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

- Rogue Medic

Corrections of Misleading Charts Comment – Part III

Continued from Corrections of Misleading Charts Comment – Part I and Corrections of Misleading Charts Comment – Part II.

3. Giving NTG to a hypotensive patient who DOES have CHF.

Is this inappropriate?


If we believe that we have caused the hypotension by giving NTG (NiTroGlycerin) to a CHF (Congestive Heart Failure) patient, then the answer would be, Yes. Much more likely is that we have a patient who was initially hypotensive. That is – before we ever met the patient, he was hypotensive.

Would it be a mistake to treat this hypotensive CHF patient with NTG?


In Most Survive with Mystery Treatment for Cardiac Arrest, I wrote about patients with no detectable blood pressure resuscitated with . . . . ?

If NTG is so practically death by ridiculously excessive hypotension, how do most of these patients with no detectable blood pressure improve after NTG?

NTG is supposed to be the final nail in the coffin.

The straw that breaks the camel’s back.

The coup de grâce.

After NTG, these patients are just mostly dead, they are all dead.

At least, that is if we believe the things we are told about NTG and hypotension.

Click on the image to make it larger.

This is what I posted in Most Survive with Mystery Treatment for Cardiac Arrest.

The drug is high-dose NTG.

High doses of NTG were used in 22 patients, including 14 patients with acute MI and eight patients with advanced HF. All patients had critically low BP measured by cuff, and 18 had an unmeasurable BP and pulse. They all had cold and mottled skin and increased central venous pressure. Eleven patients had rales in the lungs, three had pulmonary edema, and one had anasarca. The doses of NTG used in each patient, as well as the times of infusions, are listed in Table 1. BP became obtainable or increased in 20 of 22 patients immediately after intravenous NTG was administered. In the end, 13 patients survived.[1]

If we believe the NTG = hypotension fear mongers, the number surviving to discharge would be zero.

If we believe the NTG = hypotension fear mongers, the percent surviving to discharge would be zero.

The number is 13 patients out of 22.

The percent surviving to discharge neurologically intact is 59%.

The obvious question is –

How much do we not understand Nitroglycerin?

Why do we tolerate the IRBs refusing to allow studies of this?

How ignorant do we want to be?

For Valentine’s Day maybe we should demand investigation of what is potentially the most effective drug for resuscitating the heart.


[1] High dose nitroglycerin treatment in a patient with cardiac arrest: a case report.
Guglin M, Postler G.
J Med Case Reports. 2009 Aug 10;3:8782.
PMID: 19830240 [PubMed – in process]

Free Full Text from PubMed Central . . . . . Free Full Text PDF from PubMed Central


TOTWTYTR vs. Indoctrination in Iatrogenesis

Too Old To Work, Too Young to Retire has an excellent post about, well his title gives it away.

The One where he Rants about EMS Education

TOTWTYTR is right on target with this latest post. Mandatory reading for everyone involved in EMS.

In paramedic school, which is ALS (Advanced Life Support), the approach to airway management seems to be that medics will intubate the patient, so they do not need to be good at the BLS (Basic Life Support) aspects of airway management. The result is medics who do not understand the most essential part of airway management. There is nothing more important than competence in BLS airway management. Assessment is critical to competent BLS airway management, but there are plenty of medics who do not recognize esophageal tubes. Do they understand airway? Even a little bit? No.

Where is the assessment? Playing peek-a-boo with the life of the patient. Now it’s here! Now it’s not!

There should not be ALS without excellence in BLS. Teaching ALS without confirming and reinforcing excellence in BLS is bad instruction.

The medical directors for these schools should not allow this. The instructors should not, either. Nor should the students allow this.

Of course as you move from sentence to sentence, in the previous paragraph, the order of responsibility is dramatically decreasing. We should not expect the students to take responsibility for the curriculum. A bunch of people think that the medical director, the one who says that idiocy is permitted or that idiocy is not permitted, should not be held accountable for the results of his actions.

We allow medical directors to set up a system that proclaims:

Idiocy, Incompetence, and Iatrogenesis are permitted here.


If you look at what happens when these students have graduated and are developing as medics, the next big influence on the way they treat people is, surprise, surprise, the EMS medical director.

I believe that the difference between the ALS services that have excellent quality and the rest . . . .

What do you mean the rest?

There is no bronze medal in medical care, unless you believe in the government quality indicator rankings.

There are places that uniformly provide excellent care.


After excellent it is just a matter of naming the abuses the patient may suffer.

Statistically, many of these patients will arrive at the hospital unharmed, but there will be plenty who do not escape harm. So, what method of medical misadventure will they come up with this time?

I believe that the difference between the ALS services that have excellent quality and the rest lies in the involvement of the medical director.

An absentee medical director means that on a regular basis these are some of the medical misadventure menagerie that the medics will be inflicting on patients:

  • Unrecognized esophageal tubes,
  • Furosemide (Lasix) for pneumonia,
  • Delayed transport for IVs,
  • Patients treated according to the dispatch information instead of their actual medical condition,
  • Poor pain management,
  • Et cetera.
Absentee = Not being there.

  • Performing chart review is the same thing as not being there, because you aren’t.
  • OLMC (On Line Medical Command) requirements are the same as not being there, because you aren’t.
  • Having monthly/quarterly/yearly continuing education is the same as not being there, because you aren’t.
  • Telemetry (transmitting ECGs to be read by the doctor) is the same thing as not being there, because you aren’t.
  • Et cetera.
Being there to take report from medics at the hospital, showing up on calls, following up (with the patient and with hospital staff) on all unstable patients, . . . . are part of being there.

Do you know your medics?

Investing in some smart technology is a good thing (waveform capnography) when it is part of improving the abilities of the medics. Investing in telemetry is just a waste of money, an admission that you are trying to keep it stupid, and that you don’t know how to run ALS. Spending money on technology instead of a medical director, who WILL be there, is a waste of money.

Idiocy, Incompetence, and Iatrogenesis are permitted here.

Would you want this inscription on your certificate/diploma/degree?

Would you want this inscription on the side of your ambulance?

Would you want this inscription on your EMS patch?

The NR (National Registry of EMTs) should come up with a nice round patch EMT-P-III?

This is not the New York level of EMT-III (intermediate). It is quite a bit different.

Iatrogenesis = inadvertent and preventable induction of disease or complications by the medical treatment or procedures of a physician.

Being There, the book or movie, is not the same as a medical director being there.


Dead VT vs Not Quite Dead, Yet VT.


In my post The Three Flavors of VT (VT = Ventricular Tachycardia),[1] I described some of the problems we have when assessing death.

The heart can be beating so quickly that no palpable pulse is produced,, or it can be beating so slowly that no pulse is produced or it might not be beating at all.

The heart that is beating too quickly or beating too slowly is not stopped. This heart is producing so little output that the person assessing for a pulse is not able to feel a pulse.

The carotid artery is the place to assess for death.

So, there’s dead and there’s dead?

Let’s go back to ACLS class and listen in on some more bad teaching .

Are we going to take the Wayback Machine?


During a scenario the student is presented with an unstable VT patient.

Student – I want to give this unstable VT patient some epinephrine.

Instructor – You killed him!


Gee. That’s one way to make sure they remember.

Depends on what you want them to remember and it is bad science.

What do you mean “bad science?”

Do you know of any controlled studies of patients being treated with epinephrine vs. placebo for unstable VT?


Then how would you be able to say with any certainty what the result of such treatment would be?

Well, it is a good guess.

It may be a good guess, but it is not science and it is very bad teaching.

Why is it bad teaching?

It teaches that we know what will happen to the patient when we give a treatment.

We don’t.

But there are some treatments that we know will produce certain effects when we give them.

Even that is wrong. Most of the time the medication may produce the expected response, but not always.

To suggest otherwise is very bad medicine.

We have a good idea of what will happen when we give epinephrine to a patient with unstable VT.

Based on what?

Everyone knows that epi –

Stop! Sentences that start with “Everybody knows” often end with the speaker looking like a fool. When they do not, it may be because the audience is even more foolish than the speaker.

But epinephrine will cause the heart to beat too fast, and overstimulate the heart, and maybe cause the rhythm to change to V Fib (Ventricular Fibrillation).

Maybe it will overstimulate the heart.

Then you would be wrong to give epinephrine to VT.

What about when the pulse can no longer be felt?

Then you give epinephrine!

But the rhythm is still VT, just pulseless instead of unstable.

There is a big difference between a living patient with VT and a dead patient with VT.

The difference can be really very subtle.

With unstable VT someone is able to feel a pulse, so we know there is cardiac output.

With pulseless VT, someone is not able to feel a pulse, so we think that the cardiac output is much less.

What do you mean think? Pulseless means NO cardiac output.


The heart can be beating, there is probably blood that is circulating due to the heart beating, but the amount circulating is so little that there is no palpable pulse.

The heart normally beats slowly enough that the ventricles fill completely before each beat. When the heart accelerates, the cardiac output increases, but only as long as the heart is able to keep filling up. Eventually the heart is beating so quickly that the heart does not have time to fill when the next contraction of the ventricles occurs. Since the heart is not full, the amount that leaves is less. The blood pressure will start to fall if this continues. If the heart keeps accelerating, eventually the blood pressure, or the work of the heart, or the filling of the coronary arteries, or something else will catch up with the patient and they will exhibit signs of being unstable. If the heart is beating even faster the pulse may disappear.

What was that about the coronary arteries?

They fill between heart beats, so as the heart beats faster – even though the heart is working harder – the ability of the heart to supply blood to itself decreases.


Do you remember our criteria for unstable tachycardias?

What were those criteria, again?

Acute altered mental status (not their 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).[2],[3]


But the pulseless patient is not like that – the pulseless patient is dead!

So the first category – acute altered mental status would not apply?

Yes, but this person is unresponsive.

Usually – and unresponsive is probably not their normal level of consciousness.

And the other categories do not apply.

Well the chest pain probably does not, but do you think the patient is hypotensive?

They don’t have a blood pressure!

No. The patient does not have a palpable pulse – that just means that the blood pressure is too low for the person attempting to measure the pulse to be able to feel enough evidence of the pulse.

But they aren’t showing signs of shock.

You’ve been watching too much TV. The signs of shock do not go away just because you can no longer feel a pulse.

OK. Let me see if I understand this. The patient just has less cardiac output when pulseless than when unstable. Isn’t that what I said before?

If the same person is attempting to feel the pulse, yes. You were generalizing that all pulseless patients would have lower blood pressures than all unstable patients. There is too much variability among patients to make any such broad statement.

Give me an example.

A well conditioned athlete may tolerate a heart rate of 200 for an extended period and never show signs of instability. Someone with heart problems may be pulseless with a rate of 200 showing on the heart monitor. One patient is exercising and the other is assessed as dead.

Or a person with a blood pressure of 70/38 may be stable, while another patient is unstable even with a much higher blood pressure.

But the dead guy with VT needs to get epinephrine to help his heart start beating again.

His heart appears to be beating – just much to quickly to produce a pulse.

Then epinephrine would not be a good idea?

Well, if the biggest difference between the two might be the ability of the person assessing for the presence of a pulse to feel a pulse, then we aren’t really treating a difference in the patients, but our ability to assess our patients.

How did Schroedinger’s Cat get in this conversation?

Why don’t we just leave the cat in a state of uncertainty, for now.

So, his heart is beating, just too quickly?

Probably. The heart may not be contracting at all, but still producing a VT-looking rhythm on the heart monitor.

But if his heart is beating, just much too quickly, how is this different from the unstable patient the instructor said would be killed with epinephrine?

Not very different at all. Depending on who is assessing the patient, it could be the same patient.

Then epinephrine could be the worst thing we could give the patient.

It could be.

Was the point of this to drive me crazy?

No, just to point out another reason why epinephrine in cardiac arrest[4] may not be such a great idea.

And the part where you drive me crazy is just a bonus?

See also –

Epinephrine in Cardiac Arrest

More on Epinephrine in Cardiac Arrest.


[1] The Three Flavors of VT
Thu, 03 Apr 2008
Rogue Medic

[2] Cardioversion – I’m not doing that, you do it!
Mon, 24 Mar 2008
Rogue Medic

[3] Initial Evaluation and Treatment of Tachyarrhythmias
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

[4] Epinephrine in Cardiac Arrest
Sun, 06 Apr 2008
Rogue Medic


The Three Flavors of VT.


Why is VT (Ventricular Tachycardia) so complicated?

It isn’t really much different from the other rate related arrhythmias.

Rate related?

The heart rate is the problem, not the arrhythmia.

But there are 3 different treatments for VT and none of the other rate related arrhythmias have that many different treatments.

The AHA simplified the rest of the tachycardias and bradycardia.

Please explain.

With an SVT we have stable, unstable, and pulseless – we just don’t have that written explicitly in the algorithms.

But there is no pulseless SVT treatment.

Are we claiming that a rhythm that usually produces a rate much faster than VT cannot produce pulselessness?

What does the rate have to do with it? It’s the rhythm, and VT is just really bad! I don’t know why they even pretend that there is such a thing as stable VT. VT is a lethal rhythm. Everyone knows that.

VT does look worse than SVT.

It is ugly.

We’ve been told how bad VT is.

We have to learn somehow.

We spend a lot of time on the perfect antidote for VT.

That amiodarone is great stuff!

No, it isn’t, but let’s go over the rhythm differences first. What causes the VT to be so bad?

Well, it wants to be VF (Ventricular Fibrillation).

The heart does produce its own electrical activity, but it does not think, so it doesn’t want anything.

How long do we expect someone to stay in VT?

Until the VT spontaneously resolves, or until the VT becomes unstable, or until the VT resolves with treatment, or maybe for hours or days without becoming unstable.

Days? Impossible.

All patients had recurrent spontaneous episodes of ventricular tachycardia that were typically sustained for minutes to days.[1]


This is from 1978, so we can see that very long periods of VT are nothing new.

But VT does not have an atrial kick.

Do we even know what an atrial kick is?

The atria help the heart beat.

Yes, the atria help to fill the ventricles. They help to push more blood into the ventricles than would enter otherwise. This stretches the heart muscle and allows it to contract more forcefully. When someone is trying to add force to a muscular contraction one effective method is to wind up, as a pitcher does. The muscles are stretched out and when they contract more force is produced. This is what the heart is getting from the atria. When the atria are not coordinated with the ventricles, or are not contracting at all, this extra force is lost and the heart has to work harder to fill up and harder to contract.

Right. VT gets rid of that extra force, so the heart has to work harder to produce the same circulation.

And SVT does not?


With an SVT, the sinus node is not in charge, so coordination between any atrial contractions and the ventricular contractions is not going to happen. The electrical activity in the atria may also be preventing the atria from contracting.

So, what is the difference between SVT and VT.

Well, the causes are different. VT is often caused by a heart attack in older people, so the heart is naturally weaker. The medications are quite a bit different, too.

And you mentioned that VT spontaneously resolves?

VT probably goes away on its own more often than it does with any of our treatments. Just because we started giving something to the patient does not mean that the treatment is the reason the patient’s condition improved.

OK, what are the 3 flavors of SVT?

The same as the flavors of VT – stable, unstable, and PEA (Pulseless Electrical Activity).

But PEA and pulseless VT are entirely different.

Pulseless VT is just one type of PEA. VF is a PEA with electrical activity that is disorganized. We would not expect it to produce a pulse. Since rapid defibrillation is critical for treatment of VF, it is treated differently from PEA. Pulseless VT is treated the same as VF, so the two are lumped together in one algorithm. SVT can be fast enough to produce a pulseless condition. Bradycardias can be slow enough to produce a pulseless condition. Since pulseless bradycardias are treated pretty much the same way as asystole, they are lumped together with asystole. This makes treatment easier to remember.

So, what do we do for a pulseless SVT?

What do we do for an unstable SVT?


The same as for an unstable VT, so what do you think we should do for a pulseless SVT?


Sure. If we are comfortable enough with cardioversion that using the cardioverter will not delay the shock, go ahead and cardiovert. Since pulseless SVT is not something we will see often, we may want to keep it simple and defibrillate as if it were VF.

But the drugs are different.

Yes, but that is a topic for another post. And there are really 6 flavors of VT. Polymorphic VT is treated differently from monomorphic VT.

That sounds like another post, too.

Of course.


[1] Recurrent sustained ventricular tachycardia. 1. Mechanisms.
Josephson ME, Horowitz LN, Farshidi A, Kastor JA.
Circulation. 1978 Mar;57(3):431-40.
PMID: 624152 [PubMed – indexed for MEDLINE]

Free Full Text Download in PDF format from Circulation.


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.