Hands-Only CPR

Now@NEJM just posted an article detailing the results of two new studies on Hands-Only or Compressions-Only CPR or Cardiocerebral Resuscitation (CCR). These studies[1,2] look very promising, in fact they showed no appreciable difference in overall survival-to-discharge for traditional CPR versus CCR. Moreover, when one of the studies, by Rea et al[1], compared using CCR to CPR survival-to-discharge of cardiac arrest victims of a primary cardiac etiology there was an increase from 12.3% to 15.5%, although it was not statistically significant. However, when comparing CCR to CPR to non-cardiac etiologies, there was a higher percentage of survivability in the CPR group (7.2% vs. 5.0%), although this as well was not statistically significant.

So what does this mean?

The researchers in Rea et al[1] note that while there was no statistically significant difference between the two, there was a clinically significant trend towards higher survival-to-discharge numbers using compressions alone. Additionally, 80.5% (n=981) of callers given compressions-only instructions began compressions versus 72.7% (n=960) given traditional CPR instructions. Overall 76.7% (n=1941) of callers began either CCR or CPR, which means 1 in 4 callers declined to perform some form of resuscitation.

Taking a closer look at the efficacy of the caller instructions, there is a nearly 8% increase in initiation of compressions under compressions-only instructions. Applying that increase to the CPR-instructions group would have meant nearly 75 more patients would have received compressions! Potentially another 9 people could have gone home from the hospital. Rea et al went as far as saying this was a clinically significant difference, but we all know how big of a difference it makes having just one more person walk home.

So what should we do?

I think progressive systems with tight integration between first responders, EMS, and dispatch need to get the Hands-Only word out to the public. Start using Hands-Only dispatch instructions along with an aggressive public information campaign. I feel in just a 60-90 second TV advertisement, Hands-Only CPR could be demonstrated to the public effectively. You could even throw in your favorite prime time TV cast to really capture those eyeballs.

I've not been in EMS very long, but my heart sinks every time I walk into a house and there has been no attempt at CPR. Our response times are often in the 8-9 minute range which means most of our attempts are futile. I understand the psychological barriers are high, but we need something to improve the rates of bystander CPR. If these studies have shown one thing, it is that Hands-Only CPR has a good chance of doing just that.

References
1. Rea TD, et al. CPR with Chest Compression Alone or With Rescue Breathing. N Engl J Med 2010; 363: 423-433. [at nejm.org]
Conclusions: Dispatcher instruction consisting of chest compression alone did not increase the survival rate overall, although there was a trend toward better outcomes in key clinical subgroups. The results support a strategy for CPR performed by laypersons that emphasizes chest compression and minimizes the role of rescue breathing.


2. Svensson L, et al. Compression-Only CPR or Standard CPR in Out-of-Hospital Cardiac Arrest. N Engl J Med 2010; 363: 434-442. [at nejm.org]
Conclusions: This prospective, randomized study showed no significant difference with respect to survival at 30 days between instructions given by an emergency medical dispatcher, before the arrival of EMS personnel, for compression-only CPR and instructions for standard CPR in patients with suspected, witnessed, out-of-hospital cardiac arrest.

Morphine Equivalents Visualized

My day job involves the creation of visualization software to help engineers evaluate complex systems. In my last post detailing Morphine Equivalents there was math, and numbers, and eyes glazing. So, as an aide to the previous post I submit to you a graph of the three narcotic dosing schedules. I pulled the half-lives from Wikipedia and assumed a bioavailability of 100% for the IV route.

The half-lives used are:

• Morphine: 2-3 hours
• Fentanyl: 2-4 hours
• Dilaudid: 2-3 hours

Morphine Equivalents

A pretty hot topic lately has been prehospital pain control and how for the most part it is viewed as a failure. Granted, the perception of how well prehospital providers handle pain control is not what I'm looking to talk about, Rogue Medic and the bloggers at Paramedicine 101 have touched on this topic quite a number of times.

What I'd like to do is add a little math to the discussion. Over at Street Watch: Notes of a Paramedic there is an excellent post about a new study on Fentanyl versus Morphine combined with a more liberal pain control protocol. The protocol mentioned "Morphine Equivalents," something of which I was only tangentially aware.

"Morphine Equivalents" are basically a unit of measure used to compare the efficacy of opiods. After a trivial amount of Googling I came across an easy to follow guide from the University of Alberta's Multidisciplinary Pain Centre which listed conversion factors between various opiods. Using these conversion factors, we could compare how equivalent various pain control protocols are.

In North Carolina our 2009 EMS protocols allow 3 opiods for the treatment of pain: dilaudid, morphine, and fentanyl. Per the conversion guide, these drugs compare as follows:

• 1 mg of Fentanyl is equivalent to 100 mg of Morphine
• 1 mg of Dilaudid is equivalent to 5 mg of Morphine

So let's examine the 2009 NC Protocols for Pain Control:

• Morphine: 4 mg IM/IV/IO bolus, may repeat with 2 mg every 3-5 minutes to a max 10 mg or clinical improvement
• Fentanyl: 50-75 mcg IM/IV/IO bolus, may repeat with 25 mcg every 20-30 minutes to a max 200 mcg or clinical improvement
• Dilaudid: 1-2 mg IM/IV/IO bolus, may repeat with 1 mg every 20-30 minutes to a max 5 mg or clinical improvement

Now let's do the conversion to Morphine Equivalents (MSeqv hereafter):

• Fentanyl: 5-7.5 MSeqv bolus, may repeat with 2.5 MSeqv every 20-30 minutes to a max 20 MSeqv
• Dilaudid: 5-10 MSeqv bolus, may repeat with 5 MSeqv every 20-30 minutes to a max 25 MSeqv

Both the Fentanyl and Dilaudid protocols allow for a higher loading dose in Morphine Equivalents. They both offer a much higher maximum dosage as well. However, if we look at the rebolus schedule they compare poorly to Morphine. Fentanyl's maintenance schedule is 5x weaker, and Dilaudid's is 2.5x weaker than the equivalent Morphine schedule.

Moreover, when you compare the amount of Morphine Equivalents per minute allowed by the protocol, assuming you had the maximum time required to deliver each medication, you find both Fentanyl and Dilaudid compare poorly to Morphine:

• Morphine: 0.8 MSeqv/minute (max reached in 12 minutes)
• Fentanyl: 0.2 MSeqv/minute (max reached in 120 minutes)
• Dilaudid: 0.3 MSeqv/minute (max reached in 80 minutes)

Take this with a huge grain of salt, because this mathematical comparison does not take into account bioavailability, half-life, side effects, rate of administration, and probably a whole host of other important factors. However, what this comparison does show is that while pain control protocols have improved and prehospital providers have options, they aren't all necessarily equal!

Updated 20 July 2010: For a visual representation of their "strength of schedule" see Morphine Equivalents Visualized.

Something for my tag line

"...and sometimes you get to shake someone's hand."

 It's a great feeling.

Question about my Job Description

"Paramedics are not there to determine what is or isn't a life and death situation."

I must have missed something in paramedic school.

Improving BLS to ALS Patient Handoff in Cardiac Arrest

One of the benefits of my software engineering job is access to a large corpus of journals through ScienceDirect. About once a month I pick a topic and pull the latest research. This month I did a journal search for "paramedic" AND 2010 which returned many interesting articles. One that particularly piqued my interest was Berdowski J, et al: Delaying a shock after takeover from the automated external defibrillator by paramedics is associated with decreased survival [1]. The authors found that if the paramedics switched from using the AED to their monitor and a shock was delayed, for whatever reason, there was a decrease in patient survivability to admission.

Currently I work for two services in two different counties, one is a BLS industrial fire brigade and the other is an ALS combined Fire/EMS department. Both services have AEDs for their BLS providers with pads that are interchangeable with the monitors predominantly carried by the ALS units in their respective counties (Philips in one, Physio in the other). The standardization on pads obviously makes BLS to ALS patient handoff simpler during cardiac arrest. However, I had not considered at what point in resuscitation would be the most appropriate to make the pad switch.

As the research showed, in nearly two thirds of the cases where a switch from the AED to the ALS monitor was made, the delivery of an appropriate shock was delayed. Barring equipment or operator malfunction, an AED and a paramedic are both going to defibrillate the same rhythms. Paramedics can still place the patient on their monitor with a 3-Lead even if they have not changed the pads over. The study authors conclude that the appropriate time to switch the pads would be after the AED delivers a shock or advises that no shock should be delivered.

Schematic timeframe of the ALS takeover period (Berdowski J, et al)

The mechanics of a patient handoff from a BLS unit to an ALS unit during cardiac arrest are not something touched on in paramedic school or ACLS [2]. The handling of compressions versus defibrillation is rightfully stressed, but this appears to have missed another factor critical to patient survival. In retrospect this factor is obvious and thankfully easily correctable perhaps simply through recognition. ACLS classes geared towards pre-hospital providers can add this into scenarios used for testing and EMS protocols can include:

Minimize interruptions in compressions or appropriate defibrillation delivery by first responders when initiating ALS treatments in cardiac arrest.

This minor change is low hanging fruit compared to the benefit to our patients!

References

1. Berdowski J, et al: Delaying a shock after takeover from the automated external defibrillator by paramedics is associated with decreased survival. Resuscitation 2010; 81: 287-292.
2. American Heart Association: 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Part 5: Electrical Therapies - Automated External Defibrillators, Defibrillation, Cardioversion, and Pacing. Circulation 2005; 112: IV-35 – IV-46.

Common and Uncommon Usages of Glucagon in the Field (Part 2)

In the pre-hospital setting, Glucagon primarily plays a role in the management of hypoglycemic patients. Emergency Medical Technicians carry Glucagon as an alternative or adjunctive therapy to dextrose administration for these patients. However, this is not the only usage of Glucagon in the field. Many ALS protocols include Glucagon in the treatment of symptomatic bradycardia for patients who have overdosed on β-blockers or are refractory to standard ACLS treatments. As we will find, there are a number of alternative usages of Glucagon which could be considered in the field under online medical direction.

This is a continuation of a two part series: Part 1 contains the pharmacodynamics and common clinical applications of Glucagon.

Uncommon Clinical Applications of Glucagon

• Steakhouse syndrome
• Refractory anaphylaxis
• Severe asthma (little support)
• Refractory CHF (little support)

Steakhouse Syndrome

Steakhouse syndrome, otherwise known as an esophageal food bolus obstruction, is a medical emergency occurring when a foreign body becomes stuck in the esophagus either due to spasms, strictures, or rings. Standard treatment includes endoscopy, digestive enzymes (such as papain), or Glucagon. An interesting property of Glucagon is that it can overcome smooth muscle spasms of the lower esophagus and lower esophageal sphincter pressures. Glucagon has been used in various radiological studies since the 1970s and its hypotonic effects on the esophagus are well documented.

Usage in the ED began formalization in the 1990s with studies on determining an effective treatment protocol. The most common protocol begins with fluoroscopy studies to determine the extent of the obstruction. Next, the patient is laid supine and 1 mg of Glucagon is given over 1 minute via IV push (to lessen the chance of nausea and vomiting). Finally, the patient is sat upright and encouraged to drink 200 cc of water and an effervescent solution. The combination of Glucagon’s spasmolytic effects, the hydrostatic pressure of the column of water, and the esophageal dilation secondary to the effervescence is very successful at passing obstructions.

In the field, patients will present with an inability to swallow, excessive salivation, drooling, and will probably be distressed. If prompt medical attention is not sought, aspiration, esophageal rupture or perforation may occur. A trial of 1 mg Glucagon slow IVP under medical direction may be an effective means of terminating any spasms and passing the obstruction. Glucagon could also be considered in the case of a recent clearing of a foreign body airway or esophageal obstruction with excessive coughing or spasms. Unfortunately the use of Glucagon in the field to treat true esophageal food bolus obstructions is limited by an inability to conduct radiological studies, so unless transport times are long or the EMS system rural, safe and expeditious transport should not be delayed.

Refractory Anaphylaxis

Prompt recognition and management of anaphylactic shock is constantly stressed in EMS education as it is both rapidly fatal and reversible. Treatment protocols include epinephrine, antihistamines, corticosteroids, inhaled β2-agonists, and aggressive fluid resuscitation. However, in certain patient populations the use of epinephrine may not be desired or outright contraindicated. Additionally, some patients may just not respond to β-adrenergic stimulation. Due to its orthogonal cardiovascular mechanism of action, Glucagon is an appropriate choice as supplemental treatment in these patients.

In the field, dosages for Glucagon in refractory anaphylaxis should begin at 1 mg IV every 5 minutes as needed. If the patient has a known β-blockade or is refractory to epinephrine, doses as high as 3-5 mg may be required. If hypotension continues in spite of aggressive fluid resuscitation, a maintenance infusion of 1-5 mg/hr should be started, titrated to effect. As discussed in β-blocker overdoses, most ALS units do not carry enough Glucagon for prolonged treatment and additional units should be requested for an intercept. As before, safe and expeditious transport to an ED should not be delayed for treatment with Glucagon.

Severe Asthma

Treatment of asthma in the field is relatively straightforward, involving nebulized β2-agonists and parasympatholytics, IM sympathomimetics, and IV corticosteroids. However, if a patient has a β-blockade or is in status asthmaticus, the condition may be so severe that standard treatments are not effective on their own. Studies were conducted in the late 1980s and early 1990s on the use of IV and nebulized Glucagon for the adjunctive treatment of bronchospasm. They showed that the smooth muscle relaxation of Glucagon, which is independent of β-adrenergic pathways, provides some clinical benefit when compared against using β2-agonists alone. Current clinical guidelines for the management of asthma note that "last ditch" treatments such as magnesium sulfate or Glucagon have little support in the literature and may even be harmful. However, Glucagon has been shown to be safe even if the additive benefit is negligible.

In the field, patients presenting with severe asthma or status asthmaticus should be treated aggressively using current protocols. Albuterol, ipratropium, epinephrine, and corticosteroids should all be administered prior to the consideration of "last ditch" treatments such as Glucagon. Dosages for Glucagon in severe asthma vary based on the route of administration; 1-2 mg slow IV push or 2 mg nebulized have been shown to be effective in small studies in addition to aggressive β2-agonist treatment. Do not delay safe and expeditious transport or definitive airway management in a decompensating asthmatic.

Refractory CHF

In a patient with acute Congestive Heart Failure, if they are refractory to inotropes Glucagon can be considered as a potential treatment. Studies conducted in the 1960s and 1970s showed promise for Glucagon as a supportive agent in CHF, but only for NYHA Class I and Class II heart failure. Recent studies, however, do not show strong for a support for Glucagon in CHF, reserving its usage for refractory shock states. Dosages in the field of Glucagon for refractory CHF should be 0.01-0.05 mg/kg IV bolus with a maintenance infusion of 1-3mg/hr. The paucity of literature in support of Glucagon for CHF relegates this treatment to a last ditch effort with close medical direction.

Conclusion

Glucagon is one of the most common items in an ALS drug box and as the literature shows surprisingly versatile. Beyond its hyperglycemic effects, Glucagon is a positive inotropic and chronotropic agent. This oft overlooked mechanism of action arms pre-hospital providers with new treatments without adding additional medications. While medical control will be required for nearly all of the alternate indications, both rural and urban providers can make more informed treatment choices for their patients especially when the standard treatments fail.

Potential Utility of Glucagon in the Field

• Hypoglycemia: Adults: 1 mg SQ, IM, IV; 2 mg IN. Peds: 0.5 mg SQ, IM, IV; 1 mg IN. Neonates: 50 mcg/kg SQ, IV. (should accompany glucose resuscitation)
• Symptomatic bradycardia secondary to β-blocker overdose: 10 mg IV bolus, 1-5 mg/hr maintenance infusion. (should supplement standard treatment)
• Symptomatic bradycardia secondary to Ca-channel blocker overdose: 2-10 mg IV bolus; consider maintenance infusion. (should supplement standard treatment)
• Steakhouse syndrome: 1 mg SQ, IM, IV, may repeat.
• Refractory anaphylaxis: 1 mg IV q 5 min; consider 3-5 mg IV; consider maintenance infusion. (should supplement standard treatment)
• Severe asthma: 1-2 mg IV; 1-2 mg nebulized. (paucity of literature to support this use)
• Refractory CHF: 0.01-0.05 mg/kg IV bolus, 1-3 mg/hr maintenance infusion. (paucity of literature to support this use)

References

• Pollock CV: Utility of Glucagon in the Emergency Department. J Emerg Med 1993; 11: 195-205.
• Rosenfalck AM, et al: Nasal glucagon in the treatment of hypoglycaemia in type 1 (insulin-dependent) diabetic patients. Diabetes Research and Clinical Practice 1992; 17: 43-50.
• Love JN, Howell JM: Glucagon Therapy in the Treatment of Symptomatic Bradycardia. Ann Emerg Med January 1997; 29:181-183.
• American Heart Association. Part 7.3: Management of Symptomatic Bradycardia and Tachycardia. Circulation 2005; 112; IV-67-IV-77.
• Stadler J, et al: The "steakhouse syndrome". Primary and definitive diagnosis and therapy. Surg Endosc 1989; 3(4):195-8.
• Glauser J, et al: Intravenous Glucagon in the Management of Esophageal Food Obstruction. JACEP June 1979; 8: 228-231.
• Handal KA, Riordan WM, Siese J: The lower esophagus and glucagon. Ann Emerg Med November 1980; 9: 577-579.
• Galvagno, Samuel M. (2003). Emergency Pathophysiology: Clinical Applications for Prehospital Care (pp. 195-200). Jackson, Wyoming: Teton NewMedia.
• Lieberman MD, et al: The diagnosis and management of anaphylaxis: An updated practice parameter. J Allergy Clin Immunol 115 (2005); 3: S483-S523.
• Gavalas M, Sadana A, Metcalf S: Guidelines for the management of anaphylaxis in the emergency department. J Accid Emerg Med 1998; 15: 96-98.
• Compton J: Use of glucagon in intractable allergic reactions and as an alternative to epinephrine: An interesting case review. J Emerg Nurs 1997; 23: 45-7.
• Wilson JE, Nelson RN: Glucagon as a Therapeutic Agent in the Treatment of Asthma. J Emerg Med 1990; 8: 127-130.
• Melanson SW, Bofante G, Heller MB: Nebulized Glucagon in the Treatment of Bronchospasm in Asthmatic Patients. Am J Emerg Med 1998; 16: 272-275.
• Marik PE, Varon J, Fromm R: The Management of Acute Severe Asthma. J Emerg Med 2002; 23: 257-268.