Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

Comment on With Conflicting Evidence, What Should We Do? – Oxygen


In the comments to With Conflicting Evidence, What Should We Do? – Oxygen is the following from Dr. Brooks Walsh.

The importance of this study is that it may suggest that hyperoxia may be beneficial at different points in critical illness, and that we need to be careful before acting too broadly.


The way to find out what works is with prospective studies.

We do not have any shortage of cardiac arrests to study. We only have a shortage of research and therefore a shortage of understanding.

We should not attempt to make up for that ignorance with wishful thinking.

Homeopathy, epinephrine, chiropractic, oxygen, Reiki, amiodarone, prayer, lidocaine, acupuncture, vasopressin, et cetera. There is no shortage of possible treatments that lack evidence of benefit.

Where do we start?

Homeopathy probably has more research than all of the other treatments combined.

Howevere, homeopathy is just playing the numbers. There is no real treatment, but if we study a placebo enough times, there will be some statistically significant results.

This is just the same as flipping a coin. If we flip a coin enough times, we will produce a series of heads that is so long that it will have a p value that has an impressive bunch of zeroes in it.

Image credit. Click on image to make it larger. Below is the mouse-over text from this – xkcd 882.

So, uh, we did the green study again and got no link. It was probably a–‘ ‘RESEARCH CONFLICTED ON GREEN JELLY BEAN/ACNE LINK; MORE STUDY RECOMMENDED!


The important point is to pretend that the other studies do not matter. Except that the other studies do matter. All that is being done is throwing feces at a wall and hoping that something sticks.

We have been pretending that, with our understanding of physiology, we are too smart to have too study oxygen.

We have been very arrogant and very stupid.

We haven’t even bothered to find out how dangerous our treatments are.

Perhaps there is an analog to the past studies that looked at the treatment of sepsis. Initial studies of sepsis therapy, using aggressive fluid resus and pressors, were conducted in the ICU, hours after admission. Although these studies were based on strong physiologic evidence, the clinical studies were negative. However, when these same interventions were started in the ED, minutes after arrival, we found a huge drop in mortality. Timing matters.


I should have linked to an mp3 recording of Dr. Mervyn Singer pointing out that hypoxemia is probably not as dangerous as we have been told.[1]

Dr. Singer also has a presentation pointing out the problems with catecholamines in sepsis and questioning the research showing benefit from dopamine.[2]

Dr. Singer raises some interesting questions. the only way to find out the answers is to do the research, not to claim that a lack of proof of harm is evidence of benefit.

Very few treatments have been proven to be harmful, so we could use anything. If enough people follow suit, we have a standard of care that probably is much more harmful than we image and probably not helpful at all.

And so it may be with oxygen. It doesn’t help that most of the studies out there are retrospective, and so are suggestive, but they require confirmation with prospective trials. Some “common-sense” changes in practice have already been implemented, but we need to be careful before extending this reasoning to all clinical situations.


We do not have any high-quality data of benefit. We have a lot of anecdotes of kitchen sink treatment.

When we throw the kitchen sink at the patient, sometimes the patient dies and sometimes the patient lives. We cannot tell if there is any benefit from the kitchen sink, or from any element of the kitchen sink, but we don’t let that stop us.

Our ignorance is unstoppable.

We already have an avalanche of excuses for continuing to harm patients.

We need to stop making excuses and figure out what we are doing.


[1] Permissive hypoxaemia – the way forward
2011, Critical Care, Manchester Critical Care Conference
2011-04-28 at 09:30
Dr. Mervyn Singer
Free Emergency Medicine Talks
Free page with link to free mp3 of presentation.

[2] Catecholamines Should Be Banned
2009, Critical Care, Manchester Critical Care Conference
2009-04-24 at 15:45
Dr. Mervyn Singer
Free Emergency Medicine Talks
Free page with link to free mp3 of presentation.


The Parachute Study as an Objection to Studying Ventilations in Cardiac Arrest

The use of ventilations in cardiac arrest is an example of a treatment that some of us defend by reference to the parachute study.

We assume that we understand all we need to know about physiology, thus we overestimate our ability to understand what we are doing.

Is it impractical to compare the effects of compression-only CPR with standard CPR?

It doesn’t take a PhD physiologist to know that at SOME point you have to provide some ventilation, or 02 sats will decrease, CO2 will increase, etc., to unsurvivable levels. Before you buy the “never been researched ergo must be bad,” you have to read http://www.bmj.com/content/327/7429/1459.full

No, there has never been a prospective, randomized trial of the parachute, but does that make the use of parachutes any less valid?


Is compression-only CPR the same as throwing the patient from a plane without a parachute?

Of course not, but suggesting that traditional treatments are not essential does seem to encourage the use of logical fallacies in otherwise intelligent people, even those trained to the doctorate level especially those trained to the doctorate level.

How much bias is necessary to jump to the conclusion that the criticism of our evidence-free traditional treatments is the same as claiming that the treatment must be bad?

The decision to continue to use treatments of unknown benefit and unknown harm is what is bad.

The list of treatments we have abandoned after we finally examined the treatments, and found out the traditional treatments were harmful, is not short.

We killed a lot of people with ignorance and appeals to common sense.

We still do.


The decision to remain ignorant is a bad decision for us, but a much worse decision for our patients.

What evidence do we have that ventilations improve survival from cardiac arrest?


We assume this.

Is any ventilation provided by continuous chest compressions?

The comment above suggests that there is no ventilation, or that the ventilation is completely inadequate for the physiologic needs of a dead patient.

Is it reasonable to treat patients based on those assumptions?

Is it ethical to treat patients based on those assumptions?

It doesn’t take a PhD physiologist to know that at SOME point you have to provide some ventilation, or 02 sats will decrease, CO2 will increase, etc., to unsurvivable levels.

Is that point at any time before ROSC (Return Of Spontaneous Circulation)?


Maybe not.

This report demonstrates that if powerful cardiac compressions are started early, in this case less than two minutes after normothermic arrest, it is possible to maintain circulation and a sort of spontaneous respiratory movements resulting in gas exchange for more than 25 minutes. For this patient, this kind of respiration was sufficient for survival without neurological damage.

Favourable outcome after 26 minutes of “Compression only” resuscitation: a case report.
Steen-Hansen JE.
Scand J Trauma Resusc Emerg Med. 2010 Apr 16;18:19.
PMID: 20398354 [PubMed – indexed for MEDLINE]

Free Full Text from PubMed Central


Unless there is evidence of benefit, an intervention should not be presumed to be benign.



Potentially Reversible Causes of Cardiac Arrest and the Futility of CPR for Trauma Arrest – comment from DocXology


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.[1]

This is a non sequitur.

Where is there any evidence that CPR in any pulseless trauma patients is not futile?[2]


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.

Image credit.

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.[3]


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.

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).[5]


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 [6]


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


[1] 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

[2] Potentially Reversible Causes of Cardiac Arrest and the Futility of CPR for Trauma Arrest
Mon, 14 Nov 2011
Rogue Medic

[3] Oxygen and resuscitation: beyond the myth.
Lefkowitz W.
Pediatrics. 2002 Mar;109(3):517-9. No abstract available.
PMID: 11875151 [PubMed – indexed for MEDLINE]

[4] 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]

Free Full text from Pediatrics.

[5] 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]

Free Full Text from JAMA.

[6] 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]

Free Full Text from Circulation.


The Myth that Narcan Reverses Cardiac Arrest


We are supposed to search for the potentially reversible causes of cardiac arrest and treat those causes. Since naloxone (Narcan) is the most familiar antidote out there, many people assume that we should be giving naloxone.

Narcan is in the ACLS (Advanced Cardiac Life Support) guidelines!

What do the ACLS guidelines actually state about naloxone?

Naloxone is a potent antagonist of the binding of opioid medications to their receptors in the brain and spinal cord. Administration of naloxone can reverse central nervous system and respiratory depression caused by opioid overdose. Naloxone has no role in the management of cardiac arrest.[1]


Naloxone has no role in the management of cardiac arrest.

Yes. Naloxone is in the ACLS guidelines, but the guidelines say naloxone is not for cardiac arrest.

But what if I really, really, really want to give Narcan?

We can give naloxone, but we shouldn’t pretend that we are following ACLS guidelines.

What about the Hs and Ts?

ACLS does state that we are supposed to consider the potentially reversible causes and to give a treatment that has the potential to improve the outcome. ACLS clearly states that naloxone is not one of those treatments.

Opioid overdose is a potentially reversible cause of cardiac arrest, but naloxone is not the recommended treatment. Opioids do not require administration of an antidote for resuscitation.

But at least Narcan is safe!

Opioid Depression
Abrupt reversal of opioid depression may result in nausea, vomiting, sweating, tachycardia, increased blood pressure, tremulousness, seizures, ventricular tachycardia and fibrillation, pulmonary edema, and cardiac arrest which may result in death (see PRECAUTIONS).


That is not a description of safe.

Safety depends on the context.

Yesterday I wrote about giving naloxone to an intubated patient who had good vital signs after a couple of minutes of chest compressions.[3] There are many ways that naloxone could have made things worse and only one way that it might have helped. That is not the kind of context where naloxone is safe. The medic got lucky.

Why go looking for trouble?

We get invited to enough trouble already.

In normal subjects anaesthetised with morphine and nitrous oxide,3 and in patients addicted to narcotics, pulse rate and blood pressure increase appreciably after reversal of the effects of opiates. Presumably naloxone antagonises opiate suppression of the sympathetic system resulting in a sudden increase in its activity.[4]


We could protect against this unwanted sympathetic stimulus by giving another drug, but how many drugs are we going to give to a patient who is already stable to try to produce a stable patient?

Clonidine might possibly be useful because it abolishes increases in pulse and blood pressure after reversal of opiate effects with naloxone.5 [4]


I am very aggressive in treating many things (e.g. high doses of nitrates for CHF, high doses of opioids and/or benzodiazepines), but these are supported by documentation of safety in the way that I use them.

Why go looking for trouble?

Naloxone has no role in the management of cardiac arrest.


[1] Opioid Toxicity
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 12.7: Cardiac Arrest Associated With Toxic Ingestions
Free Full Text from Circulation

[2] NALOXONE HYDROCHLORIDE injection, solution
[Hospira, Inc.]

Adverse reactions
Opioid toxicity
FDA Label

[3] To Narcan or not Narcan
Tue, 11 Dec 2012
Rogue Medic

[4] Cardiac arrest after reversal of effects of opiates with naloxone.
Cuss FM, Colaço CB, Baron JH.
Br Med J (Clin Res Ed). 1984 Feb 4;288(6414):363-4. No abstract available.
PMID: 6419929 [PubMed – indexed for MEDLINE]

Free Full Text from Pubmed Central.


Optimizing Outcomes in Cardiac Arrest


One more of the great presentations at EMS Expo was on improving outcomes from cardiac arrest.[1]

Lake Sumter EMS does not follow the AHA (American Heart Association) ACLS (Advanced Cardiac Life Support) guidelines.


One member of the audience kept asking about the threat of law suits – the mediocrity response.

But you’ll get sued!

Tell me what to do to avoid getting in trouble.

There is a great scene in The Eiger Sanction. Clint Eastwood (Dr. Jonathan Hemlock) is an art professor and a pretty student wants to flirt her way to a passing grade. Eastwood responds to the suggestion with –

Dr. Jonathan Hemlock: Are you busy this evening?
Art Student: No.
Dr. Jonathan Hemlock: You live alone?
Art Student: My roommate’s gone for the week.
Dr. Jonathan Hemlock: Good. Then… go on home, break out the books and study your little ass off. That’s the best way to maintain a “B” average. Don’t study it all off.[2]


We have too many people in EMS who think a magic pill will keep them out of trouble. The right connections or some magic phrase. Scene safe! BSI!

They don’t want to have to be competent at patient care. They just want to stay out of trouble. Perhaps the best way to avoid trouble is to provide competent patient care.

If they don’t know what competence is, they should stay out of EMS to stay out of trouble.

Dr. Banerjee responded politely to mediocrity fan boy. His results are better than what the ACLS guidelines would produce. You need to show evidence of harm to win a law suit. Evidence of non-conformity is irrelevant.


Fewer than 10 systems produce better than 20% VF (Ventricular Fibrillation) survival to discharge.

We need to stop listening to the defenders of mediocrity and stop killing so many patients.

If we are more worried about the lawyers, than we are about our patients, then we should not be making patient care decisions.


Do these numbers suggest that Dr. Banerjee has any reason to worry about law suits for not following the ACLS guidelines?

No. His only concern would be if he were to start following ACLS guidelines.

No ventilations until resuscitated. Eventually, removing ventilations will the ACLS recommendation, but they part with voodoo tradition slowly. Ventilations are not based on research.

Dr. Banerjee is a fan of pressors (epinephrine and vasopressin), but he is also not going to go against the research if research ends up showing that epinephrine is harmful.

The PEA (Pulseless Electrical Activity) protocol is interesting – treat for many of the potentially reversible causes automatically. I do not remember if it is already part of their protocol, but if it is not, they might want to add bilateral needle decompressions to rule out tension pneumothorax.

Why do the defenders of mediocrity fight so hard against progress?

Maybe they just don’t want progress.


[1] Optimizing Outcomes in Cardiac Arrest
Nov 2 2012 1:15PM
Pushpal (Paul) Rocky Banerjee, MD, Medical Director, Lake EMS, FL; Assistant Medical Director, Aviation One – Medical Transport Services
Friday schedule

Cardiac arrest is a medical emergency that is potentially reversible if treated early. With fast, appropriate medical care, survival is possible. Administering continuous chest compressions, along with early defibrillation, can improve the chances of survival until emergency personnel arrive. Lake EMS has developed an innovative approach to cardiac arrest care. Dr. Banerjee will demonstrate why the cardiac arrest resuscitation rates at Lake EMS are among the highest in the world.

[2] The Eiger Sanction
Movie quote at IMDb


More evidence that interrupting chest compressions kills


This article starts with a misunderstanding of evidence that is common in medicine, and very deadly.

The trend of treating patients on-site — instead of en route — has become the latest standard in Maine, but until now, there was only anecdotal evidence of its effectiveness widely available.[1]

By cutting out the placement of patients on stretchers and transporting them in an ambulance, responders also are cutting out 30- and 40-second gaps of time in which nobody is administering CPR or other treatments, Kooistra said. Those extra seconds, when the heart needs consistent and regular compressions to restart, are making the difference between life and death, he said.[1]


They have it backwards. There is no evidence that transporting cardiac arrest patients improves outcome.

Transport is an intervention. We should not be providing interventions without evidence.

The biggest killer in medicine may be providing interventions without evidence. The problem is that we do not know how dangerous many of our interventions are, because we avoid finding out.

In Portland, Maine, they were killing almost 2/3 of cardiac arrest patients by interrupting compressions just to transport the patient to the hospital.

Is preventing resuscitation the same as killing?

Think of it this way. Your child has a cardiac arrest. GOBSAT methods are used. The GOBSAT methods reduce resuscitation by 2/3. If your child is not resuscitated because of these GOBSAT methods, do you think your child was killed?

What is GOBSAT? Good Old Boys Sitting Around Talking – the way much of medicine is practiced.

Why transport, rather than treat on scene? Maybe because the slightly more effective way of ensuring death, dropping a house on the patient doesn’t look like trying to help. Racing around with lights and sirens gives the appearance of doing something good, but only to those who don’t know what they are doing.

Image credit.

This is a big part of the reason we have so many dangerous standards of care. A bunch of people think that something makes sense, so they start using the treatment, except –

They just don’t care enough to find out how dangerous it is.

Why do we continue to put up with this corruption?

Because we are hopeless optimists. We really do think that this time the GOBSATs will get something right – after all they mean well.

We probably kill more patients with good intentions, than with anything else.

We just don’t care enough about our patients to want to know the truth.

This is not meant as a criticism of EMS in Portland, because they have stopped doing something that never had any evidence to support it. This is meant as criticism of all of us still doing things without evidence to support it.

The AHA (American Heart Association) does not recommend interrupting compressions for transport. The 2005 guidelines did not recommend interrupting compressions for transport. The 2010 guidelines do not recommend interrupting compressions for transport.

Why do so many people claim that they are forced to follow the guidelines, when the guidelines hurt patients, but ignore the guidelines when the guidelines protect patients?

Minimize interruptions in effective chest compressions until ROSC or termination of resuscitative efforts. Any unnecessary interruptions in chest compressions (including longer than necessary pauses for rescue breathing) decreases CPR effectiveness.[2]


Longer than necessary?

Ventilations are not necessary.

Rapid transport is also not necessary.

No intelligent medical personnel should still be rushing to transport cardiac arrest patients before ROSC (Return Of Spontaneous Circulation).

For those who do not understand the simple concept that interruptions in chest compressions kill, please pay attention.

There is only one interruption in chest compressions that has evidence of improved outcomes.

That interruption is for defibrillation.

Not for charging the defibrillator.

Not for ventilation.

Not for intubation.

Not to move the patient.

Only for defibrillation.

Unless the patient is in a location that makes treatment difficult, or dangerous, we should not be moving the patient before ROSC.

The AHA guidelines still recommend that professional rescuers provide worse CPR than bystander. We need to recognize that there was no evidence for including ventilations in CPR and most of us did not care enough to find out what really works until recently.

When will the AHA correct this mistake?

When will the AHA correct these other mistakes?

When will the AHA demand evidence of improved survival to continue to recommend epinephrine in cardiac arrest?

When will the AHA demand evidence of improved survival to continue to recommend vasopressin in cardiac arrest?

When will the AHA demand evidence of improved survival to continue to recommend magnesium in cardiac arrest?

When will the AHA demand evidence of improved survival to continue to recommend phenylephrine in cardiac arrest?

When will the AHA demand evidence of improved survival to continue to recommend amiodarone in cardiac arrest?

When will the AHA demand evidence of improved survival to continue to recommend lidocaine in cardiac arrest?

The AHA cites a lot of evidence.

There is no evidence of improved survival with good neurological function from cardiac arrest using any of these drugs recommended by the AHA.

Alternative medicine has no evidence. Why not use alternative medicine?

We are using alternative medicine. We just don’t admit this fraud to patients.

Why is the AHA continuing to recommend that we use treatments that cannot be shown to work?


[1] Portland paramedics skip the ambulance rides, save three times as many lives
By Seth Koenig, BDN Staff
Posted Nov. 27, 2012, at 3:14 p.m.
Last modified Nov. 27, 2012, at 3:29 p.m.
Bangor Daily News

[2] Key Points of Continued Emphasis for the 2010 AHA Guidelines for CPR and ECC
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 1: Executive Summary
Highlights of the 2010 Guidelines
Free Full Text from Circulation


Is a half a bottle of nitro too much for a single dose?

In what I last wrote about the emergency treatment of CHF (Congestive Heart Failure) and furosemide (Lasix – frusemide in Commonwealth countries) being a bad drug,[1] I also mentioned what Peter Canning had written about Hero Medic and a very high dose of NTG (NiTroGlycerin – GTN GlycerylTriNitrate in Commonwealth countries).

How much NTG?

The hero medic opened the nitro, pulled open the patient’s mouth and poured in what seemed like half the container. The hero medic closed the patient’s mouth, and then told the new medic. “You should be all set.”[2]


What seemed like half the container of something we are warned not to give chest pain patients more than one at a time and never more than 3 tabs of – ever!

That does seem like a lot, but how much is half of a bottle?


How much is a lot?


For the typical bottle pictured, the label states that the total is 25 of the 0.4 mg tabs.

That is a total of 10 mg. Half of that is easy math – 5 mg.

What seemed like half the container is probably less than half, but it was just such a shocking visual for the narrator, that all he could do was estimate.

Is 5 mg a large dose?


Is 5 mg a dangerous dose?

That depends on the patient presentation.

a patient in severe pulmonary edema who was circling the drain[2]


I would like to know his blood pressure, but even hypotensive CHF patients do well with huge doses of NTG.

The patients below were more than just circling the drain.

All were hypotensive, or pulseless.

Click on the image to make it larger.[3]


Almost all of the massive dose NTG patients survived.

The highest blood pressure before NTG was 80/70.

The lowest dose of NTG was 1 mg – and that was the only patient who received less than 5 mg NTG.

Almost every hypotensive patient received much more than 5 mg NTG.

Is 5 mg NTG a dangerous dose?

Probably not.

Is 5 mg a scary dose?

Of course. We have been trained to be scared of NTG.

That dose is just much larger than most people are comfortable with, because of fear and inexperience.

You can talk about the hero medic acting off protocol and being a cowboy, etc, but the story still resonates for me.[2]


Would it be appropriate to just drop in, give a large dose of anything, and then not stick around?

No. If the original medic is not comfortable with that treatment, the Hero Medic should be there to hold the nitrophobic medic’s hand and reassure the medic to follow his assessment, rather than to follow his anxiety. That is the way we learn.

The story of Hero Medic is told through hyperbole – exaggeration to make an important point.

I have done this with others. Look, not only am I giving a much larger dose than you claim is safe – I am going to add a few more tabs – just to make a point.

If the scare stories about NTG were true, the patients would bottom out their blood pressures, but it is only the witnesses who bottom out their blood pressures, due to over-stimulation of their vagal nerves. The patients improve.

Some people learn from this clear demonstration that they have been lied to, but others choose to believe the dogma even after seeing clear evidence that the dogma is a lie.

Doctors, nurses, medics, et cetera. They are equally susceptible to dogma.

Is the Hero Medic a cowboy?

No, the Hero Medic s a teacher.

We need to be smart enough to learn.


[1] Lasix Kills: Better Therapy for CHF
Wed, 07 Nov
Rogue Medic

[2] NTG and the Hero Medic
Street Watch
November 7, 2012

[3] High dose nitroglycerin treatment in a patient with cardiac arrest: a case report.
Guglin M, Postler G.
J Med Case Reports. 2009 Aug 10;3:8782.
PMID: 19830240 [PubMed]

Free Full Text from PubMed Central


Details on NIPPV for CHF Works, ACLS Algorithms Do Not at the 1-Union-801 Podcast


I have forgotten to post about a podcast that was kind enough to have me as a guest on the topic of CPAP (which works) and ACLS (Advanced Cardiac Life Support) drugs (which don’t work).

John Broyles, the host of 1-Union-801, had me on back in October.[1] This was about something I wrote reviewing an article by Dr. David Newman.[2],[3]

What is NIPPV – Non-Invasive Positive Pressure Ventilation?

What is CPAP?

Is there evidence that CPAP improves outcomes?

What are contraindications to CPAP?

The real problem with disoriented patients using CPAP is that they may not be able to trigger a breath by taking a deep enough breath.

CPAP should be a BLS skill everywhere.

CPAP is required BLS equipment in Pennsylvania.[4]

Et cetera.

What do we do for cardiac arrest according to ACLS that is based on evidence?

What do we do for cardiac arrest according to ACLS that is not based on evidence?

Where is the evidence that ACLS drugs improve any outcome that matters?

ACLS Medications for Cardiac Arrest[5]

What does the epinephrine research show?


I added the two most recent studies to this, since they were not yet published when the review of vasopressors was published.[6] The quality and outcome of the added studies is my interpretation, but I think that others will rank them similarly.

If your idea of a good outcome is a temporary pulse in a patient who lives in a coma for a few seconds, or minutes, or hours, or days, then your priorities are screwed up.

My idea of a good outcome is the ability to wake up and talk with the people I care about.

ACLS drugs DO get pulses back more often than not using drugs, but the drugs decrease the chances that these patients will wake and be able to think.

Why do we poison our patients’ brains just to get some temporary pulses?

Because we are giving the drugs for the satisfaction of getting a pulse back, not for bringing a living, thinking human back.

We value a zombie resuscitation over resuscitation of a thinking patient.

If the patient could walk, and talk, and make sense before the cardiac arrest, not being able to walk, and talk, and make sense after the cardiac arrest is not a good outcome.

Any standard of care that does not have evidence of survival benefit needs to have an expiration date.

If your idea of a good outcome is to be one of The Walking Dead, but without the walking, then you will want epinephrine for your cardiac arrest.

Go listen to the podcast.

I apologize for not being more lively during the podcast, but part of the reason is that there were people sleeping near by.


[1] NIPPV with CHF works…ACLS does not
by 1 Union 801 TheWebcast
Sat. October 13, 2012

[2] NIPPV for CHF Works, ACLS Algorithms Do Not
by David Newman, MD
September 26, 2012
Emergency Physicians Monthly

[3] NIPPV for CHF Works, ACLS Algorithms Do Not
Thu, 04 Oct 2012
Rogue Medic

[4] Required Ground and Air Ambulance Equipment and Supplies
[39 Pa.B. 6167]
[Saturday, October 17, 2009]
Web Page.

Required Equipment and Supplies

 Approved equipment and supplies shall be carried and readily available in working order for use on both ground and air ambulances. Some patients and crewmembers of an ambulance service may have allergies to latex. Latex free supplies are recommended, where possible. The following equipment and supplies must be carried on each ground and air ambulance, as indicated.

62. CPAP Ventilation-portable equipment X X X

[5] ACLS Medications for Cardiac Arrest
August 19, 2010

[6] Vasopressors in cardiac arrest: a systematic review.
Larabee TM, Liu KY, Campbell JA, Little CM.
Resuscitation. 2012 Aug;83(8):932-9. Epub 2012 Mar 15.
PMID: 22425731 [PubMed – in process]

CONCLUSION: There are few studies that compare vasopressors to placebo in resuscitation from cardiac arrest. Epinephrine is associated with improvement in short term survival outcomes as compared to placebo, but no long-term survival benefit has been demonstrated. Vasopressin is equivalent for use as an initial vasopressor when compared to epinephrine during resuscitation from cardiac arrest. There is a short-term, but no long-term, survival benefit when using high dose vs. standard dose epinephrine during resuscitation from cardiac arrest. There are no alternative vasopressors that provide a long-term survival benefit when compared to epinephrine. There is limited data on the use of vasopressors in the pediatric population.