Answers

Answers



Case 1



1. a) Type 1 respiratory impairment (moderate)

b) Uncompensated respiratory alkalosis


2. Yes

3. Yes

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


= 15 kPa


A-a gradient = 15 – 10.3


= 4.7 (norm <2.6 kPa)


OR


PAO2 = (0.21 × 713) – (29.3 × 1.2)


= 150 – 35


= 115


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


2. Yes

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


2. No!

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

3. Severe

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


2. PO2

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.

Related posts:

  1. Common ABG values
  2. When and why is an ABG required?
  3. Making ABG interpretation easy
  4. Acid–base balance: the basics

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Dec 18, 2016 | Posted by in CARDIOLOGY | Comments Off on Answers

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