There are plenty who … claim to be competent at intubation even though their last intubation was months ago on the third attempt and if the patient had not already been dead – that would have finished the patient off …

- Rogue Medic

The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia

ResearchBlogging.org
 

This is a very interesting trial that may surprise the many outspoken amiodarone advocates, but it should not surprise anyone who pays attention to research.

ALPS showed that we should stop giving amiodarone for unwitnessed shockable cardiac arrest. The lead researcher is still trying to spin amiodarone for witnessed shockable cardiac arrest, even though the results do not show improvement in the one outcome that matters – leaving the hospital with a brain that still works.[1],[2],[3]

There is an excellent discussion of the study on the podcast by Dr. Salim Rezaie and Dr. Anand Swaminathan REBELCast: The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia.

One problem with the study that they do not address on the podcast is that the patients in the study appear to have had time to watch Casablanca before treatment started. Here’s looking at you, while we’re waiting, kid. This is apparently unintentional one way of doing a placebo washout. If we wait long enough . . . .
 

Time from arrival to start of infusion was 87 ± 21 min for procainamide and 115 ± 36 min for amiodarone patients (P = 0.58).[4]

 

If nothing else, this demonstrates how little we need to worry about immediately pushing drugs for stable monomorphic VT (V Tach or Ventricular Tachycardia). Should we expect much from antiarrhythmic treatment?

Research shows that for stable monomorphic VT (V Tach or Ventricular Tachycardia) amiodarone is not very likely to be followed by an improvement. Only 29%[5] or only 25%[6] or only 15% within 20 minutes, but if we don’t mind waiting an hour it can be as much as 29%.[7] For those of you who are not good at math, that means amiodarone is about the same as doing nothing, only it comes in a syringe. Even though these poor outcomes ignore the side effects, they are the best evidence in favor of amiodarone, so what Kool-Aid are the advocates drinking?

Adenosine, yes adenosine the SVT (SupraVentricular Tachycardia) drug, appears to be more effective at treating ventricular tachycardia than amiodarone – and adenosine is faster and safer than amiodarone.[8]

What if the patient becomes unstable? First start an IV (IntraVenous) line. Then sedate the patient. Then apply defibrillator pads. After the patient is adequately sedated, then cardiovert. We do not need the pads on the patient first. If it takes a while to put the pads on, that is a problem with the ability of the doctors and nurses, not a medical problem.

It does not appear as if any patient received amiodarone or procainamide until after waiting in the ED (Emergency Department) for over an hour. Were some patients cardioverted in well under an hour? Probably. The important consideration is that the doctors and nurses be able to apply the defibrillator pads properly and quickly and deliver a synchronized cardioversion in less than a minute. If the patient has not yet been sedated, the cardioversion should be delayed until after the patient is adequately sedated, so the intervention that depends most on time is the sedation of the patient.
 

VT + Amiodarone Cardioversion
 

Is there a better treatment than amiodarone? Sedate the patient before the patient becomes unstable, then cardiovert. How do the MACEs (Major Adverse Cardiac Events) compare with sedation and cardioversion vs. antiarrhythmic treatment.
 

5.4 Proarrhythmia
Amiodarone may cause a worsening of existing arrhythmias or precipitate a new arrhythmia. Proarrhythmia, primarily torsade de pointes (TdP), has been associated with prolongation, by intravenous amiodarone, of the QTc interval to 500 ms or greater. Although QTc prolongation occurred frequently in patients receiving intravenous amiodarone, TdP or new-onset VF occurred infrequently (less than 2%). Monitor patients for QTc prolongation during infusion with amiodarone. Reserve the combination of amiodarone with other antiarrhythmic therapies that prolong the QTc to patients with life-threatening ventricular arrhythmias who are incompletely responsive to a single agent.
[9]

 

All antiarrhythmic drugs can cause arrhythmias. In the absence of information about a specific problem that is best addressed by a specific drug (amiodarone is the opposite of specific), we should avoid treatments that have such a high potential for harm.

Amiodarone doesn’t even do a good job of preventing arrhythmias.
 

Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion.[10]

 

Is anything worse than amiodarone? Even epinephrine, yes epinephrine the inadequately tested cardiac arrest drug, has been followed by improved outcomes from V Tach after amiodarone failed.[11]
 

What is best for the patient?

Sedation, search for reversible causes, apply defibrillator pads, and be prepared to cardiovert.

Maybe sedation isn’t that important? This is by Dr. Peter Kowey, one of the top cardiologists in the world.
 

The man’s very first utterance was, “If it happens again, just let me die.”

As I discovered, the reason for this patient’s terror was that he had been cardioverted in an awake state. Ventricular tachycardia had been relatively slow, he had not lost consciousness, and the physicians, in the heat of the moment, had not administered adequate anesthesia. Although the 5 mg of intravenous diazepam had made him a bit drowsy, he felt the electric current on his chest and remembered the event clearly.

The patient’s mental state complicated the case considerably.[12]

 

How unimportant is sedation? How unimportant is consent?

For sedation, I would recommend ketamine, but etomidate was recommended in the podcast. Both work quickly and the most important obstacle to immediate treatment of a patient who suddenly deteriorates is the time to effect of sedation. Neither drug is expected to interfere with perfusion, which is the main excuse given for avoiding sedation for cardioversion.

This study is very small (not the fault of the authors), but it adds to the evidence that amiodarone is not a good first treatment for the patient.
 

Go listen to the podcast by Dr. Salim Rezaie and Dr. Anand Swaminathan REBELCast: The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia

 

Over the years, I have written a bit about cardioversion and the importance of sedation –

Cardioversion – I’m not doing that, you do it! – Mon, 24 Mar 2008

Cardioversion – 2010 ACLS – Part I – Mon, 25 Oct 2010

Cardioversion – 2010 ACLS – Part II – Sun, 31 Oct 2010

Cardioversion – 2010 ACLS – Part III – Thu, 11 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part I – Thu, 11 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part II – Fri, 12 Nov 2010

Synchronized Cardioversion Without Sedation – Part II Scallywag’s Response – Sun, 14 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part III – Tue, 16 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part IV – Wed, 24 Nov 2010

Comments on Cardioversion – 2010 ACLS – Part II – Mon, 16 Apr 2012
 

I have also written a bit about amiodarone –

Merit Badge Courses, Amiodarone, and tPA – Fri, 17 Sep 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part I – Wed, 01 Dec 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part II – Fri, 03 Dec 2010

Is Nexterone the Next Amiodarone? – Sat, 04 Dec 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part III – Mon, 06 Dec 2010

Where are the Black Box Warnings on These Drugs – I – Mon, 05 Dec 2011

Where are the Black Box Warnings on These Drugs – II – Sun, 11 Dec 2011

Is Amiodarone the Best Drug for Stable Ventricular Tachycardia – Wed, 14 Dec 2011

V Tach Storm – Part I – Wed, 28 Dec 2011

V Tach Storm – Part II – Thu, 29 Dec 2011

Nifekalant versus lidocaine for in-hospital shock-resistant ventricular fibrillation or tachycardia – Wed, 04 Jan 2012

NIH launches trials to evaluate CPR and drugs after sudden cardiac arrest – Sun, 29 Jan 2012

What Will Be the Next Standard Of Care We Eliminate – Wed, 28 Mar 2012

Happy Adenosine Day – Tue, 12 Jun 2012

Too Much Medicine and Evidence-Based Guidelines – Part I – Tue, 26 Jun 2012

Too Much Medicine and Evidence-Based Guidelines – Part II – Tue, 03 Jul 2012

Ondansetron (Zofran) Warning for QT Prolongation – is Amiodarone next? – Part I – Mon, 02 Jul 2012

Ondansetron (Zofran) Warning for QT Prolongation – is Amiodarone next? – Part II – Thu, 05 Jul 2012

Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium – Part I – Mon, 17 Sep 2012

Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium – Part II – Tue, 18 Sep 2012

How do we measure the QT segment when there are prominent U waves? – Thu, 13 Dec 2012

Woman with Risks for Torsades de Pointes Dying within Hours of Leaving the Emergency Department – Wed, 02 Jan 2013

Examples of Ventricular Tachycardia Caused by Amiodarone – Part I – Tue, 28 May 2013

Publication Bias – The Lit Whisperers – Tue, 11 Jun 2013

Standards Of Care – Ventricular Tachycardia – Wed, 31 Jul 2013

Footnotes:

[1] Dr. Kudenchuk is Misrepresenting ALPS as ‘Significant’
Tue, 12 Apr 2016
Rogue Medic
Article

[2] Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest
Mon, 04 Apr 2016
Rogue Medic
Article

[3] Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest.
Kudenchuk PJ, Brown SP, Daya M, Rea T, Nichol G, Morrison LJ, Leroux B, Vaillancourt C, Wittwer L, Callaway CW, Christenson J, Egan D, Ornato JP, Weisfeldt ML, Stiell IG, Idris AH, Aufderheide TP, Dunford JV, Colella MR, Vilke GM, Brienza AM, Desvigne-Nickens P, Gray PC, Gray R, Seals N, Straight R, Dorian P; Resuscitation Outcomes Consortium Investigators.
N Engl J Med. 2016 May 5;374(18):1711-22. doi: 10.1056/NEJMoa1514204. Epub 2016 Apr 4.
PMID: 27043165

CONCLUSIONS
Overall, neither amiodarone nor lidocaine resulted in a significantly higher rate of survival or favorable neurologic outcome than the rate with placebo among patients with out-of-hospital cardiac arrest due to initial shock-refractory ventricular fibrillation or pulseless ventricular tachycardia.

[4] Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study.
Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J; PROCAMIO Study Investigators.
Eur Heart J. 2016 Jun 28. pii: ehw230. [Epub ahead of print]
PMID: 27354046

Free Full Text from European Heart Journal.

[5] Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison.
Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, Ellinor PT.
Acad Emerg Med. 2010 Mar;17(3):297-306.
PMID: 20370763 [PubMed – indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine.

[6] Amiodarone is poorly effective for the acute termination of ventricular tachycardia.
Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, Ruskin JN.
Ann Emerg Med. 2006 Mar;47(3):217-24. Epub 2005 Nov 21.
PMID: 16492484 [PubMed – indexed for MEDLINE]

[7] Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment?
Tomlinson DR, Cherian P, Betts TR, Bashir Y.
Emerg Med J. 2008 Jan;25(1):15-8.
PMID: 18156531 [PubMed – indexed for MEDLINE]

[8] Adenosine for wide-complex tachycardia – diagnostic?
Thu, 23 Aug 2012
Rogue Medic
Article

[9] AMIODARONE HYDROCHLORIDE- amiodarone hydrochloride injection, solution
DailyMed
5 WARNINGS AND PRECAUTIONS
FDA Label

[10] Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction.
Kułakowski P, Karczmarewicz S, Karpiński G, Soszyńska M, Ceremuzyński L.
Europace. 2000 Jul;2(3):207-15.
PMID: 11227590 [PubMed – indexed for MEDLINE]

Free Full Text PDF + HTML from Europace

[11] Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia.
Bonny A, De Sisti A, Márquez MF, Megbemado R, Hidden-Lucet F, Fontaine G.
World J Cardiol. 2012 Oct 26;4(10):296-301. doi: 10.4330/wjc.v4.i10.296.
PMID: 23110246 [PubMed]

Free Full Text from PubMed Central.

[12] The calamity of cardioversion of conscious patients.
Kowey PR.
Am J Cardiol. 1988 May 1;61(13):1106-7. No abstract available.
PMID: 3364364

Kudenchuk PJ, Brown SP, Daya M, Rea T, Nichol G, Morrison LJ, Leroux B, Vaillancourt C, Wittwer L, Callaway CW, Christenson J, Egan D, Ornato JP, Weisfeldt ML, Stiell IG, Idris AH, Aufderheide TP, Dunford JV, Colella MR, Vilke GM, Brienza AM, Desvigne-Nickens P, Gray PC, Gray R, Seals N, Straight R, Dorian P, & Resuscitation Outcomes Consortium Investigators (2016). Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. The New England journal of medicine, 374 (18), 1711-22 PMID: 27043165

Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J, & PROCAMIO Study Investigators (2016). Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. European heart journal PMID: 27354046

Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, & Ellinor PT (2010). Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 17 (3), 297-306 PMID: 20370763

Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, & Ruskin JN (2006). Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Annals of emergency medicine, 47 (3), 217-24 PMID: 16492484

Tomlinson DR, Cherian P, Betts TR, & Bashir Y (2008). Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emergency medicine journal : EMJ, 25 (1), 15-8 PMID: 18156531

Kułakowski P, Karczmarewicz S, Karpiński G, Soszyńska M, & Ceremuzyński L (2000). Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology, 2 (3), 207-15 PMID: 11227590

Bonny A, De Sisti A, Márquez MF, Megbemado R, Hidden-Lucet F, & Fontaine G (2012). Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia. World journal of cardiology, 4 (10), 296-301 PMID: 23110246

Kowey PR (1988). The calamity of cardioversion of conscious patients. The American journal of cardiology, 61 (13), 1106-7 PMID: 3364364

.

Ketamine For Anger Management

 

I have been meaning to write about this ketamine study, but Greg Friese wrote about one of the comments on a review of the paper –
 

Most intriguing is this reader comment “talk to your damn patients calm them down and you can avoid this knee jerk, sedate first ask questions later whilst risking side effects, response ,that seems to be coming the norm” which seems disconnected to the actual syndrome of ExDS and the danger to medics, cops, and the patient when a patient’s behavior is out of control.[1]

 

Intriguing?
 

Tasmanian Devil - from outbackcooking dot blogspot dot com 1
 

The review was by Dr. Ryan Radecki of Emergency Medicine Literature of Note (the best quick and to the point reviews of research I know of on line). Did Dr. Radecki even suggest that we should avoid attempts at talking the patient down?
 

From the land of “we still have droperidol”, this case series details the use of ketamine as “rescue” treatment for “agitated delirium”. In lay terms, the situation they’re describing is the utterly bonkers patient being physically restrained by law enforcement for whom nothing else has worked.[2]

 

No.

Did the authors of the original paper suggest that we should avoid attempts at talking the patient down (verbal de-escalation)?
 

The sedation of agitated and aggressive patients in the emergency department (ED) and other acute care areas is a major problem for health care workers. Patients with acute behavioral disturbance may respond to verbal de-escalation or oral sedation, but a substantial proportion of this group requires parenteral sedation and mechanical restraint.1, 2, 3, 4, 5 [3]

 

No.

What about the studies cited above?

This is from one –
 

Combined pharmacological sedation and physical restraint were required on 66 (46%) occasions, pharmacological sedation alone on 20 (14%), physical restraint alone on 14 (10%) and neither on 43 (30%) occasions.[4]

 

30% of patients did not require physical and/or chemical restraint.

What does require mean?

How many patients can be managed by just talking them down? Should we avoid preparation for chemical and physical restraints, just because we are trying to talk the patient down?
 

There is indirect evidence from pharmacologic studies of agitation that verbal techniques can be successful in a substantial percentage of patients. In a recent study, patients were excluded from a clinical trial of droperidol if they were successfully managed with verbal de-escalation; however, the specific verbal de-escalation techniques were not identified or studied.12 [5]

 

Research on chemical management of excited delirium should not be interpreted as discouraging us from talking patients down.
 

Clinicians who work in acute care settings must be good multitaskers and tolerate rapidly changing patient priorities. In this environment, tolerating and even enjoying dealing with agitated patients takes a certain temperament, and all clinicians are encouraged to assess their temperament for this work.[5]

 

There is a lot of good information in the article, but approaching every patient with the expectation that verbal de-escalation will work is unrealistic. A lack of preparation sets everyone up for a worse outcome in the cases where verbal de-escalation does not work. Injuries and death become more likely, when we are not prepared to switch to sedation and have only physical restraint to respond to rapidly changing patient priorities.

We need to be able to adapt to the agitated patient. Verbal de-escalation and excited delirium do not get enough attention. This paper does not address the use of verbal de-escalation, because the enrolled patients had to fail to respond to other chemical sedation first. The patients who failed chemical sedation are also the ones who failed to respond to whatever attempts at verbal de-escalation were used.
 

Read the full paper on verbal de-escalation.

Footnotes:

[1] Sunday morning reader – coffee, ketamine, and EMS news
Everyday EMS Tips
by Greg Friese
March 6, 2016
Article

[2] Ketamine For Anger Management
Emergency Medicine Literature of Note
Friday, March 4, 2016
Posted by Ryan Radecki
Article

[3] Ketamine as Rescue Treatment for Difficult-to-Sedate Severe Acute Behavioral Disturbance in the Emergency Department.
Isbister GK, Calver LA, Downes MA, Page CB.
Ann Emerg Med. 2016 Feb 10. pii: S0196-0644(15)01562-0. doi: 10.1016/j.annemergmed.2015.11.028. [Epub ahead of print]
PMID: 26899459

[4] Structured team approach to the agitated patient in the emergency department.
Downes MA, Healy P, Page CB, Bryant JL, Isbister GK.
Emerg Med Australas. 2009 Jun;21(3):196-202. doi: 10.1111/j.1742-6723.2009.01182.x.
PMID: 19527279

[5] Verbal De-escalation of the Agitated Patient: Consensus Statement of the American Association for Emergency Psychiatry Project BETA De-escalation Workgroup.
Richmond JS, Berlin JS, Fishkind AB, Holloman GH Jr, Zeller SL, Wilson MP, Rifai MA, Ng AT.
West J Emerg Med. 2012 Feb;13(1):17-25. doi: 10.5811/westjem.2011.9.6864.
PMID: 22461917

Free Full Text from PubMed Central.

.

How Bad is the Evidence for the New 2015 ACLS Guidelines?

ResearchBlogging.org
 
    The new ACLS guidelines are out. How bad is the evidence?

    The short answer – The Advanced Cardiac Life Support guidelines could be worse.

How does the American Heart Association determine that a recommendation is not beneficial?
 

Class III: No Benefit, is a moderate recommendation, generally reserved for therapies or tests that have been shown in high-level studies (generally LOE A or B) to provide no benefit when tested against a placebo or control.[1]

 

The tobacco enema has been used successfully as a treatment for cardiac arrest, so the evidence of lack of benefit is poor.[2] Clearly, the Advanced Cardiac Life Support guidelines cannot claim that the tobacco enema is Class III. Successfully? The treatment was used and a dead person was no longer dead. In other words, just as successfully as most of the ACLS treatments.
 

From Eisenberg, MS. Life in the balance: emergency medicine and the quest to reverse sudden death. 1997; Oxford University Press. [betterworldbooks][3]

 

This is one way to make excuses for justify doing something just because of ideology. In the absence of good evidence of benefit, we should not harm our patients to protect our ideology. We used to do this with blood-letting, which was defended even after there was clear evidence of harm. That is just the best known example, but this dishonesty continues and continues to be defended.

Why don’t we hold anyone accountable, when we have the evidence that our treatments are harmful? Because we all seem to go along to get along.

The 2015 ACLS guidelines are not all bad, but they clearly do not encourage withholding harmful treatments until we have obvious evidence of harm. Should we assume that a treatment works just because the explanation appeals to some experts as much as the explanation for blood-letting appealed to the experts when that was in vogue?

This is not medicine. This is a fashion show. Our patients are the ones harmed.
 

Footnotes:

[1] 2015 AHA Classes of Recommendation
2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 2: Evidence Evaluation and Management of Conflicts of Interest
Development of the 2015 Guidelines Update
Circulation.
2015; 132: S368-S382
Free Full Text from Circulation.

[2] Tobacco smoke enemas
Ghislaine Lawrence
Volume 359, No. 9315, p1442,
20 April 2002
Lancet
Abstract with link to Full Text PDF download.

[3] Ever tried smoking?
by Chris Nickson
Life in the Fast Lane
Article

Morrison LJ, Gent LM, Lang E, Nunnally ME, Parker MJ, Callaway CW, Nadkarni VM, Fernandez AR, Billi JE, Egan JR, Griffin RE, Shuster M, & Hazinski MF (2015). Part 2: Evidence Evaluation and Management of Conflicts of Interest: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation, 132 (18 Suppl 2) PMID: 26472990
 

Lawrence, G. (2002). Tobacco smoke enemas The Lancet, 359 (9315) DOI: 10.1016/S0140-6736(02)08339-3

.

Will the Upcoming Pennsylvania Paramedic Protocols Eliminate Our Use of Not-So-Therapeutic Hypothermia?

 
Will Pennsylvania continue its trend of rejecting treatments that do not work and medicine that is not medicine?

One place to get a clear indication is the Post-resuscitation Care protocol, which has encouraged testing the ice waters of therapeutic hypothermia as an optional treatment that requires medical command orders. Backing away from further use of cold IV fluid for no known benefit to patients should be easy to do without political backlash from those more interested in doing something than in protecting patients from treatment for the sake of treatment.
 

Possible Medical Command Orders:

A. In adult patient, cold (4º C) NSS bolus of 20-30 mL/kg, if available, may be ordered if patient not following commands after ROSC from nontraumatic cardiac arrest.[1]

 

But wait.

      I know that therapeutic hypothermia works.

That is misleading. There is plenty of evidence that cooling patients in the hospital improves outcomes, but for prehospital patients the use of cold IV fluids has only been shown to improve outcomes for asystole/PEA (Pulseless Electrical Activity) patients and only in one study.[2]

For the patients most likely to survive cardiac arrest, the initial rhythm is V Fib (Ventricular Fibrillation). For these patients we need to stop the ice water infusions. Prehospital cold IV fluids following resuscitation of V Fib patients has been studied to death – more deaths in the treatment groups than in the no treatment groups. There has been no evidence of any benefit from IV ice water.[3],[4],[5]
 


Image credit.
 

This method of administration would probably be better for V Fib patients than IV ice water, because the adverse effects of IV ice water appear to be due to fluid overload.

I do not mean that prehospital therapeutic hypothermia is always a bad idea for V Fib patients – only that we need to find a way that is less harmful than dumping ice water into these recently dead patients for no benefit.
 


Click on image to make it larger.[3]
 

First, do no harm.

If the treatment is not beneficial, there is no good reason to expose patients to the adverse effects of the treatment for no known benefit.

Will we stop making excuses for endangering our patients with treatments that do not work?

Science teaches us to learn from our mistakes, while human nature encourages us to make excuses and continue to make the mistakes. Will we make the mistake of continuing to dump cold ice water into these recently dead patients for no good reason?

Footnotes:

[1] Post-Resuscitation Care
Pennsylvania Statewide ALS Protocols 2013
pp. 34-36 – 3080 – ALS – Adult/Peds
Protocols in PDF Download format.

[2] Induction of prehospital therapeutic hypothermia after resuscitation from nonventricular fibrillation cardiac arrest*.
Bernard SA, Smith K, Cameron P, Masci K, Taylor DM, Cooper DJ, Kelly AM, Silvester W; Rapid Infusion of Cold Hartmanns Investigators.
Crit Care Med. 2012 Mar;40(3):747-53. doi: 10.1097/CCM.0b013e3182377038.
PMID: 22020244 [PubMed – indexed for MEDLINE]

[3] Induction of therapeutic hypothermia by paramedics after resuscitation from out-of-hospital ventricular fibrillation cardiac arrest: a randomized controlled trial.
Bernard SA, Smith K, Cameron P, Masci K, Taylor DM, Cooper DJ, Kelly AM, Silvester W; Rapid Infusion of Cold Hartmanns (RICH) Investigators.
Circulation. 2010 Aug 17;122(7):737-42. doi: 10.1161/CIRCULATIONAHA.109.906859. Epub 2010 Aug 2.
PMID: 20679551 [PubMed – indexed for MEDLINE]

Free Full Text from Circulation.

[4] Effect of Prehospital Induction of Mild Hypothermia on Survival and Neurological Status Among Adults With Cardiac Arrest: A Randomized Clinical Trial.
Kim F, Nichol G, Maynard C, Hallstrom A, Kudenchuk PJ, Rea T, Copass MK, Carlbom D, Deem S, Longstreth WT Jr, Olsufka M, Cobb LA.
JAMA. 2013 Nov 17. doi: 10.1001/jama.2013.282173. [Epub ahead of print]
PMID: 24240712 [PubMed – as supplied by publisher]

Free Full Text from JAMA.

[5] Targeted temperature management at 33°C versus 36°C after cardiac arrest.
Nielsen N, Wetterslev J, Cronberg T, Erlinge D, Gasche Y, Hassager C, Horn J, Hovdenes J, Kjaergaard J, Kuiper M, Pellis T, Stammet P, Wanscher M, Wise MP, Åneman A, Al-Subaie N, Boesgaard S, Bro-Jeppesen J, Brunetti I, Bugge JF, Hingston CD, Juffermans NP, Koopmans M, Køber L, Langørgen J, Lilja G, Møller JE, Rundgren M, Rylander C, Smid O, Werer C, Winkel P, Friberg H; TTM Trial Investigators.
N Engl J Med. 2013 Dec 5;369(23):2197-206. doi: 10.1056/NEJMoa1310519. Epub 2013 Nov 17.
PMID:24237006[PubMed – indexed for MEDLINE]

Free Full Text from NEJM.

.

Dextrose in Cardiac Arrest – More Kitchen Sink Medicine

 
Should we treat hypoglycemia in a dead person?

How do we determine hypoglycemia in a dead person?

Is there any evidence that giving dextrose, in any concentration, will help to resuscitate a dead person?

Should we treat patients based on the philosophy of Who knows? Maybe it could work? Bleach enemas are currently in fashion among the alternative to medicine crowd,[1] so we could use the same reasoning to give bleach enemas in cardiac arrest. Who knows? Maybe it could work.

Is Kitchen Sink Medicine significantly different from any other alternative to medicine?

The dead person is not breathing, so we have to provide ventilations.[2], [3], [4]

The dead person is dead, so we have to do something.

We do compressions and (when indicated) defibrillation, because those are the only treatments that have been demonstrated to work.

 


 
 

The foundation of successful ACLS is high-quality CPR, and, for VF/pulseless VT, attempted defibrillation within minutes of collapse. For victims of witnessed VF arrest, early CPR and rapid defibrillation can significantly increase the chance for survival to hospital discharge.128–133 In comparison, other ACLS therapies such as some medications and advanced airways, although associated with an increased rate of ROSC, have not been shown to increase the rate of survival to hospital discharge.31,33,134–138 [5]

 

Ventilations are only a part of high-quality CPR for children and people who have a respiratory cause of cardiac arrest.

But what about dextrose for hypoglycemic cardiac arrest?

We may already be raising the blood sugar with epinephrine.
 

Epinephrine causes a prompt increase in blood glucose concentration in the postabsorptive state. This effect is mediated by a transient increase in hepatic glucose production and an inhibition of glucose disposal by insulin-dependent tissues.[6]

 

We seem to have trouble understanding that dead people do not respond to treatments the same way that living people do.
 

Pharmacologic insults are just so massive and normal metabolism and physiology so deranged that no mere mortal can make a meaningful intervention. The seriously poisoned who maintain vital signs in the ED have the best, albeit never guaranteed, chance of rescue from a modicum of antidotes and intensive supportive care.[7]

 

Maybe we should find out what we are doing and not blindly throw kitchen sinks at dead people based on hunches.

Dr. Brooks Walsh gave a good review of the evidence in his article written three years ago.[8]
 

What about my original questions?

Should we treat hypoglycemia in a dead person?

There is no evidence that giving dextrose is safe or effective for any cardiac arrest patients.

How do we determine hypoglycemia in a dead person?

We guess or check a capillary blood sugar, which is not reliable.

Is there any evidence that giving dextrose, in any concentration, resuscitates a dead person?

No.
 

Go read Using Dextrose in Cardiac Arrest at Mill Hill Ave Command.
 

Footnotes:

[1] Bleaching away what ails you
Science-Based Medicine
David Gorski
May 28, 2012
Article

[2] Cardiocerebral Resuscitation: An Approach to Improving Survival of Patients With Primary Cardiac Arrest.
Ewy GA, Bobrow BJ.
J Intensive Care Med. 2014 Jul 30. pii: 0885066614544450. [Epub ahead of print]
PMID: 25077491 [PubMed – as supplied by publisher]

[3] Cardiocerebral resuscitation is associated with improved survival and neurologic outcome from out-of-hospital cardiac arrest in elders.
Mosier J, Itty A, Sanders A, Mohler J, Wendel C, Poulsen J, Shellenberger J, Clark L, Bobrow B.
Acad Emerg Med. 2010 Mar;17(3):269-75.
PMID: 20370759 [PubMed – indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine.

[4] Cardiac Arrest Management is an EMT-Basic Skill – The Hands Only Evidence
Fri, 09 Dec 2011
Rogue Medic
Article

[5] Management of Cardiac Arrest
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8.2: Management of Cardiac Arrest
Overview
Free Full Text from Circulation.

[6] Effect of epinephrine on glucose metabolism in humans: contribution of the liver.
Sherwin RS, Saccà L.
Am J Physiol. 1984 Aug;247(2 Pt 1):E157-65.
PMID: 6380304 [PubMed – indexed for MEDLINE]

[7] 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

[8] Using Dextrose in Cardiac Arrest
Wednesday, March 14, 2012
Mill Hill Ave Command
Dr. Brooks Walsh
Article

.

Proposed 2015 ACLS Chest compression only CPR vs conventional CPR Recommendation


 
The AHA (American Heart Association) and ILCOR (International Liaison Committee On Resuscitation) 2015 resuscitation guidelines evidence reviews appear to be merely justifications for continuing to use treatments that do not improve survival with good neurological function, which is the only outcome that matters. What do the AHA and ILCOR intend to recommend for ventilation of patients who appear to be adults and pulseless due to non-respiratory conditions?
 

Full Question:
Among adults who are in cardiac arrest outside of a hospital (P), does provision of chest compressions (without ventilation) by untrained/trained laypersons (I), compared with chest compressions with ventilation (C), change Survival with Favorable neurological/functional outcome at discharge, 30 days, 60 days, 180 days AND/OR 1 year, Survival only at discharge, 30 days, 60 days, 180 days AND/OR 1 year, ROSC, bystander CPR performance, CPR quality (O)?
[1]

 

Do we really want to increase the rate of survival of permanently comatose patients?
 


Image credit.
 

That is not a goal. That is only a first step if we can do something to change the outcome for this comatose patient. There is no reason to believe that ventilations during CPR will do anything to improve the neurological outcome of these patients. We want to improve the survival of neurologically intact patients, not fill nursing homes with comatose patients until sepsis finishes them off.
 

We suggest performing chest compressions alone for trained laypersons if they are incapable of delivering airway and breathing manoeuvres to cardiac arrest victims (weak recommendation, very low quality of evidence).[1]

 

The AHA and ILCOR want us to provide this intervention that is based on tradition and disproven pathophysiology, rather than based on any valid evidence, except if we are incapable of providing the intervention.

Ventilations do not improve outcomes. However, ventilations may be harmful, so we should avoid using them in all cases where ventilations are not supported by valid evidence. Ventilations are not supported by valid evidence for non-respiratory causes of adult cardiac arrest.
 

We suggest the addition of ventilations for trained laypersons who are capable of giving CPR with ventilations to cardiac arrest victims and willing to do so (weak recommendation, very low quality of evidence).[1]

 

Each study cited to support ventilations showed no significant difference between compression only and standard CPR according to the AHA/ILCOR evidence review. That is the way to imitate Rube Goldberg. That is not support for any kind of medical intervention.
 

This recommendation places a relatively high value in [1] harm avoidance (not performing CPR or performing ineffective chest compressions and ventilations) and [2] simplifying resuscitation logistics, than potential benefit of an intervention of routine ventilations and compressions.[1]

 

That statement misrepresents harm avoidance and simplification of resuscitation logistics, since it encourages the potentially harmful treatment that has no valid evidence that the intervention increases any benefit that matters. How does adding ventilations simplify resuscitation logistics?

There is no evidence that passive ventilation provides inadequate oxygenation during chest compressions.

There is no evidence that passive ventilation provides inadequate removal of carbon dioxide during chest compressions.

Where is the need for any positive pressure ventilation to decrease blood return to the heart and increase the likelihood of vomiting?

Why continue to recommend doing something harmful for no benefit to the patient?

Footnotes:

[1] Chest compression only CPR vs conventional CPR
ILCOR Scientific Evidence Evaluation and Review System
Questions Open for Public Comment
Closing Date – February 28, 2015
Question page

.

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.

.

Should ACLS Recommend the Unknown Based on Weak Evidence?


 
The AHA (American Heart Association) and ILCOR (International Liaison Committee on Resuscitation) will be meeting tomorrow to finalize the recommendations for the 2015 ACLS (Advanced Cardiac Life Support) guidelines. Here is the comment I submitted on the proposed recommendation for epinephrine (Adrenaline in Commonwealth countries) in cardiac arrest.

I have not received any information about where to submit SEERS comments, so I am sending this to you. Please forward it to whomever is supposed to receive comments.

Vasopressors for cardiac arrest (1. Epi v Placebo)
 

Consensus on Science:
For all four long term (critical) and short term (important) outcomes, we found one underpowered trial that provided low quality evidence comparing SDE to placebo (Jacobs, 2001, 1138).
[1]

 

As a trial that is stated to be underpowered (through no fault of Dr. Jacobs),[2] is there any valid reason the Jacobs study should be considered to be superior to observational studies?
 

Among 534 subjects, there was uncertain benefit or harm of SDE over placebo for the critical outcomes of survival to discharge [RR 2.12, 95% CI 0.75-6.02, p=0.16] and good neurological outcome defined as CPC of 1-2 [RR 1.73, 95% CI 0.59-5.11, p=0.32].[1]

 

We do not have good evidence to tell us if this is harmful or beneficial and we do not have any way of determining which patients will be harmed or helped by administration of epinephrine.


 

However, patients who received SDE had higher rates of the two important outcomes of survival to admission [RR 1.95, 95% CI, 1.34-2.84, p=0.0004] and ROSC in the prehospital setting [RR 2.80, 95% CI 1.78-4.41, p<0.00001] compared to those who received placebo.[1]

 

Are these surrogate endpoints important?

How do we know?

If these surrogate endpoints are important, why is there no valid evidence to support this claim?

We have a history of being misled by surrogate endpoints. We used to bleed patients and that produced a number of clear benefits in surrogate endpoints.
 

Physicians observed of old, and continued to observe for many centuries, the following facts concerning blood-letting.

1. It gave relief to pain. . . . .

2. It diminished swelling. . . . .

3. It diminished local redness or congestion. . . . .

4. For a short time after bleeding, either local or general, abnormal heat was sensibly diminished.

5. After bleeding, spasms ceased, . . . .

6. If the blood could be made to run, patients were roused up suddenly from the apparent death of coma. (This was puzzling to those who regarded spasm and paralysis as opposite states; but it showed the catholic applicability of the remedy.)

7. Natural (wrongly termed ” accidental”) hacmorrhages were observed sometimes to end disease. . . . .

8. . . . venesection would cause hamorrhages to cease.[3]

 

We don’t do that any more, because medicine is not supposed to just create a superficial improvement.

We should not be making any recommendation to treat based on such weak evidence.
 

The evidence for the routine use of adrenaline is perceived to be at equipoise within the international community of resuscitation scientists requiring re-evaluation19 as suggested by this comprehensive systematic review and meta-analysis. There is a need for well-designed, placebo-controlled, and adequately powered RCTs to evaluate the efficacy of adrenaline and to determine its optimal dosing.11,16,54 The question as to the efficacy of adrenaline for OHCA remains unanswered.[4]

 

Since the question as to the efficacy of adrenaline for OHCA remains unanswered, we should avoid substituting a bad answer for We don’t know.

Maybe we should bring back the indeterminate class for these unanswerable questions.
 

Treatment Recommendation
Given the observed benefit in short term outcomes, we suggest Standard Dose Epinephrine be administered to patients in cardiac arrest.(weak recommendation, low quality)
[1]

 

The benefit is considered important, but that is just an expert opinion, which is the lowest level of evidence.

A weak recommendation to give a treatment of unknown benefit and unknown harm, based on evidence that is admitted to be of low quality, should not set the standard of care. Even if the guidelines are explicitly stated to not be standards of care, they are adopted as standards of care by the emergency medicine community and by the EMS community.

We don’t know enough to make a recommendation about epinephrine, or most other treatments, in cardiac arrest.

We do not need to keep making the same recommendation just because we have made it before. We can leave it up to the treating physician or to the medical director writing the protocols for EMS.
 
 

See also – Proposed 2015 ACLS Epinephrine Recommendation – Vasopressors for cardiac arrest (1. Epi v Placebo)

Footnotes:

[1] Vasopressors for cardiac arrest (1. Epi v Placebo)
ILCOR Scientific Evidence Evaluation and Review System
Questions Open for Public Comment
Closing Date – February 28, 2015
Question page

[2] Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL.
Resuscitation. 2011 Sep;82(9):1138-43. Epub 2011 Jul 2.
PMID: 21745533 [PubMed – in process]

Free Full Text PDF Download of In Press Uncorrected Proof from xa.yming.com

 

This study was designed as a multicentre trial involving five ambulance services in Australia and New Zealand and was accordingly powered to detect clinically important treatment effects. Despite having obtained approvals for the study from Institutional Ethics Committees, Crown Law and Guardianship Boards, the concerns of being involved in a trial in which the unproven “standard of care” was being withheld prevented four of the five ambulance services from participating.

 

In addition adverse press reports questioning the ethics of conducting this trial, which subsequently led to the involvement of politicians, further heightened these concerns. Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate.

 

[3] Blood-Letting
Br Med J.
1871 March 18; 1(533): 283–291.
PMCID: PMC2260507

[4] Adrenaline for out-of-hospital cardiac arrest resuscitation: a systematic review and meta-analysis of randomized controlled trials.
Lin S, Callaway CW, Shah PS, Wagner JD, Beyene J, Ziegler CP, Morrison LJ.
Resuscitation. 2014 Jun;85(6):732-40. doi: 10.1016/j.resuscitation.2014.03.008. Epub 2014 Mar 15.
PMID: 24642404 [PubMed – in process]

.