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

- Rogue Medic

Keeping ALS Out of Resuscitation

Why do we work so hard at keeping resuscitation rates low?

Rates of bystander cardiopulmonary resuscitation (CPR) in the United States are dismal. A national study showed that only 31% of patients with cardiac arrest treated out-of-hospital received CPR from a bystander.1 The low rates of bystander CPR, a procedure developed over 50 years ago, is particularly notable when compared with the great progress that has been made in making a much newer technology—percutaneous coronary angioplasty—highly accessible.[1]

We could recognize this dismal level of bystander CPR chest compressions.

In America, we seem to be trying to demonstrate how much more intelligent people are in other countries. Here, we have only isolated pockets of high bystander CPR rates.

We spend our time making excuses for the higher resuscitation rates is these places. Seattle is #1, again – and again – and again – and again – . . . .

But they call fine V Fib (Ventricular Fibrillation) asystole!

Is there any validity to that claim?

Probably not.

Is there any evidence that fine V Fib is in any way more responsive to defibrillation than asystole?

Is there any difference between what the critics of Seattle think of as a shockable rhythm and what is programmed into AEDs (Automated External Defibrillators)?

If these critics are so offended by Seattle’s high resuscitation rates, maybe they should submit their own resuscitation rates with their version of fine V Fib and without. Will removing their fine V Fib result in results that compare to Seattle’s resuscitation rates?

Or is the secret of Seattle not the way they measure V Fib, but the way they encourage bystander CPR chest compressions?

Is a cath lab useful without bystander chest compressions?

Is adding more cath labs an expensive way of avoiding the real problem – low rates of bystander CPR chest compressions?

In addition, angioplasty fits our medical model. A person has a medical problem. A subspecialty physician treats it with a high-technology intervention in a hospital setting. Interventions that can be performed by laypersons in nonhospital settings tend to receive less attention.[1]

A medical model of cardiac arrest treatment?

The medical model would not be the BLS treatments. Treatments that we know improve outcomes.

The medical model would be the ALS treatments. Treatments that we only hope improve outcomes.

What has dominated our attention in resuscitation?

Drugs, tubes, ventilations, . . .

We still do not have any evidence that these improve survival with good brain function. Is there any other valid way to measure outcomes?

We know that low rates of bystander CPR limit resuscitation rates, but we continue to make excuses for pushing the drugs, for pushing the tubes, and for squeezing the bag.

The captain of that engine is running that cardiac arrest. His job is to make sure there are good chest compressions and to make sure that the medics, when they arrive, don’t get in the way of good chest compressions.

It is an EMT-Basic skill to run a cardiac arrest now. The paramedics just get in the way.[2]

We can improve resuscitation or we can support paramedic egos.

As a paramedic, I think the choice is easy. We need to improve the rate and quality of bystander chest compressions.

Bystander chest compressions save lives.



[1] Increasing bystander CPR rates: the chest compression-only method puts the goal in easier reach.
Katz MH.
Arch Intern Med. 2011 Jan 10;171(1):87-8. No abstract available.
PMID: 21220665 [PubMed]

[2] Medical Direction Issue
Medical Direction Issue.

Dr. Sporer Interview.


Asymptomatic Sustained Ventricular Fibrillation in a Patient With Left Ventricular Assist Device


Also posted over at Paramedicine 101 and at Research Blogging.

Go check out the rest of the excellent material at both sites.

There’s a big difference between mostly dead and all dead. There are even other not quite dead yet categories that we tend to ignore. Asymptomatic Sustained Ventricular Fibrillation is not a group of words that appear to be appropriate together in a sentence. The old Sesame Street segment on which of these doesn’t belong would have a lot of people yelling Asymptomatic.

Sustained Ventricular Fibrillation is something we are familiar with, but in symptomatic patients – symptomatic to the point of being dead. We provide chest compressions to make up for the lack of cardiac output.

The first-generation assist devices are volume-displacement pumps. Consisting of a chamber filled passively or by suction and compressed by externally applied pressure, they provide a pulsatile flow, thereby mimicking the cyclic systole and diastole of the heart. The second generation has been developed with axial-flow, rotary-pump technology, providing a continuous blood flow.[1]

What does continuous flow mean, when assessing a patient?

No pulses, at least no pulses from the device.

On the day of admission, the patient noticed 3 consecutive discharges of the implantable cardioverter defibrillator, prompting him to call emergency medical services. On-site findings showed an alert and asymptomatic patient despite electrocardiographic analysis, exhibiting sustained ventricular fibrillation. Blood pressure measurement using a sphygmomanometer was not successful.[1]

Not an unusual 911 call. My AICD has been shocking me. My doctor told me to call 911 when that happens.

Typically, the AICD has shocked the heart back to the patient’s normal rhythm. A bit of hand holding and a discussion about possible prescriptions for a sedative and an antiarrhythmic, or an adjustment to the doses of these.

This patient is pulseless. Pulseless patients are not rare. A 911 call for a pulseless patient is usually because the pulseless patient is dead.

Contrariwise, a patient talking to me has a pulse. I have had several patients who were awake and talking, but without any palpable pulses. The absence of palpable pulses is different from the absence of pulses. All of these patients, with no palpable pulses, were significantly symptomatic.

conceivably the cardiac output had decreased substantially because of ventricular fibrillation, whereas intra-arterial monitoring revealed a continuous mean arterial pressure of 80 mm Hg (Figure 1B).[1]

respiratory rate (12 breaths/min), body temperature (36.8°C, 98.2°F), and peripheral O2 saturation (92%) were normal. Physical examination revealed a constant precardiac noise derived from the left ventricular assist device pump, whereas heart sounds were not audible. Lungs were clear and peripheral edema was not present.[1]

In other words, asymptomatic and pulseless, but with a more than adequate blood pressure and a good SpO2.

Under these circumstances, pulseless VF (Ventricular Fibrillation), the use of the term VAD (Ventricular Assist Device) is not really accurate. The VAD is working as the pump. The cardiac output is zero with VF. There is nothing to assist.

All of the blood flow is due to the VAD.

Implantable cardioverter defibrillator memory function yielded several adequate but unsuccessful electric shocks delivered in response to ventricular fibrillation, which had developed from multifocal ventricular tachycardia.[1]

Would we be more aggressive with the same presentation, if the patient were still in multiform VT (Ventricular Tachycardia)?

I think that a lot of people would, because they would want to prevent the rhythm from deteriorating to VF. Once the patient is in a rhythm that cannot get any worse, we may relax and be less aggressive.

Can this become worse?

This VF can become symptomatic. Almost all of the labs were within normal ranges. The exceptions were the electrolytes, which were low normal, or low, troponin I at 0.2 ng/mL (normal <0.03 ng/mL) and creatine kinase at 187 U/L (normal <145 U/L).

After supplementation of potassium and magnesium, amiodarone treatment was started, but first followed by 2 unsuccessful attempts of internal cardioversion. Eventually, after 3.5 hours, ventricular fibrillation could be terminated with external electrical biphasic cardioversion at 200 J, resulting in a stable rhythm with atrioventricular sequential pacing (Figure 1C). The intra-arterially determined mean blood pressure of 80 mm Hg remained unchanged.[1]

3 1/2 hours of documented asymptomatic VF.

They have this to state about the increasing use of VADs and the possible interaction/interference of VADs with AICDs (Automated Implantable Cardioverter Defibrillators).

Ventricular fibrillation is a fatal arrhythmia in the absence of circulatory support and inevitably results in death if not treated immediately. Whereas implantable cardioverter defibrillators have been proven to significantly reduce sudden cardiac death caused by ventricular tachycardia and ventricular fibrillation in severe congestive heart failure, their role in patients with left ventricular assist devices remains to be determined. 7,9 In fact, left ventricular assist devices might have a direct effect on implantable cardioverter defibrillator devices with alteration of lead parameters, ventricular tachycardias, and electromagnetic interference, thereby reducing the effectiveness of the implantable cardioverter defibrillator. 11 However, left ventricular assist devices may be able not only to support circulation but also to effectively substitute cardiac pump function in the presence of a malignant arrhythmia, even over a longer period, as previously reported with pulsatile-flow devices. 12-15[1]

Occurrence of sustained ventricular fibrillation in a patient with left ventricular assist device reflects a challenging situation that might be observed more frequently in the future: In 2008, about 4,000 left ventricular assist devices were implanted in the United States, but the numbers are expected to increase significantly. This is particularly true for the use of left ventricular assist devices in destination therapy of congestive heart failure, with the first device (HeartMate II; Thoratec Corporation) recently approved by the Food and Drug Administration for this indication.[1]

The HeartMate II LVAS includes a pump implanted inside the patient’s body and components that remain outside the patient’s body. The pump controller and batteries are worn outside the patient’s body. The system also includes a battery charger/power supply and monitor that remain outside the body..[2]

The extra equipment should be apparent, when assessing a patient with one of these devices. Smaller, less noticeable VADs may soon be available, but they will all probably have external equipment that we should notice.

Seven of the patients (all biventricular; diagnoses: four cardiomyopathy, two acute myocardial infarction, one end-stage coronary artery disease plus acute myocardial infarction) had prolonged arrhythmias that normally would have been lethal (six cases of ventricular fibrillation from 2 to 22 days, one asystole for 3 hours), but complete support of the systemic and pulmonary circulations was maintained in all seven patients with biventricular devices. Mean systemic blood flow during this period (4.6 +/- 0.6 l/min) was unchanged compared with that during sinus rhythm. Six of these patients survived to receive heart transplants.[3]

Up to 22 days of (continuous?) VF.

Blood flow during arrhythmias was not significantly different from blood flow during sinus rhythm.

It remains unclear, however, if sustained ventricular fibrillation during a longer period would have affected hemodynamics and outcome in our patient. Because left ventricular assist device patients are at high risk of developing malignant arrhythmias, which in turn can affect the cannulas’ position, effective treatment of ventricular tachycardias and ventricular fibrillation is recommended in this situation. In fact, slightly increased creatinine and troponin levels, although transient, were suggestive of some end-organ damage in our patient.[1]

Even though the patient was asymptomatic, there may have been damage occurring in the patient’s organs.

It is important to know that cardiopulmonary resuscitation (CPR) with chest compression may be performed in patients with a left ventricular assist device, if deemed clinically indicated. However, this intervention needs to be viewed cautiously because CPR may result in dislocation or damage of the cannulas or ventricle rupture, requiring emergency thoracotomy and heart surgery. CPR may be considered only in some patients who have substantial right ventricular failure, along with severe left ventricular dysfunction. Those patients may not be able to tolerate ventricular fibrillation because the right ventricle cannot deliver blood to the left side of the heart. In these cases, CPR may be necessary to prevent death while waiting for internal or external defibrillation, which can be performed without risk. Further studies are needed to determine the role of serious ventricular arrhythmias and implantable cardioverter defibrillators in patients with left ventricular assist devices.[1]

For the patient who has enough cardiac output to produce signs of life, CPR is probably a bad idea. Rapid transport to a hospital capable of treating patients with a VAD, or capable of transferring a patient with a VAD to a specialty center (just about any hospital), is probably a much better idea.

In theory, patients with sustained VF would not benefit from univentricular support because of the ineffective blood flow across the right heart associated with this dysrhythmia. In patients with refractory VT, particularly VT with a rate of less than 150 beats/min, univentricular mechanical support should be capable of sustaining adequate hemodynamics, because the right heart contributes some forward flow. Two of the most important factors affecting the physiologic flow across the pulmonary vascular bed are the status of the right ventricle and the pulmonary vascular resistance (PVR). If the PVR is elevated, whether because of VT or VF, the flow across the pulmonary vascular bed will be compromised, resulting in diminished LVAD flow. Conversely, if the PVR is low or normal, the LVAD should provide satisfactory flow. Therefore, selective agents to reduce the workload of the right ventricle and decrease the PVR, such as nitric oxide, could be useful in this setting.[4]

With a single chamber VAD, during VF, there might not be adequate blood flow. Compromised blood flow through the right ventricle might explain the elevated troponin and creatinine levels.


[1] Asymptomatic sustained ventricular fibrillation in a patient with left ventricular assist device.
Busch MC, Haap M, Kristen A, Haas CS.
Ann Emerg Med. 2011 Jan;57(1):25-8. Epub 2010 Jul 31.
PMID: 20674087 [PubMed – in process]

[2] Thoratec HeartMate II LVAS – P060040/S005
FDA (Food and Drug Administration)
Device Approvals and Clearances
Device Approval Notice with links to FDA Approval Letter

[3] Successful biventricular circulatory support as a bridge to cardiac transplantation during prolonged ventricular fibrillation and asystole.
Farrar DJ, Hill JD, Gray LA Jr, Galbraith TA, Chow E, Hershon JJ.
Circulation. 1989 Nov;80(5 Pt 2):III147-51.
PMID: 2680160 [PubMed – indexed for MEDLINE]

I could not find this paper on Circulation’s site, not a link to the abstract. Maybe the Pt 2 means a part of a supplement, that is not included in the archives.

[4] Ventricular assist device support for management of sustained ventricular arrhythmias.
Fasseas P, Kutalek SP, Samuels FL, Holmes EC, Samuels LE.
Tex Heart Inst J. 2002;29(1):33-6.
PMID: 11995847 [PubMed – indexed for MEDLINE]

Free Full Text Article from PubMed Central with links to Free Full Text PDF download

Busch MC, Haap M, Kristen A, & Haas CS (2011). Asymptomatic sustained ventricular fibrillation in a patient with left ventricular assist device. Annals of emergency medicine, 57 (1), 25-8 PMID: 20674087

Farrar DJ, Hill JD, Gray LA Jr, Galbraith TA, Chow E, & Hershon JJ (1989). Successful biventricular circulatory support as a bridge to cardiac transplantation during prolonged ventricular fibrillation and asystole. Circulation, 80 (5 Pt 2) PMID: 2680160

Fasseas P, Kutalek SP, Samuels FL, Holmes EC, & Samuels LE (2002). Ventricular assist device support for management of sustained ventricular arrhythmias. Texas Heart Institute journal / from the Texas Heart Institute of St. Luke’s Episcopal Hospital, Texas Children’s Hospital, 29 (1), 33-6 PMID: 11995847


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]

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