ACLS | Rogue Medic

If you have a BVM (Bag Valve Mask resuscitator), you should not need naloxone. The problem is inadequate respiration, not inadequate naloxonation.

- Rogue Medic

NIH launches trials to evaluate CPR and drugs after sudden cardiac arrest

Sun, 29 Jan 2012 06:30:21 +0000 By Rogue Medic 3 Comments

The NIH (National Institutes of Health) announced two new resuscitation studies. This is not the kind of research to find any private sponsorship, but it is important – well, one study is.

The CCC trial will compare survival-to-hospital-discharge rates for two CPR approaches delivered by paramedics and fire fighters. Persons experiencing cardiac arrest will be randomly assigned to receive continuous chest compressions, or standard CPR by emergency responders. Standard CPR, the approach recommended by the American Heart Association (AHA) for use by emergency responders, includes chest compressions with short pauses for assisted breathing. This approach has been called into question by emerging data suggesting that stopping chest compressions to provide assisted breathing interrupts overall blood flow, thereby lowering survival.^[1]

The AHA wants to find some evidence to justify their preferred method of combining chest compressions with ventilations.

There is no evidence that ventilations improve survival from adult cardiac arrest of cardiac origin.

There is evidence that any interruption to compressions decreases survival.

The only known interruption that does not decrease survival is defibrillation.

Not for ventilation.

Not for intubation.

Not for any medication.

Not for application of any CPR machine.

Not for transport.

Not for acupuncture.

Trained emergency personnel will give all participants in the CCC trial three cycles of CPR followed by heart rhythm analysis and, if needed, an electrical shock (defibrillation), applied to the chest. Half will be randomly assigned to receive continuous compressions combined with pause-free rescue breathing and half will receive standard professional CPR.^[1]

Why only three cycles?

This suggests that the hypothesis presumes some benefit from ventilations.

Based on what?

Apparently based on tradition and wishful thinking – a deadly combination.

Tradition and wishful thinking have been a deadly combination for thousands of years.

The Amiodarone, Lidocaine, or neither (Placebo) for Out-Of-Hospital Cardiac Arrest Due to Ventricular Fibrillation or Tachycardia study (ALPS) will determine whether amiodarone or lidocaine improves survival-to-hospital-discharge rates for participants with shock-resistant ventricular fibrillation. Participants will receive one or the other drug or a placebo.^[1]

We already know that these drugs do not improve survival from V Fib (Ventricular Fibrillation). The only questions are

Image modified from Paramedicine 101 – 2010 AHA Updates.

How many resuscitations does lidocaine prevent?

How many resuscitations does amiodarone prevent?

The CCC trial will enroll up to 23,600 participants at eight major regional locations across the U.S. and Canada.^[1]

That number of patients should be enough for clear results.

The ALPS trial will enroll up to 3,000 participants at nine locations across the U.S. and Canada.^[1]

That ridiculously small number of patients should allow those who base treatment on tradition and wishful thinking to continue to pretend that their treatments do not make things worse.

Almost 60 fire and EMS organizations will participate in the ALPS trial, and approximately 125 EMS organizations will participate in the CCC trial.^[1]

Maybe the number 3,000 is a misprint. That would be only 50 V Fib (Ventricular Fibrillation) cardiac arrests per EMS organization.

Estimated Enrollment: 3000 ^[2]

How will that produce statistically significant results, while the CPR study requires 8 times as many patients?

Footnotes:

^[1] NIH launches trials to evaluate CPR and drugs after sudden cardiac arrest
Embargoed for Release
Thursday, January 26, 2012
11 a.m. EST Contact:
NHLBI Communications Office
(301) 496-4236
NIH
Press Release

^[2] Amiodarone, Lidocaine or Neither for Out-Of-Hospital Cardiac Arrest Due to Ventricular Fibrillation or Tachycardia (ALPS)
ClinicalTrials.Gov
Last Updated on September 21, 2011
ClinicalTrials.gov Identifier: NCT01401647
Trial data

Filed Under: ACLS, Heresy, Research

Is the Drug Shortage an Excuse for Incompetence – Part II

Sat, 07 Jan 2012 06:30:25 +0000 By Rogue Medic 6 Comments

Continuing from Part I.

A hospital, or ambulance company, should not allow doctors, nurses, or paramedics to give substitute medications without educating them about the medication. Different concentrations. Different dosages. Different side effects. Different drug interactions. Different indications. Different routes of administration. Et cetera. Even for nearly identical drugs.

Likewise, a doctor, nurse, or paramedic should not give any medication without being familiar with the drug – concentrations, dosages, side effects, drug interactions, indications, et cetera.

Gosh, I’ve never given this before. Let’s play with it. It’s not like anything bad could happen.

Do doctors do this?

Do nurses do this?

Do paramedics do this?

Is this the kind of behavior that any hospital wants/accepts from its employees?

Is this the kind of behavior that any ambulance company wants/accepts from its employees?

“In our mind, that’s just the tip of the iceberg,” Vaida says of the 15 deaths. “No one may be attributing a death because they really aren’t aware that a drug actually caused the death. If someone is notaware of the potency of one medication and gives too much so that the patient goes into respiratory arrest and dies, they may attribute it to the fact that the patient came into the hospital with respiratory problems.”^[1]

Ex-Dr. Conrad Murray is going to prison for similar behavior.

How can any administrator claim that Conrad Murray behavior is to be expected from their employees, but not end up being investigated.

If I give a medication and the patient stops breathing, I should still be able to ventilate and oxygenate the patient. The same is true for any first responder, or basic EMT.

If the problem is respiratory depression

and the result is death,

is the problem the drugs,

the people giving the drugs,

or the oversight of the people giving the drugs?

Why hire people who can tell the difference between one and 100?

How is a death, under these circumstances, any different from the death of Michael Jackson under similar circumstances?

What are the circumstances of these deaths?

So far, 15 deaths attributed to the drug shortage have occurred nationwide, an Associated Press study found.^[1]

One code-blue patient in an undisclosed city died because the preloaded emergency syringe epinephrine wasn’t available.^[2]

In cardiac arrest, epinephrine, does NOT save lives.

Epinephrine does help to just get a pulse back, but that is not saving a life. If just getting a pulse back were saving a life, then we would not have large awards to the families of patients who went in to the hospital without impairment, but came out with just a pulse. That would be considered a good outcome.

If the doctors, nurses, and medics do not know what medications they are using, they should not proceed until they do know what they are doing.

Footnotes:

^[1] Shortage of Lifesaving Drugs Reaches Epic Proportions
Beverly Ford Source: Telegram & Gazette (Worchester, MA)
December 21, 2011
EMS World
Article

^[2] Oklahoma EMS Face Drug Shortage
by Sonya Colberg
The Oklahoman
Monday, October 4, 2010
Article at JEMS.com

Filed Under: ACLS, Heresy, Pharmacology

Is the Drug Shortage an Excuse for Incompetence – Part I

Fri, 06 Jan 2012 06:30:14 +0000 By Rogue Medic 2 Comments

Continuing from Shortage of Lifesaving Drugs Reaches Epic Proportions.

It’s how to provide the best patientcare while at the same time preventing medical mix-ups when administering drug substitutes, many of which have different potencies than their more commonly used counterparts. Fentanyl, for example, which isused as a substitute for morphine, is 10 times stronger than the opiate. A wrong dose, hospital officials worry, could cause death.^[1]

Fentanyl is 100 times as potent per mg (not 10 times), but the packaging is generally single dose packaging. A syringe of fentanyl with 100 mcg is roughly the same strength as a syringe of morphine that contains 10 mg. I would need to get 99 more syringes of fentanyl to give the same dose in milligrams.

In what hospital is this not going to require a trip to the pharmacy? What ambulance company carries 10 mg fentanyl (10,000 mcg fentanyl) on any ambulance?

This 10 mg of morphine -

Image credit.

Is not the same as this 10 mg of fentanyl –

Image credit. Click on images to make them larger.

Hold on. That isn’t 10 mg fentanyl. We need more –

We still need more –

We aren’t there yet –

Just a teensy-weensy bit more –

There is more than a subtle difference between the one syringe and the 100 syringes. If you missed it, go back and look again. Can you tell the difference between 100 syringes and 1 syringe? Are you sure?

Have carpal tunnel symptoms developed from repeatedly pushing the plunger on these syringes? Is each syringe being followed by a flush? If 2 ml fentanyl is followed by a 10 ml flush, that is 1,200 ml for what should have been 1 ml of morphine. The syringes are the same size, although the fentanyl syringes contain 2 ml each and the morphine syringes contain 1 ml each.

There may be other concentrations available, but 50 mcg/ml is the most common concentration of fentanyl. The variation in concentrations is much more common with morphine. The 10 mg/ml concentration is what I carry, which is 10 mg in one 1 ml syringe (as pictured). Everyone should check the concentration at least once before giving any medication.

To be continued in Part II.
-

Footnotes:

^[1] Shortage of Lifesaving Drugs Reaches Epic Proportions
Beverly Ford Source: Telegram & Gazette (Worchester, MA)
December 21, 2011
EMS World
Article

Filed Under: ACLS, Heresy, Pharmacology

Shortage of Lifesaving Drugs Reaches Epic Proportions

Fri, 30 Dec 2011 06:30:42 +0000 By Rogue Medic 2 Comments

I did not come up with the title – Shortage of Lifesaving Drugs Reaches Epic Proportions – that was the title of the article I am criticizing, but not for any lack of hyperbole.

“It’s a perfect storm of conditions with a rapidly consolidating marketplace, a health care system that is trying to control costs, an issue with raw materials and a marketplace that doesn’t have a good redundancy system in place to handle things when a plant shuts down,” says Allen Vaida, executive vice president of the Institute for Safe Medication Practices. “No question about it. It’s a national crisis.”^[1]

In EMS, we are worried about a shortage of drugs, when we should see this as an opportunity to improve patient care.

Among the drugs Fox found that were in short supply during 2011 were injectable versions of calcium gluconate, used by first responders to regulate heart rhythm in patients suffering cardiac arrest; succinylcholine, a muscle relaxer used to intubate patients; naloxone hydrochloride, which reverses drug overdoses; and propofol, an anestheticused in emergency surgery better known for causing the death of singer Michael Jackson. Most of those medications are older generic injectables that are widely used in emergency situations. Some of those shortages, among them propofol and succinylcholine, have since been resolved but others continually crop up, creating a gap in emergency drug stockpiles.^[1]

calcium gluconate, used by first responders to regulate heart rhythm in patients suffering cardiac arrest

It could be, but that does not make sense. ACLS (Advanced Cardiac Life Support) discourages the routine use of calcium, but in true emergencies we should be using calcium chloride, rather than the slow infusion of calcium gluconate.

Routine administration of calcium for treatment of in-hospital and out-of-hospital cardiac arrest is not recommended (Class III, LOE B).^[2]

naloxone hydrochloride, which reverses drug overdoses

Naloxone is only indicated for life-threatening respiratory depression due to an opioid overdose. However, a response to naloxone is definitely not diagnostic for an opioid overdose.

Suppose that EMS has no naloxone (Narcan), so what? The essential treatment for opioid overdose, and for benzodiazepine overdose, is just supportive care.

and propofol, an anesthetic used in emergency surgery better known for causing the death of singer Michael Jackson.

Propofol did not cause the death of Michael Jackson. The lack of airway management by Dr. Conrad Murray killed Michael Jackson. Opening his airway, and maybe some painful stimulus, would have kept Michael Jackson alive.

“Gray market” suppliers, usually small wholesalers or individuals who closely monitor and react to pharmaceutical trends, are scooping up medications as soon as a shortage becomes apparent then selling back the products to drug distributors, other wholesalers or hospitals at inflated prices that can sometimes top more than 1,000 percent of a drug’s original cost.^[1]

What is the original cost used for these calculations? Is it the cost to the manufacturer? The list price? The wholesale price to hospitals? The cost per dose to the patient? Why use percentages? Do most people realize that 1,000% as much means ten times as much.

Image credit.

“We’re not getting any complaints regarding any infringement on care because of the shortages,” she says. “That doesn’t guarantee it isn’t happening, but we usually see that fairly quickly when there seems to be an uptick in problems. What I surmise is that providers are doing what they are supposed to do under the circumstances.”^[1]

Is it possible for people to actually do what they are supposed to do?

If we are not doing what we are supposed to be doing, why not?

“Patient access to innovative treatments is the cornerstone of our industry. That is why the critically important issue of drug shortages demands our collective attention to ensure patients can access themedicines they need in the most expeditious manner possible,” says John Castellani, chief executive officer and president of The Pharmaceutical Research and Manufacturers of America, a trade group comprised of pharmaceutical research and biotechnology companies.^[1]

No.

“Patient access to ~~innovative~~ safe and effective treatments is the cornerstone of our industry.

Safe and effective are essential. Innovative is desirable, but not essential.

Dr. Conrad Murray killed Michael Jackson with incompetence, not with any drug. Is blaming deaths on a drug shortage any different from blaming deaths on a drug?

To be continued in Is the Drug Shortage an Excuse for Incompetence – Part I on 01/06/2012.

Image credit.

Footnotes:

^[1] Shortage of Lifesaving Drugs Reaches Epic Proportions
Beverly Ford Source: Telegram & Gazette (Worchester, MA)
December 21, 2011
EMS World
Article

^[2] Interventions Not Recommended for Routine Use During Cardiac Arrest
Part 8: Adult Advanced Cardiovascular Life Support
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 8.2: Management of Cardiac Arrest
Free Full Text Article with links to Free Full Text PDF download

Filed Under: ACLS, Heresy, Pharmacology

The Danger of ROSC – Return Of Spontaneous Circulation

Tue, 20 Dec 2011 06:30:30 +0000 By Rogue Medic 11 Comments

JB responded to Where is the Evidence for Epinephrine in the 2010 ACLS Guidelines with the following comments about the benefits of ROSC (Return Of Spontaneous Circulation) -

The difference being…

ROSC tends to be a useful starting point for return of normal life, even if it doesn’t always lead there.

This is a problem. Any evidence of benefit is given much more weight than evidence of harm.

Suppose you are trying to get into a locked room. You own the room, but you do not have your key. You left $50 in the room. You want to go shopping for groceries.

If you do not get into the room (if you do not get ROSC – Re-Open Shut Chamberdoor), you cannot get your money and buy groceries.

If you use the dynamite that is mysteriously outside your door, you can get in the room (ROSC). Remember, that getting in the room (ROSC) is a prerequisite to getting your money.

Do you use the dynamite on the door?

If Dynamite = ROSC, do you give it a go?

Image credits.

Oh, but this is different!

Is it really different?

We have a problem. We could approach this problem in the least destructive way possible and not use the explosives until we have thoroughly searched for the key.

But we are in a hurry.

Are we providing any real benefit by using epinephrine to blast the heart into action, regardless of the damage epinephrine causes to the brain and heart?

We have no evidence of improved survival with epinephrine, but we do have evidence of worse survival with epinephrine.

Why are we choosing worse survival?

Even if the survival were identical, choosing the more complicated treatment is very bad medicine.

Until there is evidence of a benefit with epinephrine, we should only use epinephrine in randomized, placebo-controlled trials. If there is any benefit from epinephrine, it will probably be small and only in a specially selected group of patients, but we will not know, unless we study it. Maybe epinephrine should only be used after 20 minutes of attempted resuscitation, but if we aren’t improving survival, we are just increasing the hospital costs.

In this post hoc analysis the actual use of adrenaline was associated with increased short-term survival, but with 48% less survival to hospital discharge. This negative association with survival is very similar to the multivariate analysis of observational Swedish registry data where patients receiving adrenaline were 57% less likely to be alive after one month.⁶ ^[1]

Highlighting is mine.

Unless you know of a method of achieving return of normal life without first achieving ROSC? I’d be interested to hear it.

You are looking at this backward.

Where is the evidence of improved survival with epinephrine?

Where is the evidence of even survival that just as good as no epinephrine?

ROSC is not the goal. ROSC is just a surrogate endpoint. ROSC can be curing the disease, but killing the patient.

If those x amounts of time was going to turn to death anyway, is it not in the patient’s best interests to give it a go?

If Dynamite = ROSC, do you give it a go?

You assume a lot for a drug that shows decreased survival and worse neurological outcomes in those who do survive.

The burden of proof is on those proposing a treatment.

Show that the treatment is safe.

Show that the treatment works better than placebo.

Don’t just show that the treatment is better at a surrogate endpoint (ROSC), but show that the treatment is better at improving meaningful survival.

Everything else is a distraction – a dangerous distraction.

If you are just resuscitating me to a coma, followed by death in the ICU. Don’t do it.

If you are resuscitating me to a life in a nursing home in front of a TV, wearing diapers and unaware of my surroundings. Don’t do it.

Epinephrine kills brains, when it doesn’t kill the whole patient.

Patient care is not about giving it a go.

Image credit.

In the absence of any studies showing *diminished* return of normal life with adrenaline or other drugs that improve rates of ROSC, I would say that increasing ROSC is giving people the best chance of then taking the next steps along the path to return of normal life (or as I’ve seen it abbreviated – RONF – “return of neurological function”). And thus ethically, at least to my mind, adrenaline is a good idea.

No.

Nonetheless, I agree with your main point. More research needed, and providers/governments/ethics committees/wherever the hold up is need to have the balls to do some proper adrenaline vs placebo studies!

On that we do agree.

I do not see any reason to assume that epinephrine will improve outcomes.

We are just punishing families with false hopes and huge hospital bills and even the torture of having to care for a family member who does not even recognize them anymore.

If we want to convince people that resuscitation is a bad idea, so they sign DNR (Do Not Resuscitate) orders, epinephrine is one way to do it.

Is epinephrine safer than dynamite?

Footnotes:

^[1] Outcome when adrenaline (epinephrine) was actually given vs. not given – post hoc analysis of a randomized clinical trial.
Olasveengen TM, Wik L, Sunde K, Steen PA.
Resuscitation. 2011 Nov 22. [Epub ahead of print]
PMID: 22115931 [PubMed - as supplied by publisher]

Filed Under: ACLS, Ethics, Heresy, Pharmacology, Research

Where is the Evidence for Epinephrine in the 2010 ACLS Guidelines

Mon, 19 Dec 2011 15:36:45 +0000 By Rogue Medic 17 Comments

What evidence did the AHA (American Heart Association) use to decide to keep epinephrine (adrenaline) in the 2010 ACLS (Advanced Cardiac Life Support) guidelines?

Since most drug trials have, at most, demonstrated only short-term outcome advantage, it may be important to evaluate long-term outcome when these drugs are combined with optimized post–cardiac arrest care.^[1]

Let me translate that –

We have only looked at short-term outcomes (ROSC – Return Of Spontaneous Circulation), perfusion pressure, and other surrogate endpoints.

We have never done a study large enough to find out if epinephrine works.

Even though surrogate endponts are only a preliminary basis for treatment, we refuse to insist on better evidence to continue with this uncontrolled, unapproved experiment on patients.

We have been pumping dead people full of epinephrine according to ACLS since 1974 and only now think that it may be important to evaluate long-term outcome.

What have we been waiting for?

Where is our ethical obligation to patients?

Based on this complete failure to show that epinephrine produces any improvement in outcomes that matter, what does the AHA recommend?

Treatment Recommendation
Although there is evidence that vasopressors (epinephrine or vasopressin) may improve ROSC and short-term survival, there is insufficient evidence to suggest that vasopressors improve survival to discharge and neurological outcome. There is insufficient evidence to suggest the optimal dosage of any vasopressor in the treatment of adult cardiac arrest. Given the observed benefit in short-term outcomes, the use of epinephrine or vasopressin may be considered in adult cardiac arrest.^[1]

We should stop and reconsider our complete failure to improve survival with drugs. We should not keep procrastinating.

Given the observed benefit in short-term outcomes, the use of epinephrine or vasopressin may be considered in adult cardiac arrest.

How can we ethically come to that conclusion?

This is the kind of fraud that is used to justify homeopathy, Reiki, acupuncture, and every other kind of alternative medicine.

Knowledge Gaps
Placebo-controlled trials to evaluate the use of any vasopressor in adult and pediatric cardiac arrest are needed.^[1]

And they are long overdue.

What if we look at it this way?

Given the absence of benefit in long-term outcomes,

the use of epinephrine or vasopressin

may be considered FUTILE in adult cardiac arrest.

The medical condition is cardiac arrest.

The goal is a Return Of Normal Life.

We have limited ourselves to just looking at Return Of Spontaneous Circulation for 36 years of ACLS guidelines.

How many people who take ACLS will be told that the strongest recommendation for epinephrine the AHA could come up with is really only that the use of epinephrine or vasopressin may be considered in adult cardiac arrest.

If I were writing an EMS protocol, this is the way I would use that suggestion from the AHA –

OK. I did consider epinephrine.

I considered that there is no evidence that in any way justifies automatically giving epinephrine to every cardiac arrest patient.

I could not ethically continue to include epinephrine in any treatment of cardiac arrest outside of a large scale randomized placebo-controlled trial that is designed to produce statistically significant results.

What do we hope for when we treat cardiac arrest?

Return Of Spontaneous Circulation.

Or –

Return Of Normal Life.

We are asking the wrong question and we are satisfied with an irrelevant answer.

We are dangerous.

Footnotes:

^[1] Supporting the Circulation During Cardiac Arrest
2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations
Part 8: Advanced Life Support
Free Full Text from Circulation with link to PDF Download

Filed Under: 2010 AHA Guidelines, ACLS, Heresy, Mythology, Pharmacology

Intraosseous Versus Intravenous Vascular Access During Out-of- Hospital Cardiac Arrest – A Randomized Controlled Trial

Thu, 15 Dec 2011 06:30:00 +0000 By Rogue Medic 4 Comments

Also posted over at Paramedicine 101 (now at EMS Blogs) and at Research Blogging. Go check out the excellent material at these sites.

For treatment of medical cardiac arrest patients, which is better – IO (IntraOsseous) or IV (IntraVenous) access for medication administration?

Since no medications have ever been demonstrated to improve survival from cardiac arrest (only chest compressions and defibrillation have), the most important consideration will be what method results in the least interruption of compressions and the least interference with defibrillation.

All patients eligible for inclusion in this study had their ﬁrst attempt at vascular access randomized to one of 3 locations: proximal tibial intraosseous, proximal humeral intraosseous, or peripheral intravenous. The proximal tibial insertion site was located medial to the tibial tuberosity, or just below the patella along the ﬂat aspect of the tibia. The proximal humerus insertion site was deﬁned as the greater tubercle of the anterior humeral head 1 cm proximal to the surgical neck of the humerus. Peripheral intravenous catheter placement could occur at any accessible peripheral vein but preferably at the antecubital fossa; the external jugular vein was not an option provided for catheterization.^[1]

Proximal tibial access points.

Proximal humeral access point.
Images credit.

Does this hurt? No. The patients are unresponsive and pulseless (dead), but even live patients and EMS personnel (who have tried this on themselves) report very little pain.

Overall success took into account a failure to maintain initial vascular access during the course of resuscitation, which included needle dislodgement or the inability to successfully administer medications or ﬂuid at any time during the resuscitation.^[1]

Those would interfere with the one claimed benefit – ability to deliver medication.

There was no difference in time to success for either of the intraosseous routes compared with the peripheral intravenous route.^[1]

Click on images to make them larger.

The time to success is interesting. The times for the humeral site are similar to the tibial IO and the IV for placement and first drug administration – at least at the low end of the IQRs (InterQuartile Ranges). The problem is that the upper end of the IQRs is much longer than for the other methods. This is in part due to the low number of patients, which is partially explained by the 13 protocol violations – all in favor of the tibial IO site. The lack of familiarity of paramedics probably also contributes, resulting in much longer times for some of the paramedics.

Finally, there were 13 protocol violations that favored the tibial intraosseous route, which may have been an indicator of bias among paramedics for that route and therefore could have resulted in confounding of the study results.^[1]

It may be that this group of paramedics was much more comfortable with the tibial IO, than with the humeral IO and this led to a greater likelihood of coming up with excuses for protocol violations. This may also have led to the performance differences. I have seen similar differences with the introduction of a new type of IV catheter to some services. There can be a lot of conscious and unconscious resistance to the new method, but after some familiarity develops, things tend to return to normal.

In the literature, intraosseous needle insertions have been linked to local wound infections, osteomyelitis, fat emboli, and compartment syndrome.^18-20 During this study, there was no mechanism in place for EMS or hospital personnel to report complications in the use of the intraosseous device.^[1]

That would be good to know, but this was not one of the goals of the study.

The average weight of patients in the humeral intraosseous group was greater than that of individuals in either of the other 2 arms of the study. This increased weight may have been associated with a difﬁculty in obtaining or maintaining vascular access.^[1]

Weight can be a problem for any method of IV/IO access, so this is a very important limitation.

Weight – mean (SD)

Overall – 97.3 kg (2.7)

Humeral IO – 103.9 kg (6.5)

IV – 97.7 kg (3.8)

Tibial IO – 91.5 kg (3.9)

An average weight of 228.6 pounds (103.9 kg) in the humeral IO group, but only 201.3 pounds (91.5 kg) in the tibial IO group? 27.3 pounds difference (13.8% difference).

That strongly suggests a problem.

The proximal humerus can also prove tenuous during cardiac arrest because it is centered near the upper torso, where resuscitation efforts are occurring, including airway management, ongoing chest compressions, and rescuer interchange. The constant activity creates a tremendous amount of movement and further increases the risk of unintentional needle dislodgement, which was veriﬁed during the debrieﬁng session after each out-of-hospital cardiac arrest, with paramedics frequently citing entanglement of the humeral intraosseous line, leading to dislodgement.^[1]

The peripheral intravenous site is the most commonly used vascular access by all health care providers, yet it proved successful in less than 50% of cases in this study.^[1]

No matter how bad the success of the humeral IO was, the IV success was even worse – less than 50% first attempt success.

Do IOs improve outcomes?

IOs may make it less likely that compressions will be interrupted, but we cannot tell from this study.

IOs may make it more likely that potentially harmful medications will be given.

The most interesting numbers I saw were the total fluid infused – twice as much in the IV group as in either IO group. No explanation is given, other than the possible slower flow rate for an IO. This may help to prevent fluid overload for those patients not in need of having an IV line accidentally left wide open.

There is no evidence that IOs, IVs, tubes, or medications improve survival to discharge with a working brain.

ACLS drug therapy during CPR is often associated with increased rates of ROSC and hospital admission but not increased rates of long-term survival with good neurologic outcome.^[2]

Will this make the Three Stooges Pit Crew concept less of a comedy of errors to implement?

Probably not, but we can hope that the AHA does the right thing and eliminates all of the treatments that don’t work – ventilation, intubation, IV access, IO access, epinephrine, amiodarone, lidocaine, ~~atropine~~ – wait, they actually did remove atropine, so there is hope.

Footnotes:

^[1] Intraosseous Versus Intravenous Vascular Access During Out-of-Hospital Cardiac Arrest: A Randomized Controlled Trial.
Reades R, Studnek JR, Vandeventer S, Garrett J.
Ann Emerg Med. 2011 Dec;58(6):509-16.
PMID: 21856044 [PubMed - in process]

^[2] Medications for Arrest Rhythms
Part 8: Adult Advanced Cardiovascular Life Support
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 8.2: Management of Cardiac Arrest
Free Full Text Article with links to Free Full Text PDF download

Reades R, Studnek JR, Vandeventer S, & Garrett J (2011). Intraosseous Versus Intravenous Vascular Access During Out-of-Hospital Cardiac Arrest: A Randomized Controlled Trial. Annals of emergency medicine, 58 (6), 509-16 PMID: 21856044

Filed Under: 2010 AHA Guidelines, ACLS, Heresy, Paramedicine 101, Research Blogging

Is Amiodarone the Best Drug for Stable Ventricular Tachycardia

Wed, 14 Dec 2011 06:30:47 +0000 By Rogue Medic 6 Comments

Is Amiodarone the Best Drug for Stable Ventricular Tachycardia?

What do the cardiologists recommend?

D. Sustained Monomorphic Ventricular Tachycardia
Recommendations

Class I

1. Wide-QRS tachycardia should be presumed to be VT if the diagnosis is unclear. (Level of Evidence: C)

2. Direct-current cardioversion with appropriate sedation is recommended at any point in the treatment cascade in patients with suspected sustained monomorphic VT with hemodynamic compromise. (Level of Evidence: C)

Class IIa

1. Intravenous procainamide (or ajmaline in some European countries) is reasonable for initial treatment of patients with stable sustained monomorphic VT. (Level of Evidence: B)

2. Intravenous amiodarone is reasonable for patients with sustained monomorphic VT that is hemodynamically unstable, refractory to conversion with countershock, or recurrent despite procainamide or other agents. (Level of Evidence: C)

3. Transvenous catheter pace termination can be useful to treat patients with sustained monomorphic VT that is refractory to cardioversion or is frequently recurrent despite antiarrhythmic medication. (Level of Evidence: C)^[1]

Class I –

Cardioversion.

Class IIa –

1. Procainamide.
2. Amiodarone.
3. Transvenous pacer.

OK, but that is not from the current ACLS.

Amiodarone must have been moved up in the rankings in the current ACLS, because that is what we were taught.

The guidelines above came out in 2006.

Amiodarone was was not moved up, but was downgraded to Class IIb in the current (2010) ACLS Guidelines.

Image modified from Paramedicine 101 – 2010 AHA Updates.

For patients who are stable with likely VT, IV antiarrhythmic drugs or elective cardioversion is the preferred treatment strategy. If IV antiarrhythmics are administered, procainamide (Class IIa, LOE B), amiodarone (Class IIb, LOE B), or sotalol (Class IIb, LOE B) can be considered. Procainamide and sotalol should be avoided in patients with prolonged QT. If one of these antiarrhythmic agents is given, a second agent should not be given without expert consultation (Class III, LOE B). If antiarrhythmic therapy is unsuccessful, cardioversion or expert consultation should be considered (Class IIa, LOE C).^[2]

Class I -

Still cardioversion.

Class IIa –

Procainamide.

Class IIb -

Amiodarone.

Maybe in the 2015 ACLS Guidelines there will not be any mention of amiodarone, except as a historical footnote. Maybe amiodarone will be replaced by something more effective at treating ventricular tachycardia, such as adenosine.

More likely is that we use more procainamide, but we should also consider being much more aggressive in sedating patients in anticipation of cardioversion. Amiodarone is associated with improvement from ventricular tachycardia in less than 30% of patients with stable ventricular tachycardia.

We need better sedatives. Ketamine would probably be the safest sedative for EMS to use.

Why don’t more of us have ketamine?

Footnotes:

^[1] D. Sustained monomorphic ventricular tachycardia
XIII. Acute management of specific arrhythmias
ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death–executive summary: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.
Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, Gregoratos G, Klein G, Moss AJ, Myerburg RJ, Priori SG, Quinones MA, Roden DM, Silka MJ, Tracy C, Blanc JJ, Budaj A, Dean V, Deckers JW, Despres C, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Tamargo JL, Zamorano JL, Smith SC Jr, Jacobs AK, Adams CD, Antman EM, Anderson JL, Hunt SA, Halperin JL, Nishimura R, Ornato JP, Page RL, Riegel B; American College of Cardiology/American Heart Association Task Force; European Society of Cardiology Committee for Practice Guidelines; European Heart Rhythm Association and the Heart Rhythm Society.
Eur Heart J. 2006 Sep;27(17):2099-140. No abstract available.
PMID: 16923744 [PubMed - indexed for MEDLINE]

Free Full Text from European Heart Journal with link to PDF Download

^[2] Therapy for Regular Wide-Complex Tachycardias
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.3: Management of Symptomatic Bradycardia and Tachycardia
Wide-Complex Tachycardia (Figure 4, Boxes 5, 6, and 7)
Free Full Text from Circulation with link to PDF Download