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

- Rogue Medic

The association between emergency medical services staffing patterns and out-of-hospital cardiac arrest survival

Also posted over at Paramedicine 101 and at Research Blogging. Go check out the rest of the excellent material at both sites.

A recent study looks at The association between emergency medical services staffing patterns (the number of paramedics dispatched on an ambulance) and out-of-hospital cardiac arrest survival. They make some interesting observations.

We tested the hypothesis that two or more paramedics at the scene of OHCA would be correlated with a higher rate of survival to hospital discharge.[1]

Since there were at least 2 paramedics on scene, they really compared the presence of 2 medics with the presence of 3 medics and with the presence of more than 3 medics. OHCA is Out-of-Hospital Cardiac Arrest.

Paramedic treatment of cardiac arrest is provided by protocol and direct medical oversight.[1]

An interesting interpretation of the word direct. A medical command physician is available by phone or radio for consultation/orders. This is historically the way direct medical oversight has been interpreted, but it requires some flexibility in the interpretation of the meaning of direct. The word oversight requires similar flexibility, since the physician depends entirely on what the medic says, except for the medical command physicians who perversely just say no to everything.

Cardiac arrests resulting from a drug overdose, suicide, drowning, hypoxia, exsanguination, stroke, or trauma were excluded from the study. Also excluded were cases in which no crew configuration or responding unit information was available, cases in which no resuscitation effort was attempted, and cases in which no time data were available.[1]

It is reasonable to exclude some of these causes, since they are not standard medical cardiac arrests and do not contribute significantly to resuscitation statistics. The intent of the study seems to be the effect of the number of medics on standard cardiac arrest. Trauma is reasonable to exclude, since resuscitation from traumatic arrest is, for all practical purposes, zero percent. Movies and TV suggest otherwise, but there is nothing about chest compressions that reverses blood loss, TBI (Traumatic Brain Injury), pneumothorax, cardiac tamponade, or other traumatic causes of sudden death. On the other hand, there are some causes of cardiac arrest that do respond to chest compressions, such as commotio cordis[2], [3] or lightning strike,[4] that might appear to fall into the trauma category. Cardiac arrest due to stroke may have resuscitation outcomes as dismal as trauma.

Why exclude cardiac arrest due to hypoxia? Are they looking only at airway obstruction as a cause of hypoxia? Does this include anaphylaxis or asthma? What about CHF (Congestive Heart Failure), which could be categorized as hypoxic or as cardiac? These are questions that were not addressed.

There is no explanation for any of these exclusions anywhere in the paper. Are these excluded because the authors consider resuscitation to be so unlikely that they would only contribute a more zeros to the data?

If a paramedic responded as part of the first response unit’s crew, the paramedic was not counted as being part of the crew configuration. The independent variable was categorized solely on the number of paramedics present in the responding ALS unit crew. Milwaukee County EMS operates with a minimum of two paramedics on ALS ambulances. During the study period, there were no cases treated by one paramedic.[1]

In other words, although we are looking at whether more medics lead to better outcomes, we will set aside cases where the medics are first responders, unless those first responders are responding on an ambulance. Interesting, but it is difficult to tell if this would have any influence, since no numbers are reported. If medic first responders are rare, it probably will not have any effect on outcomes. Not having data, we do not know if it is rare. If medic first responders are common, this should not be ignored as a variable.

It might be nice to evaluate the effect of paramedic first responders. Even though there does not appear to be any benefit from having paramedics treating cardiac arrests, as first responders or otherwise, some systems are adopting the practice of having every responder be a paramedic. These systems seem to encourage the belief that, even though paramedic treatments do not improve outcomes, the sight a lot of paramedics on scene is more important than anything that might actually improve outcomes. There is no need to address things that matter, when we can put on an impressive show, unless survival is important.

Neurologic status at discharge was not available.[1]

Too bad. That could be useful information to have.

There were sufficient data to analyze 10,057 (98%)cases.[1]

That is very good.

FIGURE 2. Frequencies of cardiac arrest outcome by year in Milwaukee County.
ROSC = Return Of Spontaneous Circulation.
I added the red circles and green squares to make it easier to identify the lines. Nothing else was changed about this chart.

The most interesting thing that I notice is that increases in one of the surrogate end points (ROSC) seems to indicate drops in the end point that matters – survival to discharge. While they did not have access to the neurological status at discharge, this information seems to contradict what everyone claims is important about resuscitation – If we don’t have ROSC, we cannot improve survival to discharge.

In the above chart, as ROSC increases, survival to discharge decreases. Is this statistically significant? I don’t know, but it appears to be pretty consistent. The numbers are not provided by years, but the trend can be determined from the chart. Below, I list the the changes from year to year in ROSC (Return Of Spontaneous Circulation) and in Survival (survival to discharge from the hospital).
= year to year decrease. = increase. = no change. More arrows = more change.

1993 to 1994         ROSC               Survival

1994 to 1995         ROSC               Survival          

1995 to 1996         ROSC ⇑⇑⇑⇑     Survival              

1996 to 1997         ROSC ⇑⇑            Survival            

1997 to 1998         ROSC ⇑⇑            Survival          

1998 to 1999         ROSC ⇓⇓⇓        Survival

1999 to 2000         ROSC ⇑⇑            Survival

2000 to 2001         ROSC ⇓⇓⇓        Survival            

2001 to 2002         ROSC ⇑⇑            Survival ⇓⇓        

2002 to 2003         ROSC ⇑⇑            Survival ⇑⇑

2003 to 2004         ROSC               Survival

2004 to 2005         ROSC               Survival ⇑⇑        

I need to point out that this study was not designed to examine any connection between ROSC and survival to discharge. The yearly data are not included, so I am only looking at the direction of change of the bars connecting one year to the next. Out of 12 years, the change in percentage of ROSC is the same as the change in percentage of survival only 5 times. Sometimes these divergences are dramatic. Almost every big change in ROSC had an opposite change in survival.

As percentage of ROSC improves, percentage of survival seems to decrease. Maybe we need to stop obsessing about improving ROSC and just work on the more complicated problem of improving long term survival, which is all that really matters.

it appears that even though there was a medication change in the treatment protocol, changes to the American Heart Association guidelines, advances in abilities, training, equipment, CPR performance, and variation in hospital care, survival to hospital discharge remained stable during the study period. This may indicate that we have not yet identified the factors that are crucial to improving survival and that more research is needed to find the ideal treatment for cardiac arrest.[1]

Contrariwise, it may indicate that we have already found the most effective paramedic/ALS (Advanced Life Support) treatment. We are just unwilling to accept it, because we cannot believe it is that simple. Excellent continuous compression CPR interrupted only by rapid defibrillation.

We do not need paramedics for this. Therefore the number of paramedics on scene may only lead to interference with effective treatment.

It is important to note that, as is shown in Table 1, crews with two paramedics treated fewer cardiac arrest cases with an initial rhythm of ventricular fibrillation or pulseless ventricular tachycardia than crews with three or more paramedics. Yet the unadjusted and adjusted odds ratios demonstrated that two paramedics conferred a survival advantage. This seems counterintuitive and may indicate an even stronger association between crew size and survival.[1]

If there is a bias in the data, it is likely one that hides the magnitude of the harm to patients from more paramedics.

The Milwaukee County EMS system operates with a minimum of two paramedics on ALS ambulances. During the study period, no cases were treated by one paramedic. A single paramedic’s influence on outcome was not able to be evaluated.[1]

The data do appear to be stating that the more paramedics on scene, the less likelihood that the cardiac arrest patient will leave the hospital alive.

When adjusted for variables previously correlated with cardiac arrest survival and referenced against crews with two paramedics, patients treated by crews with three paramedics (0.83, 95% confidence interval [CI] 0.70 to 0.97, p = 0.02) and crews with four or more paramedics (0.66, 95% CI0.52 to 0.83, p < 0.01) were associated with reduced survival to hospital discharge.[1]

The number of paramedics does not appear to interfere with ROSC, only with long term meaningful outcome.

The studies of ALS interventions keep pointing out the increased ROSC with ALS interventions. Unfortunately, the surrogate endpoint of ROSC does not appear to lead to improved survival to discharge.

Standard cardiac arrest treatment has led to more of an emphasis on continuous compressions and defibrillation. Standard cardiac arrest treatment still includes epinephrine, amiodarone, atropine, intubation, and intravenous access – treatments that have repeatedly failed to show improved survival to discharge.

During cardiac arrest, basic CPR and early defibrillation are of primary importance, and drug administration is of secondary importance. Few drugs used in the treatment of cardiac arrest are supported by strong evidence. After beginning CPR and attempting defibrillation, rescuers can establish intravenous (IV) access, consider drug therapy, and insert an advanced airway.[5]

By supported by strong evidence, they mean that there is not any evidence of improved survival to discharge with drugs, IVs, endotracheal tubes – anything other than good continuous compressions and defibrillation.

Maybe this study means that the more people capable of performing less-than-helpful treatments, the more likely that less-than-helpful treatments will be given.

Perhaps, with the next revision of the cardiac arrest guidelines, we will make the ethical decision to limit treatments to those that have been shown to improve survival, rather than subjecting everyone to these treatments that have not been shown to improve survival.


[1] The association between emergency medical services staffing patterns and out-of-hospital cardiac arrest survival.
Eschmann NM, Pirrallo RG, Aufderheide TP, Lerner EB.
Prehosp Emerg Care. 2010 Jan-Mar;14(1):71-7.
PMID: 19947870 [PubMed – indexed for MEDLINE]

[2] An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis)
Link MS, Wang PJ, Pandian NG, Bharati S, Udelson JE, Lee MY, Vecchiotti MA, VanderBrink BA, Mirra G, Maron BJ, Estes NA 3rd.
N Engl J Med. 1998 Jun 18;338(25):1805-11.
PMID: 9632447 [PubMed – indexed for MEDLINE]

Free Full Text from NEJM         Free PDF from NEJM

[3] Protecting our children from the consequences of chest blows on the playing field: a time for science over marketing.
Link MS, Bir C, Dau N, Madias C, Estes NA 3rd, Maron BJ.
Pediatrics. 2008 Aug;122(2):437-9. No abstract available.
PMID: 18676560 [PubMed – indexed for MEDLINE]

Free Full Text from Pediatrics         Free PDF from Pediatrics

[4] Electric Shock and Lightning Strikes
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 10.9: Electric Shock and Lightning Strikes
Free Full Text         Free PDF

[5] Management of Cardiac Arrest
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.2: Management of Cardiac Arrest
Access for Medications: Correct Priorities
Free Full Text         Free PDF

Eschmann, N., Pirrallo, R., Aufderheide, T., & Lerner, E. (2010). The Association between Emergency Medical Services Staffing Patterns and Out-of-Hospital Cardiac Arrest Survival Prehospital Emergency Care, 14 (1), 71-77 DOI: 10.3109/10903120903349820


Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.

Also posted over at Paramedicine 101. Go check out the rest of what is there.

This study has received a lot of attention. I will interchangeably use the terms the IV (IntraVenous) group and the epinephrine group depending on the terminology I think is more relevant at the time. The distinction is not one that I believe is important. This is a study of IV medication in cardiac arrest. Epinephrine is the stated focus of the study.

There has never been any evidence to suggest that medication leads improved resuscitation outcomes. Unless your idea of an improved resuscitation outcome has nothing to do with quality of life.

Beneficial short-term effects of epinephrine have been shown in animal studies,3-5 but there is increasing concern for increased myocardial dysfunction6,7 and disturbed cerebral microcirculation after cardiac arrest.8[1]

Some people argue that the short-term effects are important. If we do not get a pulse back, we will not resuscitate anyone. This is true, but the problem is how much long-term damage do we inflict just to obtain that short-term improvement?

High-dose epinephrine is no longer recommended, even though it was better than standard-dose epinephrine at producing ROSC (Return Of Spontaneous Circulation). The current recommendation for epinephrine is based on this same misconception. More ROSC = better outcomes – except that the dogma is not supported by any evidence.

CONCLUSIONS–High-dose epinephrine (HDE) significantly improves the rate of return of spontaneous circulation and hospital admission in patients who are in prehospital cardiac arrest without increasing complications. However, the increase in hospital discharge rate is not statistically significant, and no significant trend could be determined for neurological outcome. No benefit of NE compared with HDE was identified. Further study is needed to determine the optimal role of epinephrine in prehospital cardiac arrest.[2]

That study was 17 years ago. That was far from the first study of epinephrine. There has been many studies of epinephrine in cardiac arrest since then.

We still do not have any research to show improved outcomes with any dose of epinephrine to treat cardiac arrest, but rather than admit that epinephrine should only be used in well controlled studies, we continue to make excuses. We are practicing alternative medicine, not real medicine.

Absence of evidence of benefit does not mean an absence of benefit, but when does it become enough evidence to insist that we stop using this ineffective and potentially harmful drug as the standard treatment?

Back to the current study.

Because there are no randomized controlled studies showing improved survival to hospital discharge with any drugs routinely administered during CPR, we concluded such a study was warranted.[1]

This study is possible because these researchers are outside of the US. In the US, the IRBs (Institutional Review Boards) seem to have concluded that it is unethical to deviate from the standard treatment, even if the standard treatment is harmful. Of course, we can never learn if the standard treatment is harmful, or even if it is beneficial, if we are prohibited from studying the treatment. However, the IRBs’ definition of ethics seems to have been arrived at while consuming hallucinogens and reading Lewis Carroll.

Epinephrine in cardiac arrest is also firmly established outside of the US. Here is a part of their explanation of the study design.

In this prospective, randomized controlled trial of intravenous drug administration during out-of-hospital cardiac arrest, we compared outcomes for patients receiving standard ACLS with intravenous drug administration (control) and patients receiving ACLS without intravenous drug administration (intervention).[1]

ACLS is Advanced Cardiac Life Support – almost all of the treatments that would be given in the ED (Emergency Department). Not giving the drug is the intervention. Giving the drug is considered the non-intervention – the control against the effects of the treatment, which is the non-treatment.

Defibrillation was attempted in more patients in the intravenous group compared with the no intravenous group (47% vs 37%, respectively; OR, 1.16 [95% CI, 0.74-1.82]). More defibrillation shocks were delivered to those who received defibrillation in the intravenous group compared with the no intravenous group (median, 3 [range, 1-22] vs 2 [range, 1-26], respectively; P = .008). Both groups had adequate and similar CPR quality with few chest compression pauses (median hands-off ratio, 0.15 for the intravenous group and 0.14 for the no intravenous group) and the compression and ventilation rates were within the guideline recommendations (Table1).[1]

While there were no apparent differences in the quality of CPR, the more frequent defibrillations might be worth looking at. One of the important aspects of this study, as opposed to most prehospital research, is the recognition of a need to control for quality.

The explanation for the more frequent defibrillations that seems most likely is that the epinephrine produced a shockable rhythm more often than CPR alone produced a shockable rhythm. Since a shockable rhythm appears to be the next best thing to ROSC, this would not be a surprise. Many patients will change from a shockable rhythm to asystole when defibrillated. Defibrillation is a profound vagal stimulus and asystole is the ultimate vagal state. Even with similar initial rates of shockable rhythms, some of both groups would be expected to be shocked into asystole. The epinephrine, being a huge cardiac stimulus, would be expected to lead to a return of a shockable rhythm more often than just CPR. In other words, if the epinephrine is expected to produce ROSC more often, it should also produce a shockable rhythm more often. The authors came to a similar conclusion.

Without differences in the predefined primary outcome, patients in the intravenous group received more defibrillations, were resuscitated for a longer period, and more frequently had ROSC. With similar and adequate CPR quality, this is likely due to the pharmacological effects of the drugs used (epinephrine, atropine, and/or amiodarone). This finding is consistent with previous animal studies with epinephrine,6,7 and clinical studies evaluating the effects of amiodarone,23 atropine,24 and even high-dose epinephrine,25 all of which documented improved short-term effects without improving long-term outcomes.[1]

One major criticism of the methods is that they did not have a placebo to be given to keep the EMS crews blinded to the actual treatment. The authors do admit that this is a limitation. Of course, this placebo would probably not be called a placebo, since the epinephrine arm is the placebo arm, while the non-treatment arm is the active intervention arm, but that is really only an amusing problem of terminology and attitude. When the epinephrine group is the group with an IV line in place during resuscitation and the no epinephrine group is the one that does not have an IV until after return of pulses, there is not even an attempt at blinding. Did this lead to any detectable difference in the way patients were treated by EMS, other than other than the differences intended by the study design?

Our study has several limitations. First, ambulance personnel could not be blinded to the randomization. Closely related to this, only patients who were randomized to the no intravenous group could be monitored with regard to protocol compliance. If intravenous drugs were administered to a patient in the no intravenous group, violation of the study protocol could be documented. If intravenous drugs were not administered to a patient in the intravenous group, several valid reasons could exist, such as rapid ROSC. We have no reason to believe that personnel refrained from establishing intravenous access under the pretense that the procedure was unsuccessful. The ambulance personnel involved were strongly committed to testing the hypothesis presented, but we cannot totally rule out possible bias toward procedures such as intravenous access and administration of drugs, which have been important in Norwegian culture for decades.[1]

This is a reason for creating a sham drug to use for the study. Without knowledge of the contents of the syringes being used, any bias of the treating medics should not affect the results. That is the purpose of blinding.

Analysis was performed on an intention-to-treat basis regardless of which treatment was actually given.[1]

In the No IV group, 10% received IV drugs. 9% of patients received epinephrine.

In the IV group, 82% received IV drugs. 79% of patients received epinephrine.

Why did some of the No IV patients receive epinephrine, or any drug? Clearly a protocol violation. I tripped and the IV landed in the patient, is not a valid explanation.

Why did 21% of the IV group not receive epinephrine? That is not clearly explained by the authors. Were these patients resuscitated prior to initiation of an IV and administration of epinephrine?

CPR and defibrillation are indicated before drugs. Since both CPR and defibrillation have research showing that they improve the long-term outcome from cardiac arrest, it is not unreasonable to expect that cases of ROSC with only CPR and defibrillation will be the reason for some patients not receiving epinephrine.

One of the perversions of a requirement that epinephrine be given in cardiac arrest is that the 1 mg bolus dose of epinephrine, repeated every 3 to 5 minutes, is never to be given to a patient with a pulse – Never. The reason is that epinephrine is so toxic to the heart, that it could be expected to produce cardiac arrest.

There are people criticizing this study because not all of the patients in the IV group received epinephrine. They see this as a bias. Contrariwise, I see their objection as just looking for any excuse to complain about research results they do not like, even though the study’s results are consistent with all of the other research that has been done. The critics fail to consider that some patients will be resuscitated prior to the point in the algorithms where drug administration is indicated. Their apparent demand that patients resuscitated prior to epinephrine administration be given epinephrine, even though the patient is no longer in cardiac arrest, is silly.

This would also not be likely to do anything to improve outcomes in the epinephrine group. The patients resuscitated prior to epinephrine administration are likely to be the patients with the briefest periods of cardiac arrest and therefore maybe the patients with the best potential for good outcomes. Returning them to a cardiac arrest, by means of epinephrine, just to follow an algorithm, would not be a good thing and it would probably have a dramatic negative effect on the survival of the patients in the epinephrine group.

The standard dose of epinephrine for a patient with a pulse, but not in cardiac arrest, is 2 mcg/minute to 10 mcg/minute. The standard dose of epinephrine for a patient without a pulse, but in cardiac arrest, is 1,000 mcg fast push every 3 to 5 minutes. I do not know of any medical professional, or any medical organization, or any medical reference, that recommends giving a living human being the dose of epinephrine that we only give to dead patients, and repeating it every 3 to 5 minutes. I would not be surprised at murder charges if the patient were to die soon after receiving this treatment that is given indiscriminately to dead patients.

Unless we can predict which patients, if any, will benefit from epinephrine, we need to find a better way to prevent giving epinephrine to the patients who will be harmed by epinephrine. If we cannot do that, we need to admit that we do not have any basis for using epinephrine in cardiac arrest.

Until there is research to show any benefit from epinephrine in cardiac arrest, we should eliminate epinephrine from all cardiac arrest treatment algorithms that are not part of well controlled studies.

Correction posted 3/07/2010 in Correction on Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.


^ 1 Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.
Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L.
JAMA. 2009 Nov 25;302(20):2222-9.
PMID: 19934423 [PubMed – in process]

If you want to read the entire study, this link opens it in PDF.

^ 2 A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest.
Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J.
JAMA. 1992 Nov 18;268(19):2667-72.
PMID: 1433686 [PubMed – indexed for MEDLINE]

Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, & Wik L (2009). Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial. JAMA : the journal of the American Medical Association, 302 (20), 2222-9 PMID: 19934423


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?


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!


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.