M2E Too! Mellick's Multimedia EduBlog
The M2E Too! Blog by Larry Mellick, MD, presents important clinical pearls using multimedia.

By its name, M2E Too! acknowledges that it is one of many emergency medicine blogs, but we hope this will serve as a creative commons for emergency physicians.

Tuesday, August 1, 2017

Double sequential defibrillation appears to work in the electrophysiology lab, and anecdotal evidence shows that lives can be saved in the prehospital setting and in the emergency department. With all the unanswered questions swirling around it, should we use this technique? Let’s consider the evidence.

Using two sets of defibrillators fired simultaneously or in a sequential pattern to treat refractory ventricular fibrillation is a relatively new concept. A number of different names for the procedure exist, but double sequential external defibrillation (DSED) or double simultaneous defibrillation (DSD) are commonly used. This technique was first described in 1994 by Hoch, et al., in five patients who were successfully converted from ventricular fibrillation in an electrophysiology laboratory. (J Am Coll Cardiol 1994;23[5]:1141.) The patients in this report failed to convert to normal sinus rhythm with monophasic energies ranging from 200-360 joules. All of them, however, responded to double shock with a total of 720 joules. The current experience with DSD in treating atrial fibrillation is probably more robust, but the evidence for refractory ventricular fibrillation is mostly case reports and case series. Nonetheless, DSD appears to convert fibrillating hearts and save lives.

Multiple questions still surround this off-label use of defibrillators for ventricular fibrillation. There is evidence of safety based on the use of DSD in atrial fibrillation patients, but the potential risk of myocardial injury from doubling the joules administered to the patient is not completely known. Two defibrillators fired simultaneously at maximal output will deliver 400 or 720 joules depending on whether one is using a biphasic or monophasic defibrillator.

It is also unclear whether quick sequential defibrillation or simultaneous defibrillation is more beneficial. It may be a moot point, though. Simultaneously firing two defibrillators probably doesn’t ever happen when done manually, and it is possible that a short millisecond separation may allow the second set of joules to occur at the moment of greatest drop in electrical resistance following the first attempt.

It is also unclear whether the overall increase in energy levels, the addition of a second vector of current flow, or the greater amount of heart muscle lying directly under the pads is responsible for the successes. It is clear that impedance in a patient relates to body mass and that human anatomy and chest sizes vary. It is also highly likely that the fibrillating ventricles may frequently not align perfectly with a single energy vector.

Another question needing clarification is which pad placement format is best: two sets placed side by side using the traditional anatomic locations for defibrillator pads or one set of pads placed at the traditional locations and the second set placed in an anterior-posterior location. At this time, no one knows for sure which option is more effective.

It is also unknown, or at least unclear, exactly when the dual simultaneous defibrillation should be initiated. Is DSD more effective when incorporated earlier in the attempted resuscitation of a VF arrest? It is known that the longer the patient is in ventricular fibrillation, the more resistant the heart is to being defibrillated. Obviously, the sooner we have a return of spontaneous circulation, the better the cognitive outcome for the patient. It would seem obvious that incorporating DSD sooner is better than later.

What do we know for sure? Additional vectors of current flow are added, and a higher total number of joules are delivered to the flailing heart. And almost definitely a greater cardiac topography is covered by the double sets of pads. We also know that the defibrillation process is probably never going to be exactly simultaneous because of the manual process required.

Equipment:
-Two defibrillators and two sets of pads.

Steps:
-Apply a second set of defibrillation pads in the same configuration as the existing pads but adjacent or in the anterior-posterior position. (Make sure the pads are not touching or applied on top of one another.)
-Charge both monitors to their maximum energy level (200 joules for biphasic, 360 joules for monophasic). Warn all providers not to be in contact with the patient at the time of discharge, and then charge and simultaneously push the defibrillation button on each monitor. Some recommend continuing cardiac compression until just before the defibrillation buttons are pushed. Immediately resume chest compressions. Administer appropriate ACLS medications and repeat as necessary.
-Have a video of double sequential defibrillation available.

So, should we use this technique? Let’s turn to The Aphorisms of Hippocrates: “For extreme diseases, extreme methods of cure, as to restriction, are most suitable.” (http://bit.ly/2sUkilA.) In other words, desperate times call for desperate measures, and double simultaneous defibrillation in the face of refractory ventricular fibrillation easily fits that bill.​

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Monday, July 3, 2017

The time for possible salvage and survival of a torsed testicle is commonly thought to be six to eight hours, a period that is expressed with confidence by the medical and legal professions. Survival of torsed testicles with and without subsequent atrophy is known to occur outside that critical window. My colleagues recently treated a 17-year-old boy approximately three days after the onset of right scrotal pain. He reported his pain constantly as 8/10 in severity. He didn't tell his mother for several days because he was scared, embarrassed, and hoping that the pain and swelling would resolve.

The patient was taken to the operating room approximately 70 hours after the onset of his testicular torsion. The cyanotic, 360-degree torsed left testicle pinked up and was deemed viable in the OR. The patient reported a week later that he was experiencing no pain and that his testicle seemed to be completely back to normal. Consider for a minute if the urologist had elected not to take the patient to the operating room that night. The outcome would have been much different, and an otherwise salvageable testicle would have died.

The potential for subsequent testicular atrophy is acknowledged, but no one knows for sure. Is there a clear-cut time when it is futile to rush to the operating room? If there is, it probably has to be based on other physical and ultrasonographic findings in addition to time.

It is true that torsed testes have been found to be necrotic after just six or fewer hours of pain, and scores of reports describe testicular survival following significantly longer periods. Many of these salvaged testicles have subsequently atrophied, but some also appear normal despite prolonged periods of torsion. Possible explanations for variations in testicular survival include fewer twists of the spermatic cord, the relative thickness of the torsed spermatic cord, or other anatomical aspects such as the attachment level of the tunica albuginea in the bell clapper deformity that allows persistence of critical blood flow.

The importance of understanding survival time in testicular torsion is critical; failure to recognize that testicular survival can occur even after many hours and potentially days of symptoms can lead to inappropriate delays in timely management. I am working on a systematic review of testicular survival rates and duration of torsion, and a preliminary but extensive search of the literature found 1,857 patients with surprising results. These numbers may change once our systematic review is finished, but time to surgery varied. Our tallied survival was 97.8 percent in patients whose treatment was zero to six hours since onset of symptoms, 83.1 percent for seven to 12 hours, 62.9 percent for 13-18 hours, 44.6 percent for 19-24 hours, 22.5 percent for 24-48 hours, and 7.7 percent for more than 48 hours. These survivals are almost identical to those reported by Visser, et al. (BJU Int 2003;92[3]:200.) Unfortunately, no references were included to support this graphically presented data. Our systematic review has more than 2,000 patients to date, and the survival data remains pretty much unchanged.

The question remains, however, why some torsed testicles appear to be necrotic even though the pain was less than six hours. Based on evidence that suggests this is more commonly seen in younger patients and because some patients have pain honeymoons, it is my opinion that the dead testicles had actually been torsed for much longer.​

I am confident the data are going to prove that we should not give up when suspected testicular torsion patients present many hours past the commonly taught six to eight hours. We will have done our patients and their torsed testicles a huge favor if we will aggressively and expediently manage their initial care in the emergency department.

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Watch a video of Dr. Mellick discussing torsion in a 14-year-old.​


Watch a video of Dr. Mellick discussing an unusual presentation of torsion in a 15-year-old.​​


Thursday, June 1, 2017

Are you one of those clinicians who frequently finds himself frustrated with asthma patients who improve to a point but not enough to discharge home? Even though this has to be a common problem, no one seems to talk or write much about it. I was feeling deeply frustrated about these patients, and it led me to serious clinical introspection. Why does everyone write about the crashing asthma patient, but hardly anyone addresses the problematic patient with improving but recalcitrant bronchospasm?

Most articles typically cover every available therapeutic option, including the proverbial “kitchen sink” for managing severe asthma emergencies. Kitchen-sink recommendations generally include continuous albuterol nebulization, intravenous magnesium sulfate, intramuscular epinephrine or terbutaline, noninvasive (NIV) positive pressure ventilation, helium-oxygen administration, and ultimately intubation and ventilation using ketamine. It is time, however, to give “out-the-door” asthma management a little respect and attention.

Typically, emergency department asthma protocols will include repeated albuterol treatments with at least two of those treatments combined with nebulized ipratropium bromide. Corticosteroids are also administered orally or intravenously. When these initial interventions fail, most practitioners continue to treat the bronchospasm with additional doses of albuterol and ultimately continuous nebulization of the β2 agonist.

This is where logic seems to fade. Continuing to hammer the patient with the same medication and the same receptors seems a little illogical. Wouldn’t it make more sense to switch to other medications that target different pulmonary smooth muscle receptors and the inflammatory factors associated with the bronchoconstriction? Nevertheless, most clinicians maintain a relatively limited number of therapeutic tools in their toolbox when it comes to routinely managing asthma. Consequently, many patients are ultimately admitted to the hospital for ongoing management when some of them could have been discharged home.

What other options do we have? Truthfully, a lot of new magic bullets don’t really exist for acutely managing asthma. What about looking again at some of the older, proven interventions that have been benched for the newer, shinier treatments? Maybe we should be treating the known common inflammatory factors associated with asthma more aggressively. The following treatment options seem to be working anecdotally, especially for my pediatric asthma patients. Beginning with the strongest evidence first, these tools for your asthma tool box may help you get a few more patients home.

Inhaled Corticosteroids
One of the best supported asthma management options is inhaled corticosteroids. The literature is consistently positive, and appears to support nebulized steroids in addition to other systemic corticosteroids. In our pediatric emergency department, we typically give one dose of oral dexamethasone (0.6 mg/kg) up to a maximum of 16 mg for asthma exacerbations that have been ongoing for one to two days and are resistant to home management. Other options are effective, but my choice for an inhaled or nebulized corticosteroid is 0.5 mg of budesonide. A review article and a Cochrane review of the benefits of inhaled corticosteroids provide supporting evidence for routinely adding this intervention for patients with recalcitrant bronchospasm. (Respir Med 2007;101[4]:685; Cochrane Database Syst Rev 2012;12:CD002308.)

Intramuscular or Nebulized Epinephrine
Epinephrine, of course, has always worked for bronchospasm. Older clinicians will remember when subcutaneous epinephrine administered every 20 minutes was one of the few treatment options available. Despite the tears caused by the painful injections, it worked. In fact, many older papers described injected and nebulized epinephrine as being therapeutically similar to agents such as terbutaline or albuterol. (Ann Allergy 1983;50[6]:398; Clin Pharm 1983;2[1]:45.) Besides having a few more side effects, epinephrine, a nonselective β2 agonist, also fell to the wayside because it was far easier and less objectionable to nebulize medications than give painful injections to children and adults. If they use it at all, most clinicians reserve epinephrine for the patient presenting with severe and status asthma.

Nebulized epinephrine, however, probably works just as well as intramuscular epinephrine, and possibly delivers a greater quantity of epinephrine with minimal side effects. Both regular epinephrine (5 mg maximum) and racemic epinephrine (11.25 mg maximum) can be nebulized to treat asthma and croup. It seems to be much easier to use the commercially supplied preparations of racemic epinephrine for nebulization current available. Again, there is good evidence for the effectiveness of nebulized racemic epinephrine to treat asthma. (CJEM 2007;9[4]:304; Acad Emerg Med 2000;7[10]:1097; Am J Emerg Med 2006;24[2]:217; J Crit Care 2004;19[2]:99; Allergy 1980;35[7]:605.) When the effectiveness of nebulized albuterol seems to have petered out and you sense a need for something else, consider a trial of nebulized racemic epinephrine.

Antihistamines
The triggers of an asthma exacerbation are commonly divided into allergic and nonallergic etiologies. In fact, it is possible that allergies trigger asthma attacks in 60 to 90 percent of children and 50 percent of adults. (Medscape. April 13, 2017; http://bit.ly/2oXKp4s.) Mite and cockroach antigens are known to increase asthma morbidity, and are commonly found in the environment. (J Allergy Clin Immunol 2015;136[1]:38.) Histamine is a known inflammatory mediator in the pathophysiology of asthma. IgE binds to high-affinity receptors on the surface of mast cells and basophils, leading to mast cell and basophil degranulation. Mast cell mediators, histamine, pro-inflammatory cytokines, and proteases are released, leading to an early allergic response.

Consequently, it seems intuitive that antihistamines could play a role in treating asthma. Unfortunately, evidence for the benefit of first-generation antihistamines in asthma is relatively limited. This may be secondary to the fact that antihistamines were avoided in asthma for many years. Clinicians were taught to avoid antihistamines out of concerns for possible drying and inspissation of airway secretions. Current research on second-generation antihistamines suggests benefit, however. (Am J Med 2002;113[Suppl 9A]:2S; Curr Opin Allergy Clin Immunol 2002;2[1]:53; Treat Respir Med 2006;5[3]:149; J Allergy Clin Immunol 2003;112[4 Suppl]:S96.) Clinical studies have shown mixed results, but no detrimental effects were noted. Despite weaker evidence, the addition of intravenous or oral antihistamines during an acute asthma event seems safe, reasonable, and disease mechanism-based. And it is possible that antihistamines could prove to be synergistic with other anti-inflammatory interventions.

Ibuprofen or NSAIDs
Another even more controversial option is the use of the anti-inflammatory drug, ibuprofen, in asthma. Ibuprofen is a nonselective inhibitor of the enzyme cyclooxygenase (COX), which is required for the synthesis of prostaglandins via the arachidonic acid pathway. This pathway is active in the pathogenesis of asthma. (Pharmacotherapy 1997;17[1 Pt 2]:3S.) (Figure 1.)

mellick-ibuprofen.png
Figure 1. Stylized cell depicting the mechanism of action of ibuprofen. (Pharmacogenet Genomics 2015;25[2]:96.)  Pharmacodynamics ©PharmGKB. Reprinted with permission from PharmGKB and Stanford University.

Ibuprofen is often immediately rejected as a therapeutic intervention for asthma because of concerns about exacerbating asthma in the context of aspirin sensitivity. Literature analysis seems to indicate that the use of ibuprofen in the pediatric population does not exacerbate asthma morbidity. (Paediatr Drugs 2004;6[5]:267; Clin Ther 2007;29[12]:2716.) As stated by one author: "Given the infrequent occurrence of aspirin/NSAID sensitivity in children with asthma, it seems reasonable to allow the use of ibuprofen in this population unless there is a personal or family history of aspirin-induced asthma. In addition, the inflammatory pathogenesis of asthma, anti-inflammatory effect of ibuprofen, and evidence suggesting ibuprofen may reduce morbidity in children with asthma raises the intriguing possibility that ibuprofen might actually have therapeutic benefit for at least some children with asthma." (Paediatr Drugs 2004;6[5]:267.)

A paper by Lesko, et al., stated that rather than supporting the hypothesis that ibuprofen increases asthma morbidity among children who are not known to be sensitive to aspirin, their study suggested that compared with acetaminophen, ibuprofen may reduce such risks. (Pediatrics 2002;109[2]:E20.) Finally, another study recommended that ibuprofen be withheld for at least 24 hours prior to investigations utilizing allergen bronchoprovocation because a single dose of ibuprofen was found to inhibit early and late asthmatic responses to allergen bronchoprovocation. (Allergy Asthma Clin Immunol 2016;12:24.) The evidence is limited, but ibuprofen should theoretically decrease the inflammatory factors causing bronchospasm in asthma through its actions on the arachidonic acid pathway.​

If you find yourself regularly frustrated with asthma patients who only partially improve, consider putting back into the game some or all of these older, previously benched bronchodilators and anti-inflammatory treatment modalities.




Wednesday, May 3, 2017

The differential list of potential causes of abdominal pain is pretty long. Like most differentials, though, it usually boils down to a handful of more common etiologies benign and serious. Potentially life- or organ-threatening conditions such as appendicitis, diverticulitis, or ovarian or testicular torsion simply cannot be misdiagnosed and usually aren't missed.

We frequently find ourselves walking into the patient's room at the end of an extensive and exhaustive workup and announcing the good news that the cause of the pain isn't one of these more serious causes. As emergency physicians working in an uncontrolled and tactical environment, we get used to reassuring patients that it isn't something serious even though we are unable to provide a definitive diagnosis.

If we admit it, deep down we share a little bit of the frustration expressed by our internist colleagues who by self-report experience a degree of psychic pain when stuck with a differential list instead of a definitive diagnosis for a patient's complaint. We may also find ourselves quietly avoiding our frustration with having exposed the patient to the CT scan's radiation or the expense of sequential tests such as a screening ultrasound only to find "enlarged lymph nodes," "a small amount of free fluid," or a few normal appearing ovarian cysts.

Epiploic appendagitis is one diagnosis, albeit rare, that allows the emergency physician to give the patient pretty much all-around good news. Making the diagnosis of this condition caused by a twisting or necrosis of the fat appendages hanging off the colon allows us to give the patient a definitive diagnosis and the good news that they have a condition that will not require admission or surgical intervention. In fact, the treatment for this condition is ibuprofen, rest, and time. Epiploic appendagitis can be responsible for an "acute abdomen" presentation, but the associated condition is self-limited and requires only pain and inflammation management. In fact, ibuprofen is frequently sufficient. The condition is rare enough that the few times that we've made the diagnosis before confirmation by CT scan were considered "high-five" moments. Most recently, the diagnosis was made in a 17-year-old boy sent to the emergency department because of suspicion for appendicitis. (See video​.)

What's the skinny on this condition that frequently causes your colleagues and the patient to correct your suspected mispronunciation of "appendicitis"?

-Epiploic appendagitis (EA) is frequently a condition unknown to clinicians. (AJR Am J Roentgenol 2009;193[5]:1243.)
-The term "epiploic appendagitis" is attributed to Lynn, et al., in 1956 who described a primary inflammatory disease of the fatty colonic appendages. (Surg Gynecol Obstet 1956;103[4]:423.)
-EA has other aliases such as appendicitis epiploica, hemorrhagic epiploitis, epiplopericolitis, or appendagitis. (Surg Gynecol Obstet 1956;103[4]:423.)
-EA is the result of ischemic infarction of an epiploic appendage following torsion or spontaneous thrombosis of the central draining vein.
-The epiploic appendages are finger-like projections of adipose tissue typically arranged in parallel rows along the colon. (Arch Surg 1985;120[10]:1167.)
-Numbering between 50 to 100, these appendages cover the entire adult colon but are larger and most abundant on the transverse and sigmoid colon.
-Epidemiologic studies suggest that the true incidence of EA is not known, but it has been reported in two percent to seven percent of patients initially suspected of having acute diverticulitis. (Nat Rev Gastroenterol Hepatol 2011;8[1]:45.)
-This condition usually occurs more commonly in men in the fourth and fifth decades of life, but also occurs in women and children.
-Sudden focal, nonmigrating lower abdominal pain and tenderness with a dull and colicky pain that waxes and wanes may be described by the patient. (Dig Dis Sci 2004;49[2]:347.)
-Ultrasound of EA has characteristic findings and MRI appears to be a reliable tool, but CT is the current imaging study of choice.
-Classically the findings of epiploic appendagitis on CT is a fat-density oval lesion called a “ring sign” consisting of a central fatty core (between 1.4 cm and 3.5 cm in length) surrounded by inflammation and located on the anterior aspect of the sigmoid colon. (Radiol 2005;237[1]:301; AJR Am J Roentgenol 2004;183[5]:1303.) A central dot corresponding to a thrombosed appendage vein is sometimes evident. (Radiology 1997;204[3]:713.)

When your colleagues try to correct your "mispronunciation" of appendicitis, your response should be, "Heck no, I meant to say appendagitis. Go look it up!"

Watch a video interview with a young patient with epiploic appendagitis.

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Friday, March 31, 2017

Hanging out with cardiopulmonary researchers effectively imprinted on my psyche that we fail our patients during cardiopulmonary resuscitation in many ways. Unfortunately, too many patients who could have walked out of the hospital after experiencing death don't because of our mistakes in CPR. It's critical to find the resuscitation sweet spot for each patient and to never waver during a CPR event. These are the ways we can kill our patients during cardiopulmonary resuscitation:

Too Slow or Too Fast

The recommended heart rate for cardiopulmonary resuscitation was 60 compressions/minute in 1960. (JAMA 1960;173:1064.) Observational human studies relating compression rate to outcomes, however, have established a sweet spot somewhere between 100 and 120 compressions per minute. (Crit Care Med 2015;43[4]:840.) External chest compressions are the primary intervention performed in cardiopulmonary resuscitation, and not doing them correctly has the greatest impact on the outcome. Without any doubt, compressing too slow or too fast is deadly during CPR.

Too Shallow or Too Deep

Part of the problem with compressing too fast is that the depth of compressions suffers dramatically, and the compressions become too shallow. (Crit Care Med 2015;43[4]:840.) Too deep compressions simply don't appear to add any benefit to resuscitation end-points and may cause unwanted trauma such as broken ribs and increased intracranial pressure (ICP), resulting in reduced cerebral blood flow. Compressions that are too shallow are simply not effective in moving blood into and out of the heart. The AHA recommended compression depth is 2.0 to 2.4 inches or 5 to 6 centimeters. (http://bit.ly/2mZwT3U.) The evidence is strong that the depth of chest compressions makes a difference in survival outcomes. (Circulation 2014;130[22]:1962.)

Too Many or Too Slow

It is almost counterintuitive to think that breathing more frequently for a patient during CPR has the potential to guarantee the patient a trip to the morgue. Ventilating too rapidly or prolonging slower respirations has a dramatic impact on physiology that has been repeated and easily demonstrated in resuscitation laboratories. Positive pressure ventilation in the laboratory increases intrathoracic pressure and intracranial pressure and decreases venous blood return to the right heart.

A decrease in cerebral and coronary artery perfusion pressure occurs during the ventilation process. We need to look at ventilations during cardiopulmonary resuscitation as a necessary evil that they temporarily negate the benefits of our chest compressions while providing oxygen and keeping the airways open for gas exchange. Animal studies unequivocally demonstrate that high ventilation rates can be uniformly lethal in the ventricular fibrillation cardiac arrest model. (Crit Care Med 2004;32[9 Suppl]:S345; Circulation 2004;109[16]:1960.)

Leaning on the Chest

Not allowing full recoil can also be detrimental to effective CPR. It is a subtle and easy not to recognize the error of continuing to put downward pressure and prevent full recoil of the chest. This happens when the rescuer continues to lean on the chest between compressions. Incomplete chest wall recoil or leaning increases ICP and lowers right atrial pressure, decreasing cerebral and coronary perfusion pressures.

Too Many Interruptions

Too many and too long interruptions can negate the benefits of performing spot-on chest compressions. These interruptions ultimately result in the same outcomes as compressing the chest too slowly. No compressions mean no heartbeat.

Giving Up Too Soon

Just how long should we perform cardiopulmonary resuscitation? This partially depends on the patient and his condition. Longer CPR attempts are appropriate from a prehospital perspective, and excellent neurologic recovery is possible for those with the best conditions of shockable rhythms and bystander resuscitation. (Circulation 2016;134[25]:2084.) Hospitalized patients also appeared to benefit from longer CPR, which was associated with greater return of spontaneous circulation and survival to discharge even for the patients in asystole. Efforts to systematically increase the duration of resuscitation could improve survival in this high-risk population. (Lancet 2012;380[9852]:1473.)

In reality, the brain is probably a little more resilient than we think. Resuscitation researchers describe porcine research subjects that go about their activities of daily living after prolonged periods of ventricular fibrillation and delayed resuscitation. They also have scores of stories of human patients down for prolonged periods who received effective resuscitation and eventually recovered after prolonged periods of unconsciousness in the intensive care unit. (Resuscitation 2014;85[2]:211.) Reperfusion injury to the brain, however, does happen, and research on how to prevent such injuries is ongoing.

Too Slow Adaptation

It's true that adapting new technologies too soon or before they are adequately vetted with good research is potentially dangerous, but it is also true that good research based on bad CPR can slow the acceptance of potentially useful new resuscitation tools. (Resuscitation 2015;94:106; http://bit.ly/2mZSglK; N Engl J Med 2015;373[23]:2203.) Several decades of work has yielded irrefutable evidence that good things happen to the cerebral perfusion pressure and the coronary perfusion pressure with the impedance threshold device and active compression decompression CPR. (West J Emerg Med 2014;15[7]:803.) And elevating the head simultaneously with the application of an impedance threshold device also clearly improves those physiologic parameters that are associated with better outcomes. (Resuscitation 2016;102:29.) Evidence, finally, is accumulating to validate the decades of work of these resuscitation researchers. (Resuscitation 2017;110:95; Circ J 2016;80[10]:2124.)

Unfortunately, the confounding variables and uncontrolled environment of prehospital cardiac arrest research has slowed the validation and acceptance of important new techniques and technologies as well as something seemingly obvious such as continuous chest compressions during CPR. (Resuscitation 2015;94:106; http://bit.ly/2mZSglK; N Engl J Med 2015;373[23]:2203.)

A commentary by Goodloe, et al., addresses possible options to address the unique challenges of resuscitation research: "This is not to say that high-quality research attempts should not continue, but rather that treatments that appear beneficial to a consensus of resuscitation leaders should not be withheld until benefit is fully demonstrated in primary and confirmatory randomized controlled trials. The unwillingness to adopt new ideas and therapies until they are proven beyond any doubt via randomized clinical trials also holds back progress. Overwhelming evidence is often years in coming, and while we wait, patients die. The context in which resuscitation scientists work is dynamic, complex, and even sometimes chaotic, yet we have made great strides in discovering new processes and technologies that have resulted in better outcomes." (West J Emerg Med 2014;15[7]:803.)

CPR Physiology

Part of the problem with failure to perform the best CPR possible is that the vast majority of emergency health care providers probably operates with an incomplete understanding of the pathophysiology of cardiac arrest and the physiology of resuscitation. We are much more vulnerable to these mistakes without this complete understanding.

Watch a video showing how conventional CPR works — and doesn’t.​


Watch a video with tips for code team organization during​ CPR.