STILL JUST NOTES, UNDER CONSTRUCTION
The Potential Harm of Oxygen in ED Patients
Most physicians believe that high oxygen concentrations are life-saving (2). Yet, an abundance of evidence suggests the contrary even though it is common practice to administer high flow oxygen to unstable ED patients. We thought this would make for a thought-provoking clinical pearl:
ACS & CHF
In both acute ischemic cardiac syndromes and CHF, experimental evidence argues against the use of supplemental oxygen. Administration of oxygen induces a variety of potentially hazardous hemodynamic changes, largely because it induces coronary and systemic vasoconstriction. As early as 1950 it was suggested that oxygen might be deleterious, as it prolonged ECG changes during exercise tolerance testing (2). In patients with severe triple-vessel disease, administration of 6 minutes of high-flow oxygen was demonstrated to reduce coronary blood flow sufficiently to induce myocardial ischemia (3). It appears that only when patient oxygen saturations are < 85- 90%, does oxygen administration increase myocardial oxygen delivery (2).
A 2010 trial of 405 patients with COPD exacerbations compared treatment with high-concentration oxygen with titrated oxygen in a pre-hospital setting. Mortality was significantly lower in COPD patients receiving titrated oxygen rather than high-concentration oxygen (4).
Hyperoxia can cause vasoconstriction of the carotid and downstream cerebral arteries. 3 randomized trials have looked at the effect of supplemental oxygen in ischemic stroke. One showed no benefit, one showed a lower survival in non-hypoxic patients and one showed excess mortality in the hyperoxia group (2). Guidelines from the American Stroke Association do not support the use of supplemental oxygen for most patients with acute ischemic stroke.
There is evidence that patients might be managed more safely after ROSC with 30% oxygen rather than 100% (2). Clinically, hyperoxia is associated with poor neurological outcome following resuscitation (2,5).
Septic and Hemorrhagic Shock
Hyperoxia may impair oxygen delivery in patients with sepsis, and hyperoxia decreases whole-body oxygen consumption in critically ill patients (2,6). In hemorrhagic shock, data from animal studies suggest that increasing the fraction of inspired oxygen compromises hemodynamics (2).
(1) Burls A, et al. Emerg Med J 2010, 27:283-286.
(2) Cornet AD, et al. Crit Care 2013 Apr 18;17:313.
(3) Bourassa MG, et al. Am J Cardiol 1969, 24:172-177.
(4) Austin MA, et al. BMJ 2010, 341:c5462.
(5) Janz DR, et al. Crit Care Med 2012, 40:3135-3139.
(6) Rossi P, et al. Clin Physiol Funct Imaging 2007, 27:180-184.
In one study, “Apneic Oxygenation in Man,” volunteers were intubated and pharmacologically paralyzed to prevent breathing.(1) With the endotracheal tube filled with pure oxygen and connected to a circular circuit, one volunteer subject maintained a 100% oxygen saturation level for almost an hour without taking a breath. The other volunteers similarly maintained their oxygen saturation levels for extended periods of time.
While oxygenation was occurring, the patients developed an acidosis and their carbon dioxide tension increased three mmHg per minute on average. The lowest pH recorded was 6.72.
In another study, patients were pre-oxygenated before induction and, after the patients became apneic, a catheter was inserted nasally.(2) Patients were divided into two groups: the first had its pharynx insufflated through the catheter, while the second group did not. After the patients desaturated or 10 minutes had elapsed, they were pre-oxygenated manually. Then, the process was repeated while the second group received insufflation and the first did not.
The study showed that without oxygen insufflation, the participants began to desaturate at around seven minutes.(2) However, all the anesthesia providers maintained their patient’s oxygen saturation for 10 minutes with oxygen insufflation.
Note: Although there’s a mechanism to entrain oxygen into the lungs outside of breathing, there’s no mechanism toexpel carbon dioxide. The carbon dioxide in the blood stream rapidly eqiulibriates with teh carbon dioxide in the lung. For more discussion on the differences between oxygen and ventilation, see the November JEMS article, “Oxygenation & Ventilation Are Not the Same Thing.”
The goal is to increase the amount of time it takes for the patient to become critically hypoxic (less than 70% oxygen saturation) in case there are problems with intubation.
Why, When & How to Use It
Understanding the benefit of apneic oxygenation, you can see why it’s an important process to use when performing a rapid sequence intubation. Your goal is to increase the amount of time it takes for the patient to become critically hypoxic (less than 70% oxygen saturation) in case there are problems with intubation.(3) In a 2010 study, apneic oxygenation was shown to increase the time until an obese patient started to become hypoxic by about 2.5 minutes.(4)
To perform apneic oxygenation when performing a rapid sequence intubation, the patient should either be placed head up or in reverse Trendelenburg at a 20–30° angle.(3) Insert a nasal cannula and set it for at least five liters of oxygen per minute. If possible, the patient should then be pre-oxygenated by allowing three minutes of tidal volume breathing, or eight vital capacity breaths(.)3 This involves providing 100% oxygen to the patient either while they breathe or while the medical provider assists the patient’s breathing.
1. Frumin MJ, Epstein RM, Cohen G. Apneic oxygenation in man. Anesthesiology. 1959;20:789–798.
2. Teller LE, Alexander CM, Frumin MJ, et al. Pharyngeal insufflation of oxygen prevents arterial desaturation during apnea. Anesthesiology. 1988;69(6):980–982.
3. Weingart SD, Levitan RM. Preoxygenation and prevention of desaturation during emergency airway management.Ann Emerg Med. 2012;59(3):165–175.
4. Ramachandran SK, Cosnowski A, Shanks A, Turner CR. Apneic oxygenation during prolonged laryngoscopy in obese patients: a randomized, controlled trial of nasal oxygen administration. J Clin Anesth. 2010;22(3):164–168.
5. Weingart SD. Preoxygenation, reoxygenation, and delayed sequence intubation in the emergency department. J Emerg Med. 201; 40(6):661–667.
6. Mort TC, Waberski BH, Clive J. Extending the preoxygenation period from 4 to 8 mins in critically ill patients undergoing emergency intubation. Crit Care Med. 2009;37(1):68–71.