Oxygen is perhaps
the most common drug administered in medical emergencies. It requires careful
use in patients with exacerbations of chronic obstructive pulmonary disease
(COPD). This case report looks at the treatment of a patient that thought he
was “allergic” to oxygen, explores reasons for hypercapnia in certain patients
and looks at how treatment could have been improved.
· COPD is a group of lung diseases
characterised by non-reversible and progressive obstruction of airflow that interferes
with normal breathing.1 It is
a common condition and the second leading cause of emergency admission to
· Patients with COPD generally have
lower than normal SaO2 and in cases of exacerbation it is
recommended to maintain a SaO2 of 88-92% (GOLD, BTS ref, JRCALC)
This is due to the risk of hypercapnic respiratory failure in some patients
(BTS hypercapnic ref).
· Oxygen is legally a general sales
list medication that does not require a prescription. But in the context of
being administered by a healthcare professional oxygen requires accurate
documentation of dosage and clinical intentions.
· Oxygen is absorbed by passive
diffusion from alveoli into capillary beds and is distributed mostly bound to
haemoglobin. Oxygen is metabolised in cell mitochondria where it is essential
in the formation of ATP. The resulting carbon dioxide produced enables the
oxygen to be excreted via the lungs.
· Oxygen is indicated for hypoxemic
patients. Concentration is dictated by the condition being treated; guidelines
are available for common medical emergencies (JRCALC).
Patient: 58-year-old male, smoker, end-stage COPD, lives in residential
Presenting condition: Difficulty in breathing.
History of presenting condition: Struggling to breath, residential home
staff concerned. Increasing difficulty in breathing for past week, rigors, increased
cough and sputum production. Feels increasingly unwell.
Previous medical history: COPD, hypertension, diabetes.
Findings: The patient presented with low oxygen saturations (<80%), signs of respiratory distress and some red flag sepsis markers. He had bi-basal crackles and an expiratory wheeze. Unable to obtain a peak expiratory flow reading (PEFR) due to the patient's distressed state. A community first responder on scene was reluctant to give oxygen as the patient had stated he was "allergic to oxygen". It turns out that a previous episode had resulted in him being given high-flow oxygen during ambulance transport and during assessment in the emergency department. This had resulted in a reduced mental state that had distressed the patient. Treatment: The patient was given some nebulised salbutamol for the expiratory wheeze. Medium flow mask and then a nasal cannula were used to give oxygen which was titrated to response. He was given fluids as per sepsis guidelines and conveyed to hospital. Discussion The patient in this case did not have an oxygen alert card, but did think he was "allergic to oxygen" and reported symptoms for earlier treatment that would indicate CO2 retention. Causes of oxygen-induced hypercapnia may include – Ventilation/Perfusion (V/Q) mismatch – Reduced ventilation in COPD patients results in hypoxic pulmonary vasoconstriction to balance V/Q and optimise gas exchange. Increased PAO2 leads to increased perfusion to poorly ventilated alveoli and therefore increased shunt and alveolar dead space. Blocked off alveoli also can collapse as O2 is absorbed from the blood faster than dissolved nitrogen diffuses into them (absorption atelectasis). This can further increase shunt and therefore V/Q mismatch. (aubier, robinson, BTS) Ventilatory drive – PaCO2 provides the main ventilatory stimulus in healthy individuals. As COPD patients have chronically elevated PaCO2 their central chemoreceptors become tolerant to the high levels and PaO2 then provides ventilatory stimulus. Administration of oxygen will cause PaO2 to rise and ventilatory drive to reduce resulting in increasing PaCO2. This may be attributable to reduced minute volume in certain patients (7), but it has also been shown to be a temporary effect and is not attributable for increased PaCO2. Haldane effect – CO2 binds with greater affinity to deoxygenated haemoglobin and therefore increased PaO2 reduces the CO2 buffering capacity of haemoglobin. This can normally be excreted by an increase in minute volume, but COPD patients can generally not achieve this.(aubier, BTS) Rebreathing of expired gases from face masks with low flow rates. (BTS) How could this patient have been treated more effectively prehospitally? ETCO2 – ETCO2 was not monitored in this patient as he mostly received O2 through a nasal cannula as recommended by guidelines (BTS). Nasal ETCO2 monitors are not widely available in SWAST. Although the usefulness of ETCO2 (Nurettin ÖzgürDo?an) and its relationship to arterial PaCO2 monitoring in COPD patients has been questioned (Lise Piquilloud) and it is not recommend in guidines (BTS ref), trends in ETCO2 and waveform capnography can be useful to measuring a patients response to treatment and monitoring any deterioration (SWAST guideline). It has also been shown to be useful in differentiating between cases of exacerbation of COPD and congestive heart failure (hunter). Pulse oximetry – IS a useful non-invasive way to monitor SaO2 and is recommended whenever O2 is administered (BTS). When breathing room air pulse oximetry can rule out hypercapnia, but this is no longer the case when breathing supplemental oxygen (witting). Pulse oximeters do have limitations and readings are affected by poor perfusion (Phillips manual, ) and may overestimate in exacerbations of COPD (.Amalakanti). Current guidelines (BTS, JRCALC) suggest smokers over 50 who have chronic breathlessness should be treated as having COPD. In that case are you going to consider a SpO2 of 92% 'normal' for them? Venturi masks – Are recommended (BTS), relatively cheap and are able to provide a constant level of inspired oxygen which correlates with lower incidences of acidosis, hypercapnia and hyperoxia on hospital admission. (Durrington, austin) Non Invasive Ventilation – Problems caused by oxygen administration and resulting hypercapnia are generally exacerbated by a poor ventilation (brill). Studies have shown that prehospital NIV can be useful in improving vital signs, but there is not enough evidence to show any improvement in mortality. (neilson, bakke) Learning points · Oxygen is a drug which is indicated for hypoxemic patients only. Titrate to response; especially in patients at risk of hypercapnic respiratory failure. Aim for SpO2 of 88-92% in these patients. · People can't be "allergic" to oxygen, but hypercapnic respiratory failure can occur in some patients for the reasons outlined above. · Pulse oximetry is the main non-invasive way of monitoring effects of oxygen administration, although it has limitations in critically ill patients. · ETCO2 can be a useful tool in monitoring patients' response to treatment, although absolute values are of limited use in the spontaneously breathing patient as they may not correlate to PaCO2. · Venturi masks and non-invasive ventilation may be of benefit in treating patients with exacerbation of COPD but are not currently available locally. References