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Answers

Case 1

1. a) Type 1 respiratory impairment (moderate)

b) Uncompensated respiratory alkalosis

This patient has moderate type 1 respiratory impairment. Hyperventilation is an appropriate response to the hypoxaemia and sensation of dyspnoea and has resulted in a mild alkalaemia (remember that metabolic compensation does not occur in response to acute respiratory acid–base disturbance).

The correct management for his condition is supplemental oxygen to correct the hypoxaemia and appropriate antibiotics to treat the infection.

In a patient such as this, with moderate hypoxaemia and no ventilatory impairment, monitoring by pulse oximetry is more appropriate than repeated ABG sampling. Indications for further ABG analysis would include signs of exhaustion or hypercapnia (p. 23) or a further significant decline in SaO₂.

Case 2

1. a) Chronic type 2 respiratory impairment

b) Compensated respiratory acidosis

2. Chronic type 2 respiratory impairment due to morbid obesity

At first glance it may be difficult to determine whether this ABG represents respiratory acidosis with metabolic compensation or metabolic alkalosis with respiratory compensation, as both give a high HCO₃ and high PaCO₂. The best clue is the pH (or H⁺) which, although just within the normal range, is on the brink of acidaemia. This would represent overcompensation for an alkalosis and, therefore, suggests an acidosis as the primary abnormality (overcompensation does not occur). The mildly impaired oxygenation is consistent with the degree of hypoventilation.

The likeliest cause of chronic type 2 respiratory impairment in this case is severe obesity. Around 20% of individuals with a body mass index greater than 40 have chronic hypercapnia from restricted ventilation (pickwickian syndrome).

Case 3

1. a) Mild type 1 respiratory impairment (with marked hyperventilation)

b) Uncompensated respiratory alkalosis

2. Pulmonary embolism

This patient is a young, fit, non-smoker with no history of lung problems but, despite hyperventilating (low PaCO₂), has a PaO₂ below the normal range, indicating impaired oxygenation. Given the recent long-haul flight and absence of clinical and X-ray abnormalities, the most likely cause of her breathlessness and impaired oxygenation is pulmonary embolism and she must be investigated accordingly.

This is one of the clinical situations where calculation of the A–a gradient can be helpful (more so when the PaO₂ is just within the normal range). As shown below, it is significantly elevated, indicating the presence of V/Q mismatch.

A–a gradient = PAO₂ – PaO₂

PAO2 = (0.21 × 93.8) – (3.9 × 1.2)

= 19.7 – 4.7

A-a gradient = 15 – 10.3

= 4.7 (norm <2.6 kPa)

PAO2 = (0.21 × 713) – (29.3 × 1.2)

A-a gradient = 115 – 77

= 38 mmHg (norm <20 mmHg)

Case 4

1. a) Acute type 2 respiratory failure

b) Uncompensated respiratory acidosis

2. Opioid toxicity

3. Opioid antagonist

Opioids have a depressant effect upon respiration and may lead to acute ventilatory failure (type 2 respiratory failure). This elderly man has received a large amount of morphine in a short period of time and exhibits pinpoint pupils, making opioid toxicity by far the likeliest cause of his severe ventilatory failure. Since metabolic compensation takes several days to occur, the acute respiratory acidosis has produced a severe acidaemia.

His PaO₂, though within the normal range, is lower than expected for a patient breathing 28% O₂, and more or less consistent with this degree of hypoventilation.

In addition to basic life support measures, he should be administered an opioid antagonist (e.g. naloxone), to reverse the respiratory depression, then closely monitored to ensure sustained improvement.

Case 5

1. a) Type 1 respiratory impairment (moderate)

b) Normal acid-base balance

The above ABG is helpful in guiding the correct treatment for this patient with acute exacerbation of chronic obstructive pulmonary disease. Patients with this condition are often prescribed inadequate oxygen for fear of suppressing hypoxic drive (and thereby depressing ventilation), but this is only an issue in patients with chronic type 2 respiratory failure (indicated by ↑PaCO₂ and ↑HCO₃). This patient has type 1 respiratory impairment and will not rely on hypoxic drive.

Although this patient is likely to have a chronically low PaO₂, the acute deterioration in his symptoms and exercise tolerance suggests a further recent decline from his normal baseline. Importantly, even a small drop in PaO₂ around this level (steep part of O₂–Hb curve) may cause a marked reduction in SaO₂, compromising O₂ delivery to tissues. Thus O₂ is required both to alleviate symptoms and to prevent the development of tissue hypoxia, and should not be withheld for fear of precipitating hypoventilation.

Case 6

1. a) Acute type 2 respiratory impairment

b) Uncompensated respiratory acidosis

This patient with an acute exacerbation of chronic obstructive pulmonary disease has been struggling to overcome severe obstruction to airflow over a period of hours to days and is now exhausted from the increased work of breathing. As a result, his alveolar ventilation is declining, leading to acute type 2 respiratory failure. This may complicate type 1 respiratory failure from any cause, not just from chronic obstructive pulmonary disease. The rising PaCO₂ is, therefore, not due to diminished hypoxic drive and removing his oxygen will not correct it. Indeed his FiO₂ should probably be increased (in addition to other treatment) as he remains significantly hypoxaemic.

Remember that, with acute respiratory acidosis, there is no time for metabolic compensation to develop and a dangerous acidaemia develops rapidly. Adequate ventilation must be restored, as a matter of urgency, to correct the PaCO₂. Possible measures, in this case, include a respiratory stimulant (e.g. doxapram) or, preferably, non-invasive ventilation. If these fail, intubation and mechanical ventilation may be required, if considered appropriate.

Case 7

1. a) Type 1 respiratory impairment

b) Mild respiratory alkalosis balanced by mild metabolic acidosis (likely two primary processes)

2. Aspiration pneumonia

This patient has mild to moderate hypoxaemia despite receiving a high FiO₂ and therefore has severe impairment of oxygenation. The slightly low PaCO₂ indicates that ventilation is adequate, so this is type 1 respiratory impairment. The probable explanation for the mild metabolic acidosis is lactic acidosis resulting from tissue hypoxia.

The history, examination findings and chest X-ray all suggest a diagnosis of aspiration pneumonia.

This patient is severely unwell and any further decline in her PaO₂ could be catastrophic (on the steep part of the O₂–Hb saturation curve). Her O₂ therapy should be adjusted as necessary to maintain her SaO₂ above 92% and she should be managed on a high-dependency unit with close monitoring for signs of deterioration.

Case 8

1. a) Chronic type 2 respiratory impairment

b) Compensated respiratory acidosis

3. PCO₂ and HCO₃

Acute exacerbation of chronic obstructive pulmonary disease is a common medical emergency and this case illustrates key principles.

1. The ↑PaCO₂ shows the patient has type 2 respiratory impairment (ventilatory impairment).

2. The ↑HCO₃ tells us it is chronic type 2 impairment (since metabolic compensation takes time to develop).

3. Even in chronic type 2 impairment, a further acute rise in PaCO₂ would lead to an acidaemia. The pH here is normal, so the PaCO₂ has not changed appreciably in the last few days (i.e. there is no acute-on-chronic rise).

4. His PaO₂is likely to have dropped, leading to the increased breathlessness and marked decline in exercise capacity: below a PaO₂ of 8 kPa (60 mmHg) even small falls may cause a major decline in SaO₂ (steep part of the curve).

5. As this patient has chronic hypercapnia, he may rely on hypoxic drive as a stimulus to ventilation.

6. The goal is to ensure adequate oxygenation (we must not ignore his hypoxaemia) without depressing ventilatory drive.

Case 9

1. a) Acute-on-chronic type 2 respiratory impairment

b) Partially compensated respiratory acidosis

2. Excessive supplemental O₂

Care must be taken when prescribing supplemental O₂ to patients with chronic type 2 respiratory failure. The aim is to reverse any recent worsening of hypoxaemia and allow adequate tissue oxygenation, without depressing ventilatory drive through an excessive rise in PaO₂.

Most authorities recommend controlled O₂ therapy using a fixedconcentration mask at an initial concentration of 24–28%. The response to therapy must be closely monitored with frequent clinical assessment and repeated ABG measurement. Note that pulse oximetry is not an adequate substitute for ABG in these circumstances as knowledge of the SaO₂ alone does not permit assessment of ventilatory adequacy.

The latter point is well illustrated in this case as the patient now has life-threatening acute-on-chronic respiratory failure despite a normal SaO₂. The rising PaCO₂ must be rapidly checked and reversed through improving ventilation. Potential strategies include reducing inspired O₂ concentration, respiratory stimulants or assisted ventilation.

Case 10

1. a) Mild type 1 respiratory impairment

2. The PaCO₂ (high end of normal range)

3. Life-threatening attack

This patient has several features of a severe asthma attack but it is the high–normal PaCO₂ that is the most worrying aspect of her presentation and makes it a life-threatening attack. Patients with acute exacerbations of asthma should have a low PaCO₂ on account of the increased respiratory rate and effort (↑alveolar ventilation). A level >5 kPa (37.5 mmHg) suggests the patient is struggling to overcome the obstruction to airflow and, perhaps, beginning to tire from the effort of breathing. Consequently, her PaCO₂ signals a life-threatening attack.

The intensive care unit should be informed immediately of any patient with acute severe asthma and life-threatening features. Patients must receive intensive treatment and monitoring, including repeated ABG measurements to assess response and identify the need for intubation.

Case 11

1. a) Hyperventilation (primary)

b) Uncompensated respiratory alkalosis

2. Low ionized calcium

3. Psychogenic hyperventilation

This is a classic clinical picture of psychogenic hyperventilation. The ABG is entirely in keeping with this diagnosis as it reveals evidence of hyperventilation (low PaCO₂) with normal oxygenation (normal PaO₂) and a normal A–a gradient.

Note that the HCO₃ (and BE) is normal as there has been insufficient time for metabolic compensation to occur. Consequently the reduction in PaCO₂ has caused a marked alkalaemia.

Another point to note is that the concentration of ionized calcium in the blood is affected by the pH of the specimen, since H⁺ ions compete with calcium for binding sites on albumin and other proteins. Therefore, as the number of H⁺ ions drops (alkalaemia), more calcium is bound to albumin, causing serum ionized calcium levels to fall. This is the most likely cause of the numbness and tingling.

Care must be taken in ruling out other cardiovascular and respiratory pathologies before ascribing symptoms of chest pain and shortness of breath to psychogenic hyperventilation.

Case 12

1. a) Normal – but severe hypoxaemia

b) Compensated metabolic acidosis

2. Carbon monoxide poisoning

Carbon monoxide (CO) poisoning commonly presents with nausea, vomiting, headache and confusion. CO saturations correlate poorly with symptoms but levels above 50% may cause cardiac arrest and seizures.

Why is the patient hypoxaemic?

CO binds to haemoglobin (Hb) with 200 times the affinity of O₂ so is carried on the Hb molecule (as carboxyhaemoglobin) in preference to O₂. As a consequence, the percentage of Hb saturated with O₂ – the SaO₂ – is markedly reduced in CO poisoning, even when the PaO₂ is very high. Since the overall O₂ content of blood is determined by the SaO₂ and Hb concentration, O₂ delivery to tissues is inadequate (tissue hypoxia), leading to lactic acidosis.

Why does SaO₂ appear to be normal?

Most pulse oximeters are unable to distinguish carboxyhaemoglobin from oxyhaemoglobin, so fail to reflect the true SaO₂ in CO poisoning. In ABG analysis, the SaO₂ is not normally measured but simply calculated from the measured PaO₂. The latter parameter is based only on free, unbound O₂ molecules so is unaffected by the presence of CO.

Case 13

1. a) Hyperventilation – no impairment of oxygenation but hypoxaemia secondary to anaemia (P.18)

b) Uncompensated respiratory alkalosis

2. Anaemia (Haemoglobin 6.8)

3. Restore haemoglobin (Hb) concentration (e.g. blood transfusion, iron replacement)

This patient appears to have severe anaemia, most likely due to iron deficiency from chronic rectal bleeding. This should be confirmed with a formal laboratory sample (‘full blood count’).

There is no impairment of ventilation or O₂ transfer so PaO₂ and SaO₂ are normal. However the vast majority of O₂ in blood is carried by Hb, so the overall O₂content of her blood is low.

Hyperventilation is a normal response to the sensation of breathlessness and increases the PaO₂ slightly. However, in the above context, this has very little impact on blood O₂ content as the available Hb molecules are already fully saturated.

For the same reason supplemetal O₂ would also fail to improve O₂ content significantly. Indeed the only effective strategy is to increase Hb concentration. This could be achieved rapidly, by a blood transfusion or more gradually by iron replacement.

Case 14

1. a) Hyperventilation (secondary)

b) Partially compensated metabolic acidosis

2. Mesenteric ischaemia

What does the ABG tell us here? There is acidaemia due to a severe metabolic acidosis and the elevated lactate tells us it is a lactic acidosis. Lactic acid is produced by tissues receiving an insufficient supply of O₂ but oxygenation is normal (note the PaO₂ is appropriate for an FiO₂ of ∼40%) and there are no clinical signs of shock (e.g. hypotension, cold peripheries) suggesting there is no generalised problem of O₂ delivery to tissues.

In fact, the source of lactic acid here is bowel. The patient has mesenteric ischaemia, in which blood supply to the bowel wall is impaired due to occlusion of an artery by a thrombus or embolus. In the absence of an adequate blood supply, bowel tissue becomes hypoxic and must rely on anaerobic metabolism (producing lactate as a byproduct).

Mesenteric ischaemia is a difficult diagnosis to make, as presenting symptoms, signs and routine investigations are all non-specific. The diagnosis should be considered in patients with minimal abdominal examination findings despite severe pain, especially in the presence of a lactic acidosis.

Case 15

1. a) Hyperventilation (secondary)

b) Severe metabolic acidosis with partial compensation

2. Anion gap = (141 + 4.6) – (96 + 6) = 43.6 (normal = 10–12)

3. Diabetic ketoacidosis

In diabetic ketoacidosis, severe insulin deficiency leads to hyperglycaemia and increased metabolism of fats. The breakdown of fats produces ketone bodies – small organic acids – which provide an alternative source of energy but can accumulate, leading to a profound metabolic acidosis. It is the ketone bodies that account for the raised anion gap.

In this case the acidosis has overwhelmed not only the kidneys’ ability to excrete an acid load but also respiratory compensatory mechanisms. There is therefore a severe and dangerous acidaemia despite near-maximal respiratory compensation.

An equally important problem in diabetic ketoacidosis is the profound osmotic diuresis resulting from hyperglycaemia that leads to severe dehydration and electrolyte loss.

Case 16

1. a) Hyperventilation (secondary)

b) Severe metabolic acidosis with partial compensation

Methanol ingestion can be fatal in doses as small as 30 mL. Methanol is metabolised by the liver to produce formaldehyde and formic acid. Accumulation of formic acid leads to a profound acidosis with a raised anion gap. It also causes ocular toxicity and may result in permanent blindness.

Anion gap = (Na {136} + K {4.5}) – (Cl {99} + HCO₃ {9.5}) = 140.5 – 108.5 = 32

Treatment for methanol poisoning is complex but often involves the administration of ethanol, which inhibits the conversion of methanol to its more toxic metabolites.

Case 17

1. a) Slight hyperventilation (secondary)

b) Compensated metabolic acidosis

2. Anion gap = (137 + 3.0) – (109 + 18) = 138 – 125 = 13 (normal)

3. Renal tubular acidosis (type 1)

The differential diagnosis of normal anion gap acidosis is relatively narrow and, in the absence of diarrhoeal symptoms, renal tubular acidosis (RTA) is the likely cause. The history of renal stones and associated hypokalaemia also supports the diagnosis.

In type 1 RTA, the kidneys fail to to secrete H⁺ ions into the urine in exchange for Na⁺ ions. This leads to excessive loss of HCO₃ in the urine, resulting in an acidosis. To maintain electroneutrality, extra Cl⁻ ions are retained (so it is a hyperchloraemic acidosis). Because Cl⁻ is a measured rather than unmeasured anion, there is no increase in the anion gap.

Type 1 RTA is often complicated by renal stones as calcium tends to precipitate in alkaline urine, forming stones.

Hypokalaemia results because Na⁺ ions are exchanged for K⁺ ions instead of H⁺ ions.

Case 18

1. a) Hyperventilation

b) Compensated metabolic acidosis or metabolic acidosis with concomitant respiratory alkalosis

Salicylate poisoning may cause both a primary respiratory alkalosis (direct stimulation of the respiratory centre) and a primary metabolic acidosis as salicylate is an acid (it may also promote lactic acid formation). It is therefore not possible to confidently ascertain whether or not the hyperventilation is due to a primary effect of the aspirin or is a response to the metabolic acidosis.

The diagnosis would be confirmed in this instance by taking salicylate levels.

Case 19

1. a) Hyperventilation (secondary)

b) Severe metabolic acidosis with partial compensation

2. Hyponatraemia (↓Na), hyperkalaemia (↑K), hypoglycaemia (↑glucose), raised lactate

3. Intravenous corticosteroids

This patient is likely to have adrenal insufficiency, a condition in which the adrenal glands fail to produce sufficient amounts of the hormone cortisol (and, in some cases, aldosterone). It often presents non-specifically with fatigue, malaise, anorexia and weight loss can be easily overlooked or misdiagnosed.

Lack of adrenal hormones causes salt and water depletion and loss of vascular tone which, as in this case, may lead to dramatic circulatory collapse (acute adrenal crisis). The circulatory shock is the cause of the severe lactic acidosis.

Patients also have an inability to mobilise glucose reserves, hence the hypoglycaemia, and characteristic electrolyte abnormalities (↓Na: ↑K).

In addition to basic life support and fluid resuscitation, the main intervention likely to improve this patient’s condition is the administration of intravenous hydrocortisone.

Case 20

1.	a) Normal (i.e. satisfactory ventilation and oxygenation being achieved by bag and mask)
	b) Severe metabolic acidosis (uncompensated)
2.	Prognosis	Very poor

In a cardiac arrest case, the ABG has several uses. It allows one to determine the adequacy of ventilation (in this case provided manually by bag and mask), to identify the presence of hyperkalaemia (one of the reversible causes of cardiac arrest) and may provide valuable prognostic information.

Here, despite the evident success of bag and mask ventilation in eliminating CO₂ and oxygenating blood, the patient has a profound lactic acidosis secondary to overwhelming tissue hypoxia. Although this may be multifactorial (e.g. the underlying disease process; hypoxaemia prior to bag and mask ventilation), the most important cause is inadequate tissue perfusion due to loss of cardiac function.

This patient has a grave prognosis. The level of acidosis is unlikely to be compatible with life and, given his unfavourable rhythm (an agonal rhythm does not respond to DC cardioversion and often signifies a ‘dying heart’), age and co-morbidities, successful resuscitation is extremely unlikely.

Case 21

1. a) Type 1 respiratory impairment (severe)

b) Severe metabolic acidosis with partial compensation

2. 0.6–0.8 (see p. 16)

3. Acute pancreatitis

The diagnosis of acute pancreatitis is based on the history, exam findings and increased serum amylase; the main use of the ABG is in helping to assess illness severity.

The severe lactic acidosis (high anion gap and increased lactate) indicates marked tissue hypoxia. The main cause is impaired blood supply to tissues due to circulatory collapse. This occurs as part of the systemic inflammatory response in pancreatitis and must be urgently corrected with aggressive fluid resuscitation ± vasopressor agents.

A PaO₂ of 10.8 with an FiO₂ of 0.6–0.8 implies severe respiratory impairment, and together with chest X-ray appearances, suggests the development of acute respiratory distress syndrome (an inflammatory lung condition). Although PaO₂ is currently adequate, the patient may require ventilatory support if he deteriorates further or tires from the increased work of breathing.

Finally, the ABG also shows a high glucose and low calcium concentration – both of which are adverse prognostic factors in acute pancreatitis.

The patient should be transferred immediately to a critical care environment for intensive monitoring and supportive treatment.

Case 22

1.	a) Mild type 2 respiratory impairment (compensatory response)
	b) Compensated metabolic alkalosis
2.	Electrolytes	Hypokalaemia (↓K)
		Hyponatraemia (↓Na)
		Hypochloraemia (↓Cl)
3.	Treatment	Fluid and electrolyte replacement

Vomiting causes loss of H⁺ ions in gastric juice. The normal response of the kidneys to loss of H⁺ ions is increased excretion of HCO³⁻ to restore acid–base balance. So why does this not happen?

The reason is that persistent vomiting also leads to fluid, Na, Cl and K depletion. In these circumstances the overriding goal of kidneys is salt and water retention.

Under the influence of a hormone called aldosterone, Na⁺ ions are retained at the expense of either K⁺ or H⁺ ions. If K⁺ ions were plentiful, H⁺ loss could be minimised, but K is also in short supply so both are lost (worsening both the alkalosis and hypokalaemia).

Cl⁻ depletion also limits HCO₃⁻ excretion as there must be enough negatively charged ions in blood to balance the positively charged ions (electroneutrality).

Thus, in this case, intravenous replacement of fluid and electrolytes (Na, Cl, K) would allow the kidneys to excrete more HCO₃, correcting the alkalosis.

Case 23

1. a) Mild type 2 respiratory impairment (compensatory response)

b) Metabolic alkalosis with partial compensation

3. Pyloric stenosis

Congenital pyloric stenosis is due to hypertrophy of the gastric outflow tract in the first 6 weeks of life. This obstructs flow between stomach and duodenum, leading to projectile vomiting and inability to absorb nutrients.

As in the preceding case, persistent vomiting has caused significant loss of H⁺ ions, triggering a metabolic alkalosis. Again this is maintained because the associated fluid, Na, Cl and K depletion prevents the kidneys from increasing HCO₃ excretion. However, in this case there is a severe alkalaemia for two reasons.

Firstly the metabolic alkalosis is more severe. This is mainly due to the greater duration of vomiting but also because obstruction between stomach and duodenum prevents HCO₃ from the duodenum being lost in vomit.

Secondly, there is minimal respiratory compensation. Given the severe alkalaemia, one would predict a greater rise in PaCO₂. This is probably explained by the child’s distress, which provides an additional respiratory stimulus blunting the compensatory response (i.e. a mild primary respiratory alkalosis).

Case 24

1.	a) Appearance of severe type 1 respiratory impairment
	b) Normal acid-base status
2.	Explanation	Venous sample

The ABG result suggests severe, life-threatening hypoxaemia but the patient appears clinically well with only mild symptoms and no signs of major respiratory compromise. Moreover, there is a marked discrepancy between the SaO₂ as measured by pulse oximetry (99%) and that calculated on the ABG (74%). By far the likeliest explanation is that the sample was obtained from a vein rather than an artery. A repeat ABG should be performed.

It is important to ensure that an ABG sample is obtained from an artery before using it to assess the PaO₂. In addition to the points above, non-pulsatile flow and the need to draw back on the syringe at the time of sampling suggest venous blood.

Case 25

1.	a) Normal gas exchange
	b) Normal acid-base status
2.	A–a gradient	1.9 kPa/15 mmHg (normal)
3.	Yes (must exclude pulmonary embolism)

This case is included to demonstrate the limitation of ABGs and the importance of considering the clinical context. The ABG is entirely normal but the patient is at high risk of pulmonary embolism, given her recent lower-limb orthopaedic surgery and subsequent immobility. Moreover, she has now developed sudden-onset pleuritic pain, breathlessness and tachycardia, unexplained by initial investigations.

While the finding of impaired oxygenation would have lent weight to a diagnosis of pulmonary embolism, a normal ABG result never excludes it. She therefore requires appropriate imaging (e.g. ventilation–perfusion scan or computed tomography pulmonary angiogram) to rule out this diagnosis.

A–a gradient = PAO₂ – PaO₂

{(0.21 × 93.8) – (4.9 × 1.2)} – 12.1

= 1.8 kPa (normal =< 2.6 kPa)

{(0.21 × 713) – (37 × 1.2)} – 91

= 15 mmHg (normal < 20 mmHg)

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Answers

Case 1

1. a) Type 1 respiratory impairment (moderate)

b) Uncompensated respiratory alkalosis

This patient has moderate type 1 respiratory impairment. Hyperventilation is an appropriate response to the hypoxaemia and sensation of dyspnoea and has resulted in a mild alkalaemia (remember that metabolic compensation does not occur in response to acute respiratory acid–base disturbance).

The correct management for his condition is supplemental oxygen to correct the hypoxaemia and appropriate antibiotics to treat the infection.

In a patient such as this, with moderate hypoxaemia and no ventilatory impairment, monitoring by pulse oximetry is more appropriate than repeated ABG sampling. Indications for further ABG analysis would include signs of exhaustion or hypercapnia (p. 23) or a further significant decline in SaO₂.

Case 2

1. a) Chronic type 2 respiratory impairment

b) Compensated respiratory acidosis

2. Chronic type 2 respiratory impairment due to morbid obesity

At first glance it may be difficult to determine whether this ABG represents respiratory acidosis with metabolic compensation or metabolic alkalosis with respiratory compensation, as both give a high HCO₃ and high PaCO₂. The best clue is the pH (or H⁺) which, although just within the normal range, is on the brink of acidaemia. This would represent overcompensation for an alkalosis and, therefore, suggests an acidosis as the primary abnormality (overcompensation does not occur). The mildly impaired oxygenation is consistent with the degree of hypoventilation.

The likeliest cause of chronic type 2 respiratory impairment in this case is severe obesity. Around 20% of individuals with a body mass index greater than 40 have chronic hypercapnia from restricted ventilation (pickwickian syndrome).

Case 3

1. a) Mild type 1 respiratory impairment (with marked hyperventilation)

b) Uncompensated respiratory alkalosis

2. Pulmonary embolism

This patient is a young, fit, non-smoker with no history of lung problems but, despite hyperventilating (low PaCO₂), has a PaO₂ below the normal range, indicating impaired oxygenation. Given the recent long-haul flight and absence of clinical and X-ray abnormalities, the most likely cause of her breathlessness and impaired oxygenation is pulmonary embolism and she must be investigated accordingly.

This is one of the clinical situations where calculation of the A–a gradient can be helpful (more so when the PaO₂ is just within the normal range). As shown below, it is significantly elevated, indicating the presence of V/Q mismatch.

A–a gradient = PAO₂ – PaO₂

PAO2 = (0.21 × 93.8) – (3.9 × 1.2)

= 19.7 – 4.7

A-a gradient = 15 – 10.3

= 4.7 (norm <2.6 kPa)

PAO2 = (0.21 × 713) – (29.3 × 1.2)

A-a gradient = 115 – 77

= 38 mmHg (norm <20 mmHg)

Case 4

1. a) Acute type 2 respiratory failure

b) Uncompensated respiratory acidosis

2. Opioid toxicity

3. Opioid antagonist

Opioids have a depressant effect upon respiration and may lead to acute ventilatory failure (type 2 respiratory failure). This elderly man has received a large amount of morphine in a short period of time and exhibits pinpoint pupils, making opioid toxicity by far the likeliest cause of his severe ventilatory failure. Since metabolic compensation takes several days to occur, the acute respiratory acidosis has produced a severe acidaemia.

His PaO₂, though within the normal range, is lower than expected for a patient breathing 28% O₂, and more or less consistent with this degree of hypoventilation.

In addition to basic life support measures, he should be administered an opioid antagonist (e.g. naloxone), to reverse the respiratory depression, then closely monitored to ensure sustained improvement.

Case 5

1. a) Type 1 respiratory impairment (moderate)

b) Normal acid-base balance

The above ABG is helpful in guiding the correct treatment for this patient with acute exacerbation of chronic obstructive pulmonary disease. Patients with this condition are often prescribed inadequate oxygen for fear of suppressing hypoxic drive (and thereby depressing ventilation), but this is only an issue in patients with chronic type 2 respiratory failure (indicated by ↑PaCO₂ and ↑HCO₃). This patient has type 1 respiratory impairment and will not rely on hypoxic drive.

Although this patient is likely to have a chronically low PaO₂, the acute deterioration in his symptoms and exercise tolerance suggests a further recent decline from his normal baseline. Importantly, even a small drop in PaO₂ around this level (steep part of O₂–Hb curve) may cause a marked reduction in SaO₂, compromising O₂ delivery to tissues. Thus O₂ is required both to alleviate symptoms and to prevent the development of tissue hypoxia, and should not be withheld for fear of precipitating hypoventilation.

Case 6

1. a) Acute type 2 respiratory impairment

b) Uncompensated respiratory acidosis

This patient with an acute exacerbation of chronic obstructive pulmonary disease has been struggling to overcome severe obstruction to airflow over a period of hours to days and is now exhausted from the increased work of breathing. As a result, his alveolar ventilation is declining, leading to acute type 2 respiratory failure. This may complicate type 1 respiratory failure from any cause, not just from chronic obstructive pulmonary disease. The rising PaCO₂ is, therefore, not due to diminished hypoxic drive and removing his oxygen will not correct it. Indeed his FiO₂ should probably be increased (in addition to other treatment) as he remains significantly hypoxaemic.

Remember that, with acute respiratory acidosis, there is no time for metabolic compensation to develop and a dangerous acidaemia develops rapidly. Adequate ventilation must be restored, as a matter of urgency, to correct the PaCO₂. Possible measures, in this case, include a respiratory stimulant (e.g. doxapram) or, preferably, non-invasive ventilation. If these fail, intubation and mechanical ventilation may be required, if considered appropriate.

Case 7

1. a) Type 1 respiratory impairment

b) Mild respiratory alkalosis balanced by mild metabolic acidosis (likely two primary processes)

2. Aspiration pneumonia

This patient has mild to moderate hypoxaemia despite receiving a high FiO₂ and therefore has severe impairment of oxygenation. The slightly low PaCO₂ indicates that ventilation is adequate, so this is type 1 respiratory impairment. The probable explanation for the mild metabolic acidosis is lactic acidosis resulting from tissue hypoxia.

The history, examination findings and chest X-ray all suggest a diagnosis of aspiration pneumonia.

This patient is severely unwell and any further decline in her PaO₂ could be catastrophic (on the steep part of the O₂–Hb saturation curve). Her O₂ therapy should be adjusted as necessary to maintain her SaO₂ above 92% and she should be managed on a high-dependency unit with close monitoring for signs of deterioration.

Case 8

1. a) Chronic type 2 respiratory impairment

b) Compensated respiratory acidosis

3. PCO₂ and HCO₃

Acute exacerbation of chronic obstructive pulmonary disease is a common medical emergency and this case illustrates key principles.

1. The ↑PaCO₂ shows the patient has type 2 respiratory impairment (ventilatory impairment).

2. The ↑HCO₃ tells us it is chronic type 2 impairment (since metabolic compensation takes time to develop).

3. Even in chronic type 2 impairment, a further acute rise in PaCO₂ would lead to an acidaemia. The pH here is normal, so the PaCO₂ has not changed appreciably in the last few days (i.e. there is no acute-on-chronic rise).

4. His PaO₂is likely to have dropped, leading to the increased breathlessness and marked decline in exercise capacity: below a PaO₂ of 8 kPa (60 mmHg) even small falls may cause a major decline in SaO₂ (steep part of the curve).

5. As this patient has chronic hypercapnia, he may rely on hypoxic drive as a stimulus to ventilation.

6. The goal is to ensure adequate oxygenation (we must not ignore his hypoxaemia) without depressing ventilatory drive.

Case 9

1. a) Acute-on-chronic type 2 respiratory impairment

b) Partially compensated respiratory acidosis

2. Excessive supplemental O₂

Care must be taken when prescribing supplemental O₂

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Arterial Blood Gases Made Easy