Provocative Protocols

Metropolitan New York is famous for many thingsÆ’skyscrapers, burdensome taxes, beaches and high-priced baseball players, to name a few. Having just relocated to the South, I’m reminded (daily) of Northeastern idiosyncrasies that I took for granted.

Consider the ubiquitous diner. A garish, inexpensive, high-volume restaurant where you can order a cup of coffee, a seven-course meal or anything in between, the diner is as much a New York institution as overpriced real estate. The typical diner menu resembles an embossed road atlas, listing more than a hundred concoctions bearing lineage from a half-dozen culinary styles. A novice visitor might conclude this is the perfect place to sample cuisine from continents near and far.

That would be a mistake.

The first rule of diner patronage: Don’t order anything that the waiter has trouble pronouncing. (The second rule is to rely on the ample bread basket for sustenance, if you ignore the first rule.) If you insist on trying the Coq Au Vin, it’s likely that both you and the cook will experience something rare.

What does this have to do with prehospital care? As EMS novices, we spend months memorizing and reciting elaborate Ë™menusà“ of prehospital interventions known as protocols. An unintended consequence of contrived, algorithm-driven training scenarios is that many students aim for protocol proficiency, rather than mastery of the underlying medicine. Ë™Cookbookà“ technicians come of age when they discover that protocols are guidelines rather than recipes, subordinate to the art of diagnosis.

Like diner menus, protocols strain to offer something for everyone. Are more options better? How far should we push the edge of the prehospital envelope?

A Tale of Four Protocols
For this article, I reviewed the adult ALS protocols of four EMS systems, each serving populations greater than 1 million. I focused on the standing orders for seven presenting problems: paroxysmal supraventricular tachycardia (PSVT), acute pulmonary edema (APE), asthma, overdose, hypoglycemia, hypovolemia and pulseless electrical activity (PEA). Not only does the standard of care differ from North to South to East to West, but some interventions even contradict current research.

My comments are headed by abbreviated comparisons of the most distinctive standing orders for each prehospital condition. I’ve arbitrarily assigned the letters A, B, C and D to the four EMS systems reviewed. I conclude each section with questions that I’m not smart enough to answer. Perhaps you can help. After reading these, you can go to weigh in.

Paroxysmal Supraventricular Tachycardia (PSVT)
A: Adenosine 6 mg, 12 mg if Ë™stable.à“

B: Adenosine 6 mg, 12 mg, 12 mg if Ë™stable.à“

C: Valsalva, adenosine 6 mg, Valsalva, 12 mg, Valsalva, 12 mg if Ë™asymptomatic.à“

D: Valsalva, adenosine 6 mg if ˙perfusing.

A sudden, brisk arrhythmia generated by a re-entry circuit near the AV node, PSVT can cause decreased perfusion due to rapid ventricular response. However, PSVT frequently presents without any serious signs or symptoms, and is well-tolerated for short periods by many patients who don’t have underlying heart disease.

Although ACLS recommends vagal stimulation followed by adenosine to treat Ë™stableà“ SVT, neither intervention is harmless. Valsalva maneuvers have been known to cause cardiac arrest, and are rarely successful prehospitally. Adenosine may paradoxically increase the heart rate of patients with underlying Wolf-Parkinson-White (WPW) syndrome. A key question is, how likely are ALS providers to distinguish rapid atrial fibrillation (RAF) from PSVT? When treated with adenosine, RAF accompanied by WPW can lead to even faster ventricular rates and hypoperfusion.

A 10-year study that began in 1993 tracked inappropriate adenosine use resulting from inaccurate ECG interpretation by paramedics. The annual proportion of patients treated incorrectly varied from 9% to 31%, with an average of 20%. Eight other studies performed during the same decade revealed 5à41% probabilities of misidentifying rhythms.

All four of our sample EMS systems dictate administration of adenosine to patients who are Ë™stable,à“Ë™asymptomaticà“ or Ë™perfusing.à“ Those are the kinds of patients I was taught to just monitor and transport.

Despite ACLS guidelines, are we taking unnecessary risks by over-treating relatively benign arrhythmias prehospitally? Given our questionable ability to correctly interpret and treat tachyarrhythmias in the field, and the consequences of failure, would it be wiser to delay definitive care until the patient becomes symptomatic or we arrive at the hospital?

Acute Pulmonary Edema (APE)
A: Nitroglycerine (NTG), furosemide 40 mg if SBP 120.

B: NTG _ 3, furosemide 20à80 mg.

C: NTG _ 3, albuterol _ 3, furosemide 40à80 mg, if SBP > 90 and HR 50à130.

D: NTG _ 3 if SBP”ž 100, albuterol if wheezing.

When I was learning to be a paramedic in the early à‚90s, the standard of care for pulmonary edema secondary to congestive heart failure (CHF) was IV Lasix (furosemide), NTG and morphine, in that order. (Yes, I missed the glorification and subsequent discrediting of rotating tourniquets.) There were short transports where we never got past Lasix, but we were taught that the diuresis and venodilation offered by Lasix was the best treatment for sick CHFers.

Even in the late à‚90s, as research started to show that NTG was the most effective agent for prehospital preload reduction, my colleagues and I were occasionally criticized by ED nurses for administering nitro to CHF patients without chest pain. By 2003, the medical community conceded that neither furosemide nor morphine, in any combination, were as beneficial as nitrates in the setting of pulmonary edema. In fact, both agents could be harmful: Lasix, by paradoxically elevating vascular resistance through activation of the renin-angiotensin mechanism, and morphine because of its tendency to suppress respiratory drive. Subsequent studies de-emphasized Lasix as a vasodilator and illustrated the consequences of administering diuretics to respiratory patients whose etiology is something other than CHF.

Why, then, is furosemide a standing order for pulmonary edema in three of the four sample EMS systems? To what extent are protocols still driven by anecdotal, rather than evidence-based medicine?

A: Albuterol, ipratropium, albuterol.

B:”ž Albuterol _ 3 or metaproterenol _ 3.

C: Albuterol prn if HR > 180, epinephrine SQ and methylprednisolone if severe RD.

D: Albuterol prn, epinephrine SQ if severe RD and age > 40.

After albuterol, a fast-acting beta-2 agonist, there’s a lot of variation in the standing orders for exacerbated asthma. Let’s consider each of the above choices.

Ipratropium (Atrovent): Some asthmatics benefit from combining this anticholinergic agent with a bronchodilator. However, a 1998 study showed little or no advantage to adding Atrovent for mild-to-moderate asthma attacks. Further research in 2000 concluded that there was no statistical difference in clinical outcome between patients who were given Atrovent with albuterol, versus albuterol alone. One-third of the subjects in the latter study subsequently were diagnosed with CHF instead of reactive airway disease. The positive chronotropic effect of an anticholinergic medication could worsen the outcome for that subset of patients.

Metaproterenol (Alupent): Before inhaled albuterol became available, Alupent was the prehospital bronchodilator of choice. Alupent is less beta-2 specific, however. Any beta-1-mediated increase in myocardial oxygen demand could compromise patients with cardiac histories.

Epinephrine: ACLS lists subcutaneous epinephrine as a Class IIb recommendation (possibly effective) for life-threatening asthma, and encourages its use for patients who are too constricted to inhale a bronchodilator. A 1988 study downplays concern about administering epinephrine to patients over 40, provided they have no cardiac history.

Methylprednisolone (Solu-Medrol): Steroids address airway inflammation, a critical component of asthma exacerbation. However, a 1992 study didn’t show any benefit to IV methylprednisolone for patients who responded to bronchodilator treatment during the first three hours of an asthma attack or for subjects who weren’t already taking oral steroids. Given that steroids’ onset of action is at least three to four hours, it’s questionable whether Solu-Medrol has any prehospital value for asthmatics. Also, steroids can cause hypertension and fluid retentionÆ’unwelcome side effects for CHF patients.

Should our prehospital formulary include Alupent and Solu-Medrol? On what basis would the answer to that question differ by geographical region?

A: Narcan up to 2 mg Ë™if narcotic OD is suspected.à“

B: Narcan up to 2 mg if no change in mental status after D50.

C: Narcan 2 mg Ë™if narcotic use is suspected or if pupils are pinpointà“ with AMS.

D: Narcan 0.8à2 mg Ë™if hypoventilation or suspicion of narcotic overdose.

What a relief to have the daily, mind-numbing challenges of paramedic school interrupted by a Ë™no-brainerà“ scenario like an opiate overdose. As students, we were grateful for reinforcement from instructors when we verbalized our knee-jerk reaction to push naloxone (Narcan). Only when we started treating real patients did we discover that the cure was sometimes worse than the disease.

Narcan reverses opioid intoxication and is a life-saving measure for patients with profound respiratory depression. However, sudden withdrawal from narcotics, or unopposed effects of other substances accompanying an opiate overdose can create danger for both the caregiver and the patient. Experienced health-care providers learn to titrate Narcan judiciously, and to withhold it entirely in the absence of hypoventilation and hemodynamic instability.

Several examples in the literature report anticholinergic syndromes precipitated by administration of Narcan to patients who have also taken scopolamine, atropine or belladonna. More common substances mixed with narcoticsÆ’such as antidepressants, antihistamines and over-the-counter sleep medicationsÆ’can produce the same toxidrome, characterized by agitation, combativeness and even psychosis. The nausea and vomiting associated with opiate withdrawal alone can lead to airway compromise and is, at best, messy.

Why, then, does only one of the sample EMS systems (D) specify hypoventilation as a condition of Narcan administration? System B favors a generic approach, recommending the use of Narcan if the patient presents with AMS and does not respond to dextrose. Are we oversimplifying the indications for potentially dangerous opiate reversal?

D50 (50% dextrose in water) or glucagon if BSL < 80.

B: D50 or glucagon. If glucometer used, BSL < 120.

C: D50 if BSL < 60.

D: D50 or glucagon if BSL < 80 per chemstrip or BSL < 60 per glucometer.

As a young EMT, I was taught to administer oral glucose to patients with patent airways and altered mental status of unknown etiology. OK, so maybe I didn’t know what Ë™etiologyà“ meant then, but the prevailing wisdom was that treating hyperglycemia with sugar wasn’t as bad as not treating hypoglycemia.

One could argue that’s still true. Meanwhile, we’ve learned that patients suffering from stroke or head trauma can be adversely affected by hyperglycemia. Fortunately, glucometry has made its way to the field. Treating life-threatening hypoglycemia is still a prehospital priority, and now we have the technology to rule it in or out.

Or do we?

Depending on which of the sample EMS systems you work for, you have access to a glucometer, chemstrips or nothing at all to measure blood glucose. (The ancient practice of tasting urine is still frowned upon.) If you do have a glucometer, your definition of low blood sugar starts somewhere between 59 and 119 mg/dLÆ’well into the normal range.

It’s easy to adopt a cavalier attitude about administering glucose in the field. Ë™Curingà“ a hypoglycemic patient with an amp of D50 is one of the more satisfying moments in a medic’s typical workday. However, sugar is not a benign substance when administered intravenously. Extravasation can lead to tissue necrosis serious enough to warrant amputation.

The National Diabetes Information Clearinghouse recommends that both diabetics and non-diabetics treat themselves for hypoglycemia when their blood glucose falls below 70 mg/dL. Because signs and symptoms of hypoglycemia rarely present at that level, it seems reasonable to allow a further 10-point drop (i.e., 60 mg/dL) before intervening emergently in a prehospital setting.

Given the 60-point disparity in the definition of hypoglycemia among the sampled systems, is it realistic to expect a consensus at the lower end of that scale? Is there any reason not to include glucometry in the standard of care?

Titrate normal saline (NS) to SBP = 90, max of 3 L.

B: NS or LR, max of 3 L.

C: NS or LR 20 cc/kg.

D:”ž NS 10 cc/kg, then wide open.

You arrive at a grisly trauma scene and find an exsanguinating patient. WWJARD? (What Would Johnny and Roy Do?) That’s easy: punch a hole with a big needle in the A/C, thread a straw-sized catheter, and empty a liter or two of isotonic fluid into the patient en route to Rampart.

I don’t recall the medics ever asking for PolyHeme back then. In fact, we were more likely to hear about blood substitutes on”žStar Trek than”žEmergency! Are the above standing orders as outdated as Nurse Dixie McCall’s white cap?

A three-year study of blunt trauma victims, commencing in 1999, concluded that aggressive, prehospital fluid administration raised systolic blood pressure, but did not improve the odds of survival to discharge. Earlier research had shown that isotonic fluids administered to penetrating trauma patients actually increases mortality, presumably due to acceleration of hemorrhage and dilution of clotting factors. The key concept? Control the bleeding before pushing the fluids.

Despite early optimism, hemoglobin-based blood substitutes (HBBSs), such as PolyHeme, may not be a safe alternative. A 2008 study concluded that HBBSs carry a higher risk of mortality than conventional treatment. More research is needed. Meanwhile, shouldn’t we discourage the notion that aggressive fluid resuscitation is the default prehospital treatment for major trauma? Should standing orders for fluid be based on volume, the patient’s weight, the blood pressure, or none of the above?

Pulseless Electrical Activity (PEA)
A: Needle decompression, fluid, epinephrine, atropine if HR < 60.

B: Needle decompression, epinephrine or vasopressin, atropine if HR < 60.

C: Epinephrine, atropine, transcutaneous pacing (TCP). Further treatment depends on presumed cause.

D: Epinephrine, atropine if Ë™bradycardia,à“ fluid, sodium bicarbonate.

Learning to choreograph a cardiac arrest is one of the earliest challenges faced by ALS providers. It begins with memorization of ACLS algorithms, followed by management of the dreaded Ë™megacodeà“ and, ultimately, application of these rote procedures to actual patients, while dealing with the obstacles, urgency and chaos that accompanies real arrests.

All of the sample PEA protocols include the first two ACLS medications that follow BLS care: epinephrine and atropine. If you read the AHA’s Ë™fine print,à“ though, you’ll discover that neither drug has been shown to increase patients’ chances of survival to discharge after any kind of cardiac arrest.

Does this mean that resuscitation of patients in PEA is hopeless, unless we can identify a specific, treatable cause? Not according to a 2003 study, which showed that the probability of prehospital return of spontaneous circulation (ROSC) was more than twice as likely in the setting of PEA as in V-fib or V-tach. A supporting Helsinki study concluded that PEA is the most survivable, unwitnessed cardiac arrest rhythm prehospitally.

Let’s try a new way of thinking about PEA: Consider the word Ë™pulseless.à“ When we can’t feel a pulse, it doesn’t necessarily mean the patient has no perfusion. Research has shown that hearts can maintain enough electrical activity to contract weakly, without palpable pulses.

We should consider the possibility that a patient in slow PEA actually is suffering from profoundly symptomatic bradycardia. By addressing PEA as rate-related, rather than as a pump problem, we would try to improve cardiac output by increasing the rate with TCP or atropine, rather than by inducing vasoconstriction with epinephrine.

The sample standing orders for PEA include three cause-specific treatments (needle decompression, fluid and sodium bicarb) and three medications that have been shown not to work (epinephrine, vasopressin and atropine). Shouldn’t TCP be added? Is it worth including such standing orders as chest decompression and bicarb, given that the indications for those interventions are rarely detectable in the field?

Less is More
One could argue that there shouldn’t be so many differences in the standard of care from system to system. Physiology is the same, coast to coast. However, EMS protocols represent only one of many state-specific regulations with regional variations based more on local customs and practices than on logic. We deal with those quirks whenever we have to register our cars or pay taxes after an interstate move.

A bigger issue, and one that’s more specific to EMS, is whether we’re trying to do too much in the field. No invasive procedure or medication is without risk. Do some of those risks outweigh the benefits? How can we ensure quality when we stuff our Ë™menusà“ of standing orders with something for everyone, instead of focusing on what we do best? Should we be more conscientious about sticking to evidence-based medicine?

One of the best pieces of advice I got as a new medic is to go back to the ABCs when you’re not sure what to do. The ABCs are what we know best. The ABCs are what we”ždo best.

Sometimes less is more.

Sanders M. In”žMosby’s Paramedic Textbook, eds”žSt. Louis:”žMosby; 2001. p. 804-805.”ž
2.American Heart Association:”žACLS: 2005 Guidelines. 2005.
3. Davidson T. Ë™Valsalva maneuver.à“”ž
4. Slovis C, Kudenchuk P, Wayne M. Ë™Prehospital management of acute tachyarrhythmias.à“ Prehospital Emergency Care 2003;7:2-12.
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11. American Heart Association.”žACLS for Experienced Providers 2003;.”ž
12. Morell F, Orriols R, de Gracia J. Ë™Controlled trial of intravenous corticosteroids in severe acute asthma.à“ Thorax 1992;47:582-583.
13. Bledsoe B, Clayden D, Papa F.”žPrehospital Emergency Pharmacology 2001;.”ž
14. Wang H. Ë™Street drug toxicity resulting from opiates combined with anticholinergics.à“.”žPrehospital Emergency Care 2002;6:351-354.
15. Hicks S, Wolfson A, Asplin B. Ë™Anticholinergic syndrome precipitated by opioid reversal.à“.”žPrehospital Emergency Care 1998;2:328-329.
16. Wood S. Ë™Is D50 too much of a good thing?à“.”žJEMS 2007;32:103-110.
17.National Diabetes Information Clearinghouse.
18. Dula D, Wood G, Rejmer A. Ë™Use of prehospital fluids in blunt trauma patients.à“.”žPrehospital Emergency Care 2002;6:417-420.
19. Pepe P, Mosesso V, Falk J. Ë™Prehospital fluid resuscitation of the patient with major trauma.à“ Prehospital Emergency Care 2002;6:81-86.
20. Webb M. Ë™David Hoyt, MD, predicts a new world of fluid resuscitation.à“ NAEMT News July/August:12à13, 2004;.”ž
21. Natanson C, Kern S, Lurie P. Ë™Cell-free hemoglobin-based blood substitutes and risk of myocardial infarction and death: A meta-analysis.à“.”žJAMA 2008;299:2324-2326.
22. Rubin M. Ë™By the numbers: Prehospital cardiac arrest research.à“ JEMS 2004;29:68-77.
23. Hostler D, Roth R. Ë™Pulseless electrical activity: sign of life, or terminal rhythm?à“.”žPrehospital Emergency Care 2003;7:286-290.
24. Rodenberg H. Ë™The brady-PEA puzzle.à“.”žJEMS 2004;29:38.”ž

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