DocXology did not like my criticism of the futility of CPR in trauma –
I think you are setting up a straw man with your naloxone argument. There is not even biomedical plausibility for the scenario you describe.
What did I write?
While CPR in the pulseless trauma patient has overall been considered futile, several reversible causes of cardiac arrest in the context of trauma are correctible and their prompt treatment could be life-saving.
This is a non sequitur.
Where is there any evidence that CPR in any pulseless trauma patients is not futile?
Then I substituted naloxone for CPR in the argument in order to demonstrate that treatment of a potentially reversible cause has absolutely nothing to do with providing a futile treatment in the mean time.
It does not matter if the futile treatment is CPR in traumatic arrest, naloxone in cardiac arrest, or homeopathy for any medical condition. Providing a useless treatment is still useless.
Doing something useless, just for the purpose of looking like we are doing something, is not useful. This only distracts us from whatever might be useful.
One way of improving the fuel economy of a vehicle is to turn off the air conditioning and other items that make the engine work harder and burn more fuel. If the vehicle is out of fuel, then turning off the air conditioning is not going to matter. It is a futile response, just as CPR is a futile response to traumatic cardiac arrest.
The whole point of what I wrote is to demonstrate that the argument for CPR in trauma lacks biological plausibility.
Is that a straw man argument? My argument is not a straw man. Whether DocXology’s argument is a straw man, or just a misunderstanding, is not clear.
There is no RCT to say that oxygenation is good for cardiac arrest but there is a good physiological rationale for it. I presume you don’t withhold that?
That depends on the bias one uses in interpreting the evidence that is the basis for physiological hypotheses.
We started using oxygen for resuscitation because it seemed like a good idea. Now we use it because we always have.
WHAT’S KNOWN ON THIS SUBJECT:
The superiority of room air over 100% oxygen for resuscitating asphyxiated term and near-term newborns has been demonstrated. However, results of studies of preterm infants have indicated that room-air resuscitation may not be appropriate for this population.
WHAT THIS STUDY ADDS:
Resuscitation of preterm infants starting with 100% oxygen followed by frequent titration was most effective at achieving a target oxygen saturation while avoiding hyperoxemia. Treatment-failure rates were highest for those resuscitated with room air despite rapid titration of oxygen.
As with most treatments based only on the contemporary understanding of physiology, the good physiological rationale for it is being demonstrated to be an overly optimistic interpretation of what we really know.
Oxygen is a drug that should be titrated to the effect that is best for the patient.
This does not mean that physiology is unimportant, but that treatments based on physiology must be demonstrated to work in real patients before being widely adopted.
What about adult resuscitation?
Overall, 56% of patients (n = 3561) met the primary outcome of in-hospital mortality (Table 4). Mortality was highest in the hyperoxia group (732/1156; 63% [95% CI, 60%-66%]) compared with the hypoxia group (2297/3999; 57% [95% CI, 56%-59%]) and the normoxia group (532/1171; 45% [95% CI 43%-48%]). The hyperoxia group had significantly higher in-hospital mortality compared with the normoxia group (proportion difference, 18% [95% CI, 14%-22%]; P < .001). Mortality also was significantly higher in the hyperoxia group compared with the hypoxia group (proportion difference, 6% [95% CI, 3%-9%]; P < .001). On Kaplan-Meier analysis, the survival fractions for the hyperoxia and normoxia groups diverged significantly over time (log-rank P < .001; Figure). In addition, among hospital survivors, patients with hyperoxia had a significantly lower proportion of discharges from the hospital as functionally independent compared with patients with normoxia (29% vs 38%, respectively; proportion difference, 9% [95% CI, 3%-15%]; P = .002; Table 4).
Then there is the question of how much physiology really supports the use of supplemental oxygen at high flow rates, rather than just to maintain a normal oxygen saturation.
Numerous laboratory investigations have identified a paradox relative to oxygen delivery to the injured brain. Although it is intuitive that insufficient oxygen delivery can exacerbate cerebral anoxia, excessive oxygen delivery can also be harmful by exacerbating oxygen free radical formation and subsequent reperfusion injury.4,–,11 
My protocols only require that oxygen saturation be maintained at 94% or above.
Supplemental oxygen is not required if the oxygen saturation is adequate.
You suggest that the physiological rationale is unambiguous on oxygen for resuscitation.
That is not true.
I appreciate the issue of withholding ECM (Excternal Cardiac Massage) for traumatic arrest. It was raised at ICEM 2012 by Prof Harris of HEMS and he quoted animal studies with the argument the heart in hypovolaemic PEA is maximally hyper-dynamic and further mechanical augmentation is unlikely to improve output. But again no RCTs or human studies to support this.
Routine treatments should not be based on the absence of evidence of harm, otherwise we could justify anything at all that has not been demonstrated to be harmful. That is not medicine.
Medicine has evidence of efficacy.
Where is the evidence of efficacy for CPR in traumatic cardiac arrest?
Where is the physiologic rationale for CPR in traumatic cardiac arrest?
Treatments without evidence of efficacy should be limited to controlled trials.
We need to stop using wishful thinking to justify abuse of patients.
There is presentation on resuscitation by Dr. Tim Harris available as a free mp3 download at Free Emergency Medicine Talks, but I did not notice any reference to CPR for traumatic cardiac arrest. There are several skips in the recording, but the skips do not appear to obscure information necessary to understand the points Dr. Harris is making. Did he have another presentation on resuscitation?
Tim Harris (UK): Endpoints of Resuscitation
Published: JULY 25, 2012
2012-06-29 D3T3 1100 Endpoints of Resuscitation
 Part 12.8: Cardiac Arrest Associated With Trauma
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 12: Cardiac Arrest in Special Situations
Free Full Text from Circulation
 Room-air versus oxygen administration for resuscitation of preterm infants: the ROAR study.
Rabi Y, Singhal N, Nettel-Aguirre A.
Pediatrics. 2011 Aug;128(2):e374-81. doi: 10.1542/peds.2010-3130. Epub 2011 Jul 11. Erratum in: Pediatrics. 2011 Dec;128(6):1212.
PMID: 21746729 [PubMed – indexed for MEDLINE]
 Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality.
Kilgannon JH, Jones AE, Shapiro NI, Angelos MG, Milcarek B, Hunter K, Parrillo JE, Trzeciak S; Emergency Medicine Shock Research Network (EMShockNet) Investigators.
JAMA. 2010 Jun 2;303(21):2165-71. doi: 10.1001/jama.2010.707.
PMID: 20516417 [PubMed – indexed for MEDLINE]
 Relationship between supranormal oxygen tension and outcome after resuscitation from cardiac arrest.
Kilgannon JH, Jones AE, Parrillo JE, Dellinger RP, Milcarek B, Hunter K, Shapiro NI, Trzeciak S; Emergency Medicine Shock Research Network (EMShockNet) Investigators.
Circulation. 2011 Jun 14;123(23):2717-22. doi: 10.1161/CIRCULATIONAHA.110.001016. Epub 2011 May 23.
PMID: 21606393 [PubMed – indexed for MEDLINE]