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

- Rogue Medic

Safety and Effectiveness of Field Nitroglycerin in Patients with Suspected ST Elevation Myocardial Infarction


Is prehospital use of NTG (NiTroGlycerin; GTN GlycerylTriNitrate in Commonwealth countries) safe for treating prehospital suspected STEMI (ST segment Elevation Myocardial Infarction) patients?

The evidence is limited, but does not suggest that prehospital NTG produces enough harm to discourage use in suspected STEMI. These researchers looked at the emergency department assessments of patients following prehospital NTG for suspected STEMI.  

Despite the theoretical risk, the limited retrospective studies of NTG in the prehospital setting for multiple indications suggest that the medication is safe.(10-13) However, with regard to NTG use for STEMI, the AHA International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care concluded that there was not enough evidence to determine the benefit or harm of out-of-hospital use of NTG.(14) Given the high false positive rates for STEMI identified in the field, an additional concern is that many patients treated with NTG for presumed STEMI will ultimately have an alternate etiology for their pain.(15, 16) Therefore, it is not clear that the benefits outweigh the risks of administering NTG to all patients with suspected STEMI in the field.[1]

This paper helps to show the safety of prehospital NTG for suspected STEMI, providing evidence that blood pressure changes were similar in suspected STEMI patients with an SBP (Systolic Blood Pressure) of 100, or higher, regardless of whether they were treated with NTG. The study is a retrospective chart review, so we do not know why some of the patients were not treated with NTG.

One reason mentioned, but not discussed, is that only 22% (96 of 440) suspected STEMI patients not treated with NTG are documented to have had pain, but there is no information on the type of pain or other cardiac symptoms of the patients. Were the paramedics avoiding treating atypical chest pain, such as pressure, heaviness, gastric discomfort, difficulty breathing, et cetera? We do not know. Was only chest pain being documented, rather than shoulder, or arm, or jaw, pain? We do not know. Did the pain resolve prior to EMS arrival? We do not know. Were the paramedics correctly recognizing when the machine interpretation of the ECGs (ElectroCardioGrams) were wrong? We do not know.

The median Initial Pain Score is documented as 8, with an IQR (Inter-Quartile Range) of 5-9 for those treated with NTG. For those not treated with NTG the Initial Pain Score is documented as 0, with an IQR of 0-0. We do not know the Initial Pain Score of those who did have pain, but were not treated with NTG. All of these patients were in an IQR that was not documented in the paper. The good news is that the suspected STEMI patients not treated with NTG act as a control group, although possibly with important differences that are not discussed in the paper.

Click on the image of the LA County protocol to make it larger.[2]

What about the 17% of suspected STEMI patients with SPB <100 mmHg who were treated with NTG?

Was medical command (California has certified MICNs [Mobile Intensive Care Nurses] providing medical command on the radio, with physicians available, as well) contacted for authorization to deviate from the protocol? If so, that is something that should be documented in the charts, which were reviewed for this paper. That information is not included in this paper. Those patients are much more interesting to me.

I do not object to using NTG to treat suspected STEMI with an SBP below 100 mmHg, but the authors seem to think that EMS should not even consider it. Do the outcomes of those patients support the approach of the authors? We do not know.

I suspect that the fears of bottoming out the blood pressure are very exaggerated, but it would be nice to have some evidence either way.

An important secondary end point was the differences between those with inferior/right ventricular STEMI, but treated with NTG.  

By vasodilating all blood vessels, and the venous system in particular, it causes a drop in blood pressure and preload. Thus, there is concern for precipitating hypotension in ACS involving the right ventricle.(1-3) Contraindications to the use of NTG, as outlined by the American Heart Association (AHA) Guidelines on the treatment of ACS, include right ventricular infarction.(4) This raises concern for use in inferior ST-segment elevation myocardial infarction (STEMI) in the prehospital setting, since many inferior STEMI result from proximal right coronary artery (RCA) occlusion and 50% involve the right ventricle.(3) Traditional 12-lead ECG is focused mainly on the left side of the heart and typically EMS protocols do not include acquisition of right-sided ECG leads. Further, in many systems, Basic Life Support (BLS) protocols allow for administration of NTG without differentiating the location of STEMI. There is also risk of other adverse events including bradycardia and cardiac arrest.(5-9)[1]

I have aggressively promoted the use of NTG for even hypotensive CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure). Many physicians are not comfortable with that, even though the available evidence shows that aggressive IV NTG doubled the survival rate for these hypotensive patients. More research is needed on the use of NTG, especially in hypotensive patients.  

Further, we did not find an increased risk of hypotension among patients with proximal or mid RCA occlusions confirmed on coronary angiography. There are several possible reasons for our findings. First, while right ventricular involvement in inferior STEMI is common, hemodynamic instability is actually rare due to the right ventricle’s more favorable oxygen supply-demand ratio compared to the left heart and more extensive collateral flow.(3, 22) In addition, left heart occlusions may also involve the right ventricle and result in a preload dependent condition.(23-25) While limited by sample size, our results suggests that specifically avoiding NTG use in inferior STEMI, which is common in EMS systems, may be misguided. One quarter of the local EMS agencies in the state of California, for example, currently prohibit the use of NTG in inferior STEMI.(26) This analysis would benefit from additional study with a larger sample size and specific information about the infarct territory. Further studies are needed to determine which patients, in particular, are at increased risk for hypotension when treated with NTG.[1]

Perhaps NTG is also safe for treating patients with inferior ischemia and even right ventricular ischemia.


[1] Safety and Effectiveness of Field Nitroglycerin in Patients with Suspected ST Elevation Myocardial Infarction.

Bosson N, Isakson B, Morgan JA, Kaji AH, Uner A, Hurley K, Henry TD, Niemann JT.

Prehosp Emerg Care. 2018 Dec 17:1-9. doi: 10.1080/10903127.2018.1558318. [Epub ahead of print]

PMID: 30556765

[2] Treatment Protocol: Chest Pain */ Acute MI

Reference No. 1244

LA County Paramedic Protocols

Los Angeles County Department of Health Services – Emergency Medical Services



More Oxygen in the New AHA Guidelines

Just kidding. We have Less Oxygen in the New AHA Guidelines.

I had a patient who had a pulse oximetry in the 80s. The people on scene were trying, unsuccessfully, to keep a non-rebreather mask on the patient. The patient has dementia, is uncooperative, and is oxygen dependent. I switched her from high-flow oxygen by mask to a cannula at 2 LPM. Everything I did would be criticized by someone who follows the old EMS rules, but these rules are not valid rules. The patient had nice pink conjunctivae, warm extremities, strong pulses, good capillary refill, and good lung sounds, although she was rather agitated. She had kept fighting to take the mask off, but she did tolerate the cannula.

Once she was no longer fighting to remove the mask, we were able to obtain a more accurate oxygen saturation. The number had been displayed on the pulse oximeter with a waveform that was consistent with partial capture, but that does not mean that the actual oxygen saturation is higher than the number displayed. That just means that the number displayed may not be accurate. It could be inaccurately low. It could coincidentally display an accurate number. It could also display an inaccurately high number. My assessment of the patient contradicted the low oxygen saturation reading, so I chose to follow my assessment, while continuing to reassess.

We moved her to the ambulance and my partner started to drive, then the patient calmed down and we were able to see the oxygen saturation rise to the upper 90s.

No sedation. No mask. Just some hand holding and a quiet ride.

If I were concerned with the rules, I would have done things very differently and the patient would probably have been much worse off. The patient was not benefiting from wrestling with medical personnel in a fight to force an oxygen mask onto her face, just to make a number look better on the documentation. I also left a copy of the good waveform with her, when I transferred care, so that others would have some evidence that she is able to produce adequate oxygen saturation with minimal oxygen. RTs are good at paying attention to what works.

Common practice has been for basic EMT’s to administer oxygen during the initial assessment of patients with suspected ACS. However, there is insufficient evidence to ‘support or refute oxygen use in uncomplicated ACS. If the patient is dyspneic, hypoxemic, has obvious signs of heart failure, or an oxyhemoglobin saturation <94%, providers should administer oxygen and titrate therapy to provide the lowest administered oxygen concentration that will maintain the oxyhemoglobin saturation 94% (Class I, LOE C).238[1]

This patient was not complaining of anything that might be considered an ACS (Acute Coronary Syndrome), but she was not complaining of anything respiratory, either.

In what way would she have been better off with too much oxygen?

TOTWTYTR writes on the same subject in More About the New AHA CPR Guidelines.

AD writes about this in Two Steps Forward, One Step Back.


[1] Acute Coronary Syndromes
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 5: Adult Basic Life Support
Special Resuscitation Situations
Free Full Text Article with links to Free Full Text PDF download


Oxygen in the New AHA Guidelines

With all of the concern about deviating from the AHA (American Heart Association) Guidelines, will EMS agencies be as aggressive in changing their treatment with oxygen?

Will IRBs (Institutional Review Boards) be as aggressive in demanding that research not deviate from this standard of care?

Will the EMS agencies, that do not adopt this guideline, be sued by plaintiffs’ lawyers for harm that was clearly due to deviation from this standard of care?

Since everybody seems to interpret what the AHA includes in the guidelines as the standard of care, should this be any less of a standard of care than, Everybody dead gets epi?

Common practice has been for basic EMT’s to administer oxygen during the initial assessment of patients with suspected ACS. However, there is insufficient evidence to ‘support or refute oxygen use in uncomplicated ACS. If the patient is dyspneic, hypoxemic, has obvious signs of heart failure, or an oxyhemoglobin saturation <94%, providers should administer oxygen and titrate therapy to provide the lowest administered oxygen concentration that will maintain the oxyhemoglobin saturation 94% (Class I, LOE C).238[1]

In case all of those words make this seem a bit too complicated –

basic EMT’s

Not just doctors, nurses, or paramedics.

If the patient is dyspneic, hypoxemic, has obvious signs of heart failure, or an oxyhemoglobin saturation <94%

Not just because the patient is being treated for an Acute Coronary Syndrome (Chest Pain or an atypical cardiac presentation), but only with actual assessment findings that there is a probable lack of oxygen.

should administer oxygen and titrate

Not just deliver as much as they can.

administer oxygen and titrate therapy to provide the lowest administered oxygen concentration that will maintain the oxyhemoglobin saturation 94% (Class I, LOE C).

Not the highest oxygen concentration possible.

Not even in the upper 90s.

Not any mention of this being for COPD (Chronic Obstructive Pulmonary Disease) patients, who may actually be better off at lower oxygen saturations.

Not a, possibly helpful, Class IIa recommendation.

Not a, We don’t have any good evidence, but we would rather make the mistake of doing something harmful, than make the mistake of not doing something beneficial, ClassIIb recommendation.

This is a Class I recommendation.


[1] Acute Coronary Syndromes
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 5: Adult Basic Life Support
Special Resuscitation Situations
Free Full Text Article with links to Free Full Text PDF download


Early Warning For Atypical Chest Pain

There is an article[1] in yesterday’s newspaper about an early warning for chest pain. There is also a video with better explanations of the device.[2]

Why would anyone need an early warning for chest pain?

Not all chest pain is the typical crushing feeling over the middle of the chest. Actually, the chest pain considered to be typical may be the atypical presentation.

We may be doing people a disservice by convincing them that the atypical presentation is unusual. Typical chest pain is the kind of experience that is almost impossible to ignore. Anything that feels as if your chest is being crushed, is going to be difficult to ignore . . .

Difficult to ignore?

OK. It is impossible to ignore, but it is difficult to rationalize as something other than cardiac chest pain. Maybe this should be described as Typical Male Chest Pain. This isn’t about being politically correct, but women are much more likely to experience heart attacks without the typical crushing chest pain, than men.

However, the other presentations of an Acute Coronary Syndrome (ACS), or what people generally call a heart attack, can be much easier to explain as something that is not a heart attack.

I’m only 80. It can’t be a heart attack!

That is true. It does not matter what the age is. 60, 50, 40, 30, or anything else. I have worked teen-aged cardiac arrest patients that had cardiac causes for their cardiac arrest. While the lower you go in age, the less likely that you are dealing with a heart attack, there is no age at which we are immune from heart attacks.

What are the so-called atypical presentations of chest pain?

Indigestion. If there is one thing that is easy to excuse as something other than chest pain, indigestion is that thing. I just ate too much; or I ate something that didn’t agree with me; or I’m upset about whatever; or My reflux is acting up; or any of a dozen other explanations.

Difficulty breathing. Clearly difficulty breathing is a breathing problem, right? Wrong. If the heart is not working effectively to deliver blood to a part of the heart having a heart attack, the heart may be perceiving the problem as a lack of air – difficulty breathing.

Maybe if I just skip to the sidebar of the article:

Symptoms for men:

Chest discomfort lasting for more than a few minutes, or goes away and comes back. The discomfort can feel like uncomfortable pressure, squeezing, fullness, or pain.

Discomfort in other areas of the upper body, such as one or both arms, the back, neck, jaw, or stomach.

Shortness of breath.

Other symptoms may include breaking out in a cold sweat, nausea or light-headedness.

Symptoms for women:

Unusual fatigue.


Pain in either arm.



They don’t even include chest pain in the symptoms for women. There is a bunch of research on prodromal symptoms of heart attack. Perhaps this device will be able to pick up on some of what is otherwise dismissed as not feeling up to par. If these prodromal symptoms are reflected in the ECG, and th device, the Guardian System, is able to pick up on those ECG changes, that could make a big difference in outcomes from heart attacks. Those are some pretty big If’s, but this is definitely worth investigating.

In the video, Nick Nudell shows the device and explains the way it works. Nick is frequently on the EMS Garage and one of the founders of the EKG Club (along with Tom B. of Prehospital 12 Lead ECG). There is a doctor explaining things, too, but they did focus on Nick.

AngelMed has a page with some links to further information, here.


^ 1 Device to warn of heart problems tested at Memorial
By Phillip Zonkel, Staff Writer
Posted: 09/16/2009 08:53:34 PM PDT

^ 2 Long Beach Memorial Successfully Implants Cutting-Edge Heart Attack Detection Device
YouTube video of the news broadcast

From the more information section at YouTube:

MemorialCare Heart and Vascular Institute at Long Beach Memorial Medical Center (LBMMC) successfully implanted a new, cutting-edge heart attack detection device in two heart attack survivors. With the danger of a second heart attack occurring in the first year for 35 percent of female survivors and 20 percent of male survivors, the device is designed to monitor and analyze data about a patients heart, reducing the time it takes to get to the emergency room.

^ 3 Device to warn of heart problems tested at Memorial
By Phillip Zonkel, Staff Writer
Posted: 09/16/2009 08:53:34 PM PDT
This is the same as footnote [1].


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.


Call Audit in Contra Costa

In California, at least at the time this took place, OLMC (On Line Medical Command) was something that only a few hospitals provided. When it started, it was believed that they could direct paying patients to their facilities, so a bunch of hospitals were providing OLMC. At least that was the rumor. After a while the reality of the expense and the lack of the expected financial triage effect caused some to give up providing OLMC.

A Call Audit (or Tape Audit) is a California term for a review of OLMC contacts on a recorded line. It can be positive, negative, neutral, or just focus on a specific medical condition.

The most memorable one I attended was in Contra Costa County, right next door to Alameda County. Alameda County was a somewhat progressive county in California EMS (probably still is). Contra Costa would probably punish you if you used the word progress in a sentence.

The purpose of the Call Audit was to inform people of a change in protocol. The Chest Pain protocol would no longer require OLMC permission prior to starting an IV.


What year was this?

A. 1973?

B. 1983?

C. 1993?

D. 2003?

E. 2013?

Their explanation for this radical departure from sanity – actually trusting medics to start an IV on a patient with active chest pain without the recorded permission of OLMC?

First, a bit about OLMC in California (at least back then). MICNs (Mobile Intensive Care Nurses) are nurses trained to provide OLMC to the medics. The M (Mobile) is not referring to them, since they are in a radio room. The I (Intensive) does not have to do with much more than providing a vowel in the unpronounceable acronym. Not that they aren’t good nurses, but why the overly fancy title for someone to recite the OLMC-only parts of protocol to the medics?

Contra Costa was shutting down one of two OLMC facilities. The math here is not especially difficult. The remaining OLMC facility received almost double the number of OLMC calls it received when there were two OLMC facilities. If I recall correctly, the less busy facility was the one that closed.

At the Call Audit, the OLMC representative tried to put a positive spin on the development.

“We are trusting you to make this important decision. Don’t abuse it!”

They are receiving twice as many calls as they used to. Their nurses are having trouble keeping up with the volume of calls. The county EMS people decide that it is better to recognize reality and allow medics to start IVs on cardiac patients without calling for permission first.

They present this protocol change to the medics as being a tentative move to improve trust if the medics demonstrate appropriate restraint when given this huge responsibility.

When people lie, it does not encourage you to trust them.

Every medic knew that there was no way this protocol would be rescinded. The previous protocol, because of the volume of calls, was dead. Why do these administrators think medics are dumb?

Just another example of idiots micromanaging things they do not understand and making things worse (not by this change, but by resisting this appropriate change for so long).

Oh, the year was 1993. They were still practicing “Johnny and Roy call for permission for everything” EMS almost 2 decades later.

Other OLMC posts:

OLMC (On Line Medical Command) Requirements Delenda Est

OLMC for President!

OLMC = The Used Car Dealers of EMS?

OLMC For Good Medics

Fun with explosives – NTG.

Failure to communicate


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]