Your ED patient with recurrent seizures is doing much better, so why is the non-rebreather still on? It was placed half an hour ago by a well-meaning nurse, but never removed. Meanwhile, EMS brings in another patient with chest pain. You notice the patient has a nasal cannula, even though he was satting fine on room air, and breathing comfortably. If you don’t take proactive steps, that nasal cannula may stay on throughout the ACS workup.
Understanding the dangers of indiscriminate oxygenation in the ED setting
Your ED patient with recurrent seizures is doing much better, so why is the non-rebreather still on? It was placed half an hour ago by a well-meaning nurse, but never removed. Meanwhile, EMS brings in another patient with chest pain. You notice the patient has a nasal cannula, even though he was satting fine on room air, and breathing comfortably. If you don’t take proactive steps, that nasal cannula may stay on throughout the ACS workup.
Hyperoxia occurs when a patient is exposed to high levels of oxygen resulting in supra-physiologic oxygen concentrations. As with many things in medicine, dogma seems to overpower the evidence in this arena. On our boards, we are told that O2 administration is considered a “critical action,” and training programs instill the mantra “IV, O2, Monitor” into its trainees.
The concept of hyperoxia causing harm is not new. In a series of papers published in the 1940s on oxygen toxicity in US Navy Divers, the authors found signs of oxygen toxicity such as lip twitching and nausea started to take effect within a few minutes with syncope, hallucinations and convulsions following soon after [1, 2]. Furthermore, to combat the effects of hyperoxia, many neonatologists suggest using room air during resuscitations [3, 4]. Now pediatricians are finding progressively lower oxygen saturations can be well-tolerated in patients with bronchiolitis [5].
A recent study found a difference in the outcomes of patients with COPD exacerbations that were given high-flow oxygen (HFO, 14% mortality) versus those that did not receive HFO (2% mortality)[6]. Another study found patients given HFO had greater lengths of stay, and higher admission rates to the ICU6. One prehospital randomized control trial found mortality in patients with COPD exacerbations that were provided HFO was 9% compared to patients given titrated oxygen to a saturation of 88-92% was 4% [7].
Other studies have sought to evaluate the effects of HFO on patients with asthma exacerbations. One study found fewer patients with asthma exacerbations who were given 28% supplemental oxygen experienced a rise in their PaCO2 compared to patients given 100% supplemental oxygen [8]. That same group also experienced a greater improvement in their peak expiratory flow rate (PEFR).
A similar effect holds true in non-respiratory diseases. In a recent study on ventilated patients diagnosed with a stroke, mortality of patients with hyperoxia (60%) was higher than both the normoxia group (47%) and the hypoxia group (53%) [9]. Similar results were found in a 6300 patient study of cardiac arrest patients with an in-hospital mortality of 63% in the hyperoxia group compared to 57% and 45% in the hypoxia and normoxia groups respectively [10].
A recent Cochrane Review suggests a possible harm from routine oxygen use, but more importantly calls for larger randomized controlled trials before oxygen should be routinely recommended [11]. Until larger controlled trials evaluating patient-centered outcomes are published, we must rely on studies evaluating surrogate markers. A recent meta-analysis of 6 trials evaluating coronary blood flow in patients receiving room air versus HFO all demonstrated the same thing – decreased coronary blood flow after the administration of HFO12. The ACC and AHA guidelines recommend against the routine use of oxygen in patients suffering an uncomplicated AMI or ACS without evidence of hypoxemia or acute heart failure. They recommend oxygen therapy be reserved for patients with signs of breathlessness, heart failure, shock or oxygen saturations <94% [13].
So the next time your patient arrives and is placed on oxygen, ask yourself whether they really need it and remind yourself that oxygen is a drug and when indiscriminately delivered can do harm.
In Brief
- If a patient is not hypoxic, supplemental oxygen is not indicated
- If giving oxygen to a hypoxic patient, the goal should be to use the minimum amount necessary to improve their oxygenation. Some is good, but more is not always better.
- Oxygen should be viewed as a drug. Remember that the difference between therapeutic and toxic is the dose.
- Chest pain is not an indication for oxygen administration.
1. Donald, K.W., Oxygen poisoning in man. Br Med J, 1947. 1(4506): p. 667; passim.
2. Donald, K.W., Oxygen poisoning in man; signs and symptoms of oxygen poisoning. Br Med J, 1947. 1(4507): p. 712-7.
3. Kattwinkel, J., et al., Part 15: neonatal resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation andEmergency Cardiovascular Care. Circulation, 2010. 122(18 Suppl 3): p. S909-19.
4. Drack, A.V., Preventing blindness in premature infants. N Engl J Med, 1998. 338 (22): p. 1620-1.
5. American Academy of Pediatrics Subcommittee on, D. and B. Management of, Diagnosis and management of bronchiolitis. Pediatrics, 2006. 118(4): p. 1774-93.
6. Joosten SA1, Koh MS, Bu X, Smallwood D, Irving LB. The effects of oxygen therapy in patients presenting to an emergency department with exacerbation of chronic obstructive pulmonary disease. Med J Aust. 2007 Mar 5;186(5):235-8.
7. Michael A Austin et al. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial. BMJ 2010;341:c5462.
8. Denniston, A.K., C. O’Brien, and D. Stableforth, The use of oxygen in acute exacerbations of chronic obstructive pulmonary disease: a prospective audit of pre-hospital and hospital emergency management. Clin Med, 2002. 2(5): p.
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9. Rodrigo, G.J., et al., Effects of short-term 28% and 100% oxygen on PaCO2 and peak expiratory flow rate in acute asthma: a randomized trial. Chest, 2003. 124(4): p. 1312-7.
10. Kilgannon JH et al. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA. 2010 Jun 2;303(21): 2165-71. doi: 10.1001/jama.2010.707.
11. Rincon, F., et al., Association between hyperoxia and mortality after stroke: a multicenter cohort study. Crit Care Med, 2014. 42(2): p. 387-96.
12. Russek, H.I., F.D. Regan, and C.F. Naegele, One hundred percent oxygen in the treatment of acute myocardial infarction and severe angina pectoris. J Am Med Assoc, 1950. 144(5): p. 373-5.
13. Cabello, J.B., et al., Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev, 2013. 8: p. CD007160.
14. Farquhar, H., et al., Systematic review of studies of the effect of hyperoxia on coronary blood flow. Am Heart J, 2009. 158(3): p. 371-7.
15. O’Connor, R.E., et al., Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation, 2010. 122(18 Suppl 3): p. S787-817.
Dr. Schauer is a staff physician at Bayne-Jones Army Community Hospital and the author of www.emtrends.org