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

- Rogue Medic


Go watch Episode 2 of Code STEMI – Understanding STEMI from the ground up.

Tom Bouthillet of EMS 12 Lead talks with Dr. Christopher Granger, Mayme Lou Rettig and Dr. Jamie Jollis from Duke University Medical Center. They discuss Reperfusion of Acute Myocardial Infarction in Carolina Emergency Departments (RACE).

It is nice to see that the doctors are getting what is important.

The dichotomy between STEMI and trauma triage criteria could probably keep a team of psychiatrists busy for decades.

We want EMS to call the trauma alerts and we want EMS to call a lot of them, because maintaining competence in medicine is about the number of cases you see. Less than 5% accuracy is considered acceptable, since it is a numbers game and sometimes the blind squirrel actually looks like he can see. We grant a magical exception from medical competence in EMS, where we try to dilute paramedic experience to homeopathic levels by making almost every responder a paramedic (and usually those medics are cross-trained as something else, because that almost makes sense).

Since we discourage medical competence, we have to be creative in the excuses we use. Every system is unique, so we can’t claim that a system is screwing up – they are just meeting the needs of their patients in a way that works politically, but not medically, and we have to stop getting hung up on the medical part of EMS.

We reverse the criteria for calling STEMI alerts, but revert to magic as far as activation of the STEMI alert is concerned. We can’t trust medics, because even 5% over-triage is unacceptable. Interventional cardiologists are much more important than trauma surgeons.

Rather than have the medic focus on patient care and have his partner notify the hospital that they have a STEMI, there is still this need to distract the medic from paying attention to the patient so that the medic can focus on what is important – the magic phone call.

Here is a group of people not obsessed with the sleep of the STEMI team, but is interested in what is best for the patient.

What is best for the patient is reducing delays.

We need to make sure that paramedics know what they are doing.

We need to make sure that paramedics are getting appropriate feedback on their 12 lead interpretation and their patient care.

Imagine if EMS were about excellent patient care, rather than about dumbing it down to the comfort level of the most anxious and misinformed absentee medical director.

How much of a difference could we make in survival?

Go watch Episode 2 of Code STEMI – Understanding STEMI from the ground up.

Apparently, none of the pdfs work. Disregard the links below.

For more information on RACE view the presentations below. All presentations have been converted to PDF Format. The PDF Download will begin automaticall when you click a link below

Ideal World Case Study, by Jenny Underwood, RN, BSN RACE Coordinator for Durham/Greensboro/Chapel Hill

ACS Update, by Christopher Granger, MD

Lytic Hospitals; Meeting the Mark, by Mary Printz, Eastern NC RACE Coordinator

Non PCI Featured Presenters

RACE for Reperfusion, NON PCI Center Focus
Presbyterian Hospital Matthews & Presbyterian Hospital Huntersville

North Carolina Emergency Medical Services, by Greg Mears, MD, NC EMS Medical Director

Winston Salem Regional Report EMS ECG Transmission

Optimizing Door-to-Balloon Time: Strategies for Success

Final 55 of 58 Non PCI Centers Aggregate Data


On the Cult of Mechanism – Comment from Wonder_Aloud

Over at A Day in the Life of an Ambulance Driver is a post linking to my post about MOI (Mechanism Of Idiocy Mechanism Of Injury). Kelly makes some excellent points and –

Word to your mutha, RM. In fact, I’m stealing that line. Next time one of my co-workers makes a silly decision based solely on what the vehicle looked like, I’m going to ask him, “Are you an EMT, or an auto insurance adjuster?”


Mom says, Word up!

Also, you probably are re-stealing/stealing back the line.

Kelly’s post certainly generates many more comments than my posts do, even with DISQUS rejecting some of my comments. Unfortunately, DISQUS does not let me post two comments within whatever time period. The first comment disappears into DISQUS Limbo, or something. Darn you DISQUS!

My first comment was in response to this comment from Wonder_Aloud –

But with a STEMI you can do an EKG and say STEMI vs not. If we are truly going on presentation alone, gallbladder can present like STEMI without the EKG to differentiate. There isn’t the field equivalent of the EKG for trauma yet, so pertinent history has to play a larger role.

My response was along the lines of this –

There is more to trauma than MOI.

There is more to ACS (Acute Coronary Syndromes – heart attacks and related badness) than STEMI (ST segment Elevation Myocardial Infarction).

Let us assume that a patient with chest pain presents to the ED (Emergency Department) and the doctor reads the ECG (ElectroCardioGram) as not a STEMI.

Does the emergency physician send the patient home?

If we are to believe the comment from Wonder_Aloud, then the answer is easy.


Obviously, on seeing that the 12 lead does not return a reading of STEMI, the only thing for the doctor to do is to say –

Go and never darken my towels again!

Sorry, wrong movie.

Hakuna matata.

But do any of us know competent emergency physicians who would discharge chest pain patients based solely on a 12 lead?

No troponins?

No other cardiac enzymes?

What about EMS encouraging this patient to sign a refusal?

Do not tell a patient that he is not having a heart attack based on a 12 lead.

Contrariwise, it is reasonable, based on a thorough assessment, to transport a patient to a non-trauma hospital.

It is also reasonable to apply spinal clearance criteria, which EMS in Maine have been doing “Since 1995, and at all levels, including FR”, according to TOTWTYTR.

FR means First Responder. This is not limited to medics. This is not limited to basic EMTs. This means everyone responding in an official capacity is authorized to assess patients for spinal injuries and to determine that there is no need for spinal immobilization.

Is that 12 lead as clear as Wonder_Aloud would like us to believe?

There are NSTEMIs (Non-ST segment Elevation Myocardial Infarctions) and there are also STEMI mimics that are not even MIs.

Coronary artery spasm (Printzmetal or variant angina)
Early repolarization (normal variant in many men)
Acute cholecystitis
Acute pancreatitis
Intracranial hemorrhage
Acute cor pulmonale
Tako-Tsubo cardiomyopathy
Myocardial tumors
Left ventricular hypertrophy
Left bundle-branch block[1]

Tom Bouthillet also has a good post on this, with links to similar posts, at EMS 12 Lead ECG in ECG Mimics of Acute STEMI.

The suggestion was that STEMI is a simple assessment like MOI.


Trauma is more than MOI.

Heart attack is more than STEMI.

Let me know if that is too subtle.


[1] Myocardial infarction mimics ST segments.
Jacobson C.
AACN Adv Crit Care. 2008 Apr-Jun;19(2):245-8. No abstract available.
PMID: 18560293 [PubMed – indexed for MEDLINE]

Free Full Text PDF


Beta vs. Beta Blocker – comment

In the comments to Beta vs. Beta Blocker, Anonymous wrote . . .

Gang, is it time to review pharmacology?


It is almost never a bad time to learn more about pharmacology.

Dopamine acts as a beta agonist, but because it’s not terribly selective, it also acts as an alpha agonist. Metoprolol acts as a beta blocker and, because it’s highly selective, has relatively few alpha effects. So we might expect a patient who received appropriate doses of both dopamine and metoprolol to experience no net change in his beta activity. But his alpha activity would increase. Wouldn’t some peripheral vasoconstriction push our patient’s central blood pressure upwards?

But does the patient need any help with blood pressure?

If we are giving drugs to this patient, why use untested combinations?

I did not find any studies that examined the use of dopamine combined with metoprolol for the pure alpha effects of dopamine. Is there any research to support this?

Dopamine alone probably would have been harmful to TOTWTYTR’s patient. Metoprolol alone might also have been harmful (depending upon the heart’s position on the Starling curve.) But the combination seems potentially useful to me — and well within an emergency physician’s scope of practice to order.

It is interesting that you state that Dopamine alone probably would have been harmful. I agree that it is not a good idea under the circumstances.

TOTWTYTR describes it this way

an 80 year old gentleman complaining of dyspnea and chest pain (6/10). He’s conscious, alert, and oriented. He had “the look”. The one that we know when we see it, but can only describe as “looks like s@#$”. Which, come to think of it should be an official medical term. His skin is 2+ diaphoretic and pale, his respiratory rate is 28, lungs are clear. He is able to speak full sentences without difficulty. His radial pulse is 150, his BP is 68/P. His 12 lead EKG shows ST elevation in V1-4, with reciprocal changes in II, III, AVF.

Those circumstances are –

1. The patient had good radial pulses, even when the blood pressure is measured at 68 by palpation. A palpated pressure tends to run lower than an auscultated pressure, so this is probably a systolic pressure in the 70s.

2. The patient has received ASA (AcetylSalicylic Acid – Aspirin)[1] and oxygen. Since the patient’s lungs are clear, he was given 250 ml of NS (Normal Saline solution), but his 12 lead appears to rule out RVI (Right Ventricular Infarction).[2] We would expect ST elevation in leads II, III, and AVF if this were an RVI. While it is possible that the right ventricle is infarcting, we just do not have anything to support that conclusion.

3. After the 250 ml NS, the blood pressure is measured at 88/palp. So, probably a systolic pressure in the 90s.

Is this rise in pressure because of the fluid? Maybe.

Is this rise in pressure because of the oxygen? Maybe.

Is this rise in pressure because of the ASA? Maybe.

Is this rise in pressure because of placebo effects? Maybe.

Is this rise in pressure because of a homeopathic remedy? Sorry – kidding, I already mentioned placebo effects.

Has the patient’s pressure been labile (bouncing around with a very wide range)? Maybe.

Is this an example of spontaneous resolution of symptoms? Maybe.

Is this some combination of the above? Maybe.

We do not know. We are only guessing.

We only have 2 blood pressure data points to go by. This is not information that any conclusions should be based on. The least harmful interpretation appears to be – fluid helped, so try more fluid. But constantly reassess for signs that this is not the right treatment.

People are biased. We look for signs that we are doing something right, rather than signs we are doing something wrong. This patient appears to be close to dying. He needs for us to not make any mistakes.

Some patients do survive in spite of everything we do to them. We should not count on that.

The more treatments we use, the greater the chance that we will make a mistake. We are already treating this patient with 3 different treatments. I need a very good reason to add treatments at this point. He appears to be improving with the treatments already given. He may be improving in spite of the treatments already given.

Why are we giving the treatments?

Some may only want to get the pressure up so that they may give NTG (NiTroGlycerin, or GTN – Glyceryl TriNitrate in Commonwealth countries).[3] I am not in favor of this approach. Anyone with chest pain and a pressure that is not elevated is behaving abnormally. I am hesitant to throw a potent vasodilator into a patient, who recently had a pressure so low that I felt the need to treat it. My goal is not to see how close to death I can get him and still have him survive, even though that could make for some interesting blog posts.

If this is an RVI, then the approach is quite different. I am dumping as much fluid into the patient as I can. Part of the reason is to keep the pressure from dropping too much when I give NTG. RVI is different from the other heart attacks. RVI combined with another area of infarction is even more uncommon. Not having a V4R or MCR4 lead to look at, we cannot rule out RVI, even then we cannot be certain, but it seems very unlikely. On the other hand, the response to fluid is consistent with RVI. Could leads have been misplaced? Always a possibility, but unlikely to produce this result. My goal is to get the patient to the hospital in the best condition for him to survive. That does not mean the best looking vital signs. Although I am more comfortable looking at normal looking vital signs, I do not make them my goal. Vital signs are only some of the indicators of the patient’s condition. Their meaning is open to interpretation. There is still the possibility that this is an SVT (SupraVentricular Tachycardia), but I do not consider that likely, based on what TOTWTYTR wrote.

What might metoprolol (Labetolol)[4] do to this patient? Slow the heart rate and lower the blood pressure; Slow the heart rate and raise the blood pressure;[5] Or something else?

But the combination seems potentially useful to me — and well within an emergency physician’s scope of practice to order.

Now, the last sentence. With this patient, I am more worried about potentially harmful, than potentially useful. Where is the research to support this type of treatment? The theoretical and possibly illusory benefit does not make me feel comfortable with the many significant risks. The risks are all of the risks of metoprolol, all of the risks of dopamine, and any other risks that may result from combining these medications. I do agree that this should be within the emergency physician’s scope of practice to order. I am continually amazed at EMS protocols that place limits on the dosages or combination of drugs that may be ordered by a physician. Usually these limitations are on drugs that are dosed by titration – the initial dose should be estimated based on the weight, age, health, . . . of the patient. All subsequent doses should be based on the apparent response of the patient to the previous doses.

Opioids and benzodiazepines are the medications usually treated with these artificial limitations on the ability of the physician to give appropriate orders. If anything tells you that a treatment is poorly understood, it would be EMS protocols that do not allow physicians to give an order for that treatment, or EMS protocols that limit the orders the physician may give. Opioids and benzodiazepines are safe when given by competent paramedics – not paramedics with tons of experience, just competent paramedics. Why do these physicians prevent competent paramedics from giving these drugs? Because they know that they allow incompetent paramedics to work in their system. Such reckless physicians should not have anything to do with EMS.

Unfortunately, EMS is poorly understood. It is as much like the emergency department as the emergency department is like the ICU. On the other hand, things do appear to be improving. Is it hard to get paramedic students experience pushing benzodiazepines and opioids? If you are an emergency physician, you probably gave orders for both in your last shift. How hard is it to get a paramedic student some supervision and experience pushing these, reassessing, and finding out where the paramedic student’s assessment is leading him? That would be in a back woods EMS system. If you are near a burn center (even a trauma center), there are far more opportunities to give repeated and large doses of these medications. Repeated doses require reassessment, but so does the individual dose – otherwise, how do you know when it is it appropriate to stop, or pause, administering these medications? They should be given slowly, the patient should be reassessed, and they should be repeated until there is a reason to stop, or pause. The only time to stop at a maximum dose, would be because you have run out of the medication. The only way to determine too much/enough/not enough is by reassessments.

So, that is one view of the problem of protocols limiting physician orders. This is a different case. Medicine is a combination of Art and Science. A scientifically practiced art may apply more to EMS. Physicians should be aiming for something a bit higher – artfully practiced science. Too many do not get this. Some ignore the art and the science, in favor of a discipline in which they are not trained – law.

What I want to know, for this patient, who is looking better and has only a 4 minute ride to the hospital, is why mess with that? There is little reason to believe that this will help and a lot of reason to believe it will hurt. Where is the research to show that the dopamine/metoprolol combination is effective in the hospital? Where is the research to show that the dopamine/metoprolol combination is effective when used in EMS?

Surely TOTWTYTR knows his medical command physician better than we do; perhaps he’s a numbskull, perhaps not. We could second-guess the appropriateness of hanging a drip only 4 minutes from the ED. But on its face, the physician’s order does not seem utterly unreasonable to me.

The difference between a good idea and utterly unreasonable, to me, is whether it is supported by research. Theories are nice, but lead us into traps of overconfidence. CAST (the Cardiac Arrhythmia Suppression Trial) gave us a great example of that. The theory was that since, after a heart attack, people with PVCs tend to drop dead more often than those without PVCs. Therefore, getting rid of the PVCs will keep a lot of those people from dying. The opinion of the experts in cardiology was that this was going to save a lot of lives. The results of the trial were –

During an average of 10 months of follow-up, the patients treated with active drug had a higher rate of death from arrhythmia than the patients assigned to placebo. Encainide and flecainide accounted for the excess of deaths from arrhythmia and nonfatal cardiac arrests (33 of 730 patients taking encainide or flecainide [4.5 percent]; 9 of 725 taking placebo [1.2 percent]; relative risk, 3.6; 95 percent confidence interval, 1.7 to 8.5).[6]

Those taking encainide and flecainide were about 3 1/2 times more likely to die of arrhythmia. The drugs were supposed to have the opposite effect. The drugs were supposed to prevent death from arrhythmia. Since then, prophylactic use of antiarrhythmic drugs has pretty steadily decreased. Except for the thrall over amiodarone.

Expert opinion is important. Unfortunately, if the experts are misinterpreting some of the information, even though it is the state of the art science, at the time, bad treatments can result. Encainide and flecainide did a great job of getting rid of PVCs, but PVCs were not killing the patients. PVCs were just an indication of an injured heart. People with injured hearts and PVCs may have arrhythmic events more frequently than those without PVCs, but getting rid of the PVCs does not cure the heart. It just changes the conduction of electricity in the still injured heart.

So, while the emergency physician is the expert, I am hesitant to treat based on a theory of how things should work. If there is well done research of the effects of a combination of drugs in humans, then I am much more likely to just follow orders.

[Updated 8/11/2019 to correct grammar, spelling, and dead links]


[1] Aspirin

[2] Recognition and treatment of right ventricular myocardial infarction.
Gandy WE.
EMS Mag. 2008 Mar;37(3):69-73, 100.
PMID: 18814636

Free Full Text from EMS World

[3] Nitroglycerin

[4] LABEL: METOPROLOL TARTRATE- metoprolol tartrate injection, solution
FDA Label

[5] Dynamic left ventricular outflow tract obstruction in acute myocardial infarction with shock: cause, effect, and coincidence.
Chockalingam A, Tejwani L, Aggarwal K, Dellsperger KC.
Circulation. 2007 Jul 31;116(5):e110-3. Review. No abstract available.
PMID: 17664378

Free Full Text from Circulation

[6] Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction.
Cardiac Arrhythmia Suppression Trial (CAST) Investigators.
N Engl J Med. 1989 Aug 10;321(6):406-12.
PMID: 2473403

Beta vs. Beta Blocker


RM has a good head, a good EMS head. Maybe we should just call him that from now on. EMSH.

Emergency Medical S@#$ Head?

Them’s pooping words!

Well, enough bathroom humor. TOTWTYTR presents the case of a patient who is sick

His radial pulse is 150, his BP is 68/P. His 12 lead EKG shows ST elevation in V1-4, with reciprocal changes in II, III, AVF.

He has no significant medical history, takes 81 mg ASA daily, and has no known drug allergies.

IV, EMS aspirin (it isn’t likely to hurt if we give more, but not getting enough aspirin would be a bad thing), oxygen, and some normal saline solution (standard EMS IV fluid).

After 250ml of saline, the patient is still tachycardic, still has chest pain, but his BP is now 88/p.

Here is where it becomes interesting.

Medical control orders Dopamine at 5mcg/kg/min. He also orders Lopressor 5mg IV.

You and your partner are concerned about the effect the Lopressor might have on the BP and try to defer the drug until you are at the hospital. The doctor repeats his orders and tells you that he doesn’t want to delay the patients trip to the cath lab.

So, what do you do now? You are four minutes from the ED door.

There were some creative responses to the situation, even the suggestion of a new name for me. :)

Here is the way I look at this patient. I like to keep things simple. There is very little research to show that EMS is truly beneficial to this patient. There is research that has been done in hospitals, but I don’t know of any studies that looked at the specific combination of medications listed.

The initial BP (Blood Pressure was) 68/palp (palpated).

A palpated systolic pressure is generally a bit lower, maybe 10 points lower, than an auscultated systolic pressure. Palpation of the blood pressure is feeling the pulse, keeping the fingers in the place the pulse can be felt, inflating the BP cuff to the point where the pulse can no longer be felt, letting the cuff deflate slowly until the pulse can be felt again. Auscultation is using a stethoscope to listen for the changes in sounds that are produced when deflating the cuff.

The initial BP of 68/palp is uncomfortably low. The patient presentation does nothing to alter that perception. This patient appears to be having a heart attack. The most important drug is the one he takes every day – aspirin. More is given by EMS. No problem there. Some oxygen is given, how much is not specified, but the AHA (American Heart Association) recommends –

EMS providers may administer oxygen to all patients. If the patient is hypoxemic, providers should titrate therapy based on monitoring of oxyhemoglobin saturation (Class I).[1]

The use of dopamine is mentioned on the label for metoprolol (Lopressor) – as a treatment for metoprolol overdose –

Hypotension: A vasopressor should be administered, e.g., levarterenol or dopamine.[2]

On the dopamine label, there is mention of dopamine and metoprolol drug interaction –

Cardiac effects of dopamine are antagonized by beta-adrenergic blocking agents, such as propranolol and metoprolol.[3]

Maybe Dr. Rumble Fish at medical command was not looking for any cardiac effects from dopamine.

I suppose that it would be interesting to throw them into a patient to watch them fight it out. Not nice. Not civilized. Not ethical. Not humane. Just interesting.

On the other hand, there is a case report that brings up the question of LVOTO (Left Ventricular Outflow Tract Obstruction) in AMI (Acute Myocardial Infarction) with shock.[4] One of the points of this article is that the use of inotropes, such as dopamine, is not to be encouraged if LVOTO is suspected; beta blockers may calm things down and by lowering heart rate, improve BP and patient presentation. I suspect that Dr. Rumble Fish (medical command) was trying to accomplish two tasks, but refusing to acknowledge the problems of trying to combined treatments that antagonize each other.

Some other suggestions for treatment were for the antiarrhythmic drugs – amiodarone and lidocaine.

Amiodarone is not known for being a systolic enhancing drug. Its tendency toward producing hypotension may increase the need for cardioversion of otherwise stable arrhythmia patients. Yes, even VT (Ventricular Tachycardia) can be stable for extended periods.

Lidocaine is just plain ineffective. A placebo would probably be as effective. With a narrow complex, lidocaine is not indicated. With a wide complex, you need to avoid bi-fascicular blocks, which are not common, but they tend to develop into a much more stable rhythm. Asystole.

Eventually, I will complete at least one of my antiarrhythmic posts.

Back to our unstable patient. If the BP goes from 68/p to 88/p with 250 ml, why are we not happy with the progress?

Why are we throwing different drugs at the patient? Possibly very dangerous drugs.

Are the lungs still clear? 250 ml might be enough – with this patient – to cause problems.

Another 250 ml is not exactly going to land you a spot on the next Medics Gone Wild video.

The beta blocker is supposed to slow the heart rate, rather than vasodilate. By slowing the heart rate, the blood pressure is expected to drop. On the other hand, it is possible that the patient’s blood pressure is so low because of the heart rate. If you look at the calculation for maximum heart rate (220 – age = maximum heart rate), you will see that this patient is breaking the law. What does that mean?

This is a formula for predicting what the maximum heart rate of the average person will be. It is based on a complex set of variables that include all of the following: Age.

OK, the formula is not at all complex and does not take any variables into effect, except for age. There is at least one ED physician on the lecture circuit, who teaches management of tachyarrhythmias and uses this formula to demonstrate where the dividing line between ST (Sinus Tachycardia) and SVT (SupraVentricular Tachycardia) resides for narrow complex tachycardias.

This may work for Dick and Jane Call 911 and Watch Adults Treat a Tachycardia. As long as Dick and Jane are just calling 911, this is probably not dangerous. It is when you progress beyond Dick and Jane Don’t Do Diddly to a higher level, such as EMT, that you need to recognize how flawed this bi-polar approach is. Tachycardia is not a word that belongs in a Dick and Jane book. Likewise, those limited to monosyllabic expression should not be treating tachycardias. Duh!

For the young man described by TOTWTYTR, the age is 80 years. Using this formula, we can see that his heart rate is greater than his calculated maximum heart rate. 220 – 80 = 140. His rhythm is narrow complex. The rate is 150. Therefore, according to the Formula for Oversimplification and Execution, he has an SVT (possibly a rapid Atrial Fibrillation or VT).

If you approach this patient as having any of those conditions, you would be justified in zapping his heart to a standstill. This is because the arrhythmias listed can be improved with cardioversion. The problem with this patient, although I cannot see the rhythm to identify it, is probably not one of these arrhythmias. Mr. Geezer appears to be having a heart attack. This is something that may cause significant stress. His heart is racing. Perhaps trying to get as many beats in before retirement.

Another example of the folly of this simplistic rule of maximum calculated heart rate is a bit more personal for me. While working out, I often get my heart rate well above my calculated maximum heart rate for extended periods. And yet, I manage to cool down afterward without adenosine, without amiodarone, without cardioversion. It is almost as if I were not violating rules of nature. :)

What are the options?

Antiarrhythmic drug/cardioversion – bad ideas in my opinion.

Beta agonist (dopamine) – bad idea in my opinion.

Beta blocker (Lopressor) – if you have strong reasons for suspecting LVOTO, this may be a good idea. If you believe that the heart rate is the primary problem and fluid is not a problem, ditto.

Fluid – BP of 68/palp (which might translate to an auscultated BP of 78/?) appears to have brought the pressure up to 88/palp (which might translate to an auscultated BP of 98/?).

Mr. Geezer has had aspirin. He is receiving oxygen. He received fluid and now his pressure is probably above 90 systolic.

Why would dopamine be a good idea?

Dopamine is for people who do not improve with fluids.

Is there a more basic understanding of the use of dopamine than that? True, dopamine is used when fluids are contraindicated, but that does not mean that dopamine comes before fluids in other cases.

Dopamine should be used only with reluctance for patients experiencing a heart attack. Dopamine can be a very dangerous drug for a patient having a heart attack. Mr. Geezer appears to be having a heart attack. He appears to be improving with fluids. He does not appear to be someone who would benefit from dopamine – unless things change.

Do we have enough information to decide about LVOTO? I don’t think so.

The patient appears to be improving enough to take the 4 minute ride to the hospital without further treatment, in my opinion.

Perhaps Dr. Rumble Fish (medical command) should avoid the martial arts orders. This patient has a huge potential to get worse, a short transport time, appears to be improving with treatment, and no good reason to explore experimental therapy.


^ 1 (Circulation. 2005;112:IV-58 – IV-66.)
© 2005 American Heart Association, Inc.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Part 8: Stabilization of the Patient With Acute Coronary Syndromes

^ 2 Lopressor (metoprolol tartrate) injection, solution; DailyMed

^ 3 Dopamine hydrochloride and dextrose (Dopamine Hydrochloride and Dextrose) injection, solution; DailyMed

^ 4 Dynamic Left Ventricular Outflow Tract Obstruction in Acute Myocardial Infarction With Shock: Cause, Effect, and Coincidence
Anand Chockalingam, Lokesh Tejwani, Kul Aggarwal, and Kevin C. Dellsperger
Circulation. 2007;116:e110-e113, doi:10.1161/CIRCULATIONAHA.107.711697
FREE Full Text | FREE PDF – At least they appear to give full access for free.


Every Drug in the Box

The problem of using every relevant, but perhaps not necessary, drug is something medics, nurses, and doctors are bad at. The major exceptions to this are sedation and pain management. Then the problem is getting the doctor to allow the box to be opened. Both demonstrate a lack of understanding of pharmacology and assessment.

I was discussing, with some doctors, a journal article about an anaphylactic patient, who received about a dozen different medications. I suggested that some of the problems the patient experienced were probably from all of the drugs being pushed.

“Horse feathers. There is nothing wrong with giving all of the potentially indicated drugs to the patient.” OK, not the exact wording of the doctors, but it seems to capture the sentiment.

Potentially indicated and indicated are worlds apart.

It isn’t as if there is any research on the administration of all of these medications combined. There are far too many variables to control for, much too small an incidence of anaphylaxis that does not respond to standard treatments, and apparently not enough interest in questioning the just dump the box into the patient philosophy demonstrated.

In cardiac arrest algorithms, it is nice to be moving away from the let’s get rid of all of the expiring drugs approach. We still have a long way to go in recognition of the lack of benefit of ALS (Advanced Life Support) treatment of dead people. It is a start.

Currently, the AHA (American Heart Association) does not feel that an IV is that important. They have been gradually moving in this direction over the past couple of decades. Eventually, they will probably only recommend medications specifically indicated for potentially reversible causes, rather than everybody dead gets epi – and/or vasopressin.

For victims of witnessed VF arrest, prompt bystander CPR and early defibrillation can significantly increase the chance for survival to hospital discharge. In comparison, typical ACLS therapies, such as insertion of advanced airways and pharmacologic support of the circulation, have not been shown to increase rate of survival to hospital discharge.

After beginning CPR and attempting defibrillation, rescuers can establish intravenous (IV) access, consider drug therapy, and insert an advanced airway.

One of the problems with research, on a bunch of drugs given to the same patient, is that there are so many variables involved. This does not only affect the research, but the administration, too. When patient presentation changes, how do you know what the likely cause was?

Is it the effect of medication?

Is it a side effect?

Is it spontaneous remission?

Is it an erroneous assessment?

Is it the last medication given?

The first?

The third?

Is it a combination of the medications?

We do not know. How do most people deal with this? They act as if it must be the most recently given medication.

Is there a reason to believe that this is the correct approach?


Here is the logic that is applied by those, who insist that the drugs are essential:

1. Successful resuscitation is having the patient leave the hospital in about the same condition as they were before the cardiac arrest.

2. Having a pulse is necessary for a successful resuscitation.

3. Therefore, anything that leads to pulses is good, or one step closer to #1.

Unfortunately, things are not that simple. While it is hard to resist the I’m going to Disneyland! response at this point. The most common outcome for patients who have a return of a pulse is that the pulse goes away again. At some point during the resuscitation, the pulse usually goes away permanently.

Getting a pulse back is the almost immediate response that is similar to what a crack addict feels – a rush. There is a need to replicate that, and it is easy, you give enough epi to a corpse and you often get a pulse.

There is a quote above supporting the focus on excellent chest compressions and rapid defibrillation. It is immediately followed by a quote that points out the futility of the mistaken, but persistent, focus on ALS in cardiac arrest. I include both sentences together, now. the italics are mine.

For victims of witnessed VF arrest, prompt bystander CPR and early defibrillation can significantly increase the chance for survival to hospital discharge. In comparison, typical ACLS therapies, such as insertion of advanced airways and pharmacologic support of the circulation, have not been shown to increase rate of survival to hospital discharge.

If the patients who never get drugs are leaving the hospital (with an intact brain) at least at the same rate as the patients who received drugs, then maybe the drugs do not help.

If we only focused on things that produce a pulse, would we include defibrillation?

Defibrillation produces a pulse.

No. Defibrillation produces asystole. During the asystole, it is hoped that the patient’s heart has at least one pacemaker that initiates an organized rhythm. It is further hoped that the rhythm does produce a pulse.

Resuscitation is about resuscitating the heart and the brain, not about giving enough drugs to get a pulse.

Perhaps cerebral resuscitation is about a little bit more.

And the medic, with his medic-feet ice-cold in the snow,
Stood puzzling and puzzling:

How could it be so?

It came without drugs! It came without tubes!
It came without gadgets, IVs or drips!

And he puzzled three hours, till his puzzler was sore.
Then the medic thought of something he hadn’t before!

Maybe Resuscitation,

he thought

doesn’t come from a drug store.
Maybe Resuscitation… perhaps… means a little bit more!

And what happened then…? Well… in BLS-ville they say
That the medic’s understanding grew three sizes that day!

And the minute the patient’s heart didn’t feel quite so tight
He whizzed with his load away from the bright dying light

He brought back the brain! And the heart for the pulse!


The medic got a real save!

To paraphrase a great doctor.

Adapted from How the Grinch Stole Christmas.

Theodor Seuss Geisel, better known as Dr. Seuss.


A Case of Very Rapid Cath Lab Activation.

Last week Dr. Wes wrote The Race is On! about an article Saving a Life in 14 Minutes in the Boston Globe.

The article is interesting for a few reasons. It includes a time line, one that does not omit the EMS times. That is what I am going to focus on.

There are a few important questions from the time line.

8:31 EMS is dispatched.

8:34 EMS meets him at his front door. It should only take a couple of minutes to get to the ambulance and start transporting while assessing and treating. A 3 minute response time is good.

8:42 He is wheeled into the ambulance. 8 minutes later. It only took 3 minutes to “hop into an ambulance for the half-mile trip to Rosen’s house moments after his 911 call.

8:50 The ambulance is en route and notifying the ED of a STEMI. Why not notify when the first 12 lead was done, if the goal is to reduce delays? Although in this case it does not seem to have mattered, not all hospitals will respond as quickly. Yet, another 8 minutes apparently on scene.

8:57 Arrival at the ED.

9:01 Wheeled through ED doors. It took 4 minutes to get from the ambulance to the ED doors? It took less time to drive to the residence and meet the patient at the front door.

Interesting that the only ED contact mentioned is on the radio. The 12 lead ECGs are handed to a cardiology fellow, who works in the cath lab. They go straight through the ED to the cath lab, without stopping. Is there any improvement to the care of the patient that might be contributed by stopping in the ED? No.

The rest of the time line is in the story, but does not relate to EMS as much.

In the ambulance bay, the paramedics perform a second EKG to hone in on the site of the attack. As Rosen’s pain intensifies, they insert IVs and give him morphine and fluids.

They are referring to the interior of the ambulance as the ambulance bay, not the area at the ED where ambulances park. A 2nd 12 lead is nice, but all of this can be done en route – including IVs and drugs. 12 leads can be done while moving. Shaving the chest, if necessary for application of leads, can be done with an electric razor while moving. Using benzoin makes a big difference in getting leads to stick, which can otherwise cause a lot of delays in obtaining a readable 12 lead.

The description of treatment suggests that this was an RVI (Right Ventricular Infarction), since no NTG (NiTroGlycerin in the US, or GTN – Glyceryl TriNitrate elsewhere) was given, but fluids were given (perhaps I am just reading too much into it). There is not much reason to sit on scene for this stuff. Things that do matter are access to the front door of the residence with the stretcher. Was this a reason for delay? Why morphine, when fentanyl is a safer drug – especially with RVI?

If “Kevin and I recognized his heart attack immediately,” why does it take so long to get going?

A study in The Journal of the American College of Cardiology looked at the best practices for improving door to balloon times.

The ideal process (Fig. 1) represents a synthesis of the best practices found in the sample of 11 hospitals and is not meant to reflect the specific process of any single hospital in the study. The door-to-balloon process for patients transported to the ED with a prehospital ECG performed and read by a paramedic before hospital arrival is depicted by Path #1 in Figure 1.

For patients with a pre-hospital ECG indicating STEMI, the benchmark door-toballoon time is 60 min (Fig. 2).

For patients arriving without a pre-hospital ECG, the benchmark door-toballoon time is 80 min (Fig. 3).

No need for telemetry to further delay patient treatment.

Looking at the times:

8:31 response, 8:34 patient contact at front door, 8:42 in ambulance, 8:50 en route with STEMI notification by radio, 8:57 at ED, 9:01 rolling through ED doors and by-passing the ED.

8 minutes from the patient’s door to the ambulance. He met EMS at the door.

8 minutes from entering the ambulance until en route (not sure if I am reading this correctly).

4 minutes from the ambulance arrival at the ED to the ED doors.

There are 20 minutes that could not be completely eliminated, but should be dramatically reduced.

The time from door to balloon is less than the amount of the apparently avoidable EMS delays.

I realize that this article may not be accurate, that these times can never be completely eliminated, that I am reading a bit into this article, but WTF?

Historically, almost all of the unnecessary delays have been in the hospital. Here, it is the hospital that seems to have its act together. Ideal timing does seem to be one thing working in the favor of this patient. He arrived at 9 AM on a week day. The cath lab may have been preparing to take their first scheduled, non-emergency patient of the day and just had to defer that case for a while.

The cardiology fellow is waiting in the ED for the patient. There is little reason for the ED to be involved in the care of this patient. Look at the amount of time saved by the EMS notification of a cath lab patient and by the cath lab staff coming to the ED to take the patient directly to the cath lab.

Let’s add in the 4 minutes that the ambulance was at the ED, but not yet through the doors – 18 minutes door to balloon.

Just to complicate things we can put some butter on the fingers of Dr. Shah, who took just 6 minutes from initiating femoral access to inflating the balloon. How about adding 30 minutes – adding 5 times as long as it actually took. This would still give a door to balloon time of 48 minutes. The AHA and JCAHO goal is less than 90 minutes. This is just a smidge more than half of that goal.

If we can by-pass the ED, difficult if the cath lab team is not in the hospital, the amount of time saved is tremendous. This is not a criticism of the ED – we do the same thing with trauma. The cath lab team needs to be prepared to take the patient right away.

Bradley EH, Roumanis SA, Radford MJ, Webster TR, McNamara RL, Mattera JA, Barton BA, Berg DN, Portnay EL, Moscovitz H, Parkosewich J, Holmboe ES, Blaney M, Krumholz HM.
Achieving door-to-balloon times that meet quality guidelines: how do successful hospitals do it?
J Am Coll Cardiol. 2005 Oct 4;46(7):1236-41.
PMID: 16198837 [PubMed – indexed for MEDLINE]

More on Epinephrine in Cardiac Arrest.

In Epinephrine in Cardiac Arrest and Dead VT vs Not Quite Dead, Yet VT I wrote about some of the reasons that epinephrine may not be a good idea in cardiac arrest. It does improve ROSC (the Return Of Spontaneous Circulation – getting a pulse back).

If you were having a heart attack, but now are experiencing cardiac arrest, is epinephrine good for you?

Here is what AHA (American Heart Association) states about ACS (Acute Coronary Syndrome – heart attacks and related conditions).

Acute myocardial infarction (AMI) and unstable angina (UA) are part of a spectrum of clinical disease collectively identified as acute coronary syndromes (ACS).

Sudden cardiac death may occur with any of these conditions. ACS is the most common proximate cause of sudden cardiac death.6–10

“Everybody dead gets Epi,” is what I tell students. It seems to help them remember the initial part of the arrest algorithms. Things have changed with the use of vasopressin as an alternative to epinephrine. Still, the thought process that goes into giving epinephrine is as mindless as ever.

If epinephrine is the wonder drug in cardiac arrest, and “ACS is the most common proximate cause of sudden cardiac death.6–10″ Then why is there not a single mention of epinephrine in the treatment of ACS. Go, search the document. Nothing.

Cardiac arrest is part of the expected progression of the ACS.

Cardiac arrest appears to be happening most often to those with ACS.

Epinephrine is the first IV drug given for all cardiac arrests.

Why is there no consideration of treating ACS with epinephrine, even accidentally?

Even if ACS is not the cause of cardiac arrest, but only coincidentally present, this is an important consideration.

How do these ACS patients benefit from epinephrine?

AHA does not even mention epinephrine, when discussing ACS treatment.

Is a vasopressor, such as epinephrine, essential for resuscitation?

Although epinephrine has been used universally in resuscitation, there is a paucity of evidence to show that it improves survival in humans. Both beneficial and toxic physiologic effects of epinephrine administration during CPR have been shown in animal and human studies.44–50

To date no placebo-controlled trials have shown that administration of any vasopressor agent at any stage during management of pulseless VT, VF, PEA, or asystole increases the rate of neurologically intact survival to hospital discharge. There is evidence, however, that the use of vasopressor agents favors initial ROSC.

The placebo controlled trials of epinephrine in cardiac arrest have not shown any improvement in meaningful survival with epinephrine. So, epinephrine has not been shown to be better than a fake treatment.

Epinephrine is full of side effects. These are not considered to be good for ACS. It is not unreasonable to expect that most of the patients treated with epinephrine in cardiac arrest have ACS at the time of arrest.

Shouldn’t we be careful in giving epinephrine to these patients?

It may be that epinephrine does produce a long term benefit to some of these patients, but shouldn’t we find some way of discriminating among these patients to determine who might benefit?

Instead we indiscriminately give epinephrine to all patients in cardiac arrest.

The research does not support using epinephrine in cardiac arrest.

The physiology of giving epinephrine to someone with ACS is ignored.

(Circulation. 2005;112:IV-89 – IV-110.)
© 2005 American Heart Association, Inc.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Part 7.2: Management of Cardiac Arrest

Part 8: Stabilization of the Patient With Acute Coronary Syndromes