Discretionary orders for Hyperkalemia

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Continuing Medical Education News & InformationOctober, 2006 - Volume 12, Issue 10

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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
mailto:[email protected]:[email protected]


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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]
mailto:[email protected]:[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/


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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:


19/24

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


23/24

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


24/24

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

Discretionary orders for Hyperkalemia

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