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| Nathanson L A, McClennen S, Safran C, Goldberger AL. ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu. |
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| The Philips HeartStart FRx is a great first responder AED as this author has learned through personal experience. |
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| ECG 1 |
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| ECG 2 |
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?
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)
"Paramedics are not there to determine what is or isn't a life and death situation."I must have missed something in paramedic school.
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.
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
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
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
References
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
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.
HypoglycemiaAs 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
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!
