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

- Rogue Medic

FDA takes steps to improve reliability of automated external defibrillators


 

Why improve the reliability of AEDs (Automated External Defibrillators)?

AEDs are important, much more important than the epinephrine I wrote about yesterday, because AEDs actually work – at least when the AEDs work as they are supposed to.

AEDs fail much more often than they should.
 

From January 2005 through September 2014, the FDA received approximately 72,000 medical device reports associated with the failure of these devices. Since 2005, manufacturers have conducted 111 recalls, affecting more than two million AEDs. The problems associated with many of these recalls and reports included design and manufacturing issues, such as inadequate control of components purchased from other suppliers.[1]

 

72,000 reports over ten years. In the US, there are about 300,00 cardiac arrests a year where treatment is considered and an AED might be applied. Out of those, how many times is an AED applied? 1/3?

If I use that ballpark number guess, then 72,000 out of 1,000,000 is 0.72%. The reporting of problems that are identified during equipment checks and maintenance should also decrease the rate of failure in the treatment of real patients. Maybe I decrease that guess at a failure rate during cardiac arrest treatment/assessment to 0.5% or 0.1%?

A decrease to 0.1% is one out of every 1,000 uses. Is that a tolerable level of failure for a device that has only two tasks, but has to remain ready to perform those tasks at all times? The two tasks are to differentiate between ventricular fibrillation/ventricular tachycardia and any other cardiac rhythm and to deliver a shock to the patient after ventricular fibrillation or ventricular tachycardia has been identified.
 


Image credit.
 

There are only a few moving parts and the designs may vary from what I describe. The wire that is manually attached to the defibrillator pads. The lids that is opened, turns on the AED, and triggers the voice prompts. The buttons that are pressed to turn on the AEDs not turned on by opening the lid, to analyze the rhythm, and to deliver the shock.

Would Do we accept a similar failure rate from an ambulance, which has many more moving parts?

Do we accept similar failure rates from our personal vehicles, which have many more moving parts?

Do we accept similar failure rates from aircraft, which has many more moving parts?

Yes and no.

We deal with the failures in these vehicles by building in redundancies and paying attention to maintenance, but the result is that the failures rarely cause death, or the lack of resuscitation that could have occurred with a properly functioning AED.
 

For example, NASA management claimed that they had an isty-bitsy teeny-weeny failure rate. They were shown to be wrong in a very dramatic, and deadly, fashion. Twice.
 

If a reasonable launch schedule is to be maintained, engineering often cannot be done fast enough to keep up with the expectations of originally conservative certification criteria designed to guarantee a very safe vehicle. In these situations, subtly, and often with apparently logical arguments, the criteria are altered so that flights may still be certified in time. They therefore fly in a relatively unsafe condition, with a chance of failure of the order of a percent (it is difficult to be more accurate).

Official management, on the other hand, claims to believe the probability of failure is a thousand times less. One reason for this may be an attempt to assure the government of NASA perfection and success in order to ensure the supply of funds. The other may be that they sincerely believed it to be true, demonstrating an almost incredible lack of communication between themselves and their working engineers.

. . . .

For a successful technology, reality must take precedence over public relations, for nature cannot be fooled.[2]

 

We need to understand what the actual failure rates are. We also need to work on the failure rate that comes from operator error.

The reason people are able to lie to us with statistics (statistics do not lie, but statistics can be used by liars) is that we choose to remain ignorant of the appropriate use of statistics. We ask to be lied to.
 

What is an acceptable failure rate? It isn’t zero, because a zero failure rate is a lie.

Footnotes:

[1] FDA takes steps to improve reliability of automated external defibrillators
January 28, 2015
Food and Drug Administration
FDA News Release

[2] Volume 2: Appendix F – Personal Observations on Reliability of Shuttle
Report of the Presidential Commission on the Space Shuttle Challenger Accident (Also known as The Rogers Commission Report)
by R. P. Feynman
Conclusions
NASA report

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When is a double dose of defibrillation a good idea?

 
In the comments to Double simultaneous defibrillators for refractory ventricular fibrillation, NCMedic and Ambulance Driver write that they have already begun using variations on double defibrillation.
 

That     is     excellent.

 


 

The changes in when to implement the change, as well as the vector to use, are reasons we need to have people publishing results on what is being done. Please, work with your medical directors and/or others to publish some results.

We have had epinephrine (Adrenaline in Commonwealth countries) in ACLS (Advanced Cardiac Life Support) guidelines, and our protocols, for decades, but we still do not know the best dose or even which patients benefit.

NCMedic writes –
 

Has been in our protocols for sometime now, we are finding it more beneficial sooner than later for obvious reasons, next protocol revision will most likely have it on the 4th shock with the 2nd set of pads placed A/P to cover from a different vector.

 

Epinephrine seems to be harmful when given later, or is epinephrine less beneficial later, or is epinephrine always harmful, just much more harmful later, or something else.[1]

The problem is that we do not know when, or for whom, epinephrine is indicated.

Epinephrine is probably indicated in some patients, but which patients, at what dose, and at what time? If epinephrine should be repeated all of the same questions apply to all further doses. Dr. Scott Weingart points out how little we know about the use of epinephrine, because his approach makes more sense than what ACLS recommends and the evidence is equally lacking.[2]

There are many things in the presentation to discuss, such as Dr. Weingart’s misunderstanding of what nihilism means, but that is for another time.
 

There does not appear to be any harm from double defibrillation. As we use more current more often, we should expect to learn of harms, as we do with almost every intervention. However, as NCMedic states, we may be doing harm by waiting too long to deliver the double dose.

Should it be a double dose?

What about 1 ½ times the maximum?

300 j bi-phasic or 540j mono-phasic or maybe some combination of bi-phasic and mono-phasic, and if a combination, what combination, with drugs or without, which drugs if with drugs, . . . ?

What about 3 times the maximum?

600 joules bi-phasic or 1,080 joules mono-phasic or . . . ?

Should the higher-dose defibrillation be after the fifth shock with a return to VF/pulseless VT (Ventricular Fibrillation/pulseless Ventricular Tachycardia)? After the fourth shock? After the third shock? After the second shock? After the first shock?

Is waiting longer to increase joules making it more likely that epinephrine will be given? Is epinephrine more harmful than a double shock, less harmful than a double shock, or roughly the same?

The amount we do not know is huge.

We should learn what we are doing to our patients and not arrogantly choose to remain ignorant, as we have chosen with epinephrine. That is changing, but some still defend the arrogance of ignorance at the expense of our patients.[3]

Footnotes:

[1] Does Faster Epinephrine Administration Produce Better Outcomes from PEA-Asystole?
Sun, 25 May 2014
Rogue Medic
Article

[2] Podcast 125 – The New Intra-Arrest from SMACCgold
EMCrit
Dr. Scott Weingart
Web page with video and show notes.

[3] Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL.
Resuscitation. 2011 Sep;82(9):1138-43. Epub 2011 Jul 2.
PMID: 21745533 [PubMed – in process]

Free Full Text PDF Download of In Press Uncorrected Proof from xa.yming.com
 

This study was designed as a multicentre trial involving five ambulance services in Australia and New Zealand and was accordingly powered to detect clinically important treatment effects. Despite having obtained approvals for the study from Institutional Ethics Committees, Crown Law and Guardianship Boards, the concerns of being involved in a trial in which the unproven “standard of care” was being withheld prevented four of the five ambulance services from participating.

 

In addition adverse press reports questioning the ethics of conducting this trial, which subsequently led to the involvement of politicians, further heightened these concerns. Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate.

 

.

Double simultaneous defibrillators for refractory ventricular fibrillation

 
It looks as if the next generation of defibrillators will go to 11. This patient received a double dose of defib.

Is 720 joules too much?

If your answer is Yes, please explain how 720 joules is worse than death.

What about 400 joules? Some older mono-phasic defibrillators go to 400 joules, but we might see 400 joule bi-phasic defibrillators.

Until then, there is the possibility of using two defibrillators to deliver shocks at the same time, or milliseconds apart. By the time that this is a relevant treatment, the patient has been down for several shocks and is still in a shockable rhythm, but a supervisor or second medic unit should have arrived with a second defibrillator.
 


 

It is important to not put the pads from the same defibrillator next to each other.

The paper describes a patient with a BMI (Body Mass Index) of 40, a STEMI, and an onset of VF (Ventricular Fibrillation) in the presence of EMS.

CPR (being performed by the son when EMS arrived at the ED?), 200J x 3, epi x a bunch, amio x 1 by EMS.

High-quality CPR, a bunch more epi, 200 J x 2, lido x 1, bicarb x 1 (bicarb might have been indicated by the patient’s astrological sign), then the shock at 400 joules.
 

The patient then regained a palpable pulse and blood pressure. He had another brief episode of ventricular tachycardia that responded to a second defibrillation with 400 J. The patient had a wide QRS rhythm that quickly narrowed into normal sinus.[1]

 

Maybe the patient was not told about the concerns of some people that too much is too much. If he had been told, he would have remained dead, like a good scenario patient.

Next time he can follow the approved scenario.
 

Five studies have demonstrated safety in patients receiving 720 J of monophasic energy for cardioversion of atrial fibrillation (17,22–25).[1]

 

Five papers demonstrate the safety of 720 joules in living patients with atrial fibrillation, but many in EMS will tell us that it is too dangerous to use on dead people after the failure of standard doses of energy.

Lake Sumter EMS has been providing compression-only CPR, even adding 720 joule defibrillation, and they may have the best resuscitation rates in America. The rest of us should consider catching up. I wonder how things have gone for LEMS, since I wrote about them a couple of years ago.[2]
 

 

While ROSC (Return Of Spontaneous Circulation) is not the right outcome to use to evaluate a treatment, 70% suggests that we should pay attention to what they are doing in Lake Sumter. 46% ROSC in those who could not get ROSC any other way by EMS.

You can’t be too safe is still a lie.

Also read –

When is a double dose of defibrillation a good idea?

Footnotes:

[1] Double simultaneous defibrillators for refractory ventricular fibrillation.
Leacock BW.
J Emerg Med. 2014 Apr;46(4):472-4. doi: 10.1016/j.jemermed.2013.09.022. Epub 2014 Jan 21.
PMID: 24462025 [PubMed – in process]

[2] Optimizing Outcomes in Cardiac Arrest
Mon, 10 Dec 2012
Rogue Medic
Article

.

A Recalled AED is Better Than No AED


 
Cardiac arrest. CPR in progress. Do not use the AED, because it has been recalled!

Wrong.
 


 

HeartStart automated external defibrillators from Philips Healthcare have been recalled.

What does the FDA (Food and Drug Administration) mean by recall?

Well, why was the recall issued?
 

Certain HeartStart automated external defibrillator (AED) devices made by Philips Medical Systems, a division of Philips Healthcare, may be unable to deliver needed defibrillator shock in a cardiac emergency situation, the U.S. Food and Drug Administration said today in a new safety communication for users of these previously recalled devices.[1]

 

A shock might not be delivered.

What does the FDA recommend?
 

“The FDA advises keeping all recalled HeartStart AEDs in service until you obtain a replacement from Philips Healthcare or another AED manufacturer, even if the device indicates it has detected an error during a self-test,” said Steve Silverman, director of the Office of Compliance in the FDA’s Center for Devices and Radiological Health.[1]

 

Do not take these AEDs out of service service until a replacement is present.

Why?

What about the lawyers?

But it’s defective!

Thinking is dangerous!
 

“Despite current manufacturing and performance problems, the FDA considers the benefits of attempting to use an AED in a cardiac arrest emergency greater than the risk of not attempting to use the defibrillator.”[1]

 

The benefit is greater than the risk.

There is risk with everything.

Anyone who tells you otherwise is selling something.

There is not benefit with everything.

Since the detection of an error during the self-test does not guarantee that the AED will not deliver a shock when needed, removing the AED without a replacement is more dangerous than leaving the AED in service.

These recalled AEDs are better than no AED.
 

Of course, if needed for use in an emergency, make every attempt to clear the error and use the device normally, as described in the Owner’s Manual.[2]

 

The manufacturer and the FDA agree that, in the case of these AEDs, something is better than nothing.

Are we really going to make a dead patient more dead by using a defective AED?

Footnotes:

[1] FDA issues safety communication on HeartStart automated external defibrillators from Philips Healthcare
FDA News Release
For Immediate Release: Dec. 3, 2013
Media Inquiries: Jennifer Rodriguez, 301-796-8232, jennifer.rodriguez@fda.hhs.gov
Consumer Inquiries: 888-INFO-FDA
News Release

[2] Philips HeartStart FRx and OnSite (HS1) automated external defibrillators (AEDs)
Phillips Healthcare
Maintenance Advisory

.

Charging the Defibrillator While Continuing Chest Compressions – Part II


ResearchBlogging.org
Also posted over at Paramedicine 101 (now at EMS Blogs) and at Research Blogging. Go check out the excellent material at these sites.

Continuing, after a 6 month delay, a discussion of an EMS 12 Lead article from Part I. ACLS (Advanced Cardiac Life Support) recommends charging the defibrillator during compressions. This is no less of a recommendation than giving epinephrine. How many people ignore ACLS guidelines for compressions during charging, but claim that it is evil to disobey anything ACLS recommends on epinephrine, amiodarone, or ventilations?

Analyses of VF waveform characteristics predictive of shock success have documented that the shorter the time interval between the last chest compression and shock delivery, the more likely the shock will be successful.141 A reduction of even a few seconds in the interval from pausing compressions to shock delivery can increase the probability of shock success.142 [1]

Extra pauses in compressions add to the time without compressions.

If the medic/nurse/doctor using a manual defibrillator recognizes a shockable rhythm, why not provide compressions while charging the defibrillator?

Some people will say that this is dangerous.


Image credit.

But if someone accidentally delivers a shock during compressions, people will be killed!

In a systematic review, Hoke et al. summarized 29 reports of accidental defibrillator discharges, of which only 15 occurred during resuscitation attempts.21 Symptoms included tingling sensations, discomfort, and minor burns, but no long term effects or major consequences were reported.[2]

Where are the dead bodies we hear so much about?

Where are the medics/nurses/doctors needing to be defibrillated back to life?

There was only one incident where a shock was delivered while a rescuer was actively performing chest compressions. However, the compression transcript continued without any visible change to CPR administration, suggesting that the rescuer was unaffected by the event. Review of clinical records and audio transcripts revealed no evidence of inadvertent shocks to rescuers. In addition, there was no significant difference in the incidence of inappropriate shocks to patients associated with charging during compressions (20.0% vs 20.1%; p = 0.97). [2]

In this study, there was one case of a shock being delivered during compressions, but nobody seems to have been affected by this shock.

What happened to the automatic death that ACLS instructors spend so much time describing?

Where is the evidence?

In the current study, charging during compressions decreased median pre-shock pause by over 10 s, which previous studies suggest could have a dramatic effect on clinical outcomes. We previously reported an almost two-fold increase in the chances of successful defibrillation for every 5 s reduction in the pre-shock pause.9 Similarly, Eftestøl et al. found that a 10 s hands-off period prior to defibrillation would roughly halve the probability of obtaining ROSC.6 [2]

The risk to rescuers appears to be minimal, but the possible benefit to patients may be dramatic.


Click on image to make it larger.

The difference in time without compressions is significant.

Interestingly, we found that the most efficient technique with regard to minimizing pauses was not the AHA recommended method of pausing to analyze, resuming CPR to charge, and then pausing again to defibrillate. Rather, charging at the end of every 2 min CPR cycle in anticipation of a shockable rhythm and then pausing only once, briefly, to both analyze and either shock or disarm was associated with significantly shorter total pause duration in the 30 s preceding defibrillation. [2]

If we see asystole, we do not deliver a shock. We cancel the shock.

If we see PEA (Pulseless Electrical Activity, such as sinus rhythm, sinus tachycardia, sinus bradycardia, or any other non-shockable rhythm), we do not deliver a shock. We cancel the shock.

Cancelling the shock is not going to be the same for each defibrillator, but we do need to know how to cancel the shock for each machine we use. We can read the instructions.

How?

We can turn on the monitor, charge it up to the setting we would use to defibrillate, and try to figure out ways to get the charged defibrillator to turn the shock off. We should already know how to do this.

All that appears to be required is competence. Why is that so difficult?

Why do we keep making excuses for misbehavior?

Footnotes:

[1] CPR Before Defibrillation
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Rhythm-Based Management of Cardiac Arrest
Defibrillation Strategies
Free Full Text from Circulation with links to Free Full Text PDF

[2] Safety and efficacy of defibrillator charging during ongoing chest compressions: a multi-center study.
Edelson DP, Robertson-Dick BJ, Yuen TC, Eilevstjønn J, Walsh D, Bareis CJ, Vanden Hoek TL, Abella BS.
Resuscitation. 2010 Nov;81(11):1521-6.
PMID: 20807672 [PubMed – indexed for MEDLINE]

Edelson, D., Robertson-Dick, B., Yuen, T., Eilevstjønn, J., Walsh, D., Bareis, C., Vanden Hoek, T., & Abella, B. (2010). Safety and efficacy of defibrillator charging during ongoing chest compressions: A multi-center study Resuscitation, 81 (11), 1521-1526 DOI: 10.1016/j.resuscitation.2010.07.014

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


ResearchBlogging.org

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.

Footnotes:

[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

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Cardiac Arrest Video – I

There has already been a bit of blogging about this on-camera cardiac arrest. Another soccer player experiences sudden cardiac arrest on camera at Prehospital 12 Lead ECG, Salamanca Soccer Player Miguel Garcia’s Sudden Cardiac Arrest at Dr. Wes, as well as Sudden cardiac arrest in a soccer player – a happy ending at Electrophysiology Fellow.

[youtube]bEwirY_BsHQ&[/youtube]

Ignore the guy on the ground at the beginning. The guy behind him, kneeling and tying his shoe is the one to pay attention to.

The NYT article that Electrophysiology Fellow links to is an important read. The Indelible Pain of Watching an Athlete Fall.

Were there sufficient safety and security measures in place, considering that no official apparently noticed Crippen’s distress and that another U.S. swimmer, Christine Jennings, said she had raised her arm for assistance late in the race (after having vomited earlier) and gotten no help, not from a safety boat nor officials on jet skis?

The safety officials did not even find the dead guy until after the race, after one of the other swimmers told officials Crippen was missing.

We seem to do a very poor job of recognizing signs of serious medical problems.

Maybe these videos can help point out that things can change quickly. All of the other soccer players seemed to be aware of the seriousness of the medical condition. Videos can also point out the benefits of prompt action for a witnessed arrest. While it is difficult to tell what is going on with all of those people there, less than 4 minutes after a cardiac arrest, he apparently has pulses back. From

This is also one of the benefits of having audio recording of every arrest. This is the best way to learn. Yes. some states do have laws against this, but this is just one more reason to have these laws thrown out. also, the importance is in reviewing the call afterward, not in calling medical command for permission to do something. One is competent oversight. The other is not.

“He was dead for 20 seconds,” Garrido told reporters after embracing Calero.

This is confusing. Most likely, he was dead when he hit the ground. While it is difficult to tell what is going on most of the time. From about 1:30 to 1:55 somebody is doing compressions (for some reason there seems to be an attempt to apply a cervical collar at this time), then there is a pause, then more compressions. At around 2:40, compressions stop and everyone moves back a bit. Probably a shock is delivered, but it is followed by more compressions after 3:00. Was he resuscitated, but then arrested again? The statement is from the team doctor, not from one of the players, so there should be more than a layman’s understanding of the medical term dead.

This is also an example of too many people on scene. They aren’t going to use up all of the oxygen, but they will get in the way. Then they run off the field? Running with a patient endangers the patient.

This is one of the reasons we give so many drugs during cardiac arrest. It gives more people things to do to look busy.

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Every Drug in the Box

The problem of using every relevant, but perhaps not necessary, drug is something medics, nurses, and doctors are bad at. The major exceptions to this are sedation and pain management. Then the problem is getting the doctor to allow the box to be opened. Both demonstrate a lack of understanding of pharmacology and assessment.

I was discussing, with some doctors, a journal article about an anaphylactic patient, who received about a dozen different medications. I suggested that some of the problems the patient experienced were probably from all of the drugs being pushed.

“Horse feathers. There is nothing wrong with giving all of the potentially indicated drugs to the patient.” OK, not the exact wording of the doctors, but it seems to capture the sentiment.

Potentially indicated and indicated are worlds apart.

It isn’t as if there is any research on the administration of all of these medications combined. There are far too many variables to control for, much too small an incidence of anaphylaxis that does not respond to standard treatments, and apparently not enough interest in questioning the just dump the box into the patient philosophy demonstrated.

In cardiac arrest algorithms, it is nice to be moving away from the let’s get rid of all of the expiring drugs approach. We still have a long way to go in recognition of the lack of benefit of ALS (Advanced Life Support) treatment of dead people. It is a start.

Currently, the AHA (American Heart Association) does not feel that an IV is that important. They have been gradually moving in this direction over the past couple of decades. Eventually, they will probably only recommend medications specifically indicated for potentially reversible causes, rather than everybody dead gets epi – and/or vasopressin.

For victims of witnessed VF arrest, prompt bystander CPR and early defibrillation can significantly increase the chance for survival to hospital discharge. In comparison, typical ACLS therapies, such as insertion of advanced airways and pharmacologic support of the circulation, have not been shown to increase rate of survival to hospital discharge.

After beginning CPR and attempting defibrillation, rescuers can establish intravenous (IV) access, consider drug therapy, and insert an advanced airway.

One of the problems with research, on a bunch of drugs given to the same patient, is that there are so many variables involved. This does not only affect the research, but the administration, too. When patient presentation changes, how do you know what the likely cause was?

Is it the effect of medication?

Is it a side effect?

Is it spontaneous remission?

Is it an erroneous assessment?

Is it the last medication given?

The first?

The third?

Is it a combination of the medications?

We do not know. How do most people deal with this? They act as if it must be the most recently given medication.

Is there a reason to believe that this is the correct approach?

No.

Here is the logic that is applied by those, who insist that the drugs are essential:

1. Successful resuscitation is having the patient leave the hospital in about the same condition as they were before the cardiac arrest.

2. Having a pulse is necessary for a successful resuscitation.

3. Therefore, anything that leads to pulses is good, or one step closer to #1.

Unfortunately, things are not that simple. While it is hard to resist the I’m going to Disneyland! response at this point. The most common outcome for patients who have a return of a pulse is that the pulse goes away again. At some point during the resuscitation, the pulse usually goes away permanently.

Getting a pulse back is the almost immediate response that is similar to what a crack addict feels – a rush. There is a need to replicate that, and it is easy, you give enough epi to a corpse and you often get a pulse.

There is a quote above supporting the focus on excellent chest compressions and rapid defibrillation. It is immediately followed by a quote that points out the futility of the mistaken, but persistent, focus on ALS in cardiac arrest. I include both sentences together, now. the italics are mine.

For victims of witnessed VF arrest, prompt bystander CPR and early defibrillation can significantly increase the chance for survival to hospital discharge. In comparison, typical ACLS therapies, such as insertion of advanced airways and pharmacologic support of the circulation, have not been shown to increase rate of survival to hospital discharge.

If the patients who never get drugs are leaving the hospital (with an intact brain) at least at the same rate as the patients who received drugs, then maybe the drugs do not help.

If we only focused on things that produce a pulse, would we include defibrillation?

Defibrillation produces a pulse.

No. Defibrillation produces asystole. During the asystole, it is hoped that the patient’s heart has at least one pacemaker that initiates an organized rhythm. It is further hoped that the rhythm does produce a pulse.

Resuscitation is about resuscitating the heart and the brain, not about giving enough drugs to get a pulse.

Perhaps cerebral resuscitation is about a little bit more.

And the medic, with his medic-feet ice-cold in the snow,
Stood puzzling and puzzling:

How could it be so?

It came without drugs! It came without tubes!
It came without gadgets, IVs or drips!

And he puzzled three hours, till his puzzler was sore.
Then the medic thought of something he hadn’t before!

Maybe Resuscitation,

he thought

doesn’t come from a drug store.
Maybe Resuscitation… perhaps… means a little bit more!

And what happened then…? Well… in BLS-ville they say
That the medic’s understanding grew three sizes that day!

And the minute the patient’s heart didn’t feel quite so tight
He whizzed with his load away from the bright dying light

He brought back the brain! And the heart for the pulse!

And he…HE HIMSELF!

The medic got a real save!

To paraphrase a great doctor.

Adapted from How the Grinch Stole Christmas.

Theodor Seuss Geisel, better known as Dr. Seuss.

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