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Recertified Zoll AED Plus
The Zoll AED Plus’ unique graphical interface – pictures combined with text displays and voice prompts – helps rescuers every step of the way.
Curaplex Glucose Kits
The Curaplex® Glucose Start kit allows you to have the ease and convenience of having a ready-to-use set of products for checking glucose levels at your disposal.
Precision Xtra Test Strips
The Precision Xtra blood glucose test strips, designed with TrueMeasure Technology have a small 0.6 microliter sample size and simple blood application.
July 1, 2012
Can oxygen hurt our patients?
Updated October 24, 2016
EMS providers began giving oxygen not because it had medically or scientifically demonstrated benefits for patients, but because they could. Yet, inarguably, hypoxia is bad.
John Scott Haldane, who formulated much of our understanding of gas physiology, said in 1917, “Hypoxia not only stops the motor, it wrecks the engine.”
Patients begin to suffer impaired mental function at oxygen saturations below 64 percent. People typically lose consciousness at saturations less than 56 percent, giving airplane passengers no more than 60 seconds to breathe supplemental oxygen when an airplane flying at 30,000 feet suddenly depressurizes [1-3].
More recent studies suggest that hyperoxia, or too much oxygen, can be equally dangerous. Hence the drug EMS providers administer most often may not be as safe as originally thought.
Studies on benefits and dangers of oxygen therapy are not new; intensive care practitioners have long recognized the adverse effects of using high concentration oxygen 
The Amercian Heart Association Guidelines for Emergency Cardiac Care and CPR in 2000 and 2005 recommended against supplemental oxygen for patients with saturations above 90 percent. The 2010 ECC Guidelines called for supplemental oxygen only when saturations are less than 94 percent . Though the AHA continues to recommend high-flow oxygen administration when CPR is in progress.
Research on patient outcomes after hyperoxia
What is new are prehospital research studies comparing outcomes of patients treated without oxygen or with oxygen titrated to saturations versus patients routinely given high flow oxygen. These data are frightening; they invariably show impressive patient harm from even short periods of hyperoxia.
We’ve known since 1999 that oxygen worsened survival in patients with minor to moderate strokes and made no difference for patients with severe stroke . In fact, the American Heart Association recommended in 1994 against supplemental oxygen for non-hypoxemic stroke patients.
The dangers from giving oxygen to neonates have also been long appreciated . The most compelling outcome studies of neonates published in 2004 and repeated in 2007 showed a significant increase in mortality of depressed newborns resuscitated with oxygen (13 percent) versus room air (8 percent) . This led to the current neonatal resuscitation recommendations for use of room air positive pressure ventilation.
In 2002, a study of 5,549 trauma patients in Texas showed prehospital supplemental oxygen administration nearly doubled mortality . A Tasmanian study of prehospital difficulty breathing patients published in 2010 compared patients treated with oxygen titrated to saturations of 88 to 92 percent to patients treated with non-rebreather oxygen masks.
It showed a reduction in deaths during subsequent hospitalization of 78 percent in COPD patients and 58 percent in all patients . New studies are showing a troubling pattern of worse outcomes associated with hyperoxia post cardiac arrest .
Why would oxygen worsen patient outcomes?
One mechanism may be absorption atelectasis. Gas laws mandate that increases in the concentration of one gas will displace or lower the concentration of others. Room air normally contains 21 percent oxygen, 78 percent nitrogen, and less than 1 percent carbon dioxide and other gases.
Nitrogen, the most abundant room air gas, is responsible for secretion of surfactant, the chemical that prevents collapse of the alveoli at end expiration. Premature infants often are not developed sufficiently to produce surfactant and require endotracheal administration of animal surfactant.
“Washout” of nitrogen in adult lungs occurs when high concentration oxygen is administered. Lower concentrations of nitrogen can lead to decreased surfactant production with subsequent atelectasis and collapse of alveoli, significantly impeding oxygen exchange.
Oxygen is also a free radical, meaning that it is a highly reactive species owing to its two unpaired electrons. From a physics perspective, free radicals have potential to do harm in the body.
The sun, chemicals in the atmosphere, radiation, drugs, viruses and bacteria, dietary fats, and stress all produce free radicals. Cells in the body endure thousands of hits from free radicals daily.
Normally, the body fends off free radical attacks using antioxidants. With aging and in cases of trauma, stroke, heart attack or other tissue injury, the balance of free radicals to antioxidants shifts.
Cell damage occurs when free radicals outnumber antioxidants, a condition called oxidative stress. Many disease processes including arthritis, cancer, diabetes, Alzheimer’s and Parkinson’s result from oxidative stress.
The concept of free radical damage suggests the old EMS notion that, “high flow oxygen won’t hurt anyone in the initial period of resuscitation” may be dead wrong.
Tissue damage is directly proportionate to the quantity of free radicals present at the site of injury. Supplemental oxygen administration during the initial moments of a stroke, myocardial infarct (MI) or major trauma may well increase tissue injury by flooding the injury site with free radicals.
Finally, consider this: five minutes of supplemental oxygen by non-rebreather decreases coronary blood flow by 30 percent, increases coronary resistance by 40 percent due to coronary artery constriction, and blunts the effect of vasodilator medications like nitroglycerine . These effects were demonstrated dramatically in cath lab studies  published in 2005.
Now you know why the ECC Guidelines recommend against supplemental oxygen for chest pain patients without hypoxia. Supplemental oxygen reduces coronary blood flow and renders the vasodilators ALS providers use to treat chest pain ineffective.
Where do we go from here?
Knowing that both hypoxia and hyperoxia are bad, EMS providers must stop giving oxygen routinely. Oxygen saturations should be measured on every patient.
Protocols need to be aligned to reflect the current ACLS and BLS ECC guidelines: administer oxygen to keep saturations between 94 and 96 percent. No patient needs oxygen saturations above 97 percent and in truth, there is little to no evidence suggesting any clinical benefit of oxygen saturations above 90 percent in any patient.
Modifications in prehospital equipment will be inherent in controlling oxygen doses administered to patients. In all likelihood, the venturi mask will make a comeback, allowing EMS providers to deliver varied concentrations of oxygen as needed to keep oxygen saturations between 94 and 96 percent.
Few patients will require non-rebreather masks which are prone to deliver too much oxygen (hyperoxia). CPAP (Continuous Positive Airway Pressure) devices will also need redesign as most conventional EMS CPAP delivers 100 percent oxygen. A study conducted by Bledsoe, et al in Las Vegas found that prehospital CPAP using low oxygen levels (28 to 30 percent) was highly effective and safe .
Bottom line: the drug we use most often can cause harm if we give it without good reason. In the absence of low saturations, oxygen will not help patients with shortness of breath and it may actually hurt them. The same holds true for neonates and virtually any patient with ongoing tissue injury from stroke, MI or trauma. Indeed, oxygen can be bad.