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

- Rogue Medic

2016 – Amiodarone is Useless, but Ketamine Gets Another Use

amiodarone-edit-1
 

I didn’t write a lot in 2016, but 2016 may have been the year we put the final nail in the coffin of amiodarone. Two major studies were published and both were very negative for amiodarone.

If we give enough amiodarone to have an effect on ventricular tachycardia, it will usually be a negative effect.[1]

Only 38% of ventricular tachycardia patients improved after amiodarone, but 48% had major adverse cardiac events after amiodarone.

There are better drugs, including adenosine, sotalol, procainamide, and ketamine for ventricular tachycardia. Sedation and cardioversion is a much better choice. Cardioversion is actually expected after giving amiodarone.

For cardiac arrest, amiodarone is not any better than placebo or lidocaine. What ever happened to the study of amiodarone that was showing such wonderful results over a decade ago? It still hasn’t been published, so it is reasonable to conclude that the results were negative for amiodarone. It is time to make room in the drug bag for something that works.[2],[3]

On the other hand, now that we have improved the quality of CPR by focusing on compressions, rather than drugs, more patients are waking up while chest compressions are being performed, but without spontaneous circulation, so ketamine has another promising use. And ketamine is still good for sedation for intubation, for getting a patient to tolerate high flow oxygen, for agitated delirium, for pain management, . . . .[4],[5]

Masimo’s RAD 57 still doesn’t have any evidence that it works well on real patients.[6]

When intubating, breathe. Breathing is good. Isn’t inability to breathe the reason for intubation?[7]

Footnotes:

[1] The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia
Wed, 17 Aug 2016
Rogue Medic
Article

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

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

[4] What do you do when a patient wakes up during CPR?
Tue, 08 Mar 2016
Rogue Medic
Article

[5] Ketamine For Anger Management
Sun, 06 Mar 2016
Rogue Medic
Article

[6] The RAD-57 – Still Unsafe?
Wed, 03 Feb 2016
Rogue Medic
Article

[7] Should you hold your breath while intubating?
Tue, 19 Jan 2016
Rogue Medic
Article

.

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

.

What do you do when a patient wakes up during CPR?

ResearchBlogging.org
 

The return of consciousness without the return of a pulse is still rare, but may be more common with our increased focus on high quality chest compressions. There is still no evidence that interrupting chest compressions, for anything other than defibrillation, improves outcomes.

Is this due to the consistency of the machine? Maybe. Maybe not. We do not have enough evidence to draw that conclusion.

Is this growing population really growing? Maybe. Maybe not. We do not have enough evidence to draw that conclusion, either.

It could be that with the ability to use a cell phone camera to record these instances, there is more credibility to the reports. There is a suggestion that this could be common.
 

Parnia et al. conducted a multi-year, multi-center, prospective study of the frequency of awareness during resuscitation by interviewing cardiac arrest survivors after discharge. They found 55/140 (39%) had perceptions of awareness of being alive and even memories that originated during that time.2 [1]

 

Should we be giving ketamine to these patients?
 

Nebraska EMS CPR Sedation Protocol - ALS
Nebraska CPR Induced Consciousness Sedation Protocol (from the PDF)[1]
 

We should find out how common it is for people to regain consciousness without regaining a pulse. This is clearly an experimental protocol that is not supported by evidence of improved outcomes that matter – just like all of the rest of cardiac arrest treatment that is not compressions or defibrillation.
 

RESULTS: The search yielded 1997 unique records, of which 50 abstracts were reviewed. Nine reports, describing 10 patients, were relevant. Six of the patients had CPR performed by mechanical devices, three of these patients were sedated. Four patients arrested in the out-of-hospital setting and six arrested in hospital. There were four survivors. Varying levels of consciousness were described in all reports, including purposeful arm movements, verbal communication, and resuscitation interference. Management strategies directed at consciousness were offered to six patients and included both physical and chemical restraints.[2]

 

6/1,997 is 0.3% – not anywhere near the 39.3% of 55/140, but it is still a large enough group that we should not ignore them.

Depression and anxiety following resuscitation are significant problems, so this might even be a way to help decrease those resuscitation side effects.
 

CONCLUSION:
One fourth of OHCA-survivors reported symptoms of anxiety and/or depression at 6 months which was similar to STEMI-controls and previous normative data. Subjective cognitive problems were associated with an increased risk for psychological distress. Since psychological distress affects long-term prognosis of cardiac patients in general it should be addressed during follow-up of survivors with OHCA due to a cardiac cause.
[3]

 

The similarity to the outcome of STEMI (ST segment Elevation Myocardial Infarction) patients do not inspire confidence in this approach, but that does not mean that it should not be examined.

It is most important that we not make the mistake that has been made with ventilations, endotracheal tubes, extraglottic airways, antiarrhythmic drugs, pressor drugs, anti-acidosis drugs, antidote drugs, anti-hypoglycemic drugs, et cetera. We should insist that there be valid evidence of some sort of benefit before the ACLS (Advanced Cardiac Life Support) Committee of Failed Treatments adds this to the ACLS algorithms because of an abundance of wishful thinking.
 

This time will be different.
 

This use of ketamine is interesting. Ketamine is a sedative that should not depress vital signs, so it may do what we expect. There may be more benefit than harm, but there may be more harm than benefit, or there may be all harm and no benefit. We will not know until we have valid research.

We have added the other treatments without finding out if they improve outcomes. We continue to remove these treatments as we obtain evidence, because they have one thing in common – they don’t improve outcomes.

These treatments have increased the ignorance of those who work in EMS (Emergency Medical Services) and EM (Emergency Medicine). We keep convincing ourselves that we know what we are doing, but evidence keeps showing that we are lying to ourselves.

Maybe ketamine sedation during compressions will be beneficial. It is such a small patient population, that it will be difficult to study. Introducing a treatment without studying it will always be a mistake. Is Nebraska studying this? Probably, but it is not stated in the paper. Has this been approved by an IRB (Institutional Review Board)? I do not know.

Footnotes:

[1] CPR induced consciousness: It’s time for sedation protocols for this growing population
Rice, D., Nudell, N., Habrat, D., Smith, J., & Ernest, E. (2016). Resuscitation DOI: 10.1016/j.resuscitation.2016.02.013
Free Full Text from Resuscitation.

[2] Return of consciousness during ongoing cardiopulmonary resuscitation: A systematic review.
Olaussen A, Shepherd M, Nehme Z, Smith K, Bernard S, Mitra B.
Resuscitation. 2015 Jan;86:44-8. doi: 10.1016/j.resuscitation.2014.10.017. Epub 2014 Nov 4. Review.
PMID: 25447435

[3] Anxiety and depression among out-of-hospital cardiac arrest survivors.
Lilja G, Nilsson G, Nielsen N, Friberg H, Hassager C, Koopmans M, Kuiper M, Martini A, Mellinghoff J, Pelosi P, Wanscher M, Wise MP, Östman I, Cronberg T.
Resuscitation. 2015 Dec;97:68-75. doi: 10.1016/j.resuscitation.2015.09.389. Epub 2015 Oct 9.
PMID: 26433116

Rice, D., Nudell, N., Habrat, D., Smith, J., & Ernest, E. (2016). CPR induced consciousness: It’s time for sedation protocols for this growing population Resuscitation DOI: 10.1016/j.resuscitation.2016.02.013

Olaussen A, Shepherd M, Nehme Z, Smith K, Bernard S, & Mitra B (2015). Return of consciousness during ongoing cardiopulmonary resuscitation: A systematic review. Resuscitation, 86, 44-8 PMID: 25447435

Lilja G, Nilsson G, Nielsen N, Friberg H, Hassager C, Koopmans M, Kuiper M, Martini A, Mellinghoff J, Pelosi P, Wanscher M, Wise MP, Östman I, & Cronberg T (2015). Anxiety and depression among out-of-hospital cardiac arrest survivors. Resuscitation, 97, 68-75 PMID: 26433116

.

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.

.

Is It Wrong To Medicate To The Point Of Needing Ventilation – Question from mpatk


Image credit.
 

In the comments to Where is the Line Between Good Pain Management and Bad, mpatk write the following –
 

To clarify, would you consider it acceptable to sedate to the point of requiring assisted ventilation for a sufficiently painful injury (e.g. multiple long bone fx’s)?

 

I have not needed to ventilate any of these patients, but I have added oxygen to keep some patients’ oxygen saturation above 93%.

Would it be wrong to medicate to the point of needing to ventilate?

There was a time when I would have taken the position that this is an indication of bad pain management/bad sedation, but I no longer agree with that.

We are there to provide appropriate care for the patient, not appropriate care for the patient up to the point of needing to assist with ventilation.

Most medical directors will probably disagree with me, but medical directors are getting better at encouraging appropriate pain management and sedation.

You, and I, do not have access to ketamine, but ketamine would be the ideal drug for many painful injuries. Ketamine provides sedation, analgesia, and dissociation, but generally does not cause any respiratory depression. Ketamine can occasionally cause laryngospasm, but that is easy to manage. I need to follow up on some earlier posts on ketamine and laryngospasm.[1],[2],[3]

But we do not have ketamine. should our patients suffer because we do not have the best drug for these patients?

No.

What is going to happen in the hospital?

The patient is going to need surgery, which generally involves ventilation through an endotracheal tube, or an LMA (Laryngeal Mask Airway). We could anticipate that and place an airway for ventilation.

We could give tiny titrated doses of naloxone (for suspected opioid-induced hypoventilation) and/or tiny titrated doses of flumazenil (for suspected benzodiazepine-induced hypoventilation).

This problem is not a lack of oxygenation, because we could treat that with a higher concentration of oxygen. This is a problem of inadequate removal of CO2 (Carbon DiOxide), or it is a combined problem of hypoxia and hypercarbia.

There is a discussion of procedural sedation by Dr. Al Sacchetti that is essential listening for anyone who provides sedation and/or pain management.[4]

Why should paramedics listen to this? Because this is important material to understand to be good at sedation and pain management.

Pay attention to the whole presentation, because Dr. Sacchetti makes some excellent points.

Most relevant to what I am writing is what he says from 27:00 to 28:15.

Would an LMA have been more appropriate? Maybe. Maybe not.

At 29:30 Dr. Sacchetti says –
 

The medication with the lowest complication rate is . . .
 
Propofol (Diprivan)?

Midazolam (Versed)?

Ketamine (Ketalar)?

Morphine?

Hydromorphone (Dilaudid)?

Fentanyl (Sublimaze)?

What do you think was the safest drug (lowest complication rate)?
 

 

 

 

 

 

 

 

 

 

ketamine.
 

Zero major complications.
 

At 30:00 he puts the safety of fentanyl and etomidate (EMS medications) in perspective, when compared with ketamine and propofol, which are often considered too dangerous for EMS.
 

Fentanyl has the highest complication rate followed by etomidate.
 


This list is in alphabetical order, not in order of complications, or number of patients, or . . . .
 

Perspective is important.

Airway management skill is essential.

Limiting EMS to the least safe medications does not protect patients.

Footnotes:

[1] Laryngospasm, hypoxia, excited delirium, and ketamine – Part I
Thu, 21 Jun 2012
Rogue Medic
Article

[2] Laryngospasm, hypoxia, excited delirium, and ketamine – Part I
Mon, 25 Jun 2012
Rogue Medic
Article

[3] Serious adverse events during procedural sedation with ketamine – Part I
Thu, 27 Sep 2012
Rogue Medic
Article

[4] Al Sacchetti: Procedural Sedation in the Community ED
April 28, 2010
Free Emergency Medicine Talks
Al Sacchetti
Page with free download of presentation in mp3 format.

The reference is to the ProSCED registry, which is described in the papers below – both are free.

Procedural sedation in the community emergency department: initial results of the ProSCED registry.
Sacchetti A, Senula G, Strickland J, Dubin R.
Acad Emerg Med. 2007 Jan;14(1):41-6. Epub 2006 Aug 31.
PMID: 16946280 [PubMed – indexed for MEDLINE]

Page With Free Full Text in PDF Download format from Academic Emergency Medicine. Click on Get PDF (97K).
 

The safety of single-physician procedural sedation in the emergency department.
Hogan K, Sacchetti A, Aman L, Opiela D.
Emerg Med J. 2006 Dec;23(12):922-3.
PMID: 17130600 [PubMed – indexed for MEDLINE]

Free Full Text from PubMed Central.

.

Face Down Restraint into a Pillow


 

This picture just shows one image from one direction at one instant. A 12 lead ECG provides much more data and many more perspectives.

but . . . .

What it appears to show raises some questions.
 

P is for pillow – best part of paramedic school.

The pillow may not completely obstruct the airway, but this is probably not part of their protocols.
 

The patient’s hands have a bit of a cyanotic appearance, but the ears do not, so I suspect that the hands are discolored due to wrist restraints, not the pillow airway maneuver.

Glove use is fantastic, although there is no apparent need for gloves, but Scene safety, BSI then airway?

Why is the patient is restrained? Probably some charm deficit.

The side of the ambulance has Advanced Life (and maybe Support outside of the image) written on the side, so they should have access to chemical restraints – charm in a syringe.

Are any medications being used for chemical restraint?

Have any medications been used for chemical restraint?

Do protocols allow for any chemical restraint?
 

If you do not think that chemical restraint is important – to protect us and to protect the patient – listen to the EMS EduCast Excited Delirium episode.[1]

After listening to the podcast, imagine how this picture might be used to persuade a jury that you are guilty of murder or negligent homicide.
 

And this is a good time to remind everyone that K is for ketamine – the fastest IM (IntraMuscular) chemical restraint drug we have (after succinylcholine [suxamethonium in Commonwealth countries]). Even laryngospasm should not produce more of an airway problem and laryngospasm is manageable.[2]
 

 

Since one of the reasons for chemical restraint is to protect the patient, since in custody deaths may be die to excited delirium, and restraint asphyxia is one possible cause, why is the airway apparently not being addressed more aggressively?

Only one person is holding a violent patient down?

If one person is capable of restraining the patient, all by himself and with just one knee, is that a good sign?

On the plus side – at least he isn’t hog tied.

Does anyone want to guess at the patient’s heart rate?

Maybe that is the next thing to be done. We cannot tell, but all we can do is guess at the heart rate.
 

The pathogenesis of excited delirium deaths is likely multifactorial and includes positional asphyxia, hyperthermia, drug toxicity, and/or catecholamine-induced fatal arrhythmias. We suggest that these deaths are secondary to stress cardiomyopathy similar to the cardiomyopathy seen in older women following either mental or physical stress.[3]

 

Sedation is my friend.

Sedation is the patient’s friend.

If I cannot handle an overly sedated person, I should not be working in EMS.

Over-sedation (under-stimulation) is a small, but easy to manage problem.

Under-sedation (over-stimulation) is a big problem complicated by a failure to understand the relative risks.

Maybe this is the rhythm –
 


 

Maybe this is the rhythm –
 


 

Maybe it is some other rhythm.

We don’t know.

We can’t tell.
 

It’s all about the little things.

Airway?

Breathing?

Circulation?

All appear to be mysteries for this patient.

Face down restraint is a bad idea.

Obstructing the airway is a bad idea – even if the patient is spitting.
 

How’s that airway?

P is for pillow!
 

Footnotes:

[1] Excited Delirium: Episode 72 EMS EduCast
EMS EduCast
September 23, 2010
Web page with link to podcast

While on the topic of podcasts, Dr. Scott Weingart provides the view of the emergency physician on chemical restraint.

Podcast 060 – On Human Bondage and the Art of the Chemical Takedown
by EMCRIT
November 13, 2011
Podcast and page with research links

[2] Laryngospasm, hypoxia, excited delirium, and ketamine – Part I
Thu, 21 Jun 2012
Rogue Medic
Article

[3] Excited delirium, restraints, and unexpected death: a review of pathogenesis.
Otahbachi M, Cevik C, Bagdure S, Nugent K.
Am J Forensic Med Pathol. 2010 Jun;31(2):107-12. Review.
PMID: 20190633 [PubMed – indexed for MEDLINE]
 

Unexpected deaths periodically occur in individuals held in police custody. These decedents usually have had significant physical exertion associated with violent and/or bizarre behavior, have been restrained by the police, and often have drug intoxication. Autopsy material from these cases may not provide a satisfactory explanation for the cause of death, and these deaths are then attributed to the excited delirium syndrome. The pathogenesis of excited delirium deaths is likely multifactorial and includes positional asphyxia, hyperthermia, drug toxicity, and/or catecholamine-induced fatal arrhythmias. We suggest that these deaths are secondary to stress cardiomyopathy similar to the cardiomyopathy seen in older women following either mental or physical stress. This syndrome develops secondary to the toxic effects of high levels of catecholamines on either cardiac myocytes or on the coronary microvasculature. Patients with stress cardiomyopathy have unique ventricular morphology on echocardiograms and left ventricular angiography and have had normal coronary angiograms. People who die under unusual circumstances associated with high catecholamine levels have contraction bands in their myocardium. Consequently, the pathogenesis of the excited delirium syndrome could be evaluated by using echocardiograms in patients brought to the emergency centers, and by more careful assessment of the myocardium and coronary vessels at autopsy. Treatment should focus on prevention through the reduction of stress.

 

.

What Can EMS Expect From 2014? #1 Ketamine Again


 

What changes need to be made in 2014, if they have not already been made?

Ketamine – for those of you who already have ketamine, great work. Continue to improve patient care. Do not let the rest of us slow you down.

Excited delirium – ketamine is the fastest way to sedate a violent patient.

Pain management – ketamine dissociates without respiratory depression.

RSI (Rapid Sequence Induction/Intubation) – ketamine dissociates without respiratory depression.

Asthma – ketamine opens the airway.

Awake intubation – ketamine dissociates without respiratory depression.

Sedation for extrication – ketamine dissociates without respiratory depression.

Seizures– ketamine stops seizures.
 

Safety – ketamine is safe.
 

Ketamine has a wide margin of safety; several instances of unintentional administration of overdoses of ketamine (up to ten times that usually required) have been followed by prolonged but complete recovery.[1]

 

Is any other sedative that safe?
 

Here are some podcasts to explain in more detail.

Dr. Mel Herbert on ketamine.
Ketamine Update.
Free mp3 Download From Free Emergency Medicine Talks

Dr. Baruch Krauss on ketamine.
Ketamine in the Emergency Department.
Free mp3 Download From Free Emergency Medicine Talks

Dr. Sergey Motov on ketamine.
Ketamine for Everything.
Free mp3 Download From Free Emergency Medicine Talks

Dr. Scott Weingart on ketamine.
Podcast 104 – Laryngoscope as a Murder Weapon Series – Hemodynamic Kills
Page with a link to the free mp3 download, but watch the video first – it is excellent.

More from Dr. Weingart.
EMCrit Podcast 40 – Delayed Sequence Intubation (DSI)
Free mp3 DownloadFrom EMCrit.

Dr. Jim DuCanto on ketamine.
Podcast 73 – Airway Tips and Tricks with Jim DuCanto, MD
Page with a link to the free mp3 download, but watch the video first – it is excellent.

Dr. Minh LeCong on ketamine myths –

PHARM Podcast 75 Ketamine MythBusters
Part 1 – Blowing your mind

PHARM Podcast 76 Ketamine MythBusters
Part 2 – Take the pressure down

PHARM Podcast 77 Ketamine MythBusters
Part 3 – Are you mad enough?

PHARM Podcast 78 Ketamine MythBusters
Part 4 – A fitting end?

 

Would you prefer to have something to read about ketamine?
 

 

Dr. Reuben Strayer on ketamine.

The Ketamine Brain Continuum
December 25th, 2013
by reuben in PSA & analgesia
Article

Awake Intubation: A Very Brief Guide
July 7th, 2013
by reuben in airway
Article

Ketamine as a suicidality reversal agent
June 4th, 2011
by reuben in psychiatry
Article

Taming the Ketamine Tiger
January 27th, 2011
by reuben in PSA & analgesia
Article

Ketamine for RSI in Head Injury
April 3rd, 2010
by reuben in .trauma-general, .trauma-head & face, airway
Article

Another reason to use ketamine for RSI in sepsis
November 24th, 2009
by reuben in airway
Article
 

Is there any good reason to not be using ketamine in EMS?

Footnotes:

[1] Ketamine Hydrochloride (ketamine hydrochloride) Injection, Solution, Concentrate
[Bedford Laboratories]

FDA Label
DailyMed
Label

.

Further Details on ‘Ambulance Mistake Killed Teen After Skateboard Accident’


Image credit.
 

Thank you to Michael Berrier for providing a link to a much more detailed account of what I wrote about in Ambulance Mistake Killed Teen After Skateboard Accident.
 

It (the law suit) alleges the hospital and/or it employees: “failed to keep Drew Hughes properly sedated and restrained; failed to properly re-intubate Andrew Davis Hughes during the transport; failed to perform standard objective tests to verify proper placement of the endotracheal tube; failed to recognize clear signs and symptoms of an esophageal intubation and respond to those signs; attempted to falsify the medical records to cover up their negligence; failed to use their best judgment in the treatment of Drew Hughes; failed to use reasonable care and diligence in the treatment of Drew Hughes and in the application of their knowledge and skill to the care of Drew Hughes; failed to possess the required skill and learning to treat Drew Hughes; failed to practice within the standard of care for respiratory therapists, nurses and/or paramedics in the same or similar communities; and were negligent in such other respects as may be shown at trial.”[1]

 

I mentioned almost all of those problems in what I wrote based on the much more limited information in the article[2] I had read. I missed attempted to falsify the medical records to cover up their negligence; and several of the comments mentioned physical restraints (which I did not mention) in addition to chemical restraint.

Was I so accurate because I am psychic?

No.

Airway disasters happen in predictable ways.

When people fail to recognize an esophageal intubation, it is not difficult to figure out why it happened.

If I were to write about a ball rolling to the edge of a table and falling due to gravity, it would be a similarly predictable scenario.

Airway disasters happen in predictable ways.

There was a failure of assessment, which is also a major part of how the tube was removed in the first place. Proper assessment should have prevented the need for re-intubation.
 

Going back to the beginning, a series of choices led up to the apparently very preventable death of a child.
 

A CT of the head was normal but doctors suspected a possible basilar skull fracture,[1]

 

Intubation seems extreme as prophylaxis for a possible basilar skull fracture without evidence of injury by CT (Competerized Tomographic scan), but there may have been a good reason.

The gold standard for airway protection is not intubation, but the patient protecting his own airway.

Was there some reason to believe that the patient would not be able to protect his airway for the entire trip to the trauma center?
 

The article mentions that the respiratory therapist . . .
 

. . . had been licensed for less than a year at this time and was not properly trained or adequately experienced in intubating a patient outside of a hospital setting.[1]

 

The next paragraph mentions stopping to pick up a paramedic, who then drove the ambulance.

Was the paramedic supposed to handle intubation?

Was the paramedic supposed to handle intubation while driving?

That would indicate great skill, but incredibly bad judgment.

Here is the timeline –
 

11:10                   Ambulance leaves the hospital.

??:??                   Paramedic is picked up.

11:15                   Sedation wears off and tube is pulled out.
 

Did the crew change distract everyone from recognizing the signs of lack of sedation?

Was the patient on a drip, which should have been adjusted up for the increased stimulation of an ambulance ride bouncing down the road in a truck?

Did the hospital just discontinue sedation because they have failed to consider the patient’s needs once the patient is out of their bed?

Was the crew supposed to provide bolus sedation en route?

Were they provided with broad enough orders and enough sedative for the ride?
 

And –

They were within 5 minutes of the sending hospital.

Why didn’t they turn around and head back?

If there are complications, the hospital has more resources to deal with those complications.

Clearly, the plan they were following was not remotely a success.

They had left the hospital, stopped to switch crew members and drivers, and the patient had burned through his sedative and pulled his tube out.

They should still have been able to see the hospital, unless there were a lot of trees, buildings, or something else blocking their view.

What were they thinking?

Things can only get better?

Things did not get better.
 

11:43                   They arrived at the trauma center. Late entry 04:10 11/15/2013 – They diverted to a closer hospital. They did not reach the trauma center until much later.
 

It appears that they could have taken the patient out of the ambulance and pushed the patient back to the sending hospital in less time – without decreasing the quality of care provided.
 

(The paramedic) pulled the ambulance off the road and, according to the ambulance report, all four crew members worked to suction and re-intubate Drew with (the respiratory therapist) being primarily responsible for the attempted re-intubation,” the complaint continues. “Drew was given paralytics and sedatives, which meant he could not breathe on his own. He was completely dependent on the oxygen from the endotracheal tube. Drew was intubated into his esophagus rather than his trachea and was not receiving oxygen and could no longer breathe on his own. At the time of the re-intubation, Drew’s parents were parked in their car immediately behind the ambulance.[1]

 

Within 5 minutes of the hospital.
 

“The crew never used objective testing, such as colormetric testing or capnography, to verify that the endotracheal tube was in his lungs and not his esophagus.[1]

 

Why is anyone still using colorimetry?

It is litmus paper that provides false positive and false negative results that many users fail to recognize as erroneous.

Moisture ruins it and there is moisture in every breath exhaled from human lungs.

Exhalation of moisture is the reason some people use moisture in the tube as an indication of proper tube placement. What they fail to realize is that moisture can also come out of the esophagus, so this is not of much help in confirming tube placement.

The only justification for the colorimetry litmus paper is if there is a malfunction of the waveform capnography that prevents the use of waveform capnography.

According to the article, the crew did not even try to use that inadequate method of tube confirmation.
 

In the comments to my original post, Christopher Watford points out –
 

In NC (this happened in North Carolina), waveform capnography is required on all RSI’s

 

RSI is Rapid Sequence Induction/Intubation – an intubation involving the use of sedatives and paralytics. The intubation in the ambulance is described as using both.

Required, but not used.
 

“Almost as soon as the attempted re-intubation was done, Drew’s heart rate began to drop and they could not find a pulse.[1]

 

What does PALS (Pediatric Advanced Life Support) state about the sudden deterioration of an intubated patient?
 

Reevaluate tracheal tube position and patency in patients who remain agitated despite effective mechanical ventilatory support and each time the patient is moved, such as into or out of a transport vehicle. If the condition of an intubated patient deteriorates, consider several possibilities that can be recalled by the mnemonic DOPE: Displacement of the tube from the trachea, Obstruction of the tube, Pneumothorax, and Equipment failure. If tracheal tube position and patency are confirmed and mechanical ventilation failure and pneumothorax are ruled out, the presence of agitation may require analgesia for pain control (eg, fentanyl or morphine) and/or sedation for confusion, anxiety, or agitation (eg, lorazepam, midazolam, or ketamine).[3]

 

The response should be very simple and obvious –

Pull the tube and ventilate with a BVM.
 


 

If deterioration is due to Displacement, the patient should improve.

If deterioration is due to Obstruction, the patient should improve.

If deterioration is due to Equipment failure, the patient should improve.

If the patient does not improve, that leaves Pneumothorax and the patient should have large bore needles of adequate length to reach the lungs stuck into both sides of the chest to decompress the apparent tension Pneumothorax.

If things deteriorate, we need to become very aggressive very quickly. This is one reason why a prophylactic intubation for transport may be a bad idea.
 

According to the ambulance records, at approximately 11:25 p.m., Andrew’s heart rate is in the 30s and he has no pulse. CPR was started and epinephrine was given.[1]

 

Pediatric bradycardia should automatically suggest one problem much more than any other problem.

Epinephrine does not treat hypoxia. The problem was not a lack of epinephrine.
 

In general, pediatric out-of-hospital arrest is characterized by a progression from hypoxia and hypercarbia to respiratory arrest and bradycardia and then to asystolic cardiac arrest.2 17 18 Therefore, a focus on immediate ventilation and compressions, rather than the “adult” approach of immediate EMS activation or defibrillation, appears to be warranted. In this age group, early effective ventilation and oxygenation must be established as quickly as possible.[3]

 

Four people in the back of the ambulance. Three of them should have taken PALS, or been familiar with the material covered in PALS.

PALS repeatedly recommends BVM ventilation.

Why?

Hypoxia -> Bradycardia -> Cardiac Arrest – > Brain Death.

BVM ventilation can interrupt that deterioration.

Ventilation can prevent the deterioration to bradycardia.

Ventilation can prevent the deterioration to cardiac arrest.

Ventilation can prevent the deterioration to brain death.
 


 

The tube does not appear to have been removed for BVM ventilation.

What would we expect to see if the patient had been ventilated with a BVM prior to losing pulses?

An increase in heart rate.

What would we expect to see if the patient had been ventilated with a BVM after losing pulses?

An increase in heart rate and ROSC (Return Of Spontaneous Circulation).

These improvements would not always happen, but they are the most likely to happen with ventilation.
 

Things get even worse
 

“According to the records a shock is given with a defibrillator at 11:38 p.m.,” the complaint alleges. “CPR was continued. Drew’s heart rate was in the 40s. More epinephrine was given. During this time, the emergency room physician at Carteret General was called to get permission to give Amiodarone. The emergency room physician told the crew to recheck the tube and suction because the arrest may be respiratory related. The crew again failed to verify the tube placement.”[1]

 

I am calling for orders.

I receive orders to do the most important and most obvious assessment – an assessment I should have done over 20 minutes ago – an assessment that should be continued throughout transport, I but still have not done it.

I ignore the orders.

Panic? Tunnel vision?

I see what I want to see – a cardiac arrest that indicates that it is time to give another drug.

I continue to ignore the reassessment that is part of the algorithm.
 

According to the complaint, “The ambulance was diverted to CarolinaEast in New Bern because Drew’s condition was deteriorating. They arrived at Carolina East at 11:43 p.m. according to the ambulance records.[1]

 

Timeline of events –
 

11:10                   Ambulance leaves the hospital.

??:??                   Paramedic is picked up.

11:15                   Sedation wears off and tube is pulled out.

11:25                   Cardiac arrest (tube probably in esophagus).

11:30                   Still dead (tube probably in esophagus).

11:35                   Still dead (tube probably in esophagus).

11:38                  Medical command contact and diversion to hospital five minutes away (tube probably in esophagus).

11:43             Arrival at hospital and tube is pulled out of esophagus following assessment of tube placement.
 

Why did the doctor pull the tube?
 

Drew had no pulse on arrival. Once at CarolinaEast, the emergency room physician documented that Drew’s color was cyanotic, there was no fogging of the ET tube and Drew had rumbling sounds in his stomach. All of these are classic signs of an esophageal intubation.[1]

 

Apparently, even without waveform capnography, it was obvious that the tube was in the wrong place.

Cyanosis and rumbling breath sounds in the stomach?

How do you assess tube placement, observe these signs of esophageal intubation, and come up with excuses to justify leaving the tube in place?

This appears to be an example of cognitive dissonance.

We believe so strongly that we are doing the right thing, that we ignore abundant evidence to the contrary.

He’s blue.

I should check the tube.

Nah! He just needs some amiodarone (which coincidentally can cause skin to turn blue).

It sounds like I am ventilating his stomach.

I should check the tube.

Nah! He just needs to be defibrillated.

Medical command told me to check the tube.

I should check the tube.

Nah! I saw the tube go through the cords.
 

“A respiratory therapist at CarolinaEast immediately extubated and re-intubated Drew on the first attempt,” the complaint continues. “Within a few minutes his blood oxygen saturation level returned to 100 percent and his vitals improved.[1]

 

It appears to have been an easy intubation.

It appears to have been an easy assessment.

Why did the paramedic, respiratory therapist, nurse, and basic EMT not check placement of the tube?
 

Cognitive dissonance theory explains human behavior by positing that people have a bias to seek consonance between their expectations and reality. According to Festinger, people engage in a process he termed “dissonance reduction,” which can be achieved in one of three ways: lowering the importance of one of the discordant factors, adding consonant elements, or changing one of the dissonant factors.[6] This bias sheds light on otherwise puzzling, irrational, and even destructive behavior.[4]

 

This is one of the reasons we need to constantly look for evidence that we are wrong, rather than evidence that we are right.

We tend to be satisfied with inadequate evidence if we only look for confirmation.

We can talk ourselves into almost anything.

At some point we all probably engage in cognitive dissonance. We need to anticipate this and aggressively seek evidence that contradicts what we want to believe.

Our patients’ lives may depend on our ability to avoid cognitive dissonance.
 


 
This is not just a problem for EMS – See also:

What Does it Take to NOT Kill a Patient – Part I – 4/03/2011

What Does it Take to NOT Kill a Patient – Part II – 4/04/2011

What Does it Take to NOT Kill a Patient – Part III – 5/20/2011

What Does it Take to NOT Kill a Patient – Part IV – 5/23/2011

What Does it Take to NOT Kill a Patient – Part V – 5/30/2011

From EMCrit –

EMCrit Podcast 47 – Failure to Plan for Failure: A Discussion of Airway Disasters – 5/09/2011

From Resus.Me –

Anaesthesia’s dirty laundry – let’s all learn from it – 4/03/2011

 

The paramedic, respiratory therapist, nurse, and basic EMT cannot change the outcome, but they can learn from it and make sure others learn the importance of ventilation for children and the importance of looking for evidence that we are wrong.

The family of Drew Hughes cannot get him back, but maybe a part of the settlement can include some attempt to educate medical personnel, so that fewer other families experience the kind of pain they live with.
&nbsp


 

Footnotes:

[1] Lawsuit filed over death of Emerald Isle youth
Posted: Wednesday, November 6, 2013 9:51 am | Updated: 9:56 am, Wed Nov 6, 2013.
22 comments
By Brad Rich, Tideland News Writer
Tideland News
Article

[2] LAWSUIT: Ambulance Mistake Killed Teen After Skateboard Accident
Updated: Wed 9:14 PM, Nov 06, 2013
WITN.com
Article

[3] Respiratory System
2000 ECC Guidelines
Part 10: Pediatric Advanced Life Support
Postresuscitation Stabilization
Free Full Text from Circulation.

[4] Cognitive dissonance
Wikipedia
Article

.