative drugs: benzodiazepines, opiate overdose

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Respiratory alkalosis

• Hyperventilation resulting in excess loss of carbon dioxide

•
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This will result in increasing pH

Causes

• Psychogenic: anxiety leading to hyperventilation

• Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high altitude
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• Early salicylate poisoning*
• CNS stimulation: stroke, subarachnoid haemorrhage, encephalitis
• Pregnancy
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*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation
of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of
salicylates (combined with acute renal failure) may lead to an acidosis
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Question 10 of 192

Which of the blood gas results listed below is most likely to fit with a patient who has acute
respiratory acidosis?

pH 7.57, PaCO2 3.5, Pa O2 24.5 (FiO2 85%), Bicarbonate 23.5, Base excess +1.8 mmol

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pH 7.19, pCO2 10.2, pO2 16 (FiO2 85%), Bicarbonate 23.8, Base excess -2.2 mmol

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pH 7.14, PaCO2 7.4, PaO2 8.9 (FiO2 40%), Bicarbonate 14 mmol, Base excess -10.6

pH 7.36, PaCO2 7.3, PO2 8.9 (FiO2 40%), Bicarbonate 30.2, Base excess 5.3
Sa
pH 7.32, PCO2 3.8, PaO2 22.2 (FiO2 40%), Bicarbonate 19.1, Base excess -7.9

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Arterial blood gas interpretation

In advanced life support training, a 5 step approach to arterial blood gas interpretation is advocated.
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1. How is the patient?

2. Is the patient hypoxaemic?

The Pa02 on air should be 10.0-13.0 kPa

3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)

4. What has happened to the PaCO2?

If there is acidaemia, an elevated PaCO2 will account for this

5. What is the bicarbonate level or base excess?

A metabolic acidosis will have a low bicarbonate level and a low base excess (< -2 mmol)
A metabolic alkalosis will have a high bicarbonate and a high base excess (> +2 mmol)

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Question 38 of 192

Which of the following arterial blood gas results would fit with chronic respiratory acidosis with a
compensatory metabolic alkalosis?

pH 7.36, PaCO2 7.3, PO2 8.9 (FiO2 40%), Bicarbonate 30.2, Base excess +5.3

pH 7.32, PCO2 3.8, PaO2 22.2 (FiO2 40%), Bicarbonate 19.1, Base excess -7.9

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pH 7.14, PaCO2 7.4, PaO2 8.9 (FiO2 40%), Bicarbonate 14 mmol, Base excess -10.6

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pH 7.57, PaCO2 3.5, Pa O2 24.5 (FiO2 85%), Bicarbonate 23.5, Base excess +1.8 mmol

pH 7.19, pCO2 10.2, pO2 16 (FiO2 85%), Bicarbonate 23.8, Base excess -2.2 mmol
Sa
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Question 4 of 116

A 67 year old male is admitted to the surgical unit with acute abdominal pain. He is found to have a
right sided pneumonia. The nursing staff put him onto 15L O2 via a non rebreathe mask. After 30
minutes the patient is found moribund, sweaty and agitated by the nursing staff. An arterial blood
gas reveals:

pH 7.15

pCO2 10.2

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pO2 8

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Bicarbonate Sa 32

Base excess - 5.2

What is the most likely cause for this patients deterioration?

Acute respiratory alkalosis secondary to hyperventilation

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Over administration of oxygen in a COPD patient
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Metabolic acidosis secondary to severe pancreatitis

Metabolic alkalosis secondary to hypokalaemia

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Acute respiratory acidosis secondary to pneumonia

This patient has an acute respiratory acidosis, however this is on a background of chronic
respiratory acidosis (due to COPD) with a compensatory metabolic alkalosis (the elevated
bicarbonate is the main clue to the chronic nature of the respiratory acidosis). This blood gas picture
is typical in a COPD patient who has received too much oxygen; these patients lose their hypoxic
drive for respiration, therefore retain CO2 and subsequently hypoventilate leading to respiratory
arrest. If the bicarbonate was normal, then the answer would be acute respiratory acidosis
secondary to pneumonia.
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Question 6 of 116

Which of the following does not cause an increased anion gap acidosis?

Uraemia

Paraldehyde

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Diabetic ketoacidosis

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Ethylene glycol

Acetazolamide Sa
Causes of increased anion acidosis: MUDPILES

M - Methanol
U - Uraemia
D - DKA/AKA
P - Paraldehyde/phenformin
I - Iron/INH
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L - Lactic acidosis
E - Ethylene glycol
S - Salicylates
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Question 31 of 116

Which of the following does not cause hyperkalaemia?

Haemolysis

Burns

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Familial periodic paralysis

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Type 4 renal tubular acidosis

Severe malnutritionSa
'Machine' - Causes of Increased Serum K+

M - Medications - ACE inhibitors, NSAIDS

A - Acidosis - Metabolic and respiratory
C - Cellular destruction - Burns, traumatic injury
H - Hypoaldosteronism, haemolysis
I - Intake - Excessive
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N - Nephrons, renal failure
E - Excretion - Impaired

Familial periodic paralysis has subtypes associated with hyper and hypokalaemia.
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Hyperkalaemia

• Plasma potassium levels are regulated by a number of factors including aldosterone, acid-
base balance and insulin levels.
• Metabolic acidosis is associated with hyperkalaemia as hydrogen and potassium ions
compete with each other for exchange with sodium ions across cell membranes and in the
distal tubule.
 • ECG changes seen in hyperkalaemia include tall-tented T waves, small P waves, widened
QRS leading to a sinusoidal pattern and asystole

Causes of hyperkalaemia

• Acute renal failure

• Drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers,
spironolactone, ciclosporin, heparin**
• Metabolic acidosis
• Addison's

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• Tissue necrosis/rhabdomylosis: burns, trauma
• Massive blood transfusion

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Foods that are high in potassium

• Salt substitutes (i.e. Contain potassium rather than sodium)

• Bananas, oranges, kiwi fruit, avocado, spinach, tomatoes
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*beta-blockers interfere with potassium transport into cells and can potentially cause hyperkalaemia
in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as
emergency treatment

**both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought to
be caused by inhibition of aldosterone secretion
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Question 39 of 116

Which of the following drugs causes hyperkalaemia?

Heparin

Ciprofloxacin

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Salbutamol

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Levothyroxine

Codeine phosphate Sa
Both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought to
be caused by inhibition of aldosterone secretion. Salbutamol is a recognised treatment for
hyperkalaemia.
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Question 58 of 116

A patient has an arterial blood gas sample which provides the following result:

pH 7.20

pO2 7.5

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Bicarbonate 22

pCO2 8.1

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Chloride 10meq

What is the most likely cause? Sa

Type II respiratory failure

Metabolic acidosis with increased anion gap

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Metabolic alkalosis

Type I respiratory failure

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Respiratory alkalosis
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This is a sign of acute type 2 respiratory failure (non compensated). This is the result of carbon
dioxide retention.
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Question 60 of 116

A 77 year old man presents to pre operative clinic for a total knee replacement. He is on furosemide
for hypertension. He is known to have multiple myeloma. He is found to have the following test
results:

Na 120

Serum osmolality 280 (normal)

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Urine osmolality normal

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Urine Na normal

What is the most likely cause?Sa

Pseudohyponatraemia

Syndrome of inappropriate ADH secretion (SIADH)

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Hypotonic hypovolaemic hyponatraemia

Psychogenic polydipsia
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Hypertonic hypovolaemic hyponatraemia

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Hyperlipidaemia and multiple myeloma are known to cause a pseudohyponatraemia, this is due to
raised protein.
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Hyponatraemia

This is commonly tested in the MRCS (despite most surgeons automatically seeking medical advice
if this occurs!). The most common cause in surgery is the over administration of 5% dextrose.

Hyponatraemia may be caused by water excess or sodium depletion. Causes of

pseudohyponatraemia include hyperlipidaemia (increase in serum volume) or a taking blood from a
drip arm. Urinary sodium and osmolarity levels aid making a diagnosis.

Classification

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Urinary sodium > 20 mmol/l Sodium depletion, renal loss Mnemonic: Syndrome of
INAPPropriate Anti-Diuretic
Hormone:

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• Patient often hypovolaemic In creased
• Diuretics (thiazides) Na (sodium)
• Addison's PP (urine)
• Diuretic stage of renal failure
• SIADH (serum osmolality low,
Sa urine osmolality high, urine Na
high)
• Patient often euvolaemic

Urinary sodium < 20 mmol/l Sodium depletion, extra-renal loss

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• Diarrhoea, vomiting, sweating
• Burns, adenoma of rectum (if
villous lesion and large)
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Water excess (patient often • Secondary hyperaldosteronism:

hypervolaemic and CCF, cirrhosis
oedematous) • Reduced GFR: renal failure
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• IV dextrose, psychogenic
polydipsia

Management

Symptomatic Hyponatremia :

Acute hyponatraemia with Na <120: immediate therapy. Central Pontine Myelinolisis, may occur
from overly rapid correction of serum sodium. Aim to correct until the Na is > 125 at a rate of 1
mEq/h. Normal saline with frusemide is an alternative method.
The sodium requirement can be calculated as follows :

(125 - serum sodium) x 0.6 x body weight = required mEq of sodium

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Question 79 of 116

A 24 year old man is involved in a road traffic accident. His right leg is trapped for 6 hours whilst he
is moved. On examination his foot is insensate and a dorsalis pedis pulse is only weakly felt. Which
of the biochemical abnormalities listed below is most likely to be present?

Alkalosis

Hypercalcaemia

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Hypocalcaemia

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Hyperkalaemia

Hyponatraemia
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In this scenario the patient will have a compartment syndrome, delayed diagnosis and muscle death.
The effect of muscle death will result in the release of potassium. It is also highly likely that there will
be a degree of renal impairment, the result of which is that the serum potassium is likely to be high.
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Question 83 of 116

An arterial blood gas sample is taken and the following results obtained;

PaO2 8kPa

PaCO2 4kPa

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pH 7.4

With which of the following are these values most consistent?

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Compensated metabolic alkalosis
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Pulmonary atelectasis

Alveolar hypoventilation

Residing at 4500M for 48 hours

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LAD occlusion
R

The patient has low oxygen tension and low carbon dioxide. The pH is normal so there is
compensation for a long standing condition in which oxygenation is reduced. There is neither
alkalosis, nor hypoventilation as the carbon dioxide is low. At very high altitude, the low oxygen
tension can exceed the anaerobic threshold and carbon dioxide levels increase.
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Question 84 of 116

Which of the following does not cause a normal anion gap acidosis?

Pancreatic fistula

Acetazolamide

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Uraemia

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Ureteric diversion
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Renal tubular acidosis

Normal Gap Acidosis: HARDUP

H - Hyperalimentation/hyperventilation
A - Acetazolamide
R - Renal tubular acidosis
C
D - Diarrhoea
U - Ureteral diversion
P - Pancreatic fistula/parenteral saline

Uraemia will typically cause a high anion gap acidosis. It is one of the unmeasured anions.
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Question 181 of 192

Which of the following statements are not typically true in hypokalaemia?

It may occur as a result of mechanical bowel preparation

Chronic vomiting may increase renal potassium losses

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It may be associated with aciduria

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It may cause hyponatraemia

It often accompanies acidosis

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Potassium depletion occurs either through the gastrointestinal tract or the kidney. Chronic vomiting
in itself is less prone to induce potassium loss than diarrhoea as gastric secretions contain less
potassium than those in the lower GI tract. If vomiting produces a metabolic alkalosis then renal
potassium wasting may occur as potassium is excreted in preference to hydrogen ions. The
converse may occur in potassium depletion resulting in acid urine.
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Hypokalemia is very commonly associated with metabolic alkalosis. This is due to 2 factors: 1) the
common causes of metabolic alkalosis (vomiting, diuretics) directly induce H+ and K loss (via
aldosterone) and thus also cause hypokalemia and 2) hypokalemia is a very important cause of
metabolic alkalosis by three mechanisms. The initial effect is by causing a transcellular shift in which
K leaves and H+ enters the cells, thereby raising the extracellular pH. The second effect is by
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causing a transcellular shift in the cells of the proximal tubules resulting in an intracellular acidosis,
which promotes ammonium production and excretion. Thirdly, in the presence of hypokalemia,
hydrogen secretion in the proximal and distal tubules increases. This leads to further reabsorption of
HCO3-. The net effect is an increase in the net acid excretion.
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Hypokalaemia
Potassium and hydrogen can be thought of as competitors. Hyperkalaemia tends to be associated
with acidosis because as potassium levels rise fewer hydrogen ions can enter the cells

Hypokalaemia with alkalosis

• Vomiting
• Diuretics
• Cushing's syndrome
• Conn's syndrome (primary hyperaldosteronism)

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Hypokalaemia with acidosis

• Diarrhoea

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• Renal tubular acidosis
• Acetazolamide
• Partially treated diabetic ketoacidosis

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Question 14 of 32

A 73 year old man presents to pre operative clinic for an elective total hip replacement. He is on
furosemide for hypertension. His investigations reveal to the following results:

Na 120

Urine Na 10 (low)

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Serum osmolality 280 (normal)

What is the most likely cause?

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Hypotonic hypovolaemic hyponatraemia
Sa
Hypertonic hypovolaemic hyponatraemia

Syndrome of inappropriate ADH secretion

Over administration of 5% dextrose

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Glomerulonephritis
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The blood results reflect extra-renal sodium loss. The body is trying to preserve the sodium by not
allowing any sodium into the urine (hence the low Na in the urine). Note with renal sodium loss the
Urinary sodium is high.
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Hyponatraemia
This is commonly tested in the MRCS (despite most surgeons automatically seeking medical advice
if this occurs!). The most common cause in surgery is the over administration of 5% dextrose.

Hyponatraemia may be caused by water excess or sodium depletion. Causes of

pseudohyponatraemia include hyperlipidaemia (increase in serum volume) or a taking blood from a
drip arm. Urinary sodium and osmolarity levels aid making a diagnosis.

Classification

Urinary sodium > 20 mmol/l Sodium depletion, renal loss Mnemonic: Syndrome of
INAPPropriate Anti-Diuretic

h
Hormone:
• Patient often hypovolaemic In creased
• Diuretics (thiazides) Na (sodium)

la
• Addison's PP (urine)
• Diuretic stage of renal failure
• SIADH (serum osmolality low, urine
osmolality high, urine Na high)
• Patient often euvolaemic

Urinary sodium < 20 mmol/l

Sa Sodium depletion, extra-renal loss

• Diarrhoea, vomiting, sweating

• Burns, adenoma of rectum (if villous
C
lesion and large)

Water excess (patient often • Secondary hyperaldosteronism:

CCF, cirrhosis
R

hypervolaemic and
oedematous) • Reduced GFR: renal failure
• IV dextrose, psychogenic polydipsia
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Management

Symptomatic Hyponatremia :

Acute hyponatraemia with Na <120: immediate therapy. Central Pontine Myelinolisis, may occur
from overly rapid correction of serum sodium. Aim to correct until the Na is > 125 at a rate of 1
mEq/h. Normal saline with frusemide is an alternative method.

The sodium requirement can be calculated as follows :

(125 - serum sodium) x 0.6 x body weight = required mEq of sodium

 Next question

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Question 22 of 192

Which of the conditions listed below is most likely to account for the following arterial blood gas
result:
pH 7.49

pO2 8.5

Bicarbonate 22

pCO2 2.4

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Chloride 12meq

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Respiratory alkalosis

Metabolic alkalosis

Metabolic acidosis
Sa
Type II respiratory failure
C
Metabolic acidosis with increased anion gap

The hyperventilation results in decreased carbon dioxide levels, causing a respiratory alkalosis (non
compensated).
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Question 23 of 192

Which of the following blood gas results would fit with metabolic acidosis with a compensatory
respiratory alkalosis?

pH 7.36, PaCO2 7.3, PO2 8.9 (FiO2 40%), Bicarbonate 30.2, Base excess +5.3

pH 7.14, PaCO2 7.4, PaO2 8.9 (FiO2 40%), Bicarbonate 14 mmol, Base excess -10.6

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pH 7.57, PaCO2 3.5, Pa O2 24.5 (FiO2 85%), Bicarbonate 23.5, Base excess +1.8 mmol

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pH 7.32, PCO2 3.8, PaO2 22.2 (FiO2 40%), Bicarbonate 19.1, Base excess -7.9

pH 7.19, pCO2 10.2, pO2 16 (FiO2 85%), Bicarbonate 23.8, Base excess -2.2 mmol
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Question 59 of 192

A 53 year old man is on the intensive care unit following an emergency abdominal aortic aneurysm
repair. He develops abdominal pain and diarrhoea and is profoundly unwell. His abdomen has no
features of peritonism. Which of the following arterial blood gas pictures is most likely to be present?

pH 7.45, pO2 10.1, pCO2 3.2, Base excess 0, Lactate 0

pH 7.35, pO2 8.0, pCO2 5.2, Base excess 2, Lactate 1

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pH 7.20, pO2 9.0, pCO2 3.5, Base excess -10, Lactate 8

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pH 7.29, pO2 8.9, pCO2 5.9, Base excess -4, Lactate 3
Sa
pH 7.30, pO2 9.2 pCO2 4.8, Base excess -2, lactate 1

This man is likely to have a metabolic acidosis secondary to a mesenteric infarct.

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Question 62 of 192

A patient is seen in clinic complaining of abdominal pain. Routine bloods show:

Na+ 142 mmol/l

K+ 4.0 mmol/l

Chloride 104 mmol/l

Bicarbonate 19 mmol/l

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Urea 7.0 mmol/l

Creatinine 112 µmol/l

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What is the anion gap?

4 mmol/L Sa
14 mmol/L

20 mmol/L

21 mmol/L
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23 mmol/L
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The anion gap may be calculated by using (sodium + potassium) - (bicarbonate + chloride)

= (142 + 4.0) - (104 + 19) = 23 mmol/L

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Anion gap

The anion gap is calculated by:

(sodium + potassium) - (bicarbonate + chloride)

A normal anion gap is 8-14 mmol/L

It is useful to consider in patients with a metabolic acidosis:

Causes of a normal anion gap or hyperchloraemic metabolic acidosis

• gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula

• renal tubular acidosis
• drugs: e.g. acetazolamide
• ammonium chloride injection
• Addison's disease

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Causes of a raised anion gap metabolic acidosis

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• lactate: shock, hypoxia
• ketones: diabetic ketoacidosis, alcohol
• urate: renal failure
• acid poisoning: salicylates, methanol
Sa Next question
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