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Continuing Medical Education News & InformationOctober, 2006 - Volume 12, Issue 10
==========================================================================
Inside this issue:
From the Editor 1
REMAC news 2
Cert & CME info 3
FDNY contacts 4
OLMC physicians 4
FDNY BOT info 5
CME Article 6
CME Quiz 18
Citywide CME 21
2006 exam calendar 23
2007 exam calendar 24
------------------------------
Journal CME Newsletter
Published monthly
FDNY Office of
Medical Affairs
From the Editor
New Medications double the dose!
This issue concludes our 4-part series New Protocols, New Questions
that explores medications added to the FDNY formulary in September.
REMAC protocol revisions introduced on August 1, 2006 return an old
friend to our drug bags, Calcium Chloride, and stress a little-used option
that has been around for a while, Amiodarone. This months CME article,
presented in two parts to reintroduce NYC paramedics to these
medications, is provided by FDNY EMS Fellow Dr. Doug Isaacs.
REMAC Certification exams will not include questions reflecting
the protocol changes until after January 1, 2007.
New feature:Ask the Academy
The Journal CME Newsletter is pleased to announce a new feature in
upcoming issues. FDNY paramedic instructor James Bubba Fallar will
h d d i di h i l Y
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REMAC News
The REMAC Certification and Credentialing Subcommittee recently introduced pilot questions to the
written exam. Analysis of your exam results revealed that most candidates are well-informed on the use
of Etomidate.
However, more than half of both original and refresher paramedic candidates tested were unfamiliar
with the inclusion criteria for CPAP as indicated in REMAC Protocol Appendix P. NYC paramedics are
encouraged to review the CPAP criteria to prepare for both patient care and the REMAC exams.
==========================================================================
Remember - effective January 1, 2007: Of the 36 hours of Physician Directed Call
Review CME required for REMAC Refresher recertification, at least 18 hours must be
ACR/PCR Review (which may include QA/QI Review). The remaining 18 hours may
include ED Teaching Rounds and OLMC Rotation.
==========================================================================
Effective August 1, 2006, NYC REMAC has issued protocol revisions that may be implemented after
medics are updated by their ambulance service. All EMS personnel must be updated by January 1, 2007.
Per REMAC, ambulance services in NYC are responsible to provide copies of the protocols to their
personnel. The REMAC Advisories are available to all at www.nycremsco.org
REMAC Certification exams will not include questions reflecting the protocol changes until after
January 1, 2007.
Questions may be referred to the REMAC Liaison at 718-999-2671 or [email protected]
Outline of August 2006 protocol changes:
General Operating Procedures: Stroke Patient Criteria has been added
403 Non Traumatic Cardiac Arrest: updated to meet AHA Guidelines
412 Stroke (CVA): GCS replaced by Stroke Patient Criteria
414 Poisoning or Drug Overdose: deletion of Syrup of Ipecac
453 Pediatric Non Traumatic Cardiac Arrest: updated to meet AHA GuidelinesSeries 503 Non Traumatic Cardiac Arrest:
Asystole and PEA protocols are combinedupdated position of Defibrillator pads one (1) inch from permanent pacemakerdeletion of High Dose Epinephrine, Lidocaine, Dextrose, Narcan, Dopamine, TCPaddition of Calcium Chloride
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Certification & CME Information
Effective January 1, 2007: Of the 36 hours of Physician Directed Call Review CME
required for REMAC Refresher recertification, at least 18 hours must be ACR/PCR
Review (which may include QA/QI Review). The remaining 18 hours may include
ED Teaching Rounds and OLMC Rotation.
Failure to maintain a valid NYS EMT-P card will invalidate your REMAC certification.
By the day of their refresher exam all candidates must present a letter from their MedicalDirector verifying fulfillment of CME requirements. Failure to do so will prevent
recertification.
FDNY paramedics, see your ALS coordinator or Division Medical Director for CME letters.
CME letters must indicate the proper number of hours, per REMAC Advisory # 2000-03:
36 hours Physician Directed Call Review- ACR Review, QA/I Session, Emergency Department Teaching Rounds, OLMC Rotation
36 hours Alternative Source CME Maximum of 12 hours per Venue- Online CME - Journal CME- Lectures/Symposiums / Conferences - Clinical- BCLS / ACLS / PALS / NALS / PHTLS
=========================================================================
REMAC Refresher (written) examinations are held monthly, and may be attended up to 6 months
before your expiration date. See the exam calendar at the end of this Journal. To register, call the
Registration Hotline @ 718-999-7074 by the last day of the month prior to your exam.
REMAC Challenge (written and orals) examinations are held every January, April, July &
October. Registration is limited to the first 50 applicants. The next available Challenge
examination is scheduled for January 24 & 31. To register, call 718-999-2671 by December 24.
REMAC CME and Protocol information is available, and suggestions or questions about the
newsletter are welcome. Call 718-999-2671 or email [email protected]
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FDNY ALS Division Coordinators
Citywide ALS: 718-999-1738Lt. Patrick Dillon
Division 1: 212-964-4518
Paramedic Andrea Katsanakos
Division 2: 718-829-6069Paramedics Steve Pilla & Cesar Escobar
Division 3: 718-968-9750Paramedics Gary Simmonds & Al Navarro
Division 4: 718-883-2150Paramedic Lisa DeSena
Division 5: 718-979-7175
Paramedic Russell Shewchuk
Bureau of Training: 718-281-8325Paramedic James "Bubba" Fallar
EMS Pharmacy: 718-571-7620Paramedic Anthony Esposito
FDNY Division Medical Directors
Division 1 and OLMC: 718-999-2665 Dr. John Freese
Division 2 and BOT: 718-281-8473Dr. Dario Gonzalez
Division 3 and 5: 718-999-2666Dr. Glenn Asaeda
Division 4: 718-999-1872Dr. Bradley Kaufman
EMS Fellows:Dr. David Ben-Eli 718-999-2670
Dr. Doug Isaacs 718-999-0749
FDNY OLMC Physicians and ID Numbers
Acosta, Juan 80286
Alexandrou, Nikolaos 80282Asaeda, Glenn 80276
Ben-Eli 80298
Cardinal, Lucien 80292Cherson, Allen 80268
Cole, Joseph 80277
Cordi, Heidi 80279
Freese, John 80293
Gonzalez, Dario 80256Hansard, Paul 80226
Hegde, Hradaya 80262
Hew, Phillip 80267Isaacs, Doug 80299
Kaufman, Bradley 80289
Lombardi, Gary 80225McIntosh, Barbara 80246
Pascual, Jay 80287
Salem, Ashraf 80291
Schenker, Josef 80296
Schneitzer, Leila 80241Silverman, Lewis 80249
REMSCO website: www.NYCREMSCO.org
NYS/DOH EMS b it H lth St t NY US
http://www.nycremsco.org/http://../delgatm/Local%20Settings/Temp/WWW.Health.State.NY.UShttp://../delgatm/Local%20Settings/Temp/WWW.Health.State.NY.UShttp://www.nycremsco.org/8/12/2019 Discretionary orders for Hyperkalemia
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News & Information from the EMS Bureau of Training
EMS Training Supervision
Chief of EMS Training Division Chief James P. Martin
Executive Officer EMS Training Deputy Chief Scott C. HollidayCommanding Officer EMS Academy Captain John Quigley
ALS Program Coordinator Lieutenant Andres RodriguezTour 2 BLS Program Coordinator Lieutenant Lillian BonsignoreTour 2 Program Coordinator Lieutenant John ScotchTour 3 BLS Program Coordinator Lieutenant Arthur LesterTour 3 BLS Program Coordinator Lieutenant David RussellEVOC Program Coordinator Lieutenant Robert Raheb
Important Contact Numbers for the Bureau of Training
EMS Academy Main Number 718-281-8325EMS Academy Fax 718-352-3954CFR Training 718-281-8405EVOC Training 718-281-8317
Haz Tac Training 718-281-8310EMS Training Administration 718-281-8460Training Schedule Coordinator 718-281-8466Registrar 718-281-8467
Academic Schedule Summer 2006
Paramedic Basic Program: The Academy currently has 110 students is paramedic basic training. Fifty
students are in class 5 which graduates in November 2006 and 60 are in class 6 which graduates in May
2007.
Trainee Orientation Program: The next TOP program will begin on October 16, 2006 and 90 studentsare expected to be trained on tour 3.
BLS Programs: EMT refresher programs have resumed. There are a total of seven classes scheduled forthe Fall semester.
ALS Programs:A total of four paramedic refreshers are scheduled for this Fall.
Haz Tac Programs:HazMat Operations for all non-HazTac personnel is being conducted at RandallsIsland Fire Academy. Please make sure your Station Commanding Officer schedules you for HazMat
Operations training.
CFR Programs: The staff of the CFR Unit continues to train and refresh FDNY firefighters in the CFR-D program. Original, refresher and probationary firefighter training is on going.
EVOC: Due to the construction of the new EVOC field there is limited parking available at the
Academy as the staff and student parking areas is being utilized for EVOC training. This is scheduled to
continue until December 1, 2006. Members attending training at the Academy this fall should seekalternate means of transport or the use of car pools.
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October 2006 Journal CME 1stDose
New Protocols, New Questions Part 3: The Return of Calcium Chloride
Calcium its ba-ack! After a brief hiatus calcium is now back in the protocols. As before, it is a
medical control option. Previously, it had been used for cardiac arrest. This time it is specifically
indicated for arrhythmias and conduction abnormalities believed to be secondary to hyperkalemia, and
as well as for the management of hemodynamically compromising calcium channel blocker overdoses.
Following the clinical pharmacology review of calcium, the pathology for its indicated use will be
reviewed.
Clinical Pharmacology
Calcium is the fifth most abundant element in the body and it serves in many physiologic roles,
specifically the functional integrity of the nervous and muscular systems, cardiac function, and blood
coagulation. The endocrine system tightly regulates calcium metabolism through its control over
absorption by the intestine, excretion via the kidney, and storage in bone. The active form, free ionized
calcium, is only a small fraction, with the remaining either protein-bound or in storage. Intracellularly,
the ionized calcium in the cytoplasm is normally maintained at a low level by the cell actively pumping
calcium out of the cell or stored within the cell either in the mitochondria or sarcoplasmic reticulum.
This creates a gradient between the extracellular and intracellular compartments. In response to various
electrical or chemical signals, influx or release of calcium from the storage units into the cytoplasm
occurs. This allows the calcium to perform its physiologic process in the functional and metabolicfunctions of the cell, for example skeletal muscle or nerve cells causing muscle contraction or nerve
conduction, respectively.
There are several pharmacologic preparations of calcium available which differ in calcium
content and permissible route of administration. The two most common intravenous preparations are
calcium chloride and calcium gluconate: Calcium chloride (CaCl2) contains three times more elemental
calcium than calcium gluconate. CaCl2 is 27% elemental calcium, while calcium gluconate is 9%.
Therefore, one gram of CaCl2 is equal to 270 mg of elemental calcium and one gram of calcium
gluconate is equal to 90 mg. REMAC protocols recommended establishing an IV in the largest vein
possible (i e antecubital fossa verses hand) Injection may cause a burning sensation which can be
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true when digoxin is within therapeutic levels, meaning that the use of calcium is not contraindicated
when a patient is routinely prescribed digoxin.
Clinical Applications: Hyperkalemia
Hyperkalemia is a common, silent, and potentially lethal metabolic disorder. The
pathophysiologic factors resulting in the accumulation of potassium are well understood and treatment is
fairly straightforward. This disorder is caused by the kidneys inability to excrete potassium, or by the
inability of potassium to move from the circulation into cells, or a combination of the two.
Two mechanisms may attempt to mitigate elevated potassium levels within the body. First, a rise
in serum potassium stimulates the pancreas to secrete insulin, which in turn, induces rapid transport of
potassium from the circulation into cells via a special pump in the cell membrane. Second, an increase in
potassium in the circulation stimulates specialized cells within the kidney to secrete the hormone renin.
Renin is part of the Renin-Angiotensin-Aldosterone system (RAS) that leads to a feedback mechanism
through the adrenal gland resulting in secretion of elevated levels of aldosterone. The RAS system
activates cells in the distal tubules of the kidney to excrete potassium. It is through a failure of one or
both of these processes that hyperkalemia results.
Such failures most often occur in patients with chronic renal failure (#1 cause) or with other
illnesses that reduce renal potassium excretion. Some of these causes are dehydration or medicines that
alter potassium homeostasis (e.g. nonsteroidal anti-inflammatory drugs, potassium-sparing diuretics,
digoxin, angiotensin-converint enzyme inhibitors). Essentially any disorders that impair renal excretion
of potassium, such as disruption of RAS feedback mechanism (adrenal insufficiency), renal
insufficiency or failure, or autoimmune disorders, may result in a hyperkalemic state. Other disorders
that cause a shift of potassium into the extracellular space include acidosis, rhabdomyolysis, burns,
tumor lysis syndrome, intravascular hemolysis, and insulin deficiency or resistance. Diagnosis,
especially in the prehospital setting, is limited. Approach should include the clinical history, review of
medications, and physical examination. In the setting of hyperkalemia the patient may demonstratesigns/symptoms of muscular weakness, flaccid paralysis, or an ileus (paralysis of the intestine). These
signs and symptoms are non-specific. A preliminary diagnosis can be made based on clinical suspicion
and characteristic progressive changes on the EKG: tall, peaked T waves, followed by the loss of P
l d PR i l id d QRS l hi h i h h b l T
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the direct toxic effects of hyperkalemia on the
cardiac cell membrane, promoting cellular uptake
for immediate lowering of potassium, and removing
potassium from the body (longer process).
Medications used to promote cellular uptake
of potassium include the co-administration of
glucose and insulin, 10 to 20 mg of 2-agonists
(albuterol), and sodium bicarbonate (NaCHO3). In
this system, the latter two medications may be
ordered by an OLMC physician as a discretionary
order in the treatment of such a patient. The use of
sodium bicarbonate has, to some degree, fallen out
of favor due to its lack of efficacy in significantly
reducing potassium levels, though it is still
reasonable to give in a known renal patient who is
acidemic. (Make sure not to co-administer it with
calcium, as it may precipitate into calcium
carbonate chalk).
To remove potassium from the body,
medications including loop diuretics (furosemide)
or cation exchange resins (kayexalate) may be used,
as well as hemodialysis.
In the prehospital setting the most rapid and effective treatment for presumed hyperkalemia is the
administration of calcium intravenously. Calcium stabilizes the myocardium by lowering the threshold
potential, thus counteracting the toxic effect of the high potassium. Calcium does not have any effect onthe level of potassium. Reversal of EKG changes should be visible within two to three minutes of
administration of calcium, with the effects lasting 30 to 60 minutes.
Clinical Applications: Calcium Channel Blocker Overdose
C l i h l bl k (CCB) h b d i h U i d S i h 1960 f
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of calcium from extracellular to intracellular sites. This inhibition of calcium influx subsequently
prevents the cell from performing its normal function, resulting in conduction system delays such as
bradycardia, first-, second-, or third-degree blocks, bundle branch blocks, junctional and ventricular
escape rhythms, decreased contractility in myocytes, vasodilation in smooth muscle cells,
hyperglycemia secondary to blocking of insulin release (calcium-mediated), and blockade of peripheral
insulin receptors. The L-type calcium channels are located throughout the body but are most clinically
significant in cardiac myocytes and conduction cells, vascular smooth muscle cells, and pancreatic -
cells.
CCB are well-absorbed orally. Their bioavailability varies. All are metabolized in the liver to
less active metabolites by an enzyme in the cytochrome P-450 family.
There are three classes of CCB approved for use in the U.S. (see table below). Each class has
varying degrees of selectivity on cells (i.e. vascular smooth muscle cells, cardiac myocytes, and
conduction cells). These differences of selectivity lead to various presentations of clinical manifestations
with toxic levels of CCB.
Class Drug Primary Toxic Effect
Benzothiazepine Diltiazem
Negative inotrope and
chronotrope > peripheralvasodilation
Phenylalkylamine Verapamil
Negative inotrope and
chronotrope > peripheral
vasodilation
DihydropyridineAmlodipine, nifedipine,
nimodipinePeripheral vasodilation
Clinical manifestations:
Patients signs, symptoms, and physical examination are dependent on the amount of
hypoperfusion. Hypotension (combination of vasodilation and negative inotropic and chronotropic
effects) is a common sign. Patients may complain of dizziness or lightheadedness with symptoms
becoming more pronounced upon standing up (i.e. orthostasis). As the level of CCB increases, the
hypotension becomes more pronounced, various heart blocks (sinus node depression and AV conduction
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medical control. For sake of completeness, included below are treatment modalities that are also
hospital-based.
History is important in managing the patient. Besides identifying the drug ingested, it is
important to assess the time of ingestion, amount, and preparation (immediate or sustained release). The
type of drug will help predict the expected toxicity, and the preparation will help determine whether
gastrointestinal decontamination will be helpful.
As with any approach to patient resuscitation, start with assessing the airway, breathing, and
circulation:
Intravenous fluids:Normal saline, 500 ml bolus (may require more fluids, potentially liters).
Calcium Therapy: Calcium salts are administered in an attempt to overcome the antagonistic
effect of the CCB. By increasing extracellular calcium, a concentration gradient is created
causing an influx of calcium into the cells. As mentioned above, several types of channels exist
other than the L-type channel blocked by CCB. Initial dose of CaCl2is 1 to 3 grams. REMAC
dosing is for 1 gram. Any further administration requires a discretionary order by OLMC
physician. Once in the hospital, patients may require several more grams of calcium and possibly
an infusion drip.
Bradycardia:
a) Atropine: initially start with 0.5 to 1 mg every two to three minutes for a total of 3 mg. This
may only be transiently effective, if at all.
b) Pacing: Often ineffective.
Glucagon: has been shown to be beneficial in -blocker overdose but questionable in CCB
overdose. An attempt can be made in patients with hypotension, when unresponsive to fluid
resuscitation. Glucagon raises intracellular cyclic adenosine monophosphate (cAMP) that in turn
opens calcium channels. Adult dose is 2 to 5 mg slow IVP, that can be repeated in 5 to 10
minutes to a total of 10 mg (most NYC ambulances are limited by a total of 3 mg with the threemedical inserts). If the patient responds, a drip can be started based on the total amount it took to
achieve a hemodynamic response, with that dose being given as an infusion per hour.
Vasopressors: Dopamine infusion may be considered but has not been studied for its benefit.
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effect by improving carbohydrate metabolism in cardiac myocytes and increase intracellular
calcium entry.
Amrinone: Prevents the breakdown of cAMP by inhibiting phosphodiesterase leading to a
positive myocardial chronotropic and inotropic effect.
Gastrointestinal Decontamination:
a) Orogastric lavage could be indicated for patients with large ingestions or patients who are
seriously ill. This technique is limited due to the size of the sustain-release pills. Caution
should also be taken due to the possibility this of worsening the patients condition by
increasing the vagal tone resulting in worsening bradycardia.
b) Activated charcoal is indicated only in those patients with protected airways who have
ingested sustained-release preparations.
c) Whole-bowel irrigation should be attempted only in those patients with extended-release
preparations ingestions.
Mechanical Support: As a last resort, when all else has failed, mechanical support using
intraaortic balloon counterpulsation, or even extracorporeal bypass, can be used. This would
hopefully give the patient more time until the transient effect of the CCB decreases.
Conclusion:
Calcium chloride is being reintroduced to the ALS protocols for the specific indication of
hyperkalemia and calcium channel blocker overdose. This life-saving medication requires the approval
of OLMC.
Written by: Doug Isaacs, MD
EMS FellowFire Department of New York
ReferencesHarris, Stuart. Case Report. N Engl J Med. 355;6. pp602-611.
Holstege, Christopher, Dobmeier S. Cardiovascular Challenges in Toxicology. Emerg Med Clin N Am 23 (2005) 1195-1217.
Barrueto, Frank Jr. Calcium Channel Blocker Toxicity. Uptodate.2006:pp1-7.
Abernethy D. R., Schwartz, J.B. Calcium-Antagonist Drugs. N Eng J Med. 341;19. pp.1447-1457.
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October 2006 Journal CME 2nd
Dose
New Protocols, New Questions Part 4: Amiodarone: Wonder Drug?
Treating cardiac arrhythmias and cardiac arrest can make even the most seasoned paramedic
weak in the knees. In the past year (September 2005 through August 2006), Fire Department of New
York paramedics managed 2,268 out of hospital cardiac arrest (OOHCA) cases. The causes of these
cardiac arrests are numerous, with ischemic cardiovascular disease being the most common in adults.
OOHCA cases are usually associated with the lethal arrhythmia of ventricular fibrillation (VF) triggered
by an acute ischemic event or infarction of myocardium or by a primary electrical disturbance.
The American Heart Association released new Advanced Cardiac Life Support guidelines in
2005 that recommended the use of amiodarone as drug of choice for refractory VF and pulseless
ventricular tachycardia (VT). This was a change from the 2000 ACLS guidelines in which Amiodarone
was a Class IIb recommendation (fair to good evidence that a treatment modality is acceptable, safe, and
useful). Traditionally, lidocaine (indeterminate recommendation) had been used with little evidence
supporting any benefit in cardiac arrest. In light of these new guidelines the NYC Regional Emergency
Medical Advisory Committee approved the use of amiodarone in the protocols for: VF/pulseless VT;
VT with a pulse/wide complex tachycardia of unknown type; supraventricular tachycardia; and atrial
fibrillation/flutter.Amiodarone, a structural analogue of thyroid hormone, was developed in the early 1960s as an
antianginal agent and was subsequently discovered to have anti-arrhythmic properties, and since 1986,
has been used for that purpose in the United States. In 1993, an intravenous formulation became
available but was not FDA approved until 1995 for the therapy of VT or resistant VF. Through its
complex pharmacodynamic and pharmokinetic properties, amiodarone has shown efficacy for treating a
broad range of arrhythmias from atrial fibrillation to malignant ventricular rhythm disturbances.
Mechanism of Action
Below is the Vaughn Williams Classification of anti-arrhythmic agents. The drugs are assigned
t f f j l b d th i b i l t h i l i ti d ti h th i ff t
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Table 2: Vaughan-Williams classification of antiarrhythmic drugs
Class Effects on action potential Examples
Depolarization Refractory period
I (sodium channel
blockers)
Depresses phase 0
depolarization
Prolongs refractory period (by prolonging
repolarization)
--
IA Moderate depression Significantly prolongs Procainamide, quinidine, disopyramide
IB Weak depression No changes or shortens Lidocaine, mexiletine (Mexitil)*, tocainide
(Tonocard), phenytoin
IC Strong depression Little effect Propafenone, flecainide
II (blockers) Slow phase 4 spontaneous repolarization (by decreasing the sympathetic
stimulus that promotes depolarization)
Propranolol, metoprolol, atenolol, esmolol, many
others
III (potassium channel
blockers)
Decrease phase 3 potassium efflux, therefore prolonging repolarization and
refractory period
Amiodarone, sotalol, bretylium, dofetilide, ibutilide
IV (calcium channel
blockers)
Affect phase 2 by decreasing calcium influx. In calcium-dependent tissues
like the sinoatrial or atrioventricular nodes, they decrease spontaneous
depolarization and conduction velocity, and increase refractoriness
Verapamil, diltiazem
*Boehringer Ingelheim Pharmaceuticals, Ridgefield, CT.AstaZeneca, Wilmington, DE.
Though amiodarone is considered a Class III anti-arrhythmic drug, it possesses
electrophysiologic characteristics of all four classes. Similar to Class I drugs it blocks the Na+channels
(phase 0), like Class II it exerts - and -adrenergic antagonism, like Class III it blocks K+channels, and
like Class IV it blocks Ca2+
channels.
Myocardial Cell
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Amiodarones multiple electrophysiologic mechanisms of action include inhibition of abnormal
automaticity, prolongation of action potential duration and decreases in conduction velocity resulting in
the prolongation of PR, QRS, QT and the potential for sinus bradycardia.
Myocardial Conduction Cell
(Klabunde, Richard E. Cardiovascular Physiology Concepts)
In contrast, lidocaine exerts its effect by blocking the myocardial Na+ channels which account
for automaticity (impulse generation-phase 4 in the above diagram). This results in reduced cardiac
automaticity (phase 4) within the action potential slope and thereby increases the threshold for
excitability. The sum result of this is a delay in conduction but not the duration of the action potential.
Therefore there is no change in the PR or QRS duration.
Amiodarone has shown to be an effective rate-controlling agent for atrial fibrillation and
supraventricular tachycardia. This is believed to be due to its antiadrenergic and calcium channel
blocking effect on slowing conduction and increasing the refractoriness on the atrioventricular node. If
not for its adverse effects, this would seem to be the ideal drug because it is well-tolerated, and lacks
proarrhythmic effect and negative inotropic activity.Wide-complex tachycardia is a diagnostic dilemma whether it is due to VT, Wolf-Parkinson-
White syndrome, or supraventricular tachycardia with aberrancy (accessory pathway), with VT being
the most concerning. In view of amiodarones properties, it has been shown to be an effective treatment
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There is no established relationship between drug concentration and therapeutic response for short-tem
use.
Amiodarone is chemically processed by the cytochrome P450 enzyme family and forms active
metabolites. Half-life is long with inter-individual variability, but usually ranges from 14 to 59 days. It is
primarily eliminated by the liver and biliary excretion. Very little of amiodarone or its metabolites are
found in the urine. Therefore, there should not be a concern when administering it to a patient with
kidney failure or in the elderly. Though not a concern in the acute prehospital setting, caution should be
taken in patients with liver disease.
Outside of the cardiac arrest setting, the amiodarone solution needs to be diluted before
administration. D5W is the preferred diluent, as amiodarone and NaCl 0.9% are not compatible at room
temperature for 24 hours. Though such prolonged storage is not a viable concern in the prehospital
setting, the use of D5W is still recommended. Do not co-administer it with sodium bicarbonate as the
amiodarone will precipitate out.
For OOHCA patients whose ventricular arrhythmia responds to initial defibrillation attempts or
for patients whose hemodynamically stable arrhythmias allow for amiodarone administration under
REMAC protocols, one 3-mL ampule (containing 50 mg/ml of amiodarone for a total of 150 mg) is
diluted into 100 ml of D5W and given over 10 minutes. For recurrent arrhythmia, an additional 150 mg
may be given, with approval of the OLMC physician. For VF/pulseless VT, 300 mg of amiodarone is
given. Two 3-mL ampules, each containing 50 mg/ml, are drawn up into a syringe, and then diluted with
D5W to 20 ml before injection.Adverse Reactions
Most adverse effects are from chronic use due to the accumulated exposure to the drug. Acutely,
hypotension and bradycardia are the most concerning. The hypotension is believed due to the effects of
polysorbate 80 or benzyl alcohol (solvents) rather than the drug itself. This should initially be treated by
slowing the infusion rate. Additional therapy may be needed and this includes vasopressor drugs,
inotropic agents, and volume expansion with intravenous fluids. Bradycardia is not dose related. It
should also be initially treated by slowing the infusion rate or discontinuing the drug. Some patients may
require pacing. Proarrhythmic effect, a risk with all anti-arrhythmics, is a rare occurrence with
i d Thi b d i ff f l i h QT i l d i l d
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optic neuritis), gastrointestinal (nausea, anorexia, and constipation), and central nervous system (ataxia,
paresthesias, peripheral neuropathy, sleep disturbance, impaired memory, tremor).
Drug interactions
Most drug interactions are from long-term oral use and are due to its inhibitory effect on the
activity of enzymes in the cytochrome P-450 of the liver. Other drugs metabolized by this system may
experience a change in their half-life and/or distribution as a result of amiodarones action within the
P450 system. These drugs include but are not limited to phenytoin, quinidine, theophylline, and certain
-blockers.
Two well-known drug interactions are with digoxin and warfarin. Amiodarone can reduce the
renal and non-renal clearance of digoxin resulting in significant increases in digoxin levels. Most often,
levels are carefully monitored and digoxin dosage decreased as required. Amiodarone also reduces the
hepatic clearance of warfarin, usually requiring a 30-50% reduction in the dosage of warfarin. These
interactions are seen within the first few days of starting amiodarone and, because they result from
continued oral amiodarone administration, are not a concern in the acute care or prehospital setting.
Contraindications
The following are contraindications to administering amiodarone: cardiogenic shock, known
hypersensitivity to amiodarone or to any of its components including iodine, second or third degree
block, severe sinus bradycardia, and severe sinus node dysfunction.
Clinical Studies
Lidocaine has been the drug of choice in the past for the treatment of shock-resistant ventricularfibrillation as well as for the prevention of recurrent ventricular arrhythmias after OOHCA. And yet the
fact is that there has been no evidence that giving any antiarrhythmic drug routinely during cardiac arrest
increases the rate of survival to hospital discharge. Traditionally, lidocaine has been used due to its ease
and simplicity of administration and its well-understood pharmacologic and adverse effect profile.
Two blinded, randomized controlled trials in adults were performed, the Amiodarone in the
Resuscitation of Refractory Sustained Ventricular Tachyarrhythmias (ARREST) trial and the
amiodarone versus lidocaine in the Prehospital Ventricular Fibrillation evaluation (ALIVE) trial in 1999
and 2002, respectively. The ARREST trial compared amiodarone to placebo in OOHCA due to VF. The
i d i i l h i l d i i hi h hi d i 44% f i i h
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Conclusion
Prior to the ARREST and ALIVE trials, antiarrhythmic drugs have never shown benefit in OOHCA.
Intravenous amiodarone has shown short-term benefit in survival in patients being admitted to the
hospital but not survival in being discharged. More studies need to be performed to further evaluate its
potential impact on survival. Because amiodarone has been shown to be a relatively safe drug, probably
effective, and superior to lidocaine with regard to short-term survival, it has replaced lidocaine as the
drug of choice. What is important to keep in mind is that the only treatment proven to impact survival
and better neurological outcome in patients with OOHCA is performing good CPR and early
defibrillation. And without quality CPR, no drug can hope to impact upon a patients outcome.
Written by: Doug Isaacs, MD
EMS Fellow
Fire Department of New York
References
Kudenchuk, P.J., Cobb, L., et al. Amiodarone For Resuscitation After Out-Of-Hospital Cardiac Arrest Due To Ventricular
Fibrillation. N Engl J Med. 1999;341:871-878.
Dorian, P., Cass, D., et al. Amiodarone As Compared With Lidocaine For Shock-Resistant Ventricular Fibrillation. N Engl J
Med.2002;346:884-890.Caron, M.F., Kluger, J., et al. Amiodarone in the New AHA Guidlines for Ventricular Tachyarrhythmias. The Annals of
Pharmacotherapy. 2001;1248-1254.
Giardina, E., Clinical Use of Amiodarone. UpToDate. 2006.
Maheswaran, A.M., Amiodarone Hydrochloride. Mosbys Drug Consult. 2006.
Sarkozy, A., Dorian, P., Strategies for reversing shock-resistant ventricular fibrillation. Curr Opin Crit Care. 2003;9:189-193.
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OCTOBER 2006 JOURNAL CME QUIZ Calcium & Amiodarone
** DO NOT RETURN THIS PAGE SEND ANSWER SHEET ONLY (page 19) BY OCT. 31**
1. Which of the following contains more elemental calcium?
a. Calcium gluconateb. Calcium chloride
2. Calcium is indicated in all of the following except:
a. Digoxin toxicity c. Hypocalcemiab. Hyperkalemia d. Calcium channel blocker overdose
3. Calcium lowers potassium levels.
a. True b. False
4. The following are treatments for hyperkalemia except:
a. Digoxin c. Calcium chlorideb. Albuterol d. Kayexalate
5. All of the following are treatments for calcium channel blocker overdose except:
a. Calcium chloride c. Glucagon
b. Lidocaine d. Intravenous fluids
6. Lidocaine has proven beneficial in OOHCA.a. True b. False
7. Amiodarone has which of the following properties:
a. Blocks Na channels c. Blocks K+ channels
c. Blocks Ca2+ d. All of the above
8. In OOHCA the correct initialdosage of amiodaone is:a. 300mg c. 100mg
b. 450mg d. 150mg
9. In rapid atrial fibrillation the correct initialdosage of amiodarone is:
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After reading the article, place your answers to the following quiz on this answer sheet.
Paramedics receiving a minimum grade of 80%will receive 1 hourof Online/Journal CME.
------------------------------------------------------------------------------------------------------------------------------
Please submit this page only once, by the following methods:
INTER-OFFICE MAIL (pony express): FDNY Office of Medical Affairs
Or FAX: 718-999-0119
Or U.S. MAIL: FDNY OMA, 9 MetroTech Center 4th
flr, Brooklyn, NY 11201
You are strongly advised to keep a copy for your records
------------------------------------------------------------------------------------------------------------------------------------------------------------------------
*Required information to receive your CME
*Name
NY State / REMAC #
*Work Location
*Email address
October 2006 Journal CME
Calcium & AmiodaroneQuiz Answers
1. _____
2. _____
3. _____
4. _____
5. _____
6. _____
7. _____
8
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WWW.NYC.GOV/FDNY 22
2006 REMAC E i ti S h d l
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WWW.NYC.GOV/FDNY 23
2006 REMAC Examination Schedule
REMAC Challenge Exam REMAC Refresher Exam
Month Part A - Written
Tuesdays@18:00
Part B Orals
Tuesdays@09:00
Exam Date
(on Wednesdays)
Registration
Begins
Registration
Deadline
NYS/DOHExam
January 1/17/06 1/24/06 1/25/06 12/1/05 12/31/05 1/19/06
February 2/15/06 1/1/06 1/31/06
March 3/22/06 2/1/06 2/28/06 3/16/06
April 4/18/06 4/25/06 4/26/06 3/1/06 3/31/06
May 5/24/06 4/1/06 4/30/06 5/18/06
June 6/21/06 5/1/06 5/31/06 6/15/06
July 7/18/06 7/25/06 7/26/06 6/1/06 6/30/06
August 8/16/06 7/1/06 7/31/06 8/17/06
September 9/27/06 8/1/06 8/31/06
October 10/17/06 10/24/06 10/25/06 9/1/06 9/30/06
November 11/15/06 10/1/06 10/31/06 11/16/06
December 12/13/06 11/1/06 11/30/06 12/21/06
Paramedics with current REMAC certification must register for upcoming refresher examinations by calling 718-999-7074 during the registration periods. Allrefresher exams are held at 07:00 or 18:00 hours at FDNY-EMS Bureau of Training, Fort Totten, Queens.
The REMAC Challenge Examination is offered quarterly. Register early as seating is limited, and at least 30 days prior to the exam.To take a ChallengeExam for expired REMAC or inadequate CME, call 718-999-2671 to register. Part A (written) is held at 18:00 and Part B (orals) at 09:00 at FDNY-EMS Bureauof Training, Fort Totten, Queens.
Send correspondence to: FDNY Office of Medical Affairs , Attn : REMAC Liaison, 9 MetroTech Center - 4th Floor , Brooklyn, New York 11201-3857
2007 REMAC E i ti S h d l
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WWW.NYC.GOV/FDNY 24
2007 REMAC Examination Schedule
REMAC Challenge Exam REMAC Refresher ExamMonth
Part A - Written
@18:00
Part B Orals
@09:00
Exam Date
(on Wednesdays)
Registration
Begins
Registration
Deadline
NYS/DOHExam
JanuaryWednesday
1/24/07Wednesday
1/31/071/17/07 12/1/06 12/31/06 1/18/07
February 2/21/07 1/1/07 1/31/07
March 3/21/07 2/1/07 2/28/07 3/15/07
April
Thursday
4/19/07Thursday
4/26/07 4/18/07 3/1/07 3/31/07
May 5/16/07 4/1/07 4/30/07 5/17/07
June 6/20/07 5/1/07 5/31/07 6/21/07
JulyTuesday7/24/07
Tuesday7/31/07
7/18/07 6/1/07 6/30/07
August 8/15/07 7/1/07 7/31/07 8/16/07
September 9/19/07 8/1/07 8/31/07
OctoberWednesday
10/24/07Wednesday
10/31/0710/17/07 9/1/07 9/30/07
November 11/14/07 10/1/07 10/31/07 11/15/07
December 12/19/07 11/1/07 11/30/07 12/13/07
Paramedics with current REMAC certification must register for upcoming refresher examinations by calling 718-999-7074during the registration periods. Allrefresher exams are held at 07:00 or 18:00 hours at FDNY-EMS Bureau of Training, Fort Totten, Queens.
The REMAC Challenge Examination is offered quarterly. Register early as seating is limited, and at least 30 days prior to the exam.To take a ChallengeExam for expired REMAC or inadequate CME, call 718-999-2671 to register. Part A (written) is held at 18:00 and Part B (orals) at 09:00 at FDNY-EMS Bureauof Training, Fort Totten, Queens.
Send correspondence to: FDNY Office of Medical Affairs , Attn : REMAC Liaison, 9 MetroTech Center - 4th Floor , Brooklyn, New York 11201-3857