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

- Rogue Medic

Potentially Reversible Causes of Cardiac Arrest – Arrhythmia

In my last post, Not Successful Resuscitation, I mentioned the potentially reversible causes of cardiac arrest. First a definition. These are conditions that can lead to sudden death as well as a more gradual death. In the case of a more gradual death, their potential for reversibility dramatically decreases. One of the reasons is that these conditions, conditions bad enough to kill you, can cause significant organ damage when they are present for an extended period. Acidosis is very destructive to the body, but if it is a sudden change, rather than a long term condition (especially one that is not responding to aggressive medical treatment), then reversing the acidosis may help to resuscitate the patient.

Why only may?

There are many factors that affect the ability to resuscitate a patient. As I mentioned, a gradual onset is not as easy to reverse. A gradual onset is because the illness is a chronic condition or a progressive condition.

But if it is a progressive condition, that has progressed to death, how can it be a reversible cause of cardiac arrest?

The potentially reversible causes tend to be sudden. That does not mean that a gradual onset rules out resuscitation, just that it becomes much more difficult to resuscitate these patients, and much more difficult to keep these patients alive if we do manage to resuscitate them. These causes tend to be overwhelming to the body. Still, a sudden onset of a potentially reversible cause of cardiac arrest may not respond to treatment, even if the patient is in the ideal treatment setting, because these causes are only potentially reversible.

Then why spend so much time on them?

All of resuscitation is about potentially reversible causes. VF/Pulseless VT (Ventricular Fibrillation/Pulseless Ventricular Tachycardia) are the easiest to reverse, the most likely to be reversed, and the easiest to diagnose.

Diagnose? Paramedics can’t diagnose.

Of course you can. You just can’t legally claim that you are diagnosing. This is purely a legal distinction. It has no basis in reality.

Arrhythmia – shocking a shockable rhythm.

Some of the arrhythmias that can cause cardiac arrest may be reversed by defibrillation. Some of the arrhythmias that can cause cardiac arrest will not improve with defibrillation. Asystole is an excellent example of an arrhythmia that will not respond to defibrillation. Asystole is caused by defibrillation. We shock patients because we want to cause asystole – temporarily.

The defibrillation is designed to send enough current through the heart to stop the heart for less than a second. The purpose of defibrillation is to get rid of the dangerous rhythm that is controlling the heart, whether it is an organized rhythm, such as VT or SVT (SupraVentricular Tachycardia), or disorganized activity, such as VF.

After the shock is delivered, and some asystole is produced, it is hoped that the heart starts again on its own and when the heart starts again, it is hoped that the sinus node will be controlling the rate and rhythm. If the patient’s normal pacemaker is not the sinus node (a couple of examples are atrial fibrillation or an implanted pacemaker), then the hope is that the normal pacemaker resumes its role of initiating a rhythm capable of keeping the patient alive.

In western movies, during a big bar fight, the sheriff may fire a gun into the air. Everyone tends to stop, at least long enough to make sure the gun is not pointed at them. This pause in the commotion is what defibrillation is supposed to accomplish. The sheriff is telling the arrhythmia to move along. As in the movies, it does not always work as planned. If the arrhythmia/chaos does not go away with defibrillation, more defibrillation may be attempted. Even if the ceiling is shot full of defibrillations, there is no maximum number of defibrillations, as long as the patient is in a shockable rhythm. Antiarrhythmic medications may be added to the treatment (after some epinephrine, the most arrhythmogenic drug we use). The search for other potentially reversible causes of cardiac arrest will contribute to treatment.


Something that causes arrhythmias. I describe problems with the use of epinephrine in Epinephrine in Cardiac Arrest, More on Epinephrine in Cardiac Arrest, and Dead VT vs Not Quite Dead, Yet VT.

What if the asystole is not temporary?

This is not unusual. The current ACLS (Advanced Cardiac Life Support) algorithms are pretty easy to use.[1] If you are using an algorithm that no longer applies, you should switch to the algorithm that does apply. I will cover asystole in another post.

Are there any other rhythms that should be defibrillated?

SVT – if the patient is pulseless. Any rhythm that would be cardioverted, if the patient were alive, should be defibrillated if the rhythm is bad enough to produce a dead patient. Although this falls into the category of PEA (Pulseless Electrical Activity), it is a shockable rhythm and will respond best to defibrillation.

One of the perversions of the algorithms is that they spend almost no time on Postresuscitation Support. There is no algorithm, flow sheet, or other easy to use chart. The 2010 ACLS Guidelines added an easy to use algorithm.[2] This is the AHA (American Heart Association), in the 2000 guidelines they were not discouraged by the possibility of an overly dense, extremely confusing 3 page tachycardia algorithm “overview” flow sheet. Pages 1, 2, and 3, followed by the individual pages for specific tachyarrhythmias. Fortunately they did learn from that, but there is still no algorithm to ease recall of postresuscitation care – something that is not well understood. That will be more than another post.

There are methods of determining if the arrest is one that may be reversed by treatment. Again, this is something for another post.

That is enough of the potentially reversible causes for this post. And I haven’t even started on the list of potentially reversible causes. 🙂

The PALS (Pediatric Advanced Life Support) potentially reversible causes of cardiac arrest list is 5 H’s and 5 T’s:

Hypovolemia; Hypoxia; Hydrogen ion (Acidosis); Hypo/Hyperkalemia; Hypoglycemia; Hypothermia.

Toxins (Drugs); Tamponade, cardiac; Tension pneumothorax; Thrombosis (coronary or pulmonary – AMI or PE); Trauma

I have changed this from what I originally wrote. My, borrowed from Jeff B of JB on the Rocks, mnemonic (memory aid) for the potentially reversible causes of cardiac arrest is now two words – COLD PATCHeD.

COLD reminds you that the C is for hypothermia – being very cold, sometimes we forget the obvious in resuscitation attempts, so it doesn’t hurt to put extra reminders in a mnemonic. O for Oxygen deficit or hypoxia. L for Lytes. This works better as a mnemonic for the in hospital crowd, but there is nothing wrong with getting EMS to think more about electroLytes. Hypokalemia and Hyperkalemia – too little and too much potassium. D for Drugs (OverDose, poison, wrong drug, wrong dose, . . .).

PATCHeD = PPE (Pulmonary Embolus); A Acidosis and AMI (Acute Myocardial Infarction); T Tension Pneumothorax; C – Cardiac Tamponade; H – Here it is still confusing, a whole bunch of Hypo’s and one Hyper. The Hypo’s: HypoVolemia; HypoThermia; HypoGlycemia; HypOxia; HypoKalemia; The Hyper: HyperKalemia; e – Everybody dead gets Epi. Just a reminder to continue CPR and other treatments. D Drugs (OD, poison, wrong drug, wrong dose, . . .); Distributive Shock.

I will have to write a post on why each of these categories matter, what the treatments are, and other ways to approach them, rather than the order of the mnemonic. This is a lot for one post.


[1] 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Volume 122, Issue 18_suppl_3;
November 2, 2010
Guidelines index

Below is the link to the old guidelines:

2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Volume 112, Issue 24 Supplement;
December 13, 2005
Guidelines index

[2] Post–cardiac arrest care algorithm.
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 9: Post–Cardiac Arrest Care
Systems of Care for Improving Post–Cardiac Arrest Outcomes
Algorithm in JPEG format

Part 9: Post–Cardiac Arrest Care
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Free Full Text From Circulation with link to Free Full Text PDF Download

Part 7.5: Postresuscitation Support
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Free Full Text From Circulation with link to Free Full Text PDF Download

Footnotes were added 5/11/2011 to include links to 2010 ACLS guidelines. Links were also updated.


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.