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

- Rogue Medic

Beta vs. Beta Blocker – comment

In the comments to Beta vs. Beta Blocker, Anonymous said…

Gang, is it time to review pharmacology?

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 the placebo effect? Maybe.
Is this rise in pressure because of a homeopathic remedy? Sorry – kidding, I already mentioned placebo effect.
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 (NiTroGlycerine, or GTN – Glyceryl TriNitrate overseas).[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 hestitant 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 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. They 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. 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.

^ 1 ASA (AcetylSalicylic Acid – Aspirin)
^ 2 Recognition and Treatment of Right Ventricular Myocardial Infarction

By William E. Gandy
Updated: July 8th, 2008 05:26 PM GMT-05:00

^ 3 NTG (NiTroGlycerine, or GTN – Glyceryl TriNitrate overseas)
^ 4 Lopressor (metoprolol tartrate) injection, solution;
^ 5 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.

^ 6 [No authors listed]
Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators.
N Engl J Med. 1989 Aug 10;321(6):406-12.
PMID: 2473403 [PubMed – indexed for MEDLINE]
Although it states “No authors listed,” many of the top cardiologists in the US were involved in this study.


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.


Cardioversion – I’m not doing that, you do it!

First a few ground rules about what “stable” is – from the 2005 ACLS (Advanced Cardiac Life Support) guidelines.


  • If the tachycardic patient is unstable with severe signs and symptoms related to tachycardia, prepare for immediate cardioversion.
  • If the patient with tachycardia is stable, determine if the patient has a narrow-complex or wide-complex tachycardia and then tailor therapy accordingly.
  • You must understand the initial diagnostic electrical and drug treatment options for rhythms that are unstable or immediately life-threatening.[1]


In the bulleted description of bradycardia they described unstable as:

produces signs and symptoms (eg, acute altered mental status, ongoing severe ischemic chest pain, congestive heart failure, hypotension, or other signs of shock) that persist despite adequate airway and breathing,[1]


Cardioversion is one of the skills that gets even some experienced ED personnel and medics to act like rookies.


When you took ACLS (and almost everyone working in the ED has had to pass ACLS prior to working in the ED) did they have you practice cardioversion?

Or did you just practice defibrillation?

After all they’re not much different.

The problem is that when faced with cardioversion most people want anyone else to do it. In PALS (Pediatric Advanced Life Support) classes there is a similar approach to intraosseous access.

This is not a problem if the patient is stable.

But, if the patient is stable, there is no need for cardioversion or intraosseous access.

So, this is the point where we try to come to the understanding that the patient’s health is more important than our squeamishness.

What were those criteria, again?

Acute altered mental status (not the patient’s normal level of consciousness).

Ongoing severe ischemic chest pain (not mild CP or palpitations).

Congestive heart failure (not just a previous diagnosis, but something that is causing real problems right now).

Hypotension (if hypotension is the only problem and they seem otherwise stable, I am not as aggressive as with the other criteria).

Or other signs of shock (not everything fits neatly into a list, this refers to things that activate the pucker factor).

OK, those things are bad. Why does shocking them help?

We want to cause asystole, of course!


Asystole is bad. Dead. This parrot wouldn’t voom if you put 4000 volts through him!


Yes, asystole is bad as a presenting condition, but it is the best treatment for many unstable tachycardias and for VF (Ventricular Fibrillation).

But asystole is worse than the things you say get better with asystole.

You surely are crazy.

Only in a good way and stop calling me Shirley!

So we are going to practice a bit of pseudo-homeopathy – give a tiny bit of something to cause the patient to improve a lot.

Asystole is not an improvement!

Look at it this way, the heart is beating much too quickly, we need to stop it so that the sinus node – the normal pacemaker for the heart – can regain control of things.

Like the TASER you wrote about?[2]


Not at all like the TASER.

This is designed to send enough current through the heart to stop the heart for less than a second. It is hoped that the heart starts again on its own and when the heart starts again the sinus node will be controlling the rate and rhythm.

When cardioverting (or defibrillating) we want as much of the current to go through the heart as possible – anything else is wasted and possibly dangerous.

We use pads that have conductive gel or we use paddles that we apply gel to. The purpose of this gel is to help the current go through the resistance of the skin and have the current reach the heart.

We place the pads (or paddles) so that the heart is on a line between the pads. The pads do not go on the thickest part of the right pectoral muscle, but on the thinnest part (if applied over a muscle). The more tissue the current has to travel through, the less current arrives at the heart. The other pad goes on the ribs, below the heart and near the mid-axillary line and not on any muscles (we are ignoring the intercostal muscles). The other possible placement is anterior-posterior; one pad goes below the left pectoral muscle and the other pad is placed as nearly opposite the first as possible; the current travels through the heart as much as possible, rather than through the other muscles.

Placement over saline implants does not improve conduction. Yes, saline is a wonderful conductor, but go to the side of the implant.

Another method of improving conduction through the skin is to apply about 20 pounds (9 kg) of pressure. The amount is not going to be precise, but you want to put enough pressure that you force a little bit of air out of the chest, just a little, nothing more. With the pads you do not touch the pads while shocking. Please, do not apply pressure to the pads.

Here are those unstable criteria again.

Acute altered mental status.

Ongoing severe ischemic chest pain.

Congestive heart failure.


Or other signs of shock.

You do know that you are repeating yourself, don’t you?

That’s OK. When the patient is behaving in one of the ways described, you need to recognize it right away, not go looking for a not-so-handy reference guide. A little repetition is a good thing.

So, if anybody has any of those unstable presentations, then I shock them?

No. We haven’t mentioned the tachycardia, yet.

Aagh! This is complicated.

What is needed tachycardia-wise is for the heart rate to be fast enough that we believe that the rate is the cause of the unstable signs and/or symptoms.

If an infant has a heart rate of 250 BPM (Beats Per Minute), that might produce signs of instability or might not.

What are the two most likely conditions to produce this heart rate?

VT is possible, but very unlikely. AFib is even less likely.

SVT (SupraVentricular Tachycardia) and ST (Sinus Tachycardia) are the main concerns.

Maybe you are not so good at ECGs – little kid hearts beat so fast that it is hard to see anything in all of that. I’m not going to try to teach you ECGs, here. Prehospital 12 Lead ECG is the place for that.

Are you telling us that we should treat the rhythm without looking at the rhythm?

No. I am recognizing the difficulty of identifying the rhythm. I am expecting you to use a bit of clinical judgment at this point.

The rhythm we want to see is a SR (Sinus Rhythm). If the patient has a very fast sinus rhythm (ST), it would not be a good idea to shock the person out of the sinus rhythm into asystole. ST is more of a symptom than a diagnosis. If the rhythm is ST, the the rhythm is telling you that there is something causing stress to the patient. This could be a lack of volume (blood loss, vomiting, excessive sweating, drugs, lack of fluid intake, . . . ), pain, agitation, fever, physical exertion, fear of you cardioverting them, . . . .

Suppose you are driving a car, you press on the gas pedal, and the gas pedal gets stuck where you pressed it. The engine starts racing, so you turn off the ignition. If you just turn the engine back on without fixing the cause of the problem (the stuck gas pedal), you will have the engine racing just as before. This is the way ST works – It isn’t a rhythm problem, but a gas problem and the heart is not very tolerant of being turned off.

If I shock unstable patients with sinus tachycardia, things will only get worse?

Pretty much.

Are there any other rhythms that should not be shocked?

Yes, but the main thing is to avoid anything that appears sinus. Those you treat by treating the cause of the tachycardia.

When in doubt – shock.

What if it is so fast that I have no idea if it is sinus?

History can be very helpful. ST is usually the result of things that develop much more slowly than the sudden onset of an arrhythmia.

There are some people who teach that if the heart rate is faster than 220 minus the patient’s age it cannot be ST. This is nonsense. A heart rate that fast is much less likely to be ST – especially at rest, but far from impossible.

So we have an unstable patient with a tachycardia, we think the rhythm is the problem (not an underlying medical condition), we have the pads on. What next?

How about some sedation?

No thanks, that makes me forget things.

Exactly the point, but let’s give it to the patient.

What kind of sedatives can we use?

There are a lot of options – remifentanyl, fentanyl, sevoflurane, ketamine, propofol, methohexital, etomidate, midazolam, . . . .

Some of these might only be available to anesthesia. Use what you are familiar with. Now is not the time to try out new drugs that you are not familiar enough with to quickly recognize the difference between bad adverse reactions and acceptable adverse reactions.

Midazolam may be most commonly used, but is likely to worsen any hypotension.

Does this mean that we shouldn’t sedate hypotensive patients prior to cardioversion?


Use caution. This is a whole discussion to itself, so I will leave it there.

What about etomidate?

It is less likely to cause, or worsen, hypotension. Etomidate may be a good choice.

How about morphine?

Morphine takes a long time to go to work, does not cause amnesia, and lasts a long time. These are good reasons to avoid morphine.

What about combining drugs for a synergistic effect?

That may work, but it is probably safer to stick to one drug when dealing with unstable patients.

If the patient is hypotensive, what about sitting the patient up quickly to use gravity for sedation?

A physician I have a lot of respect for, who is not afraid of aggressive sedation, strongly discouraged that idea. He said it is likely to cause problems with coronary steal. That doesn’t really work for me, but I don’t encourage others to try this maneuver. If you have ideas about things that might work, I would love to hear them.

One thing not mentioned is IV access. If the patient is unconscious and probably not going to feel the shock, why delay treatment, but if the patient is conscious and going to feel this, an IV for sedation is important. One of the problems of hypotensive people is that they tend to be very difficult to start lines on. Do not avoid shocking if you cannot get an IV. Preferably, the IV is already in place.

What kind of guideline do you recommend for adequate depth of sedation before shocking?

Almost everyone seems to agree that when the patient is slurring his words, it is a good time to start. You can add more sedation if that does not work for the patient.

The man’s very first utterance was, “If it happens again, just let me die.”

As I discovered, the reason for this patient’s terror was that he had been cardioverted in an awake state. Ventricular tachycardia had been relatively slow, he had not lost consciousness, and the physicians, in the heat of the moment, had not administered adequate anesthesia. Although the 5 mg of intravenous diazepam had made him a bit drowsy, he felt the electric current on his chest and remembered the event clearly.

The patient’s mental state complicated the case considerably.[3]


What’s left to cover before we shock the patient?

The amount of energy used.

For cardioversion the order of shocks with monophasic defibrillator/cardioverters is 50 J (Joules or Watt Seconds), then progress to 100 J, 200 J, 300 J, 360 J for SVT and AFlutter. For other rhythms start at 100 J and progress the same way. When reaching the maximum without conversion, then add medication appropriate to the rhythm and continue shocking every few minutes (single shock at maximum energy).

Cardioversion with biphasic waveforms is now available,132 but the optimal doses for cardioversion with biphasic waveforms have not been established with certainty. Extrapolation from published experience with elective cardioversion of atrial fibrillation using rectilinear and truncated exponential waveforms supports an initial dose of 100 J to 120 J with escalation as needed.133,134 [4]


For polymorphic VT, the AHA does not recommend cardioversion, even though the patient may have a pulse.

the patient with persistent polymorphic VT will probably not maintain perfusion/pulses for very long, so any attempt to distinguish between polymorphic VT with or without pulses quickly becomes moot. A good rule of thumb is that if your eye cannot synchronize to each QRS complex, neither can the defibrillator/cardioverter. If there is any doubt whether monomorphic or polymorphic VT is present in the unstable patient, do not delay shock delivery to perform detailed rhythm analysis—provide high energy unsynchronized shocks (ie, defibrillation doses).[5]


Now, what is sychronization?

The whole purpose of this method of shocking the patient is to avoid having the shock land on the relative refractory period of the heart and possibly induce VF. To synchronize is to have the monitor place a dot, or some other mark, on the QRS complex of each beat to indicate that, once the shock buttons are pressed and held the shock will be delivered at the next marked beat.

How do I get the machine to synchronize?

There should be a button that has SYNC written on it. Press it. If there is a rhythm on the monitor, you should now see a mark on the QRS complex (top or bottom, depending on whether it is a mostly positive or mostly negative complex in the lead you are viewing).

Why on the QRS complex?

Because it isn’t a T wave. The refractory period and the relative refractory period are part of the T wave.

How do I know if it is the QRS or the T that the monitor is marking?

The QRS complex generally comes to a much sharper point at the top, or bottom, of the QRS. T waves, even when somewhat pointed are still more round compared with QRS complexes.

What if I cannot tell what it is?

If you think it is synchronizing on T waves, turn off the synchronization and just defibrillate. Increase the energy levels to defibrillation doses. The main difference between synchronization and defibrillation is the timing (and how you use them).

You used bold italics for pressed and held above. Is that important?


When defibrillating, the shock is delivered as soon as both buttons are pressed at the same time.

When cardioverting the synchronization changes that. There is one more factor. Both buttons still have to be pressed at the same time, but now you need to hold them until the next marked beat comes along. For a fast rhythm that is not very long. At 180 BPM you should have 3 marked beats per second, unless the synchronizer is not working well, unless there is artifact, unless the gain is too low for the synchronizer to pick up on the beats, or unless the lead is not one with a prominent QRS complex (easier to change leads than to play with the gain).

So, I assess the patient as unstable, with a rhythm that is shockable, I sedate the patient (if possible), I place the pads on the patient appropriately, I press the SYNC button and the monitor marks the QRS complexes and ignores the T waves, I select the right amount of energy, now what?

You have to charge the paddles. The initial amount of energy needed for cardioversion is much less than for defibrillation, so it takes much less time to fully charge. If the patient is intubated, disconnect the oxygen from the tube and point the oxygen away from the chest (possible fire hazard). Make sure everyone is clear of the patient and anything conductive that may be touching the patient. Make sure you are clear. With everyone remaining clear press and hold the buttons until the shock is delivered. You should hear a clunk (or whatever sound effect you feel is more descriptive) and the patient should contract a lot of muscles.

Great that was a lot. It is good to be through with this.

Hold on.

You have just treated your patient, you need to reassess.

What if you see VF on the monitor?

I would defibrillate at 360 J (monophasic).


But the patient is in VF.

Are you sure?

The monitor may be picking up artifact from poorly connected electrodes or pads. How much time does it take to check a pulse to confirm that the patient is pulseless?

When applying electrodes to unstable patients, Benzoin is a great way of helping the electrodes to stick. Unstable patients are often very sweaty. A loose electrode can produce artifact that can mislead you into believing the patient is in VF.

If this truly is VF, defibrillate immediately and follow VF treatments. If the defibrillator/cardioverter you are using remains in cardioverter mode after each shock, then turn the cardioverter off by pressing SYNC again. If it turns off automatically with each shock, then just charge up to 360 J (monophasic).

If the rhythm has not changed, press SYNC again (if necessary) and charge up to the next energy level, repeating everything as necessary.

If the rhythm has changed, reassess and treat as appropriate for the new rhythm and presentation.

Anything else?

Practice with your equipment. If you do not know how to use it in an emergency, you may only make things worse. That is not what you are there for.

No horse was actually flogged in the writing of this post – it may have fallen asleep on its feet, but that is a different matter.


[1] Principles of Arrhythmia Recognition and Management
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.3: Management of Symptomatic Bradycardia and Tachycardia
Free Full Text from Circulation.

[2] TASER or Glock – Which treatment do you choose?
Tue, 18 Mar 2008
Rogue Medic

[3] The calamity of cardioversion of conscious patients.
Kowey PR.
Am J Cardiol. 1988 May 1;61(13):1106-7. No abstract available.
PMID: 3364364 [PubMed – indexed for MEDLINE]

[4] Supraventricular Tachycardias (Reentry SVT)
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 5: Electrical Therapies
Automated External Defibrillators, Defibrillation, Cardioversion, and Pacing
Free Full Text from Circulation.

[5] Ventricular Tachycardia
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 5: Electrical Therapies
Automated External Defibrillators, Defibrillation, Cardioversion, and Pacing
Free Full Text from Circulation.

Updated links and formating and switched to footnotes 10-26-10.