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

.

Was the In-Custody Death of Eric Garner Due to Police and EMS Abuse? Part I


 

In NYC Medics Restricted By FDNY Pending Investigation Into NYPD Custody Death, The Social Medic writes about the death of Eric Garner during an arrest. Death may have many different causes. Is there any one thing that would have resulted in Eric Garner still being alive – if it had not been done (or if it had been done)?

We do not know.

We probably never will know.

Did Eric Garner deserve to die? No.

Was there a valid reason for an arrest? There is nothing in this video to answer that question.

Should the police have tried to take Eric Garner down the way they did?

Is that a real choke hold, or a movie of the week choke hold?

How much choking was going on?

How much resisting was going on?

The videos only show some of what was going on, but it seems like this was not well thought out.

Eric Garner is a big man and should be approached with a well coordinated plan for the safety of everyone – for the safety of Eric Garner, for the safety of the police, and for the safety of the bystanders. Was ESU (Emergency Services Unit) there? Was a Taser available and is Taser use permitted in that jurisdiction?

A Taser might have saved Eric Garner’s life, but Eric Garner still might have died, even if the police had not arrested him. Sudden death happens hundreds of thousands of times a year in America.

When the police initially take him down, they brush up against/bounce off of a window. If it is glass, what would have happened if it broke? If it is glass, what if they had continued through the glass? If it is not glass, how do they know?

The difference between broken glass and a knife (or a sword) is not in the amount of danger they present, since all can kill you very quickly. This difference is in the perception of that danger.
 

In this video, Eric Garner repeatedly states that he cannot breathe, but this is probably not the first time that police have heard similar statements while wrestling someone into custody. EMS was not there, so no treatment was immediately available, if any treatment had been indicated. We cannot tell. His death later is not proof that he was having trouble breathing, but it does suggest that he was not breathing adequately.
 


 

The commentary from the person filming the video is useless. It is just as prejudiced and uninformed as that of any other politically motivated commentary.

All he did was break up a fight?

Unlikely, but how would the person filming this know?

Prejudiced cops on Staten Island, this is what they do?

Does that applied to the non-white cops, too? Or is that just a prejudiced comment? Prejudice does exist. Nobody is immune from it, but what is the critic basing his comments on? He appears to be basing his comments on his prejudice.

Eric Garner was beat up?

He was violently subdued/wrestled to the ground, but I did not see anyone strike him.

Eric Garner was not beat up.

The critic seems to be singing along with the music in the background, which does not really give the impression of someone who thinks he is witnessing someone being killed. He makes a lot of accusations, but his actions do not match his words. If you are singing along with Muzak, you appear to be indicating that there is nothing important distracting you from your singing. Maybe it is someone next to the critic, but that still suggests that there was not a lot of concern among those as close to events as the critic.

Did the police choke Eric Garner into submission or did one officer overestimate the effect he would have on a much larger guy by grabbing him around the neck?

Someone has written, None of the officers knew what to do in this situation on the bottom of the video. What would the film critic like the police to do? Should they put Eric Garner in the back of a police car?

What does the film critic suggest that they do?

They have called for an ambulance and they have Eric Garner in the rescue position.

Did the police use an inappropriate method of arresting Eric Garner?

The prohibition on the use of a choke hold for restraint may have more to do with the way things look to bystanders, than the effect it has on the person being restrained. Choke holds are not prohibited in most combat sport because apparently choke holds can be used safely. Did the choke hold cause death?
 


Image credit – Wikipedia article on choke holds.
 

At about 4:30 of the video, EMS enters.

I have not commented on what The Social Medic wrote about this incident, yet. I will comment on what can be seen of what EMS did (did not do) and whether excited delirium is a part of this in Part II.

.

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.

.

Where is the Line Between Good Pain Management and Bad

 

Almost everything exists on a continuum. Pain management is no different.

The idea of completely good, or completely bad, pain management may not even be appropriate in describing the extremes, because clear distinctions are imaginary.
 

Anesthesia exists along a continuum. For some medications there is no bright line that distinguishes when their pharmacological properties bring about the physiologic transition from the analgesic to the anesthetic effects. Furthermore, each individual patient may respond differently to different types of medications.[1]

 


Image credit.
 

The definitions of sedation/analgesia as Moderate or Deep provide excellent examples.
 

Moderate
 

Moderate sedation/analgesia: (“Conscious Sedation”): a drug-induced depression of consciousness during which patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation. No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function is usually maintained. CMS, consistent with ASA guidelines, does not define moderate or conscious sedation as anesthesia (71 FR 68690-1).[1]

 

Deep
 

Deep sedation/analgesia: a drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully following repeated or painful stimulation. The ability to independently maintain ventilatory function may be impaired. Patients may require assistance in maintaining a patent airway, and spontaneous ventilation may be inadequate. Cardiovascular function is usually maintained. Because of the potential for the inadvertent progression to general anesthesia in certain procedures, it is necessary that the administration of deep sedation/analgesia be delivered or supervised by a practitioner as specified in 42 CFR 482.52(a).[1]

 

Respond purposefully is in the description of both. Respond purposefully should also be in the description of minimal sedation/analgesia and the description of no sedation/analgesia. The difference is the amount of stimulus required – following repeated or painful stimulus vs. to verbal commands, either alone or accompanied by light tactile stimulation. This is the primary difference.
 

Patients may require assistance in maintaining a patent airway,

Does that mean that a patient who does not require assistance in maintaining a patent airway is not receiving Deep sedation/analgesia?

No.

and spontaneous ventilation may be inadequate.

Does that mean that a patient with adequate spontaneous ventilation is not receiving Deep sedation/analgesia?

No.
 

What if supplemental oxygen is provided in anticipation of the potential for hypoxia, but the patient never becomes hypoxic?

What if supplemental oxygen is provided in response to hypoxia, the hypoxia resolves and does not return, but no ventilatory assistance is provided?
 

Should the following be added to the moderate sedation/analgesia definition?

Because of the potential for the inadvertent progression to deep sedation/analgesia in certain procedures, . . . .

If that is true, then what about adding the following to the definition of minimal sedation?

Because of the potential for the inadvertent progression to moderate sedation/analgesia in certain procedures, . . . .

Only no sedation/analgesia does not qualify for this kind of warning, but my point is not to provide a slippery slope justification for unethically withholding sedation/analgesia.

I am pointing out what a continuum means.

All of this raises the question, What is too much?

We cannot really consider that question without also raising the question, What is not enough?
 


 

How do we differentiate among the various possibilities of sedation/analgesia?

We differentiate according to the response of the patient, not so much according to whether the patient responds to verbal, painful, or repeated stimuli, but by the response to the question, Do you want more pain/sedation medicine?

One determines how we respond to potential ventilation needs of the patient, while the other determines how we respond to the sedation/analgesia needs of the patient.

What is too much?

That seems to depend on where the patient is on the sedation/analgesia continuum as determined by someone other than the patient.

What is not enough?

That seems to depend on where the patient is on the sedation/analgesia continuum as determined by the patient.

We cannot ask one question without implying the other question, so why do we address them in isolation so often?

Footnotes:

[1] Revised appendix A, interpretive guidelines for hospitals— state operations manual, anesthesia services.
Centers for Medicare & Medicaid Services (CMS).
Effective December 2, 2011.
Free Full Text Download in PDF Format from CMS.

.

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

.

Ambulance Mistake Killed Teen After Skateboard Accident


 
Here is an article about the death of a kid that raises a lot of questions.

The article does not answer many of those questions.

What happened?
 

Melvin says Carteret General sent a respiratory therapist along in the ambulance because they decided to put a breathing tube down the child’s throat. He says Drew was not properly sedated, woke up and pulled out the tube.[1]

 

Not properly sedated?

Unfortunately, this does happen. Dr. Scott Weingart has a couple of podcasts where he rants about this problem.[2],[3]
 

Why avoid sedation?

Maybe the patient is allergic.

Use a different sedative. There are dozens available.

Maybe the patient’s blood pressure is low.

Use ketamine.

What if the patient stops breathing?

Really. This is an excuse that I have encountered with several intubated patients.

Just how stupid are some of the people who graduate from medical school?

The patient is already intubated and on a ventilator (or being ventilated by BVM [Bag Valve Mask] resuscitator).

What do we do for someone who stops breathing?

Ventilate – for example by BVM until an endotracheal tube is placed.

If an endotracheal tube has already been placed, does anyone really care if the patient stops breathing?

And . . .

. . . ketamine.

Ketamine is a sedative that usually does not depress the patient’s respiratory drive.

And there is one more minor point to consider.

Most patients are intubated with the assistance of not just sedatives, but also paralytics.

If you are breathing after receiving a paralytic, somebody did something wrong. A paralytic is supposed to stop every muscle in the body from contracting – except the heart.

It could be that there was an omission of adequate doses of more than two types of drugs – sedatives and paralytics and, as Dr. Weingart will point out, pain medicine, because sedatives do not usually provide pain relief . . .

. . . except for ketamine.

It is a versatile drug, that ketamine.
 

The patient woke up and pulled the tube out.

Which would make you happier?

1. I have to ventilate this patient through the tube that is already in place.

2. I have to place the tube back in the trachea during transport because you neglected to provide adequate sedation. Even if reintubated excellently, intubation has many complications.

That should be the antidote to the argument that sedation is a bad thing (what if he stops breathing?), because it should be obvious that not breathing, but being ventilated is much better than not being sedated and being so agitated that the patient removes his airway.

Just put it back in!

That is the response, except . . .
 

The attorney says when those in the ambulance re-inserted the tube, it went into the teen’s esophagus, rather than his trachea.[1]

 

That happens.

Esophageal intubation is no big deal.

Just ventilate and place the tube in the trache. If the tube cannot be properly placed, we can use the BVM for ventilation or perform a crichothyrotomy. Both are acceptable means of ventilation.
 

He says Drew was given sedatives, and the teen, unable to breathe on his own, went without oxygen for about 35 minutes.[1]

 

Not recognizing a tube that has been placed in the esophagus, or one that has migrated to the esophagus, is just plain bad patient care.

Nobody should be intubating without waveform capnography to confirm placement.

Even without waveform capnography, there should not be a problem. All intubated patients should have continual assessment, which should identify a problem long before brain death.

Again, the worst case is that the patient is ventilated by BVM or crichothyrotomy.

We do not have details about what happened, but the patient appears to have arrived at the hospital without brain function. Was that due to the original injury, with the esophageal intubation only complicating matters?

There is not enough information to tell, but when the tube is left in the esophagus, it is kind of like leaving your fingerprints all over a knife sticking out of a dead guy’s chest. People are not going to spend a lot of time looking for another cause of death.

Capnography has been recommended in ACLS (Advanced Cardiac Life Support) since 2000, if not earlier.[4]

How difficult is assessment for an improperly placed tube (all tubes should be considered improperly placed and continually reassessed)?[5]
 

Melvin says the ambulance crew diverted to CarolinaEast in New Bern, and the ER doctor there immediately recognized the tube was in the wrong place.[1]

 

We like to find evidence that confirms what we believe. (I believe that the tube is where I want it to be. I saw the tube go through the cords.)

This is dangerous.

We need to look for evidence that we are wrong.

If we are not constantly looking for evidence that we are wrong, we will make a lot more mistakes than we should.

Science is a method of looking for evidence that we are wrong. That is why science keeps improving.

We need to take a more scientific approach to patient care. . .

. . . and have I mentioned ketamine? Science shows that ketamine is safe and effective.
 

I have more information here – Further Details on ‘Ambulance Mistake Killed Teen After Skateboard Accident’

Footnotes:

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

[2] Intubated ED Patients are Still Not Receiving Sedation
EMCrit
by Scott D. Weingart, MD.
Podcast page

[3] ED patients being intubated and then not sedated or pain-controlled
EMCrit
by Scott D. Weingart, MD.
Podcast page

[4] You had me at ‘Controversial post for the week’ – Part I
Tue, 22 Oct 2013
Rogue Medic
Article

[5] More Intubation Confirmation
Sun, 27 Apr 2008
Rogue Medic
Article

.

Serious adverse events during procedural sedation with ketamine – Part I

ResearchBlogging.org

What contributes to adverse events with the use of ketamine for PSA (Procedural Sedation and Analgesia) in children?

The pre-PSA use of fentanyl or morphine or concomitant use of midazolam and/or atropine was not associated with an increased in adverse event in either IM or IV ketamine (Table 1).[1]

However, there was a trend toward different rates of adverse events with the use of some medications in addition to ketamine. A larger study would be able to tell if these trends are real or just normal statistical variation.

The use of morphine, fentanyl, and midazolam would be expected to cause some adverse effects, but midazolam seems to provide protection from adverse events.

Morphine and fentanyl were used so infrequently, that drawing any conclusions from such small numbers is a bad idea.

Why does midazolam appear to protect against adverse effects?

Even more interesting is the possible harm caused by atropine.

Why would atropine increase the rate of adverse events?
 

 

Why do we give atropine to children?

To prevent ourselves from being able to see the effects of hypoxia on the child’s heart rate.

 

Incompetence.
 
 
We give children atropine to prevent their heart rates from dropping when we are doing things that are expected to occasionally result in hypoxia.

The child’s heart rate is a great indicator that we are making the child hypoxic, but we prefer to not know about the hypoxia.

Should we also avoid pulse oximetry?

We even delay our ability to identify hypoxia with pulse oximetry by using supplemental oxygen. That doesn’t mean that we should not use supplemental oxygen, only that we should assess ventilation with a measurement that is not affected by supplemental oxygen – waveform capnography.

Atropine should not be used to keep the pediatric heart rate from responding to hypoxia.

The way to prevent pediatric bradycardia is to prevent hypoxia, not to put lipstick on the hypoxia.

Image credit.

What hypoxia? No hypoxia here. Just a pulchritudinous paramedic.

Atropine is also used as an antisialog, which means that it decreases salivation. That can be an appropriate use, but if the atropine prevents the recognition of hypoxia, some saliva in the mouth may not be that important or we should use suction (just as the dentist does).

However, the study was not designed to look at that and the numbers never reached statistical significance. Does that mean that we should continue to use atropine for something that is not beneficial?

Where is the evidence that there is any benefit to anything other than the ego of the person pushing the atropine?

Oh, look! Better numbers on the monitor.

We should not be harming our patients with drugs.

To be continued in Part II, which looks at the actual IM vs. IV results.

Thank you to Peter Canning, of Street Watch: Notes of a Paramedic, for this journal article.

Footnotes:

[1] Serious adverse events during procedural sedation with ketamine.
Melendez E, Bachur R.
Pediatr Emerg Care. 2009 May;25(5):325-8.
PMID: 19404223 [PubMed – indexed for MEDLINE]

Melendez E, & Bachur R (2009). Serious adverse events during procedural sedation with ketamine. Pediatric emergency care, 25 (5), 325-8 PMID: 19404223

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How to Torture Patients

Perhaps, you have watched all of the parts of Saw and wished that you could have some of that kind of fun, too. Even though we are supposed to be having the opposite effect on patients, some of us do cause that kind of pain and psychological abuse.

Dr. Weingart gives us a piece of his mind on this topic in Pain and Terror as Effective Pressors.

Does this go well with scrubs, or with an EMS uniform?
 


Image credit.

But what about the hypotension and hypoxia that occur with fentanyl?


Click on images to make them larger.[1] [2]

There is a 97% chance that, after administration of fentanyl to a critical trauma patient who is not hypotensive, the patient will still be not hypotensive.

There is a 47% chance that, after administration of fentanyl to a critical trauma patient who is hypotensive, the patient will stop being hypotensive.

If we did not have so much anxiety about fentanyl, we might consider making it the standard of care for hypotension following trauma.

Should we be double-teaming these patients with both pain and the terror of awareness during intubation with a long-acting paralytic? It probably isn’t any worse than what the traumatically paralyzed patient experiences with intubation, but that should only encourage us to be more aggressive with pain management for these patients. This is not an excuse to be tolerant of iatrogenic pain and anxiety.

Pain management in EMS seems to keep improving, but we still have a long way to go.

Pain management in the ED (Emergency Department) seems to keep improving, but we still have a long way to go.

I currently do have a protocol that allows me to give post-intubation sedation. This was only added to my protocols in the past 5 years, but it is a start. Before that, medics had to be aggressive enough to ask for medical command permission for a treatment that was outside of protocol. Treatments that are outside of protocol are discouraged.

The problem with post-intubation pain (and the expected agitation that goes with pain) this pain management sedation is not a recent development.

In an earlier podcast, Dr. Weingart describes the problems with using sedatives, rather than pain medicine, for post-intubation PAIN.

EMCrit Podcast 7 – Sedation Tirade – and listen to his other sedation podcasts.

Why do we think that a patient does not have pain unless that patient is writhing in pain?

With a paralytic on board, especially a long-acting paralytic, and even more so with a large dose of a long-acting paralytic, these patients will not writhe.

This brings up some questions –

How much evidence do we need that many of our patients are in a lot pain?

How easy is it to ignore the severe pain of our patients?

I do have one criticism.

The dose of sarcasm could be increased. This is no time to be stingy with the sarcasm treatment. I could be wrong.

Go listen to the brief Wee podcast and decide for yourself.

Footnotes:

[1] Fentanyl in the out-of-hospital setting: variables associated with hypotension and hypoxemia.
Krauss WC, Shah S, Shah S, Thomas SH.
J Emerg Med. 2011 Feb;40(2):182-7. Epub 2009 Mar 27.
PMID: 19327928 [PubMed – in process]

Full Text PDF Download at medicalscg.

Fentanyl Study: EMS Research Episode 9
EMS Research Podcast
Podcast page

[2] Chart Version – Fentanyl in the out-of-hospital setting: variables associated with hypotension and hypoxemia
Sun, 05 Jun 2011
Rogue Medic
Article

.