SummaryOxygen is perhapsthe most common drug administered in medical emergencies. It requires carefuluse in patients with exacerbations of chronic obstructive pulmonary disease(COPD). This case report looks at the treatment of a patient that thought hewas “allergic” to oxygen, explores reasons for hypercapnia in certain patientsand looks at how treatment could have been improved.Background · COPD is a group of lung diseasescharacterised by non-reversible and progressive obstruction of airflow that interfereswith normal breathing.1 It isa common condition and the second leading cause of emergency admission tohospital.
2· Patients with COPD generally havelower than normal SaO2 and in cases of exacerbation it isrecommended 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 saleslist medication that does not require a prescription. But in the context ofbeing administered by a healthcare professional oxygen requires accuratedocumentation of dosage and clinical intentions.· Oxygen is absorbed by passivediffusion from alveoli into capillary beds and is distributed mostly bound tohaemoglobin.
Oxygen is metabolised in cell mitochondria where it is essentialin the formation of ATP. The resulting carbon dioxide produced enables theoxygen to be excreted via the lungs.· Oxygen is indicated for hypoxemicpatients. Concentration is dictated by the condition being treated; guidelinesare available for common medical emergencies (JRCALC).CaseDescriptionPatient: 58-year-old male, smoker, end-stage COPD, lives in residentialhome.
Presenting condition: Difficulty in breathing.History of presenting condition: Struggling to breath, residential homestaff concerned. Increasing difficulty in breathing for past week, rigors, increasedcough 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-basalcrackles and an expiratory wheeze.
Unable to obtain a peak expiratory flowreading (PEFR) due to the patient’s distressed state. A community first responderon 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 givenhigh-flow oxygen during ambulance transport and during assessment in theemergency department. This had resulted in a reduced mental state that haddistressed the patient. Treatment: The patient was given some nebulised salbutamol for theexpiratory wheeze.
Medium flow mask and then a nasal cannula were used to giveoxygen which was titrated to response. He was given fluids as per sepsisguidelines and conveyed to hospital.DiscussionThe patient in this case did not have an oxygen alert card,but did think he was “allergic to oxygen” and reported symptoms for earliertreatment that would indicate CO2 retention. Causes of oxygen-induced hypercapnia may include – Ventilation/Perfusion (V/Q) mismatch – Reduced ventilation inCOPD patients results in hypoxic pulmonary vasoconstriction to balance V/Q andoptimise gas exchange. Increased PAO2 leads to increased perfusionto poorly ventilated alveoli and therefore increased shunt and alveolar deadspace. Blocked off alveoli also can collapse as O2 is absorbed fromthe blood faster than dissolved nitrogen diffuses into them (absorptionatelectasis). This can further increase shunt and therefore V/Q mismatch.(aubier, robinson, BTS)Ventilatory drive – PaCO2 provides the mainventilatory stimulus in healthy individuals.
As COPD patients have chronicallyelevated PaCO2 their central chemoreceptors become tolerant to thehigh levels and PaO2 then provides ventilatory stimulus.Administration of oxygen will cause PaO2 to rise and ventilatory driveto reduce resulting in increasing PaCO2. This may be attributable toreduced minute volume in certain patients (7), but it has also been shown to bea temporary effect and is not attributable for increased PaCO2.
Haldane effect – CO2 binds with greater affinityto deoxygenated haemoglobin and therefore increased PaO2 reduces theCO2 buffering capacity of haemoglobin. This can normally be excretedby an increase in minute volume, but COPD patients can generally not achievethis.(aubier, BTS) Rebreathing of expired gases from face masks with low flowrates. (BTS)How could this patient have been treated more effectively prehospitally?ETCO2 – ETCO2 was not monitored in this patient as he mostlyreceived O2 through a nasal cannula as recommended by guidelines (BTS).
Nasal ETCO2 monitors are not widely available in SWAST. Although the usefulnessof ETCO2 (Nurettin ÖzgürDo?an) and itsrelationship to arterial PaCO2 monitoring in COPD patients has beenquestioned (Lise Piquilloud) and it is not recommend in guidines (BTS ref),trends in ETCO2 and waveform capnography can be useful to measuring a patientsresponse to treatment and monitoring any deterioration (SWAST guideline). Ithas also been shown to be useful in differentiating between cases ofexacerbation of COPD and congestive heart failure (hunter).Pulse oximetry – IS a useful non-invasive way to monitor SaO2and is recommended whenever O2 is administered (BTS). When breathingroom air pulse oximetry can rule out hypercapnia, but this is no longer thecase when breathing supplemental oxygen (witting). Pulse oximeters do havelimitations and readings are affected by poor perfusion (Phillips manual, ) andmay overestimate in exacerbations of COPD (.
Amalakanti). Current guidelines (BTS, JRCALC)suggest smokers over 50 who have chronic breathlessness should be treated ashaving COPD. In that case are you going to consider a SpO2 of 92%’normal’ for them?Venturi masks – Are recommended (BTS), relatively cheap andare able to provide a constant level of inspired oxygen which correlates withlower incidences of acidosis, hypercapnia and hyperoxia on hospital admission.(Durrington, austin)Non Invasive Ventilation – Problems caused by oxygen administrationand resulting hypercapnia are generally exacerbated by a poor ventilation(brill). Studies have shown that prehospital NIV can be useful in improvingvital signs, but there is not enough evidence to show any improvement inmortality. (neilson, bakke)Learning points · Oxygen is a drug which is indicatedfor hypoxemic patients only. Titrate to response; especially in patients atrisk of hypercapnic respiratory failure. Aim for SpO2 of 88-92% inthese patients.
· People can’t be “allergic” to oxygen,but hypercapnic respiratory failure can occur in some patients for the reasonsoutlined above.· Pulse oximetry is the mainnon-invasive way of monitoring effects of oxygen administration, although ithas limitations in critically ill patients.· ETCO2 can be a useful toolin monitoring patients’ response to treatment, although absolute values are oflimited use in the spontaneously breathing patient as they may not correlate toPaCO2.· Venturi masks and non-invasiveventilation may be of benefit in treating patients with exacerbation of COPDbut are not currently available locally.