Contraindication for 02

[OzMedic]

As tniuqs wrote lung disease secondary to bleomycin therapy is a contraindication to oxygen therapy in my service. Bleomycin is an antineoplastic agent with potential for producing pulmonary toxicity, attributed in part to its free radical-promoting ability. Clinical and research experiences have suggested that the risk of bleomycin-induced pulmonary injury is increased with the administration of oxygen. Other research rejects this theory such as:

J Urol. 1998 Oct;160(4):1347-52 Bleomycin associated pulmonary toxicity: is perioperative oxygen restriction necessary?

The inappropriate prehospital administration of oxygen therapy is one of my pet peeves and a subject that interests me greatly as a research topic. One particular instance is the administration of high concentration oxygen therarpy to CVA patients. I will expand on some of my research and understanding of the issue but before I do a message to the EBM junkies out there (Bushy, that means you mate among others). Most of this stuff is theoretical and not supported by quantitative research and when you think about it why would it be? Oxygen is free, nobody owns it and there is absolutely no money to be made by researching it, especially the possible detrimental effects of it. It has been entrenched in medical practice for hundreds of years and is widely thought to be safe and benifical for almost anything. Anyway here is some information to consider:

During ischaemic brain events there is a zone around the ischaemic area that is hypo-perfused that is often referred to as the penumbra of ischaemia. In head-injured patients, this penumbra is affected by CO2 concentrations, (i.e., hyperventilation may produce more ischaemia). During ischaemic events the penumbra rapidly losses its ability to adequately deliver oxygen and glucose to its neurons. Brain lactate increases and ATP stores run very low. This upsets the normal metabolic function of the mitochondria, which are responsible for producing, then reducing free radicals. Many people use the term free radical quite loosely, but essentially these are chemicals that are looking for electrons. They usually get them from the electron transport chain in aerobic metabolism. These electronless molecules are very reactive and tend to strip electrons off anything they bump into, including proteins, enzymes and especially membranes. These radicals are hydrogen peroxide, superoxides, nitric oxide and hydroxyl radicals. When free radicals interact with stuff inside of cells, they change it. Proteins and enzymes (which are 99.99 percent proteins) fold differently. Membranes have holes punched in them which leads to cellular oedema. Also during ischemia, the pH of the ischemic cell and intracellular fluid goes down. This acidosis causes excitatory amino acids (EAAs – the common excitatory neurotransmitters in the brain) to be released. EAA release causes further leakage of ions, increasing oedema. Since there is no ATP to run the ATPase pumps, the cells get worse and worse. This is a downward graveyard spiral. Along comes "Joe-EMT/Paramedic" who has been trained that oxygen is good and therefore lots of oxygen must be better. He/she gives the ischaemic patient 100% oxygen by mask without addressing the flow problem. The oxygen filters in and before the ischemic tissue can adjust, makes lots of free radicals that the cell is not able to scavenge. The free radicals trigger further activation of the inflammatory response and we get more leakage of ions, most notably calcium. At this point we run into what is known as the "oxygen-calcium paradox". Oxygen is needed for life. Calcium is needed for life. But during ischaemia, oxygen and calcium can actually damage tissues. The free radicals (caused by oxygen) cause ischaemic mitochondria to leak. Calcium rushes in and causes mitochondria to self-destruct. The final common pathway to cell death is the loading of calcium onto an ischemic mitochondria.

Does all this mean we don't give oxygen to brain injured patients? absolutely not! Does it mean that we only administer oxygen to maintain SpO2 to normal levels? Maybe so. Is it a subject worth further research? I think so, what about you guys?

If people are interested in any of the further info I have discovered about the effects of hyperoxia I will be happy to post it. All of this is of course superfluous to the issues of administering oxygen to certain patients with COAD. This is another area which is extremely poorly understood by most of the EMS and indeed medical profession mainly due to poor education (this whole hypoxic drive BS has got to stop). Of course all this stuff is only my understanding of the relevant issues based on research and information provided by some very smart people of which I'm sure there will be plenty that will correct any inadvertent misinformation that I have given.

By the way one of my favorite EMS quotes remains "outta oxygen - outta luck" :wink:

[BushyFromOz]

I will expand on some of my research and understanding of the issue but before I do a message to the EBM junkies out there (Bushy, that means you mate among others). Most of this stuff is theoretical and not supported by quantitative research and when you think about it why would it be? Oxygen is free, nobody owns it and there is absolutely no money to be made by researching it, especially the possible detrimental effects of it.

Ha how thoughtful if you Oz!

Im an EBM junkie? Id like to think that i can at least identify the limitations of EBM and your point on why there is little evidence into oxygen therapy is well taken mate. Interestin reading, very ineresting reading. I welcome more :wink:

[tniuqs]

OzMedic"]As tniuqs wrote lung disease secondary to bleomycin therapy is a contraindication to oxygen therapy in my service.

You can call me turnip.....!

Does all this mean we don't give oxygen to brain injured patients? absolutely not! Does it mean that we only administer oxygen to maintain SpO2 to normal levels? Maybe so. Is it a subject worth further research? I think so, what about you guys?

TWTG "the way to go" TITRATION" Oxygen IS a drug!

With pulse oximetry this is entirely possible, but it would be bloody brilliant to have a means of detemining Hemoglobin levels in the gut wagon as well, one can only hope its in the future.

With Head injuries, don't forget the 30 degree head up and +5 of PEEP if intubated, Lydocaine and Fentanyl pre noxious stimuli, PLEASE..... this has been proven, I would post studies but my internet connect is not optimal (I know a poor excuse) but we did get television just last week "in Canada" so I can't complain. te he.

If people are interested in any of the further info I have discovered about the effects of hyperoxia I will be happy to post it.

Post your heart out, a good read to be certian.

(this whole hypoxic drive BS has got to stop).

AGREED IN SPADES!

During a recient conference that I attended, a researcher proposed that: HI levels of O2 admin in the post operative patient may actually contribute to post op pnemonia (s) as a direct result due to absorbtion atelectasis. Could this be true in other demographic groups that we are treating? hmmm matbe not too far feched at all?

[fiznat]

See, I wasn't totally crazy when I mentioned this today. It's amazing who lurks on the boards.

Ahhhhh!! hahahaa! Zing! Thats great Dustyn haha... imagine your suprise to find out that Shane is on these boards too! lol... Nice one. Hahaha

[jw-c152]

I'd like to add that oxygen is contraindicated in any patient who is currently on fire.

[OVeractiveBrain]

As some of you (Fiznat) might have guessed, my preceptor that told me of this is Shane. After being unable to find mention of it i doubted it was true. I should have had faith!

Though, I must admit, hearing that there might be a contraindication to 02 (other than what i hope is that rare condition in the intensive care setting) sounded a little fishy. Im glad we managed to figure out what the deal was. Im definitely going to take a look at the web sources you put up, Shane, im very interested in the mechanism in particular.

-Overactive

[OVeractiveBrain]

As some of you (Fiznat) might have guessed, my preceptor that told me of this is Shane. After being unable to find mention of it i doubted it was true. I should have had faith!

Though, I must admit, hearing that there might be a contraindication to 02 (other than what i hope is that rare condition in the intensive care setting) sounded a little fishy. Im glad we managed to figure out what the deal was.

[medic001918]

I'm glad we were able to clear that up as well. It's something that we'll most likely not see in the field, it's more an interesting little fact about a drug we carry and a demonstration that we can all always learn something.

Good luck,

Shane

NREMT-P

[OzMedic]

Just some more info in relation to my last post for those interested

"There are several reasons for our recommendations that prehospital providers give only low-flow oxygen to stroke patients. First, no data support the administration of any dose of oxygen to acute stroke patients. The only clinical data we have (from a Swedish study) suggest that 3 L of oxygen given for the first few days after a stroke in a hospital may be harmful. The differences between oxygen and no-oxygen patients, however, were not great. Additionally, the number of patients studied was not large, so this study is not definitive.

In animal models, high-flow oxygen actually worsens ischemic stroke outcome by causing oxygen free-radical formation in the ischemic penumbra (the area of still-salvageable tissue surrounding infarcted brain in the first few hours of ischemic stroke).

High-flow oxygen is also associated with hyperventilating the patient and resultant hypocapnea. This decreases cerebral blood flow and can only hurt a patient with acute ischemic stroke.

I know of no neurologists who advocate the use of high-flow oxygen for acute stroke patients. Unfortunately, few neurologists have been involved in the education of prehospital providers in the past. That's changing.

Finally, the real controversy regarding oxygen is not high-flow vs. low-flow, but low-flow vs. nothing. EMS personnel are actually right not to give oxygen to an acute stroke patient whose O2 saturation is 92%. My personal feeling, however, is that 2-4 L of oxygen for less than 30 minutes is highly unlikely to hurt any stroke patient. Some EMS personnel may not have O2 saturation capabilities, and I'm worried about mistreating patients with stroke and hypoxia. In the hospital, if the O2 saturation stays at 92%, we can remove the oxygen."

David Lee Gordon, MD

Associate Professor of Clinical Neurology & Medicine

Director, Emergency Medical Skills & Neurology Training

Center for Research in Medical Education

University of Miami School of Medicine

[OzMedic]

and some more.........................

Hemodynamic effects of supplemental oxygen administration in congestive heart failure.

Haque WA, Boehmer J, Clemson BS, Leuenberger UA, Silber DH, Sinoway LI.

Division of Cardiology, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, Pennsylvania, USA.

OBJECTIVES. This study sought to determine the hemodynamic effects of oxygen therapy in heart failure. BACKGROUND. High dose oxygen has detrimental hemodynamic effects in normal subjects, yet oxygen is a common therapy for heart failure. Whether oxygen alters hemodynamic variables in heart failure is unknown. METHODS. We studied 10 patients with New York Heart Association functional class III and IV congestive heart failure who inhaled room air and 100% oxygen for 20 min. Variables measured included cardiac output, stroke volume, pulmonary capillary wedge pressure, systemic and pulmonary vascular resistance, mean arterial pressure and heart rate. Graded oxygen concentrations were also studied (room air, 24%, 40% and 100% oxygen, respectively; n = 7). In five separate patients, muscle sympathetic nerve activity and ventilation were measured during 100% oxygen. RESULTS. The 100% oxygen reduced cardiac output (from 3.7 +/- 0.3 to 3.1 +/- 0.4 liters/min [mean +/- SE], p < 0.01) and stroke volume (from 46 +/- 4 to 38 +/- 5 ml/beat per min, p < 0.01) and increased pulmonary capillary wedge pressure (from 25 +/- 2 to 29 +/- 3 mm Hg, p < 0.05) and systemic vascular resistance (from 1,628 +/- 154 to 2,203 +/- 199 dynes.s/cm5, p < 0.01). Graded oxygen led to a progressive decline in cardiac output (one-way analysis of variance, p < 0.0001) and stroke volume (p < 0.017) and an increase in systemic vascular resistance (p < 0.005). The 100% oxygen did not alter sympathetic activity or ventilation. CONCLUSIONS. In heart failure, oxygen has a detrimental effect on cardiac output, stroke volume, pulmonary capillary wedge pressure and systemic vascular resistance. These changes are independent of sympathetic activity and ventilation.

PMID: 8557905 [PubMed - indexed for MEDLINE]