Harvard's ECG Wave Maven

I am constantly searching for resources which let me hone my electrocardiography skills and would like to share a gem I discovered a few months ago. Harvard's School of Medicine and the Beth Israel Deaconess Medical Center has an excellent resource: ECG Wave Maven: Self-Assessment Program for Students and Clinicians. You can browse their cases as a quiz or for reference, and each case includes high resolution ECGs for your inspection.

I've found their difficulty ratings to be pretty accurate, and I've found that Level 3 or less (of 5 difficulty levels) are all ECG findings that Paramedics should be able to recognize.

Nathanson L A, McClennen S, Safran C, Goldberger AL. ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu.

I encourage all of you to go spend a few hoursdays at the site brushing up on your ECG interpretation skills, your patients deserve it!

A quick look at Pulmonary Embolisms

Acute pulmonary embolism (PE) is believed to affect anywhere from 1 in 250 to 1 in 1000 persons in the US each year. Potentially 1 in 10 patients with an acute pulmonary embolism may go into cardiac arrest within the first 60 minutes[1].

The working diagnosis of a PE in the field is likely to be based solely on clinical findings. Therefore, prehospital providers should be familiar with the most common physical findings:

1. Tachycardia
2. Tachypnea
3. Dyspnea
4. Persistently low SaO2
5. Recent history of syncope
6. Hypotension
7. Cyanosis or pallor
8. Diaphoresis
9. Hemoptysis
10. Low grade fever
11. Diminished lung sounds

Additionally, prehospital providers should be familiar with the common ECG findings in acute pulmonary embolisms (in order of prevalence):

1. Sinus tachycardia (73%)
2. Prominent S1 (73%)
3. "Clock-wise" rotation (56%)
4. Negative T in 2+ precordials (50%)
5. Incomplete or complete RBBB (20-68%)
6. P-pulmonale (28-33%)
7. Axis shift, generally RAD (23-30%)
8. No significant findings (20-24%)
9. S1Q3T3 (12-25%)
10. Supraventricular arrhythmias (12%)

Note that 1 in 5 patients are likely to have no significant ECG findings. What this should stress is the field diagnosis of a PE will lean heavily on your clinical assessment and findings. Chou[2] notes that in one study only 5 patients of 64 were diagnosed with a PE based on ECG findings.

A combination of any of these physical and electrocardiographic findings strongly favor PE and prehospital providers should act accordingly. Unrecognized pulmonary embolisms may be rapidly fatal.

References

1. Galvagno SM. Emergency Pathophysiology: Clinical Applications for Prehospital Care. Teton New Media (2003). [ISBN 1591610079]
2. Surawics B, Knilans TK, Chou TC. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric. Saunders/Elsevier (2008), 6th ed. [ISBN 1416037748]

Pediatric Intranasal Fentanyl

Scenario
It's a summer afternoon and you're dispatched to a 9 year old male patient involved in an ATV accident. The nearest ALS engine company has been dispatched as well. Upon your arrival you find an ATV on its side, another ATV upright, and a crowd gathered on the porch of a nearby house. A paramedic from the engine is assessing a distraught young boy, sitting in his mother's lap, holding an obviously deformed right forearm. The officer on the engine informs you that the boy and his father were riding alongside the road, traveling at 20-30 miles per hour, when the boy lost control and was thrown from the ATV (his father insists he was wearing his helmet).

You introduce yourself to the child, assuring him you're here to help, and ask him what happened. The boy states that when he fell he put his arms out and he heard a loud pop when his right hand hit the ground. He denies passing out or any other injuries but says his arm, "really hurts". He reluctantly allows you to assess his radial pulse in the affected arm, which is rapid but easily palpable. There appears to be distal involvement of both the radius and ulna, however he does not tolerate any further assessment of the arm and screams if there is any movement. The remainder of your physical exam reveals only minor abrasions to exposed skin. The engine company reports tachypnea, tachycardia, and a normal blood pressure.

Discussion
It appears the child has suffered a Colles' Fracture of the right distal forearm. Appropriate treatment would include splinting, ice packs, and pharmacologic pain control. However, given the current state of the patient, it may not be possible to splint the extremity due to anxiety and pain. Traditional prehospital pain management would require intravenous access or intramuscular administration. Both of these routes are likely to cause increased anxiety in this patient, which is best avoided.

Pain management in the pre-hospital setting is fraught with problems. Most studies have found poor provider perception of pain, underutilization of analgesics, and a hesitance to treat pediatric pain (Thomas; Greenwald). Often times, studies find that even if patients are provided analgesia, they do not feel their pain was managed adequately at all (Thomas). For pediatric patients, this problem is compounded as pre-hospital providers are often wary to provide pain management or may be unable to obtain invasive IV access to provide pain management (Greenwald). Moreover, pre-hospital providers are often placed in situations where access to patients is limited to provide pain-management, often times resulting in painful patient movements.

The addition of a noninvasive means of pain management would be an invaluable aid to pre-hospital providers and would remove a potential barrier to care. In pediatric populations, the importance of noninvasive pain management procedures is easy to grasp, as this patient population is often unable to comprehend the benefits of initially painful procedures. Improvements in "time to analgesia" will likely lead to and have a direct, positive impact on patient care and satisfaction.

Efficacy and Safety of Intranasal Fentanyl
The efficacy and safety of intranasal fentanyl (INF) has been the focus of multiple studies, both in-hospital and pre-hospital. Finn et al conducted an in-hospital randomized double-blind placebo controlled trial and found INF to have the same efficacy as oral morphine during procedural wound care in adult burn patients (n=26, 35.5 ± 12.4 years). The concentration of INF used in this study was 50 µg/mL, initial dosages of 1.48 ± 0.57 µg/kg, and no difference in the number of adverse events. Finn et al concluded that while patients receiving INF were more satisfied with their level of pain relief (p = 0.009) that overall only half of the patients in the trial reported they were "satisfied" or "very satisfied".

In a randomized, controlled, open-label study of pre-hospital INF versus IV morphine, Rickard et al found no significant difference in efficacy or safety (n=258, 42.3 ± 13.7 years). This study differs from Finn et al in that there were a multitude of chief complaints treated due to an "all-comers" design. Moreover, the doses used of INF was significantly higher at 180 µg divided evenly between the nares with up to two repeat dosages of 60 µg. Patients in the INF group received pain medication earlier than in the IV morphine group, likely owing to the simpler route of administration. Adverse effects were noted to occur more frequently in the INF group (relative risk 2.09, 95% CI 0.92-4.78, p = 0.07), however, the Rickard et al was not powered to adequately detect any statistical difference. One incidence of a significant adverse effect required a termination of the INF protocol, but it was unclear from the study if this was related to the treatment or the patient's condition. Rickard et al concluded that given the safety and efficacy of INF, it is a valuable option in patients where intravenous access is "undesirable or impossible".

Borland et al 2005 and Borland et al 2007 were inpatient randomized double-blind crossover studies evaluating the efficacy and safety of INF versus oral or IV morphine, respectively, in pediatric patients. Borland et al 2005 studied INF in pediatric burn patients requiring daily dressing changes and found no significant difference in outcomes (n=24, median 4.5 IQR 1.8-9.0 years). The INF dosage was calculated against the bioavailability of the IN route (listed as 70%) with 1.4 µg/kg fentanyl equating to an IV dosage of 1 µg/kg. There were no incidents of significant adverse events, although this was likely due to the study size. However, sedation scores recorded found that INF patients recovered earlier than their oral morphine counterparts. Overall, Borland et al 2005 found INF to be safe and efficacious, but more importantly well tolerated by pediatric patients.

Borland et al 2007 found INF to be comparable to intravenous morphine in pediatric patients presenting to the emergency department with acute long-bone fractures (n=67, 10.9 ± 2.4 years). The median total dose was 1.7 µg/kg fentanyl with repeat doses given PRN. The impetus of the study was to find alternative methods of analgesia to intravenous narcotics in the pediatric population. The study authors note that given the comparable efficacy, INF is invaluable as a means to decrease "time to analgesia" in the pediatric population with potential for pre-hospital adoption.

Mudd conducted a systematic review of the available literature for INF in the pediatric population and graded 12 studies with evidence qualities of four Level I/A, one II/A, two II/B, one III/A, and four at III/B. There was a wide variation in dosing of INF amongst the studies, with a common range of 1-2 µg/kg fentanyl. Differences in concentrations existed as well, owing to the fact that in the US fentanyl is commonly available at 50 µg/mL and is used IV/IM/IO/IN yet overseas it is often given IN with a more concentrated 100-150 µg/mL solution. No differences in significance in pain reduction were found between concentrations, only in the volume of medication delivered. While no studies found a significant difference in adverse effects, many studies had small sample sizes and no long-term studies have been completed on the action of fentanyl on the nasal mucosa. However, the evidence in the reviewed studies demonstrated three clear points: (1) that INF is as efficacious as IV/IM/PO morphine or IV fentanyl, (2) it has no difference in adverse effects, and (3) it decreases the time to analgesia administration and pain relief.

Intranasal Fentanyl Protocol
Based on the research available and the existing 2009 NC EMS protocols, an appropriate pain management protocol for the administration of intranasal fentanyl is given below:

• Adult patients with indications for narcotic analgesia for whom intravenous access is not feasible, not available, or at the discretion of the lead Paramedic, an initial dose of 50-75 µg fentanyl may be delivered intranasally. The total volume to be administered should be divided equally between the two nares (not to exceed 1mL per nare).
  
  • If intravenous access is not available, repeat with 25 µg fentanyl delivered intranasally every 20 minutes to a maximum total dose of 200 µg.
• Pediatric patients with indications for narcotic analgesia an initial dose of 1-2 µg/kg fentanyl up to a total dose of 50 µg may be delivered intranasally. The total volume to be administered should be divided equally between the two nares (not to exceed 0.5mL per nare).
  
  • In order to decrease the anxiety of pediatric patients requiring analgesia and invasive procedures (such as intravenous access), it may be prudent to begin with intranasal fentanyl.

References

• M. Borland, I. Jacobs and I. Rogers, Options in prehospital analgesia, Emerg Med (Freemantle) 14 (2002), pp. 77–84.
• M. Borland, I. Jacobs and G. Geelhoed, Intranasal fentanyl reduces acute pain in children in the emergency department: a safety and efficacy study, Emerg Med (Freemantle) 14 (2002), pp. 275–280.
• J. Finn, J. Wright, J. Fong, E. Mackenzie, F. Wood, G. Leslie and A. Gelavis, A randomized crossover trial of patient controlled intranasal fentanyl and oral morphine for procedural wound care in adult patients with burns, Burns 30 (3) (2004), pp. 262–268.
• M. Borland, R. Bergesio and E.M. Pascoe et al., Intranasal fentanyl is an equivalent analgesic to oral morphine in paediatric burns patients for dressing changes: a randomised double blind crossover study, Burns 31 (2005), pp. 831–837.
• M. Borland, I. Jacob and B. King et al., A randomized controlled trial comparing intranasal fentanyl to intravenous morphine for managing acute pain in the emergency department, Ann Emerg Med 49 (2007), pp. 335–340.
• C. Rickard, P. O’Meara, M. McGrail, et al., A randomized controlled trial of intranasal fentanyl vs intravenous morphine for analgesia in the prehospital setting, Amer J Emerg Med 25 (2007), pp. 911-917.
• S. Thomas, S. Shewakramani, Prehospital Trauma Analgesia, J Emerg Med 35 (2007), pp. 47-57.
• M. Greenwald, Analgesia for the Pediatric Trauma Patient: Primum Non Nocere? Clin Pedi Emerg Med 11 (2010), pp. 28-40.
• S. Mudd, Intranasal Fentanyl for Pain Management in Pediatrics: A Review of the Literature, J Pedi Health Care (2010), Article in Press. doi:10.1016/j.pedhc.2010.04.011.

One Year: Thank You

One year has passed since I received my EMT-Paramedic, and I'd like to say thank you.

Firstly, to my friends and family. You have endured my absence well, or at least have hid your anger well. I'm sure this last year has been tough, but probably not as tough as paramedic school. I really could not do this job without your support, especially as a volunteer. I cannot say it enough, thank you.

To my colleagues and peers, you have surely challenged me to accomplish things I never knew I was capable of doing. You have mentored me, scolded me, and sat patiently while I fumbled with IVs. There is an entire network of you online which have been invaluable as a sounding board and a reference. I can only hope I will continue to take what you have given me and make myself a better Paramedic going forward. The fact that I feel like my feet are underneath me at all is a testament to you all, thank you.

Lastly, to my patients of whom I've met quite a few: you have taught me more than I could ever hope to tell you. Some of you were thrust into my arms, others I knelt and said goodbye. You have challenged me to better myself and I appreciate every experience. My life as a green Paramedic has been an odd mix of on-the-job training for emergencies I was never told about and connecting the dots for those I was told every day about. I thank you for your understanding. I hope that I can tell a story of that time I sat next to you on a flight, and heard about your trip to see your niece get married. That is why I am here, you are why I am here. I feel blessed to meet each and every one of you, thank you.

2010 AHA CPR/ECC Guidelines

If you haven't already heard, today the AHA released the 2010 edition of their CPR/ECC Guidelines which include updates for laypersons, BLS, ACLS, PALS, and neonatal resuscitation. If you've been following resuscitation research at all for the last few years, there are not many surprises.

1. Compressions trump ventilations in adult patients (C-A-B not A-B-C).
2. Minimize interruptions in the "flow" of a resuscitation, that is, continuous compressions are to be minimally interrupted.
3. ETCO2 is to be preferred over manual pulse checks: if you don't have a rise in ETCO2 to physiologic or near-physiologic levels, you probably do not have a perfusing rhythm.
4. AEDs are indicated for all ages, including infants and neonates, provided there are pads available which fit without overlap (>3cm gap).
5. Pharmacologic therapy has the same weight as TCP in certain bradyarrhythmias.
6. Procainamide is now first-line or at least recommended on par with Amiodarone, Lidocaine is almost off the list.
7. Atropine is no longer recommended during routine PEA/Asystole resuscitations.
8. Studies into neonatal resuscitation have shown that deep suctioning is not required in vigorously born neonates with meconium staining.
9. Routine use of naloxone in cardiac arrest secondary to opioid overdose is not recommended.

There were many other differences, including the addition of circular flowcharts documenting the new guidelines (linear flowcharts are still provided). I encourage everyone to read them.

Edit: here is a document (PDF) comparing the AHA 2005 CPR/ECC guidelines to the 2010 guidelines.

How many Automated External Defibrillators are at your place of work?

Our Industrial Fire Brigade just added 10 more AEDs to our site. By my rough calculations this means we have 1 AED for every 150 employees and 1 AED for every 80,000 sqft of floor space (we have almost 2 million sqft). To put this in perspective, the recommendations generally are for 1 AED per 100,000-150,000 sqft or building floor. We now have an AED and emergency responders within 2 minutes of every employee on site!

The Philips HeartStart FRx is a great first responder AED as this author has learned through personal experience.

How does your place of work stack up? Do you need help with corporate/management buy-in? Perhaps our site's successes can help you out. Let me know!

12-Lead ECG: What Is It?

While cleaning up my office to put in a reading chair, I found the following 12-Lead ECGs from my clinical time.  I apologize for the poor quality of the first one, but it is a copy of a copy (of probably a copy). I have limited information on the patients for each of them somewhere in my clinical binder, but I haven't found those yet.

ECG 1

ECG 2

What do these two 12-Leads show?

Do you agree with the computerized statements?

Update on ECG 1 (16 Sept 2010)


The patient's lab values include a K+ of 2.1 mEq/L. What are some of the expected ECG changes in hypokalemia? Does this ECG show a classical or atypical presentation of hypokalemia?

Pediatric Transcutaneous Pacing

Being out of school only recently, I'm often asked "book" questions which are likely to be fresh in my mind. One of these that had me stumped was simply, "what is the appropriate current settings for pediatric transcutaneous pacing?"

I had no answer.

Honestly I had no idea, but assumed it would be weight based, and along the lines of the PALS guidelines for defibrillation. However, when I researched this topic in my PALS book I found there were no answers for pediatric pacing [1]. In fact, there was little mention of TCP whatsoever! Going over to ACLS I found no answers for current settings in adults, just when it was indicated [2].

However, in Paramedic school we had been taught the appropriate current ranges for TCP in adults, which ranged from 20-200 mA. Zoll et al found that most adults responded to TCP in the range of 40-70 mA, however, some required currents up to the device maximum of 140 mA [3]. After a few hours of searching for guidelines specific to pediatrics (including the Philips, Physio-Control, and Zoll websites), I came across a study on TCP in pediatrics which focused on the current required for different electrode sizes. Much to my amazement, the current settings required for external transcutaneous pacing of pediatrics are the same as for an adult!

A total of 56 pacing trials were conducted, 53 of which were successful in obtaining capture. A mean output of 63 +/- 14 mA (range, 42-98) at threshold using the large electrodes was comparable to published adult requirements. Béland MJ et al [4]

How could this be, wouldn't a smaller heart need less energy?

It seemed paradoxical at first, but reviewing the anatomy and physiology of a myocyte with an emphasis on the physics aspect puts it into perspective [5]. Each myocyte in the heart is a part of what amounts to an big electromechanical pump. Given a sufficient input stimulus a myocyte contracts and forwards a stimulus to its neighbors, which follow suit, leading to the eventual coordination of systole and diastole.

The goal of any artificial cardiac pacemaker, whether internal or external, is to act as the primary input stimulus by applying a current to an area of the heart which exceeds the stimulation threshold, i.e. the current required to cause a response from the myocardium.

Therefore, transcutaneous cardiac pacemakers attempt to exceed the stimulation threshold of a single area. It would be hard to achieve coordinated ventricular activity if the current was too high, instead you would have defibrillation. It stands to reason that if the only threshold required to overcome is the stimulation threshold of a single area of the myocardium, the weight of the heart--generalized as the weight of the patient--would be irrelevant.

In contrast, the goal of defibrillation is to bring all electrical activity in the heart to a halt. Defibrillation is not successful unless the all of the reentrant activations of ventricular fibrillation are stopped. Therefore the therapeutic energy levels are going to be proportional to the amount of myocardium you are acting on. Hence, pediatric defibrillation energy dosages are weight based.

So what seemed counterintuitive at first, is actually fairly logical. Pediatric transcutaneous cardiac pacing has the same energy requirements as adults because myocardium has the same stimulation threshold regardless of age. This deduction is supported in the literature as well:

No correlation has been defined between transcutaneous pacing threshholds and age, body weight, body surface area, chest diameter, cardiac drug therapy, or etiology of underlying heart disease. [6]

So there we have it, transcutaneous cardiac pacing current setting ranges are universal amongst our patient population. Below is a guideline I've created as a supplement to the material contained within PALS:

Pediatric Transcutaneous Cardiac Pacing
Symptomatic bradycardia in the pediatric population is most often related to hypoxia secondary to respiratory etiologies. In rare situations it may exist in spite of adequate ventilation and oxygenation. Given the presence of a high degree heart blocks, or symptomatic bradycardia refractory to aggressive BLS and ALS treatments, transcutaneous cardiac pacing should be initiated without delay.

Indications

• High degree heart blocks
• Symptomatic bradycardia refractory to ventilation, oxygenation, chest compressions, and pharmacological treatments

Contraindications
The only contraindication of TCP is an inability to place the pads on the patient without overlap or sufficient distance between them.

Side Effects
The side effects of TCP are most frequently muscle activation and associated pain. These are dose dependent effects which are a combination of the current delivered, size of the pads, location of the pads, and width (time) of the delivered pulse [7].

To minimize these side effects use the largest available pads, placing them in an Apical-Posterior fashion. While larger pads require higher current outputs, there is a decrease in the current delivered per surface area reducing the side effects associated with TCP.

Often, management of these side effects is achieved through concurrent pharmacological treatment with analgesics and/or sedatives.

Dose
Pediatric transcutaneous cardiac pacing (TCP) is defined by two dosing parameters: output current and rate. This guideline assumes the pacemaker is in fixed mode.

Output Current
As with adult patients, the output current for pediatric transcutaneous cardiac pacing should begin at 20 mA (or the lowest setting available) and increase in 5-10 mA increments until electromechanical capture is obtained. Additionally, the current may be increased an additional 5-10 mA above the determined threshold to ensure continued capture. If the device maximum output current is reached and no electromechanical capture exists, discontinue TCP and troubleshoot. Attempt an alternative pad placement (anterio-apical or anterior-posterior) and ensure the negative pad is on the anterior aspect of the chest. If capture is still not obtained, resume CPR and obtain expert consultation.

Output Rate
In contrast to adult patients, the output rate for pediatric transcutaneous cardiac pacing is age based. The final output rate should be titrated to an adequate systolic blood pressure to resolve perfusion problems, e.g. an improvement in mental status. Care should be taken to avoid tachycardic rates or hypertension. Consult a length-based resuscitation tape (e.g. Broselow™ tape) for appropriate starting output rates and systolic blood pressure. An example table is given below, adapted from the North Carolina 2009 EMS Standards [8]:

Age	Rate (bpm)	Systolic BP (mmHg)
0-3 mo	120-150	85 (+/-25)
3-6 mo	120-130	90 (+/-30)
7-10 mo	120	96 (+/-25)
11-18 mo	110-120	100 (+/-30)
19-35 mo	110-120	100 (+/-20)
3-4 yr	100-110	100 (+/-20)
5-6 yr	100	100 (+/-15)
7-9 yr	90-100	105 (+/-15)
10-12 yr	80-90	115 (+/-20)
>12 yr	70-80	120 (+/-20)

References

1. American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: Part 12: Pediatric Advanced Life Support. Circ 2005; 112 (24): [Suppl I:] IV-167-IV-187. [Full Text]
2. American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: Part 5: Electrical Therapies. Circ 2005; 112: [Suppl I:] IV-35-IV-46. [Full Text]
3. Zoll PM, et al. External noninvasive temporary cardiac pacing: clinical trials. Circ 1985; 71: 937-944. [Full Text PDF]
4. Béland MJ, et al. Noninvasive transcutaneous cardiac pacing in children. Pacing Clin Electrophysiol. 1987 Nov; 10(6):1262-70. [PubMed]
5. Malmivuo J, Plonsey R. Bioelectromagnetism: Principles and Applications of Bioelectric and Biomagnetic Fields. 1985 New York: Oxford University Press. Chaps 15,19,23-24. [Full Text]
6. Ellenbogen KA, Wood MA. Cardiac pacing and ICDs. 2005: Wiley-Blackwell. pp 163-191. [Google Books]
7. Bocka JJ. eMedicine: External Pacemakers. 23 Sep 2009. Retrieved 17 Aug 2010. [Website]
8. 2009 NC EMS Standards Document: Color Coded Pediatric Drug List B. Retrieved 17 Aug 2010. [Full Text PDF]

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.

Common and Uncommon Usages of Glucagon in the Field (Part 1)

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 in these patients. However, this is not the only usage of Glucagon in the field. Many ALS protocols include Glucagon for the treatment of symptomatic bradycardia in 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.

Common Clinical Applications of Glucagon

• Hypoglycemia
• Symptomatic bradycardia secondary to β-blocker overdose
• Symptomatic bradycardia secondary to Ca-channel blocker overdose

Uncommon Clinical Applications of Glucagon

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

Pharmacology

Glucagon is a hormone produced by alpha cells in the islets of Langerhans of the pancreas. The primary effect of Glucagon is to promote the release of stored glucose in the liver and stimulate the release of insulin from the pancreas to promote uptake of glucose into the cells. Additional effects of Glucagon include a cascade of activations resulting in an increase of cyclic-AMP (cAMP). cAMP is an important intracellular messenger, responsible for carrying the signals of epinephrine and glucagon across the cell membrane. cAMP also regulates the flux of Ca2+ through ion channels independent of β-adrenergic receptors. This quality of Glucagon is what is thought to explain the various changes to the cardiovascular system seen after its administration.

In the field, Glucagon is commonly packaged as a powder which is reconstituted with either sterile water or D5W (5% dextrose in water) to give a final concentration of 1 mg in 1 cc. Glucagon can be administered intravenously (IV), intraosseously (IO), intramuscularly (IM), subcutaneously (SQ), or intranasally (IN). Glucagon is assigned to the pregnancy category B, therefore usage during pregnancy should be considered when the benefits outweigh the potential risks. The most common side effects are nausea and vomiting, thought to be associated with the rate of IV administration. When giving high doses of Glucagon, the usage of antiemetics such as ondansetron or promethazine should be considered. Additionally some diluents packaged with Glucagon contain phenol, which in high doses can be toxic. Therefore, reconstitution should be done in sterile water, D5W, or normal saline.

Hypoglycemia

As this article is intended for pre-hospital providers, it is assumed that the usage of Glucagon in hypoglycemia is well understood, therefore this indication will not be explored in depth. However, pre-hospital providers may be surprised to learn that the administration of 2 mg Glucagon intranasally (IN) was shown to be as safe and efficacious as an IM administration of 1 mg. Recently the administration of drugs through the IN route has gained in popularity, the most visible of those being naloxone (Narcan). In 2009, naloxone administration via the IN route was added to the scope of practice for all levels of EMTs in North Carolina, where this author practices.

Given the few side effects and complications associated with the administration of Glucagon, it would be a powerful addition to BLS providers for hypoglycemic patients in which oral glucose is not indicated. Yet the widespread adoption of intranasal Glucagon has not been seen in EMS, even though studies on intranasal Glucagon were conducted as far back as the 1980s. One potential explanation could be the relatively high cost of Glucagon. A casual and unscientific search of Internet distributors shows the average price of 1 mg Glucagon ranges from $70-150 USD. In comparison, naloxone ranges from $18-25 USD for the common pre-hospital packaging. Given the economic troubles in 2009 and 2010, it seems unlikely that the intranasal route will gain traction amongst already cash strapped BLS providers.

Symptomatic Bradycardia

Beyond hyperglycemic effects, Glucagon exerts both positive chronotropic and inotropic effects on the heart through non-adrenergic receptors. Because the cardiovascular actions are orthogonal to β-adrenergic receptors, it should be considered in any symptomatic bradycardia refractory to sympathomimetics or as an adjunct to sympathomimetic therapy. High-dose IV Glucagon has been shown to be effective when there is a known β-blocker or Ca-channel blocker overdose.

The first consideration for EMTs when using Glucagon for a patient with suspected β-blocker or Ca-channel blocker overdose is the extreme dosage to be administered. A loading dose of 2-10 mg is cited by the literature, followed by 1-5 mg/hr maintenance infusions titrated to effect if hypotension and bradycardia persist. The service at which the author works only carries two 1 mg Glucagon kits per ambulance, which is relatively common amongst ALS providers. Therefore, a second unit or ALS QRV should be requested for an intercept to supply additional Glucagon kits. This logistical concern obviates any on-scene treatment with Glucagon for symptomatic bradycardia, and should not delay safe and expeditious transport.

In part 2, we'll explore some less traditional usages of Glucagon in the field.

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.

Bigeminy

My last two shifts have included patient's with bigeminal premature ventricular contractions (PVC). Bigeminy is a condition where every other beat does not come from the primary pacemaker. In both cases my patients had sinus rhythm with bigeminal PVCs. One of the patient's had multifocal PVCs. The other had unifocal PVCs during the bigeminy, but had multifocal couplet PVCs later (I unfortunately did not get a strip with that). As you can imagine, those are some sick hearts.

My concern would be if the rate of perfusing beats is not high enough to support hemodynamics. Surprisingly, even though neither patient's PVCs were perfusing they were both stable with these rhythms, even though the perfusing rate was quite bradycardic. One of these was the patient's normal rhythm, and thankfully I was made aware of this before I treated a problem that did not exist!

60yo F C/C Abdominal Pain


55yo M C/B SOB w/ exertion

TFS and Baseless Merging

Whoever thought it was a good idea to not allow sane branching and merging and introduced in its stead "baseless merges," should probably never work on a source control project again.

I'm now relegated to losing all sorts of history in order to stage complex feature branches by just using .patch files. Thanks for wasting my afternoon. Yet another reason to use TRAC/SVN instead of TFS.