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A case of extreme hypercapnia: implications for the prehospital and accident and emergency department management of acutely dyspnoeic patients
  1. L Urwin1,
  2. R Murphy1,
  3. C Robertson1,
  4. A Pollok2
  1. 1Department of Accident and Emergency Medicine, Edinburgh Royal Infirmary, Edinburgh, UK
  2. 2Department of Intensive Care Medicine, Edinburgh Royal Infirmary
  1. Correspondence to:
 Mr R Murphy
 Department of Accident and Emergency Medicine, The Royal Infirmary of Edinburgh, Old Dalkeith Road, Little France, Edinburgh EH16 4SU, UK;

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A 64 year old woman was brought by ambulance to the accident and emergency department. She had been referred by her GP because of increasing dyspnoea, cyanosis, and lethargy over the previous four days. On arrival of the ambulance crew at her home she was noted to be tachycardic and tachypnoeic (respiratory rate 36/min) with a GCS of 5 (E 3, M 1, V 1). She was given oxygen at 6 l/min via a Duo mask, and transferred to hospital.

The patient arrived at the accident and emergency department 18 minutes later. In transit, there had been a clinical deterioration. The GCS was now 3 and the respiratory rate 4/min. Oxygen saturation, as measured by a pulse oximeter was 99%. The patient was intubated and positive pressure ventilation started. Arterial blood gas measurements taken at the time of intubation were consistent with acute on chronic respiratory failure (fig 1).

Figure 1

Arterial blood gas measurements.

Further investigations included a chest radiograph, which showed hyperinflation of the lungs and a 12-lead ECG, which showed right axis deviation and right atrial hypertrophy.

Treatment with nebulised bronchodilators, intravenous hydrocortisone, and antibiotics was started empirically with a diagnosis of carbon dioxide narcosis attributable to oxygen therapy in a patient with previously undiagnosed chronic obstructive pulmonary disease. Repeat arterial blood gas analysis was performed seven minutes after intubation and showed: Pao2 55.2 kPa, Paco2 21.74 kPa, H+ 101.0 nmol/l, HCO3 40.3 mmol/l.

The patient was transferred to the intensive care unit where mechanical ventilation was continued. Further history revealed that she had smoked 20 cigarettes/day for 40 years but had previously been able to walk as far as her local shops without becoming short of breath. She had not seen her GP nor attended hospital for the previous 16 years.

The following day the patient was much improved. Over a period of two days she was weaned from the ventilator and extubated. She was discharged from hospital to home nine days after admission. At discharge, on room air, arterial blood gas pressures were as follows: Pao2 7.52 kPa, Paco2 7.61 kPa, H+ 37.0 nmol/l, HCO3 36.7 mmol/l.


Prehospital, the emergency treatment of patients with dyspnoea must often be undertaken without the benefit of a definitive diagnosis. In the United States between 9% and 15% of patients with acute dyspnoea have chronic obstructive pulmonary disease.1 In many situations it is possible to identify these patients and modify treatment accordingly. This necessitates some access to the medical history however and on occasion, as in this case, this is not available.

Unfortunately when such a history is unavailable, no out of hospital monitoring technique exists to identify patients with, or at risk of, carbon dioxide retention. Pulse oximetry is used by many ambulance services and can be an extremely useful non-invasive technique to aid the assessment of peripheral oxygen saturation. In situations of poor perfusion, movement and abnormal haemoglobin, however, this technique may not reliably reflect Pao2 values. More importantly, and as shown in our case, there is no definite relation between Sao2 values measured by pulse oximetry and Paco2 values although it has been shown that the more oxygenated patients with chronic obstructive pulmonary disease become the higher the incidence of respiratory acidosis.2

Clearly, in patients known to have chronic obstructive pulmonary disease it is important to control oxygen therapy to ensure the correction of dangerous levels of hypoxia while minimising the risk of hypercapnia. Despite the fact that our patient deteriorated with the administration of high concentration oxygen, this case should not be used to imply that all dyspnoeic patients should be given lower concentrations of oxygen. In many situations such as acute pulmonary oedema, anaphylaxis, acute asthma, etc, high concentrations of oxygen are essential and even in some patients with acute exacerbations of chronic obstructive pulmonary disease low concentration oxygen will not provide adequate relief of hypoxia.3

This case highlights a number of useful learning points:

  • Firstly, not all patients with severe chronic obstructive pulmonary disease are identified in the community. Consequently when they become increasingly dyspnoeic there is a risk that inappropriately high concentrations of oxygen may be administered.

  • Secondly, the well known risks of inducing hypercapnia and carbon dioxide narcosis cannot reliably be judged by currently available out of hospital monitoring techniques.

  • Thirdly, extreme levels of hypercapnia, provided they are treated promptly and appropriately, are compatible with full recovery. To our knowledge, the Paco2 value of 31.05 kPa with which this patient presented, is the highest recorded in the human literature.