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

- Rogue Medic

A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest – Part I

 
Also to be posted on ResearchBlogging.org when they relaunch the site.

The results are in from the only completed Adrenaline (Epinephrine in non-Commonwealth countries) vs. Placebo for Cardiac Arrest study.
 


 

Even I overestimated the possibility of benefit of epinephrine.

I had hoped that there would be some evidence to help identify patients who might benefit from epinephrine, but that is not the case.

PARAMEDIC2 (Prehospital Assessment of the Role of Adrenaline: Measuring the Effectiveness of Drug Administration in Cardiac Arrest) compared adrenaline (epinephrine) with placebo in a “randomized, double-blind trial involving 8014 patients with out-of-hospital cardiac arrest”.

More people survived for at least 30 days with epinephrine, which is entirely expected. There has not been any controversy about whether giving epinephrine produces pulses more often than not giving epinephrine. As with amiodarone (Nexterone and Pacerone), the question has been whether we are just filling the ICUs and nursing home beds with comatose patients.
 

There was no statistical evidence of a modification in treatment effect by such factors as the patient’s age, whether the cardiac arrest was witnessed, whether CPR was performed by a bystander, initial cardiac rhythm, or response time or time to trial-agent administration (Fig. S7 in the Supplementary Appendix). [1]

 

The secondary outcome is what everyone has been much more interested in – what are the neurological outcomes with adrenaline vs. without adrenaline?

The best outcome was no detectable neurological impairment.
 

the benefits of epinephrine that were identified in our trial are small, since they would result in 1 extra survivor for every 112 patients treated. This number is less than the minimal clinically important difference that has been defined in previous studies.29,30 Among the survivors, almost twice the number in the epinephrine group as in the placebo group had severe neurologic impairment.

Our work with patients and the public before starting the trial (as summarized in the Supplementary Appendix) identified survival with a favorable neurologic outcome to be a higher priority than survival alone. [1]

 


Click on the image to make it larger.
 

Are there some patients who will do better with epinephrine than without?

Maybe (I would have written probably, before these results), but we still do not know how to identify those patients.

Is titrating tiny amounts of epinephrine, to observe for response, reasonable? What response would we be looking for? Wat do we do if we observe that response? We have been using epinephrine for over half a century and we still don’t know when to use it, how much to use, or how to identify the patients who might benefit.

I will write more about these results later

We now have evidence that, as with amiodarone, we should only be using epinephrine as part of well controlled trials.

Also see –

How Bad is Epinephrine (Adrenaline) for Cardiac Arrest, According to the PARAMEDIC2 Study?

Footnotes:

[1] A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest.
Perkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, Black JJM, Moore F, Fothergill RT, Rees N, O’Shea L, Docherty M, Gunson I, Han K, Charlton K, Finn J, Petrou S, Stallard N, Gates S, Lall R; PARAMEDIC2 Collaborators.
N Engl J Med. 2018 Jul 18. doi: 10.1056/NEJMoa1806842. [Epub ahead of print]
PMID: 30021076

Free Full Text from NEJM

All supplementary material is also available at the end of the article at the NEJM site in PDF format –

Protocol

Supplementary Appendix

Disclosure Forms

There is also an editorial, which I have not yet read, by Clifton W. Callaway, M.D., Ph.D., and Michael W. Donnino, M.D. –

Testing Epinephrine for Out-of-Hospital Cardiac Arrest.
Callaway CW, Donnino MW.
N Engl J Med. 2018 Jul 18. doi: 10.1056/NEJMe1808255. [Epub ahead of print] No abstract available.
PMID: 30021078

Free Full Text from NEJM

.

The Kitchen Sink Approach to Cardiac Arrest

 
When faced with death, we can become desperate, stop thinking clearly, and just try anything.

Alternative medicine thrives on the desperation of people who are not thinking clearly. We should be better than that, but are we?

A recent comment on The Myth that Narcan Reverses Cardiac Arrest[1] proposes that I would suddenly give kitchen sink medicine a try, if I really care about the patient.

Kitchen sink medicine? It’s better to do something and harm the patient, than to limit treatment to what works. Throw everything, including the kitchen sink, at the patient.

Mike Karras writes –
 

I will leave you with this question sir and I am interested to hear your answer. You walk in to find your 14 year old daughter that intentionally overdosed on morphine in a suicide attempt and she is in cardiac arrest. How would you treat her? Would you give her Narcan? I think you would.[2]

 

Mike, I am thrilled to read that you do not think that I care about the outcomes of my patients, unless the patient happens to be my daughter. I am even more thrilled that you made my imaginary daughter suicidal.

No, I would not use naloxone (Narcan).

I would also not use homeopathy, acupuncture, sodium bicarbonate, incantations, or magic spells to treat my daughter during cardiac arrest. Voodoo only works on believers, because voodoo is just a placebo/nocebo.[3]
 


Image credit.
 

Does really wanting something to be true make it true? If you believe in magic, the answer is Yes, believing makes it true. If you examine the evidence for that belief, you have several choices. You can acknowledge your mistake, or you can employ a bit of cognitive dissonance, or . . . . Cognitive dissonance is the way our minds copes with the conflict, when reality and belief do not agree, and we choose to reject reality.[4]

According to the ACLS (Advanced Cardiac Life Support) guidelines –
 

Naloxone has no role in the management of cardiac arrest.[5]

 

If the patient is suspected of having a cardiac arrest because of an opioid overdose (overdose of heroin, fentanyl, morphine, . . . ), the treatments should include ventilation and chest compressions. If those do not provide a response, epinephrine (Adrenaline in Commonwealth countries) is added.

An opioid overdose can produce respiratory depression and/or vasodilation. I can counter both of those with chest compressions, ventilation, and maybe epinephrine. Naloxone works on opioid receptors. What does naloxone add?

Does naloxone’s stimulation of an opioid receptor produce more ventilation than bagging/intubating?

Does naloxone’s stimulation of an opioid receptor produce more oxygenation than bagging/intubating?

Does naloxone’s stimulation of an opioid receptor produce more vasoconstriction than chest compressions and epinephrine?*

Also –
 

Don’t confuse post- or pre–arrest toxicologic interventions with the actual cardiac arrest event.[6]

 

Dead people do not respond to treatments the same way living people do.
 
 

See also –
 

Dissecting the ACLS Guidelines on Cardiac Arrest from Toxic Ingestions – Tue, 01 Nov 2011

Naloxone in cardiac arrest with suspected opioid overdoses – Thu, 05 Apr 2012

The Myth that Narcan Reverses Cardiac Arrest – Wed, 12 Dec 2012

Resuscitation characteristics and outcomes in suspected drug overdose-related out-of-hospital cardiac arrest – Sun, 03 Aug 2014
 

* Late edit – 02/17/2015 10:52 – added the word naloxone’s to the three sentences about the relative amount of stimulus provided by standard ACLS and by the addition of naloxone. Thanks to Brian Behn for pointing out the lack of clarity.

Footnotes:

[1] The Myth that Narcan Reverses Cardiac Arrest
Wed, 12 Dec 2012
Rogue Medic
Article

[2] Comment by Mike Karras
The Myth that Narcan Reverses Cardiac Arrest by Rogue Medic
Mon, 16 Feb 2015
Article

[3] Nocebo
Wikipedia
Article

A nocebo is an inert agent that produces negative effects. What this means is that nocebo effects are adverse placebo effects. There is no reason to believe that placebos only produce positive effects or no effects at all.

[4] Cognitive dissonance
Wikipedia
Article

[5] Opioid Toxicity
2010 ACLS
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

[6] Dissecting the ACLS Guidelines on Cardiac Arrest from Toxic Ingestions
Emergency Medicine News:
October 2011 – Volume 33 – Issue 10 – pp 16-18
doi: 10.1097/01.EEM.0000406945.05619.ca
InFocus
Roberts, James R. MD
Article

Read the whole article about antidotes and cardiac arrest.

.

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]

 

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.
[4]

 

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

Footnotes:

[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
Article

[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).
[2]

 

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.
 

Footnotes:

[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.]

DailyMed
Adverse reactions
Opioid toxicity
FDA Label

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

[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.

.

Potentially Reversible Causes of Cardiac Arrest and the Futility of CPR for Trauma Arrest

One caveat. This does not apply to a medical cardiac arrest that coincidentally has some trauma associated with it. V Fib (Ventricular Fibrillation) while driving leading to a car crash. That is not a trauma arrest.

What is the purpose of CPR in trauma arrest?

To put on a show.

[youtube]e7mmrF-4rUE[/youtube]

Bullwinkle is infinitely more likely to pull a rabbit out of that hat, than CPR is likely to resuscitate a cardiac arrest due to trauma.

Play the video again, it might work.

Almost.

Keep trying.

Nearly had it.

Don’t give up.

You were so close.

Maybe this time.

There was tremendous improvement on that attempt.

Never say die.

Couldn’t you feel that it was there?

Under no circumstances will we admit that our magic is futile!

Keep trying. I know you can do it. You can find that card, Charlie Brown will kick that ball, and nobody ever dies. 😉


Picture credit.

Part 12.8: Cardiac Arrest Associated With Trauma

BLS and ACLS for the trauma patient are fundamentally the same as that for the patient with primary cardiac arrest, with focus on support of airway, breathing, and circulation. In addition, reversible causes of cardiac arrest need to considered. 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. These include hypoxia, hypovolemia, diminished cardiac output secondary to pneumothorax or pericardial tamponade, and hypothermia.[1]

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?

There isn’t any.

None. That is why CPR for pulseless patients is considered futile.

This is just a case of treatment based entirely on What if . . . ?

This is alternative medicine. This is not medicine.

Here is our good friend naloxone (Narcan) to explain the non sequitur

While CPR in the pulseless trauma patient has overall been considered futileWhile naloxone 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.

Or –

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 naloxone can cause withdrawal in opioid addicts.

Are we harming trauma patients by not using naloxone?

What does naloxone have to do with traumatic arrest?

Not a thing.

What does any futile treatment for pulseless trauma patients have to do with reversible causes of cardiac arrest?

But it is only considered futile!

That is because of the difficulty in proving a negative. Hume’s problem of induction does not mean that we should assume that anything that has a snowball’s chance of working actually does work.[2]

Should we try Reiki, because What if . . . ?

Should we try acupuncture, because What if . . . ?

Should we try a medicine dance, because What if . . . ?

Should we try therapeutic phlebotomy bleeding the patient to remove the bad humors, because What if . . . ?

Should we sing silly songs, because What if . . . ?

What is the cause of pulselessness in trauma patients?

There are 2 possibilities –

1. Obstruction of circulation –

Tension pneumothorax kills by preventing circulation, not by interfering with breathing.

Cardiac tamponade also kills by preventing circulation.

2. Nothing to circulate –

Hypovolemic arrest kills because there is not enough blood to produce a palpable pulse, even though the heart is beating as well as can be expected.

If the compressions do not produce any circulation, what is the point of CPR?

Let’s not forget spinal immobilization combined with CPR for traumatic arrest –


Picture credit. Still no rabbit.

BLS Modifications
When multisystem trauma is present or trauma involves the head and neck, the cervical spine must be stabilized.
[1]

Is the outcome from traumatic arrest so good that we need to throw in this ritual? Or is it so bad, that it does not matter what we do to keep up appearances?

If we have time to strap a patient to a backboard, then we might as well just get out a shovel and have the funeral right there. Nothing says permanently dead as clearly as putting spinal immobilization and CPR for trauma together.

There must be a rabbit in here somewhere.

It works in the scenarios in school.

Footnotes:

[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 Article with links to Free Full Text PDF download

[2] Problem of induction
Wikipedia
Article

.

Naked freezing man found alive in the snow was coldest survivor ever seen by paramedic


All rest and no work makes Jack a cold boy.
All rest and no work makes Jack a cold boy.
All rest and no work makes Jack a cold boy.
All rest and no work makes Jack a cold boy.
All rest and no work makes Jack a cold boy.
All rest and no work makes Jack a cold boy.
All rest and no work makes Jack a cold boy.
😎

The 22-year-old South Korean man is in a critical condition with hypothermia, and was put into an induced coma, after being found at Falls Creek in the state’s northeast about 4.30am.[1]

It is unusual for someone to be found at 04:30, but this guy was. Given his temperature, if he had been found at 05:00, he probably would have been pulseless and he probably would not been resuscitated.

Senior intensive care paramedic Patrick Gleeson said the man’s core temperature was only 24C – compared to 37C normally.

“That’s one of the coldest patients that I’ve been to in 30 years of ambulance service,” the Ambulance Victoria clinical support officer said.[1]

24 °C is equal to 75.2 °F. Comfortable as an air temperature. Cool as a water temperature. Very, very cold for a human body.

While this does not appear to be the time of year to consider this, it is in Australia. The difference between hypothermia in the Summer and hypothermia in the Winter is the rate of cooling.

Unintentional or accidental hypothermia is a serious and preventable health problem. Severe hypothermia (body temperature <30°C [86°F]) is associated with marked depression of critical body functions, which may make the victim appear clinically dead during the initial assessment. Therefore, lifesaving procedures should be initiated unless the victim is obviously dead (eg, rigor mortis, decomposition, hemisection, decapitation).[2]

These patients need aggressive rewarming and they need to be prevented from getting cold again.

For patients with severe hypothermia (<30°C [86°F]) with a perfusing rhythm, core rewarming is often used, although some have reported successful rewarming with active external warming techniques.408,409 Active external warming techniques include forced air or other efficient surface-warming devices.[2]

“It’s typically not seen in Australia.

“The only time that these sort of temperatures are recorded in patients that have survived are perhaps in Europe and Canada and the United States.”[1]

Because the temperature does not get low enough to drop a person’s body temperature down to 75 degrees quickly? Why not?

I think that it is rare anywhere. Few of us have treated patients with body temperatures this cold, but still alive. It is important to recognize the problem quickly. Remove wet clothing and dry the patient also quickly.

ACLS management of cardiac arrest due to hypothermia focuses on aggressive active core rewarming techniques as the primary therapeutic modality. Conventional wisdom indicates that the hypothermic heart may be unresponsive to cardiovascular drugs, pacemaker stimulation, and defibrillation; however, the data to support this are essentially theoretical.429[2]

In other words, rewarming works. Beyond rewarming, we are guessing. Since the drugs do not appear to improve survival to discharge in normothermic cardiac arrest, there is no reason to expect them to suddenly improve outcomes just because the patient is cold.

See also – Potentially Reversible Causes – Hypothermia.

Footnotes:

[1] Naked freezing man found alive in the snow was coldest survivor ever seen by paramedic
by Matthew Schulz and Amelia Harris
From: AAP, Herald Sun
August 11, 2011 1:18PM
Article

There are also 2 audio segments at the bottom of the page. An interview with one of the doctors and an interview with the paramedic.

[2] Part 12.9: Cardiac Arrest in Accidental Hypothermia
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 12: Cardiac Arrest in Special Situations
Free Full Text from Circulation with links to Free Full Text PDF Download

.

EMS 12 Lead Bradycardia Post – Part II

Continuing from Part I.

This is the rest of the discussion of 82 year old male CC: Shortness of breath and 82 year old male CC: Shortness of breath – Conclusion.

Here is the 12 lead again. –

I made it a little larger, because I expect that you have already looked at it, and the other ECGs from this patient, in Tom’s post.

The first thing I notice about this 12 lead is that there are only 2 clear QRS complexes in 10 seconds.

If the heart is beating, where is the current in the leads being recorded?

This is a 12 lead. Each portion of the printout is the simultaneous recording of 3 different leads. If there is current it should show up in the other 2 leads in the same section of the 12 lead. It could be that the axis is perpendicular to that lead, but again there are 3 leads, so the axis cannot be perpendicular to all three of the leads simultaneously recorded.[1] The first 12 lead did show Low voltage QRS in the analysis, but it also did show what appear to be QRS complexes in all of the leads.

At 07:44:31 12 lead 1 is recorded with apparent QRS complexes in all leads.

At 08:01:44 12 lead 2 is recorded, but only half of the 12 leads appear to have QRS complexes.

15 minutes later and the ECG looks worse.

The patient is sweaty/clammy/diaphoretic. Whatever terminology we use, the patient is wet. Wet is the enemy of having the leads stick, although wet is an important part of the means of conduction of the electricity to the monitor. How do we quickly troubleshoot our equipment?

Check the pulse.

Is the patient’s heart rate really only 2 beats every 10 seconds?

If yes, that means a heart rate of about 12 beats per minute. The rhythm is irregular and this is a very small sample, but the important point is that a heart rate of 12 in a human is incompatible with survival.

Even extreme athletes do not get their resting heart rates below the 20s and this 82 year old hypertensive diabetic is not an extreme athlete. He is extremely unstable. Another possible explanation would be if the person were hypothermic, but there is nothing in this case presentation to suggest hypothermia.

Tom makes some important points about the way to approach an arrhythmia. One is the potentially reversible causes. This patient is not yet in cardiac arrest, but by treating the potentially reversible condition that is expected to progress to cardiac arrest, perhaps we can prevent a cardiac arrest.

What is the potentially reversible condition?

Hyperkalemia.

Consider this conversation between Stephen Smith, M.D. (from Dr. Smith’s ECG Blog) and Scott Weingart, M.D. on the EMCrit podcast:

SW: “I know I’ve learned from being burned many times, that when I have a profound bradycardia or heart block, as my residents are getting excited to place in a pacer, even if the patient has no preexisting history, I do a trial of calcium chloride or calcium gluconate because I’ve just had so many cases where it turned out to be hyperkalemia. Is that your experience as well?”

SS: “That is my experience as well and I think it’s very wise you’re giving calcium before you start pacing. By far, more common than intrinsic causes of bradycardia and heart block is hyperkalemia — so common — and so frequently overlooked. It’s a great imitator, I think. There are so many ways the ECG can manifest with severe hyperkalemia — life-threatening hyperkalemia. Again, the treatment is benign, and cheap! So how many life-threatening diseases can you treat benignly and cheaply?”[2]

SW is Scott Weingart, M.D. SS is Stephen Smith, M.D.

While calcium is not generally in EMS protocols for bradycardia, we should consider these critical statements by Dr. Smith –

 

I think it’s very wise you’re giving calcium before you start pacing.

 

and

 

Again, the treatment is benign, and cheap!

 

A lot of people do not seem to be familiar with the word benign.

adjective
Definition:

1. kindly: having a kind and gentle disposition or appearance

2. not life-threatening: not a threat to life or long-term health, especially by being noncancerous
a benign tumor

3. harmless: neutral or harmless in its effect or influence

4. favorable: mild or favorable in effect
a benign climate

[14th century. Via French< Latin benignus]

be·nign·ly adverb[3]

What if the low amplitude/no amplitude of the QRS complexes the 12 lead claims are there really are there? Would that be an indication of hypokalemia?

No.

The beats that are clearly present are not giving any indication that the patient is hypokalemic.

The beats that I do not see, but the 12 lead counts are probably not there, but definitely not being hidden by hypokalemia.

Why does the machine come up with a different heart rate from what I come up with?

The machine could be wrong.

I could be wrong.

Both of us could be wrong.

The best way to assess this is to actually touch the patient and assess for the presence of a palpable pulse.

It is interesting that the 12 lead does not make any suggestion about considering hyperkalemia, while the doctors think that unstable bradycardia is a good reason to automatically treat for hyperkalemia.

What is important about this case?

We need to anticipate the patients with unstable bradycardia.

We need to have some sort of plan for what to do with the bradycardia patient who is mostly dead.

We need to discuss this with medical directors ahead of time, so that this does not become a long conversation on a command line while the patient expires or a conversation that ends with an order to Just transport.

Footnotes:

[1] Axis Determination – Part I
EMS 12 Lead
Article

Tom continues this in Part II, Part III, Part IV, Part V, and Part VI.

This will tell you all you need to know about axis (which is very important) and it should explain better what I am trying to point out. If we understand axis and amplitude, this should be something that immediately gets our attention.

[2] EMCrit Podcast 42: A phD in EKG with Steve Smith
EMCrit
Podcast

The supplementary material covers 10 points covered in the podcast, including –

8. If you see a wide (>190 ms) QRS, think Hyperkalemia

 

9. The treatment for VT with hyper-K is Calcium, Calcium, Calcium

Dr. Smith’s EKG Blog

[3] Benign
encarta
Definition

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Excited Delirium Strikes without Warning – Part I

In the February issue of JEMS, Dr. Keith Wesley has a very important article about excited delirium and in custody deaths.

According to the U.S. Department of Justice, 47 states and the District of Columbia reported 1,095 arrest-related deaths from 2003–2005.[1]

Assuming that the 2003-2005 means January 01, 2003 through to December 31, 2005, that means 1,095/3 years or 365 in custody deaths per year. Almost an average of one a day. 2004 was a leap year with 366 days. Maybe leap days exert a protective effect against excited delirium. 🙄

Before the proliferation of such less-lethal techniques as CEDs, pepper spray and bean bag rounds, many subjects who were this aggressive met their death from the use of lethal force.[1]

In custody death is nothing new. These deaths just seem less preventable when they are the result of GSWs (Gun Shot Wounds), rather than the now he’s alive – now he’s dead – and he stays dead presentation that is typical for these patients.

Current research reveals excited delirium patients have abnormally altered levels of several neurochemicals in their brain—the most important being dopamine.(4)[1]

This can happen even among those not taking stimulant drugs.

Elevated levels of dopamine cause agitation, paranoia and violent behavior. Heart rate, respiration and temperature control are also affected by dopamine levels with elevation resulting in tachycardia, tachypnea and hyperthermia. For this reason, hyperthermia is a hallmark of excited delirium.[1]

Kind of like hyperventilation syndrome on crack cocaine.

As dopamine levels rise, in combination with the stimulant effects of drugs, the patient’s metabolic activity increases. This results in hyperthermia. The patient becomes acidotic as a result of muscle activity, which has been documented to elevate creatinine phosphokinase—a protein released from muscle death. Metabolic acidosis results in hyperkalemia, which can precipitate dysrhythmias. Therefore, when cardiac arrest occurs, it does so in an environment of severe acidosis and hyperkalemia.(6)[1]

Therefore, when cardiac arrest occurs, it does so in an environment of severe acidosis and hyperkalemia.

A study in Los Angeles reviewed 18 consecutive witnessed arrests from excited delirium. Despite receiving immediate ALS care, all patients died.(8)[1]

Despite receiving immediate ALS care, all patients died.

It may be a good idea to start treatment with calcium (chloride is preferred, but gluconate can work, too).

Why calcium?

1. If this is a case of hyperkalemia, there is no more effective initial treatment than calcium.

2. If this is a case of hyperkalemia, there is nothing that works as quickly as calcium.

3. Even with immediate ALS (Advanced Life Support), nobody seems to be able to resuscitate these patients, so there does not appear to be anything to lose. How can calcium possibly make things any worse?

The resuscitation rate for witnessed arrests should at least equal the resuscitation rate for the community as a whole. These patients do not respond to conventional ACLS (Advanced Cardiac Life Support). Therefore, these patients should not be treated as conventional cardiac arrest patients.

Given the expectation that these patients are hyperkalemic, is it responsible to treat these patients as anything other than hyperkalemic?

If hyperkalemia is left untreated, a sine-wave pattern, idioventricular rhythms, and asystolic cardiac arrest may develop.203,204[2]

ACLS Modifications in Management of Severe Cardiotoxicity or Cardiac Arrest Due to Hyperkalemia
Treatment of severe hyperkalemia aims at protecting the heart from the effects of hyperkalemia by antagonizing the effect of potassium on excitable cell membranes, forcing potassium into cells to remove it promptly from the circulation, and removing potassium from the body. Therapies that shift potassium will act rapidly but are temporary and thus may need to be repeated. In order of urgency, treatment includes the following:

Stabilize myocardial cell membrane:
· Calcium chloride (10%): 5 to 10 mL (500 to 1000 mg) IV over 2 to 5 minutes or calcium gluconate (10%): 15 to 30 mL IV over 2 to 5 minutes[3]

That is the initial treatment for hyperkalemia. That is what EMS should focus on.

Some people will say that we should start with sodium bicarbonate. Ignore them. They do not know what they are talking about. Every responsible organization should make it clear that calcium is the initial treatment for unstable hyperkalemia.

When cardiac arrest occurs secondary to hyperkalemia, it may be reasonable to administer adjuvant IV therapy as outlined above for cardiotoxicity in addition to standard ACLS (Class IIb, LOE C).[3]

Otherwise, there is no reason to believe that these patients will be resuscitated. Similarly, we should focus on calcium when treating cardiac arrest with dialysis patients.

To be continued in Excited Delirium Strikes without Warning – Part II.

Footnotes:

[1] Excited Delirium Strikes without Warning
by Keith Wesley, MD, FACEP
JEMS February 2011 Issue
Tuesday, February 1, 2011
Article

[2] Hyperkalemia
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 12: Cardiac Arrest in Special Situations
Part 12.6: Cardiac Arrest Associated With Life-Threatening Electrolyte Disturbances
Free Full Text From Circulation with link to Free Full Text PDF Download

[3] ACLS Modifications in Management of Severe Cardiotoxicity or Cardiac Arrest Due to Hyperkalemia
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 12: Cardiac Arrest in Special Situations
Part 12.6: Cardiac Arrest Associated With Life-Threatening Electrolyte Disturbances
Hyperkalemia
Free Full Text From Circulation with link to Free Full Text PDF Download

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