Pocket Reference Guide 2011 - Lakeridge Health · This pocket reference guide is to be used for reference ... Jaun Bothma Deepinder Brar Brenda Burns ... No signs of ﬂuid overload

PrimaryCareParamedicPocket Reference Guide

2011 Version 1.2

CEPCP

This pocket reference guide is to be used for reference only. Refer to the current medical directives for all

treatment decisions. If there are inconsistencies between this reference guide and the current directives always refer

to the medical directives.

For questions, comments, or suggestions for improvements, please contact us at:

Website (follow ‘contact us’ link):www.cepcp.ca

Administration Office:95A Simcoe St. S. Oshawa, ON

Mailing Address: Central East Prehospital Care ProgramLakeridge Health Oshawa1 Hospital CourtOshawa, ONL1G 2B9

Phone: (905) 433-4370Fax: (905) 721-4737

Toll free: 1-866-423-8820

2!

http://www.cepcp.ca

http://www.cepcp.ca

Table of Contents:

BHP names................................................................! 5Cardiac Arrest............................................................! 6 - 7Trauma Cardiac Arrest...............................................! 8Foreign Body Airway Obstruction...............................! 9Neonatal Resuscitation..............................................! 10 - 11Hypothermia Cardiac Arrest.......................................! 12Supraglottic Airway.....................................................! 13Return of Spontaneous Circulation............................! 14IV and Fluid Therapy..................................................! 15Cardiogenic Shock..............................................! 16 Moderate to Severe Allergic Reaction.......................! 18-19Croup..........................................................................! 20Bronchoconstriction....................................................! 21CPAP...........................................................................! 22Acute Cardiogenic Pulmonary Edema........................! 23Cardiac Ischemia.........................................................! 24 - 25STEMI Bypass............................................................! 26 - 27!Nausea / Vomiting.......................................................! 28 - 29Hypoglycemia.............................................................! 30 - 31Electronic Control Device Probe Removal..................! 32 Special Events............................................................! 33 - 37

References (section two)

Central East Prehospital Care Program For reference only 3

4 Central East Prehospital Care Program For reference only

Markham:Shobana AnanthAndrew ArcandDavid AustinLuke BearssKatherine Bingham Tara ByrneJoan Cheng Ross Claybo Nicole Kester GreeneIlana Greenwald Peter Haw Karen HeldRoberta HoodWendy IsemanPaul JacobsonDoug JangMano KanetosScott KapoorMonica KapoorBarb KingTom Leventis Bernice MittlemanPhil MoranMike Nowak Meeta PatelCristina PopaSonia Sabir Seyon SathiaseylonSam SueMichael TaylorPaul YeeJason Zitsow

Durham:Elanchellyan AmbalavanarPeter BlecherTony ChinMike EvansPing FuBenj FullerKevin GreenMichael KahnGeoff KennedyWill LotteringGetachew MazangiaFarley MossTom NovakErik PaidraAbdolreza Paki-JavanJim ShipleyRob StuparykRudy Vandersluis

Peterborough:Vince ArcieriJohn AshbourneKate BinghamJaun BothmaDeepinder BrarBrenda BurnsDavid CarrJennifer DarlingNicole DeFrancescoKirk DillonNick FerozeDale FriesenReinhart FriesenGary HillDan HouptAnthony JefferyBrian LindsayJohn Lingertat Terry MayJames McGormanTemba McWabeniMichael MunozAllen RodgersAndrew Romanowski Grant PetersMark TroughtonNancy White


Base Hospital Physician Names:

6 Central East Prehospital Care Program For reference onlyM

edic

al C

ardi

ac A

rres

t Indications

Medical Cardiac Arrest

Non-traumatic cardiac arrest

CPR ongoing throughout callMinimize Interruptions100 - 120 per minute

At least 2 inches depth30:2

Drug Dose

Epinephrine IM

King LT should be inserted where more than OPA/BVM is required, without interrupting CPR. Once inserted, begin continuous compressions and ventilate asynchronously at 6-8 breaths / min. monitor ETCO2: 10 - 15 mmHg - poor prognosis, confirm compressions are adequate 20 - 30 mmHg - improved prognosis, indicates good CPR quality > 35 mmHg - excellent CPR / prognosis, check for palpable pulse large spike to above normal values - probable ROSC, check for pulse

Analyze

every 2 minsTransport to hospital following the 4th analysis unless medical TOR

Shock if indicatedResume CPR immediately

(if suspected anaphylaxis) 0.01 mg/kg 1:1,000 (max 0.5 mg) single dose

Medical TOR • > 18 years old• Presumed cardiac origin• Arrest not witnessed by EMS• 3 analysis with no shocks delivered• No ROSC at any time


Confirmation MethodsPrimary

• Auscultation• Chest rise

Secondary• ETCO2• OtherConfirm supraglottic airway placement.

Notes:

Size Colour Patient Amt of air in cuff#3 Yellow 4-5 ft tall 45 - 60 ml #4 Red 5-6 ft tall 60 - 80 ml#5 Purple ≥ 6 ft tall 70 - 90 ml

King LT Reference

Medical TOR Patch

“This is (your name) a Primary Care Paramedic on vehicle (number) patching for Termination of Resuscitation for a cardiac arrest”

Patient is (age) years old (estimate if needed)Gender (male or female)

State the three TOR Guidelines :• we did not witness the arrest• no shocks were given, and • there has been no return of a carotid pulse.

Brief past medical history, history of current presentationThe patient was last seen at______ And was at that time complaining of___________The patient has a history of__________My interpretation of the TOR guideline is that we could consider stopping resuscitation at this time.

Ask the BHP if further information is required? Would you like further clinical information?

______________________________

Questions that may be asked:Estimated number of minutes to the arrival on scene from the time you were notified.Whether or not the cardiac arrest was witnessed by a bystanderWhether or not bystander CPR was done.Extrication problems, if any, that may delay initiating transport.Estimated number of minutes for ambulance transport to the receiving hospital.

8 Central East Prehospital Care Program For reference onlyTr

aum

a C

ardi

ac A

rres

t Indications

Trauma Cardiac Arrest

Cardiac arrest secondary to severe blunt or penetrating trauma.

If Shockable Defibrillate once

Protect C-spineBegin chest compressions

Attach SAED padsBegin PPV with BVM

After 2 minutes perform ANALYSIS

If in PEA determine drive-time to nearest

hospital

ASYSTOLE

Less than 30 minutes drive-time to nearest ER?

16 years or older?

Continue CPRImmobilize Patient

Transport to Hospital

Continue CPRPatch to BHP for possible trauma TOR

Yes No

Yes

No

If No Shock Advised Determine Rhythm


Clinical Parameters

Not obviously dead as per BLS standard

No DNR

Interventions

Attempt to clear airway with BLS maneuvers

Indications

Foreign body airway obstruction

Cardiac arrest secondary to an airway obstruction.

Analyze once and defibrillate if the patient is in a shockable rhythm

If the obstruction cannot be removed, transport to the closest appropriate facility without delay following the first rhythm analysis.

FBA

O C

ardiac Arrest

10 Central East Prehospital Care Program For reference onlyN

eona

tal R

esus

cita

tion


Ref

eren

ced

from

:N

eona

tal R

esus

cita

tion

Text

book

6th

ed.

Am

eric

an H

eart

Asso

ciat

ion

Notes:

12 Central East Prehospital Care Program For reference onlyH

ypot

herm

ic A

rres

t

Clinical Parameters

Not obviously dead as per BLS standard

No DNR

Interventions

Indications

Hypothermia Cardiac Arrest

Cardiac arrest secondary to severe hypothermia.

Analyze once Defibrillate if the patient is in a shockable rhythm

Transport to the closest appropriate facility without delay following the first rhythm analysis.


Supraglottic A/W

Clinical Parameters

• Patient in cardiac arrest• Able to clear the airway (with suctioning etc.)• No active vomiting• No airway edema• No stridor• No caustic ingestion

IndicationsNeed for ventilatory assistance OR airway control

ANDOther airway management is inadequate OR ineffective OR unsuccessful

Supraglottic Airway

Two attempts maximum. An 'attempt' is defined as the insertion of the supraglottic airway into the mouth.







Notes:

Size Colour Patient Amt of air in cuff#3 Yellow 4-5 ft tall 45 - 60 ml #4 Red 5-6 ft tall 60 - 80 ml#5 Purple ≥ 6 ft tall 70 - 90 ml

14 Central East Prehospital Care Program For reference onlyR

OSC

Clinical Parameters

Bolus (ONLY IF CERTIFIED AND AUTHORIZED IN AUTONOMOUS IV)• Clear chest / no fluid overload

SBP < 90 mmHg

Drug Initial Dose Reassess Q Max

Notes:

Titrate oxygenation to ≥ 94%

Avoid hyperventilation and target an ETCO2 of 35-40 mmHg with continuous capnography.

Consider 12 lead ECG.

Return of Spontaneous Circulation (ROSC)

Adult Doses (≥12 years)

Pediatric Doses

Bolus IV only 10 ml/kg 250 ml 1,000 ml

IndicationsROSC after resuscitation was initiated

Drug Initital Dose Reassess Q Max Bolus IV only 10 ml/kg 100 ml 1,000 ml


Clinical Parameters ≥ 2 years old (for IV start and/or bolus)

IV Start:No fracture proximal to IV siteBolus:No signs of fluid overloadSBP < 90

Drug Initital Dose Q Repeat Max

Bolus IV/IO/CVAD 20 ml/Kg Reassess q250 ml

N/A

Notes:

PATCH to BHP for authorization to administer IV bolus to patients ≥ 2 - 12 years with suspected Diabetic Ketoacidosis (DKA).

Actual or potential need for intravenous medication or fluid therapy

2,000 ml

Drug Initital Dose Q Repeat Dose Max

Adult Doses ≥ 12 years

Pediatric Doses ≥ 2 years - 12 years, Use micro drip or Buretrol

TKVO IV/IO/CVAD 30 - 60 ml/hr

Bolus IV/IO 20 ml/Kg Reassess q100 ml

N/A 2,000 ml

TKVO IV/IO 15 ml/hr

IndicationsActual or potential need for IV medication or fluid therapy

IV and Fluid Therapy (ONLY IF CERTIFIED AND AUTHORIZED IN AUTONOMOUS IV)

IV and Fluids


Clinical Parameters

Bolus:Clear Chest

SBP < 90

Drug Initial Dose Q Repeat Dose Max

Bolus IV/IO 10 ml/KgReassess q

250 ml N/A


Bolus IV/IO 10 ml/KgReassess q

100 ml N/A

Adult Doses (≥ 18 Years)

Pediatric Doses (< 18 years)

IndicationsSTEMI and Cardiogenic Shock.

Cardiogenic Shock (ONLY IF CERTIFIED AND AUTHORIZED IN AUTONOMOUS IV)

Car

diog

enic

Sho

ck

Notes:


18 Central East Prehospital Care Program For reference onlyA

llerg

ic R

eact

ion

Clinical Parameters

Drug Initial Dose Q Repeat Max

Diphenhydramine IM/IV(IV only if certified in autonomous IV)

Notes:

Epinephrine should be the first drug administered in anaphylaxis.

The epinephrine dose may be rounded to the nearest 0.05 mg.

Diphenhydramine is commonly referred to as Benadryl® and isusually supplied in a vial with a rubber stopper.


Adult Doses ( ≥ 50 kg)

Pediatric Doses

50 mg (1 ml)> 50 Kg N/A N/A 1 dose

Epinephrine IM 0.5 mg> 50 Kg N/A N/A 1 dose

Diphenhydramine IM/IV(IV only if certified in autonomous IV)

25 mg (0.5 ml)> 25-50 Kg N/A N/A 1 dose

Epinephrine IM N/A N/A 1 dose0.01 mg/kgMax 0.5 mg

IndicationsExposure to a probable allergen and signs and/or symptoms of a moderate to severe allergic reaction (including anaphylaxis).

Moderate to SevereAllergic Reaction

Epinephrine:Use for anaphylaxis only

No allergy or sensitivity to any drug administered.


Epinephrine 1:1,000 0.01 mg/kg

Rounded to the nearest 0.05 ml


Clinical Parameters

• < 8 years old• No allergy or sensitivity to epinephrine• Heart rate less than 200 / min

Notes:

The minimum initial volume for nebulization is 2.5 ml.

Drug Dose Max Pediatric Doses

Epinephrine ≥ 1 year old 1 dose5.0 mg

(5 ml)

Epinephrine< 1 year old

> 5 kg or more1 dose2.5 mg

(2.5 ml)

Epinephrine< 1 year < 5 kg

1 dose0.5 mg(mix with 2 ml of saline to make 2.5 ml)

IndicationsSevere respiratory distress and stridor at rest and current history of URTI and barking cough or recent history of a barking cough.

Croup

Cro

up


Clinical Parameters

No allergy or sensitivity to any drug administered.

Drug Initital Dose Q Repeat Max

Salbutamol Nebulized ≥ 25 kg

Notes:

Epinephrine should be the first drug administered if the patient is apneic. Salbutamol MDI may be administered subsequently using a BVM MDI adapter (if available).Nebulization is contraindicated in patients with a known or suspected fever or in the setting of a declared febrile respiratory illness outbreak by the local medical officer of health.When administering salbutamol MDI, the rate of administration should be 100 mcg approximately every 4 breaths.A spacer should be used when administering salbutamol MDI (if available).


Adult Doses

Pediatric Doses

Salbutamol MDI ≥ 25 kg 800 mcg 5-15 min 800 mcg

5 mg 5-15 min 5 mg 3 doses

3 doses

Epinephrine IM ≥ 50 kg 0.5 mg N/A N/A 1 dose

Salbutamol Nebulized < 25 kg

Salbutamol MDI < 25 kg 600 mcg 5-15 min 600 mcg

2.5 mg 5-15 min 2.5 mg 3 doses

3 doses

Epinephrine IM < 50 kg N/A 1 dose

IndicationsRespiratory distress and suspected bronchoconstriction.

Bronchoconstriction

0.01 mg/kgMax 0.5 mg

Epinephrine:• BVM ventilation is required• Must have a history of asthma

Bronchoconstriction

22 Central East Prehospital Care Program For reference onlyC

PAP

Clinical Parameters

• ≥ 18 years old• Able to sit upright and cooperate• Respiratory rate ≥ 28 / minute• SpO2 < 90% OR accessory muscle use• SBP ≥ 100, discontinue if BP falls to < 90 after initiation

• Not asthma exacerbation• Not suspected pneumothorax• No major trauma or burns to the head or torso• No Tracheostomy

Start at Increase by Q Max

Notes:

Confirm CPAP by manometer if available

Adult Doses ≥ 18 years

5 cmH20or

15 lpm if Boussignac

2.5 cmH20or

5 lpm if Boussignac5 mins

15 cmH20or

25 lpm if Boussignac

IndicationsSevere respiratory distress AND;

Signs and/or symptoms of acute pulmonary edema OR COPD

CPAP

If device has adjustable FiO2, begin at lower setting and increase to max if SpO2 remains < 92% despite treatment and/or 10 cmH2O (20 lpm if Boussignac).


Acute Pulm

onary Edema

Clinical Parameters Vital Sign Parameters

No allergy or sensitivity

No phosphodiesterase inhibitors* in past 48 hrs

If BP < 140 mmHg then must have prior nitroglycerine use, or IV initiated

HR: 60 - 159SBP ≥ 100SBP drops no more than 1/3 of initial value


Nitroglycerine BP 100 - 140 0.4 mg S/L 5 min 0.4 mg 6 doses

Adult Dose ≥ 18 years only

Notes:

Perform 12 / 15 lead

Nitroglycerine BP ≥ 140

NO History or IV

0.4 mg S/L 5 min 0.4 mg 6 doses

NitroglycerineBP ≥ 140

WITH History or IV

0.8 mg S/L 5 min 0.8 mg 6 doses

IndicationsModerate to severe respiratory distress from suspected acute cardiogenic pulmonary edema

Acute Cardiogenic Pulmonary Edema

* Phosphodiesterase inhibitors:- Sidenafil: Viagra, Revatio (for pulmonary hypertension)- Tadalafil: Cialis, Adcirca (for pulmonary hypertension)- Vardenafil: Levitra, Staxyn


Clinical Parameters

ASA:Able to chew and swallowPrior use of ASA if asthmaticNo allergy to ASA or NSAIDsNo Current, active bleedNo CVA / TBI in past 24 hrs

No allergies or sensitivity to given drug ≥18 years oldUnaltered LOA


Nitroglycerine 0.4 mg S/L 5 min 0.4 mg 6 doses

Adult Dose ≥ 18 years only

Notes:

Perform 12 / 15 lead

ASA 160 mg PO N/A N/A 160 mg

IndicationsSuspected Cardiac Ischemia

Cardiac Ischemia Medical Directive

Nitroglycerine:Prior nitroglycerine use or IV initiatedHR 60 - 159SBP ≥100. D/C if BP drops more than 1/3 of initialNo phosphodiesterase inhibitor* in past 48 hrsNo right ventricular MI

* Phosphodiesterase inhibitors:- Sidenafil: Viagra, Revatio (for pulmonary hypertension)- Tadalafil: Cialis, Adcirca (for pulmonary hypertension)- Vardenafil: Levitra, Staxyn

Car

diac

Isch

emia


Notes:

A 15 lead ECG should be obtained;• When a 12 lead shows an inferior wall MI• When there is ST depression in V1-V4• When the 12 lead is normal but the patient is

exhibiting signs or symptoms of cardiac ischemia

V4R• The V4R lead is obtained by moving V4 to the same location but on the right

chest wall. (5th intercostal space, mid clavicular line).• V4R is considered anatomically contigous with II, III and AVF• ST elevation in V4R indicates an infarct of the right ventricle.

V8 and V9• The V8 lead is obtained by moving V5 around to the posterior, left chest wall

and placing it on the mid-scapular line just below the scapula.• The V9 lead is obtained by moving V6 around to the back and placing it

between V5 and the vertebral column.• ST elevation in V8 and V9 indicates an infarct in the posterior wall of the left

ventricle.• Infarcts in the posterior wall often show up as ST depression in leads V1-V4

Lateral Left

Lateral Left

Lateral LeftInferior Left

Inferior Left Inferior Left

Lateral Left Septal

Anterior Left

Anterior LeftSeptal

12 lead versus anatomical region

26 Central East Prehospital Care Program For reference onlyST

EMI P

olic

y

Bypass the closest Emergency Departmemt and transport the patient to one of the Cardiac Catheterization labs (PCI lab) listed below.Also call and activate ‘Code STEMI”:

Southlake - call 905-895-4521 ext. 7777Centenary - call 416-287-8364Peterborough - call 705-876-5067 (directly or via CACC) and also patch to the ER

Tell them:- your EMS service- ETA- age, gender and initials- treatment provided including advanced airway, defibrillation, pacing and/or dopamine

* Where possible, initiate the IV access in the left arm*

IndicationsPatient who is experiencing continuous cardiac ischemic "chest pain" with a STEMI positive ECG

STEMI Bypass Policy

Clinical Parameters • ≥18 yrs

• Unaltered LOA• SBP≥ 80 mmHg (with intervention if required)• Secured airway, and able to ventilate• Current episode is < 12 hours in duration (when pain became constant)• 12 or 15 lead indicative of ST elevation MI;• ≥ 1 mm in two or more anatomically contiguous limb leads• ≥ 2 mm in two or more anatomically contiguous precordial leads• NO LBBB, ventricular paced rhythms, left ventricular hypertrophy or

pericarditis is present• No advanced directives indicating a restriction in care

Time Parameter The patient can be transported to the PCI Centre in ≤ 60 mins from initial contact


COMMON COMMON IMITATORS OF MIIMITATORS OF MI ’S’S IINTERPRETING NTERPRETING STST SEGMENT SEGMENT Δ’Δ’S IS NOT POSSIBLE INS IS NOT POSSIBLE IN THE FOLLOWING RYTHYMTHE FOLLOWING RYTHYMSS ((NOT A NOT A

COMPLETE LIST COMPLETE LIST –– OTHER IMITATORS EXISOTHER IMITATORS EXIS TT))

LLBBBBBB Characterised by a supraventricular rhythm (identified by the presence of P waves)

& a wide QRS complex. A LBBB will have a -ve terminal deflection in V1 and typically a secondary R wave in

V6 (seen as a notched complex seen as RsR’ below). RBBB will have a +ve terminal deflection in V1 typically with a notched complex & a

slurred or prolonged S wave in V6.

VVENTRICULAR ENTRICULAR PPACED ACED RRHYTHMHYTHM A pacer spike is typically seen immediately preceding the QRS complex which will

be wide.

LVHLVH Look at the RS complex in either V1 or V2 and count the

small boxes of the -ve deflection Then do the same with either V5 or V6, counting the small

boxes of the +ve deflection Add the two numbers together, if they equal ≥35 mm’s

then it’s likely LVH

28 Central East Prehospital Care Program For reference onlyN

ause

a / V

omiti

ng

Clinical Parameters

• Unaltered LOA• No allergies or sensitivity to dimenhydrinate or other antihistamines• Not overdosed on antihistamines, anticholinergics or tricyclic antidepressants


Dimenhydrinate IV/IM(IV only if certified in autonomous IV)

50 mg≥ 50 Kg N/A N/A 1 dose

Indications

Nausea OR Vomiting

Nausea / Vomiting

Drug Initital Dose Q Repeat Dose Max Pediatric Doses

Dimenhydrinate IV/IM (IV only if certified in autonomous IV)

25 mg≥ 25 - 50 Kg N/A N/A 1 dose

Adult Doses

Notes:

If drawing up dimenhydrinate for IV administration, dilute drug with 9 ml normal saline to a 50 mg in 10 ml solution.

Dimenhydrinate is commonly referred to as Gravol ® and usually comes supplied in a glass ampoule.


AntihistaminesActifedAstemazole (Hismanal)Azatdine (Zadine)Cetirizine (Zyrtec, Reactine) Chlorpheniramine (Chlor-Trimeton, chlortripalon) Clemastine Cyproheptadine (Periactin) DexchlorpheniramineDesloratadine (Clarinex) Dimenhydrinate (Dramamine)Diphenhydramine (Benadryl) Fexofenadine (Allegra) Hydroxyzine (Atarax, Vistaril) Loratadine (Claritin, Alavert)PhenothiazinesPromethazine (Phenergan)PiperzanesTerfenadine (Seldane)

AnticholinergicsAtropineHyoscineGlycopyrrolate (Robinul)ipratropium bromide (Atrovent)oxybutinin (Ditropan, Lyrinel XL)oxitropium bromide (Oxivent)tiotropium (Spiriva)

Tricyclic antidepressants (TCA)Amitriptyline (Elavil, Ednep, Vanatrip) Clomipramine (Anafranil)Desipramine (Norpramin), Doxepin (Sinequan, Adapin, Silenor) Nortriptyline (Aventyl, Pamelor), Protriptyline (Vivactil)Trimipramine (Surmontil)


Clinical Parameters Vital Sign Parameters

No allergy or sensitivity to given drug

Glucagon:No Pheochromocytoma

Dextrose only applies to those certified and authorized in autonomous IV

Hypoglycemia≥ 2 yrs < 4.0 mmol< 2 yrs < 3.0 mmol

Drug Initital Dose Q Repeat Max Glucagon IM ≥ 25 kg

Notes:If the patient responds to dextrose or glucagon, he/she may receive oral glucose or other simple carbohydrates.If only mild signs or symptoms are exhibited, the patient may receive oral glucose or other simple carbohydrates instead of dextrose or glucagon.If a patient initiates an informed refusal of transport, a final set of vital signs including blood glucometry must be attempted.

Hypoglycemia


Adult Doses

Pediatric Doses

Dextrose IV ≥ 50 kg 25 g 10 min 25 g

1 mg 20 min 1 mg 2 doses

2 doses

≥ 2 years to < 50 Kg Dextrose IV

D50W

1 ml/Kg0.5 g/kg

Max25 g (50 ml)

10 min 2 doses

Glucagon IM< 25 Kg

0.5 mg 20 min 0.5 mg 2 doses

IndicationsAgitation or altered LOA or seizure or symptoms of stroke

1 ml/Kg0.5 g/kg

Max25 g (50 ml)

Hyp

ogly

cem

ia


Dextrose Reference


Clinical Parameters

• ≥ 18 years old• Unaltered LOA• Probes not embedded;

Above clavicles,In the nipple(s) or in the Genital area

Indications

Electronic control device probe(s) embedded in patient

Electronic Control Device Probe Removal

Remove probes

Notes:

Police may require preservation of the probe(s) for evidentiary purposes.

This directive is for removal of ECD only and in no way constitute treat and release, normal principles of patient assessment and care apply.

ECD

Pro

be R

emov

al

Special Events DirectivesSpecial event: a preplanned gathering with potentially large numbers and the Special Event Medical Directives have been preauthorized for use by the Medical Director



Clinical Parameters


Acetaminophen PO

Notes:

Release from care.Advise patient that if the problem persists or worsens that they should seek further medical attention.

Adult Doses

325 - 650 mg N/A None 1 dose

IndicationsUncomplicated headache conforming to the patient's usual pattern.

Headache (Special Events Only)

• > 18 years old• Unaltered LOA

• No allergy or sensitivity to acetaminophen• No acetaminophen in the last 4 hours• No signs or symptoms of intoxication

Hea

dach

e


Clinical Parameters

• Unaltered LOA• No allergies or sensitivity to topical antiobiotics

Indications

Minor abrasions

Minor Abrasion (Special Events ONLY)

Notes:

Advise patient that if the problem persists or worsens that they should seek further medical attention.

Minor A

brasion


Clinical Parameters


Diphenhydramine PO

Notes:

Release from care.

Adult Doses

50 mg N/A N/A 1 dose

IndicationsSigns consistent with minor allergic reaction.

Minor Allergic Reaction (Special Events Only)

• ≥18 years old• Unaltered LOA• SBP ≥100 (and other vitals within normal limits)

• No allergy or sensitivity to diphenhydramine• No antihistamine or sedative use in the previous 4 hours• No signs or symptoms of a moderate to severe allergic reaction• No signs or symptoms of intoxication• No wheezing

Min

or A

llerg

ic R

eact

ion


Clinical Parameters


Acetaminophen PO

Notes:

Release from care.Advise patient that if the problem persists or worsens that they should seek further medical attention.

Adult Doses

325 - 650 mg N/A None 1 dose

IndicationsMinor musculoskeletal pain.

Musculoskeletal Pain (Special Events Only)

• ≥18 years old• Unaltered LOA

• No allergy or sensitivity to acetaminophen• No acetaminophen use in the last 4 hours• No signs or symptoms of intoxication

Musculoskeletal Pain

ReferenceMaterials

Stroke Prompt Card.............................! 3Rule of nines charts.............................! 4Field Trauma Triage.............................! 5ECG Basics.........................................! 6IM Injections........................................! 7End Tidal CO2.....................................! 8 - 9Overdose Levels.................................! 10Toxidromes..........................................! 11Phone Numbers..................................! 12 - 13Codes of Entry....................................! 14Pediatric References..........................! 15Medication References.......................! 16 - 32PCP Scope of Practice........................! 33ACP Scope of Practice........................! 34 - 35VSA Special Circumstances...............! 36Death Notification Tips........................! 37Blank Pages for Notes or Stickers......! 38 - 41Pounds to Kilograms Conversion Chart! 42

2

3

4

Burn Chart 'Rule of nines'

5

Field Trauma Triage Guidelines

• spinal cord injury with paraplegia or quadriplegia;

• penetrating injury to head, neck, trunk or groin;

• amputation above wrist or ankle;

• adult patients with a Glasgow Coma Scale less than or equal to 10;

• If adult GCS is greater than 10, any two of the following: (1) any alteration in level of consciousness;(2) pulse rate less than 50 or greater than 120;(3) blood pressure less than 80 systolic (or absent radial pulse); (4) respiratory rate less than 10 or greater than 24.

• Pediatric Trauma Score of less than or equal to 8;

• paramedic’s judgement that the patient requires assessment and treatment at a lead trauma centre.

6EECCGG BBAASSIICCSS

NNOORRMMAALL EECCGG PPAARRAAMMEETTEERRSS � P wave Ì Typically +ve

� QRS Complex Ì <0.12 sec

� T wave Ì May be –ve in V1

� PR Interval Ì 0.12 – 0.2 seconds

� ST Segment Ì Compared to TP

� QT Interval Ì < ½ the preceding

RR interval

RRAATTEE CCAALLCCUULLAATTIIOONN � Choose a QRS complex that falls on

the thick line and count to your right until you reach the next complex.

QQ WWAAVVEESS 11.. Pathological: Sign of MI (new or old)

�� > ¼ of accompanying R wave and/or > 0.04 sec (1 sm box)

22.. Physiological Q waves: Normal �� Less then criteria above QQRRSS NNoommeennccllaattuurree

11

22

7

Needle length:

5/8" for small infants1" for young children1.5" for school-age children and older

The insertion site is in the middle of the depicted rectangle, anterolateral aspect of the middle of the thigh.

!

!

Needle length:

1 - 1.5" for school-age children and older

Do not use this site in children < 2 years old.

Base of pictured triangle is 2 - 3 finger widths below the acromium process.

The insertion site is in the middle of the triangle.

Intra Muscular Injection Landmarking and Needle Selection

8

9

10 OOVVEERRDDOOSSEE LLEEVVEELLSS TTHHIISS��CCHHAARRTT��IISS��IINNTTEENNDDNNEEDD��OONNLLYY��AASS��AA��GGUUIIDDEE..��

NNUUMMEERROOUUSS��VVAARRIIAABBLLEESS��IINNFFLLUUEENNCCEE��TTOOXXIICC��//��LLEETTHHAALL��LLEEVVEELLSS..��ASA� Adults�&�children:�

� 300�–�500�mg/kg�is�a�severe�ingestion�� >500�mg/kg�may�be�fatal�

Acetaminophen�� Adults:�� 70�–�140�mg�/kg�may�be�toxic�� 140�mg/kg�can�be�fatal�Children:�� <�5�yr’s�old�Ͳ�100�Ͳ200�mg/kg�may�be�toxic�� >200�mg/kg�may�be�fatal�

Amphetamines� � 100�mg�(40�mg�in�children)�Atropine� � 100�mg�Benadryl�(diphenhydramine)�� 20Ͳ40�mg/kg�may�be�fatal�Barbiturates� � 1�–�3�gm�Benzodiazepines� � Toxicity�ranges�from�500�–�1500�mg’s�Cocaine�(As�ē�most�sreet�drugs,�impurities,�etc�make�predicting�toxic�levels�difficult)�

� A�rock�is�usually�100�–�200�mg�� A�typical�‘line’�is�usually�20�–�30�mg�� A�spoon�is�usually�5�–�10�mg��

Codeine� � 2�–�25�mg/kg�can�cause�toxic�effects�� 500�–�1000�mg�can�be�fatal�

Demerol� � 1�gm�may�be�fatal�Digitalis�Glycosides� � Digitalis:�2�gm�may�be�fatal�

� Digitoxin:�3�mg�may�be�fatal�� Digoxin:�10�mg�may�be�fatal�

Dilantin� � 20�mg/kg�may�be�toxic�GHB�� 30�–�60�mg�may�be�toxic�Ibuprofen� Adults:�

� 6Ͳ�54�mg�may�be�toxic�Children:�� 200�–�400�mg/kg�may�be�severe�ingestion�� >400�mg/kg�may�be�fatal�

Methadone� � 50�mg�can�be�fatal�Methamphetamine� � 1�mg/kg�may�be�fatal�Morhpine� � 200�–�250�mg�ingestion�can�be�fatal�Methanol�� 30�–�240�ml�may�be�fatal�Monoamine�Oxidase�Inhbitors�(MAOI’s)�

� 2�–�3�mg/kg�is�life�threatening�� 4�–�6�mg/kg�is�typically�fatal�

Tricyclic�AntiͲdepressants�(TCA’s)�

� 20�–�35�mg/kg�may�be�severe�� 35�–�40�mg/kg�may�be�fatal�

Valium�(Diazepam)� � 1�gm�may�be�fatal�

11

TT OOXX

II DDRR

OOMM

EE// II

NNFF OO

AA

PPPP

EEAA

RRAA

NNCC

EE

HHOO

WW UU

SSEE

DD

LL OOAA

RR

RR

HHRR

BB

PP

PPUU

PPII LL

SS

EECC

GG

MMII SS

CC

EECC

SSTT AA

SSYY

(( SSTT II

MMUU

LL AANN

TT ))

Look

s lik

e pi

lls/c

andy

P

O

Alte

r �

��

��

��

Dila

ted�

Tach

y-

Arr

hyth

mia

s �

Tº, T

eeth

gr

indi

ng, I

rrat

iona

l

MMEE

TT HH

(( SSTT II

MMUU

LL AANN

TT ))

Diff

col

oure

d po

wde

r, R

ock,

C

ryst

al

Sno

rted,

IV,

smok

ed, P

O

Alte

r �

��

��

��

Pos

s di

late

d�Ta

chy-

A

rrhy

thm

ias

Trem

ors

, Pos

s C

VA

, Sei

zure

s,

�Tº

, Sw

eaty

CCOO

CCAA

II NNEE

// CC

RRAA

CCKK

(( SS

TT IIMM

UULL AA

NNTT ))

D

iff c

olou

red

pow

ders

, R

ock,

Cry

stal

Sno

rted,

IV,

smok

ed

�

��

��

��

Dila

ted�

Tach

y-

Arr

hyth

mia

s C

P, P

rone

to

MI/C

VA

, Vio

lent

HHEE

RROO

II NN

(Opi

ate

Nar

cotic

)

Ligh

t-Dar

k P

owde

rs o

r B

lack

tarr

y su

bsta

nce

Sno

rted,

IV,

smok

ed, S

C

Alte

r �

+ �

+�

�

+C

onst

A

rrhy

thm

ias

N/V

, Res

tless

, S

eizu

res,

KKEE

TT AAMM

II NNEE

(Ana

esth

etic

) C

lear

liqu

id,

Whi

te p

owde

rS

norte

d, IV

, sm

oked

, PO

�

��

��

A

rrhy

thm

ias

Sw

eaty

, �Tº

, N

ause

a

GGHH

BB

(Dep

ress

ant)

Lo

oks

like

wat

er

Dra

nk (o

ften

mix

ed þ

ETO

H)

�+

�+

�

�

Nor

m/D

ilat

Slu

gg

Irreg

ular

N

ause

a,

Sei

zure

s,

II NNHH

AALL AA

NNTT SS

Glu

e, p

aint

, pe

tro,

Aer

osol

s In

hale

d A

lter

�

�

P

oss

dila

ted�

Arr

hyth

mia

s S

lurre

d sp

eech

, D

izzy

, H

allu

cina

tions

MMAA

RRII JJ

UUAA

NNAA

Pla

nt m

ater

ial

Sm

oked

, Mix

ed

þ fo

od, T

ea

Alte

r �

�

�

N

orm

/Dila

tS

lugg

Blo

odsh

ot e

yes,

‘M

unch

ies’

AA

nn ttii cc

hh ooll ii nn

ee rrgg ii

cc (( TT

CCAA

’’ SS// BB

EENN

AADD

RRYY

LL// GG

RRAA

VVOO

LL //AA

NNTT II

HHII SS

TT ))

Pill

s P

O, S

C,

A

lter

�

Ø¨

��

��

Dila

ted

N

, War

m, W

et,

Pos

sibl

e se

izur

es

12

Phone Numbers

!

13

Phone Numbers

!

NOTES:

14

Age Respiratory Rate Heart Rate

0-3 months 30-60 90-1803-6 months 30-60 80-160

6-12 months 25-45 80-1401-3 years 20-30 75-1306 years 16-24 70-110

10 years 14-20 60-90

< 2 Year EYE OPENING > 2 Year< 2 Year EYE OPENING > 2 Year< 2 Year EYE OPENING > 2 YearSpontaneous 4 Spontaneous

To Speech 3 To SpeechTo Pain 2 To PainNone 1 None

BEST RESPONSE TOAUDITORY / VISUAL

STIMULUS (0-2 years)

BEST RESPONSE TOAUDITORY / VISUAL

STIMULUS (0-2 years)

BEST VERBAL RESPONSE (2-5 Years)

BEST VERBAL RESPONSE (2-5 Years)

Orients to sounds, follows objects, smiles, coos, babbles 55 Oriented, appropriate words

Cries appropriately; when upset 44 Confused, inappropriate words

Inappropriate, persistent cry / Scream 33 Inappropriate, persistent cry /

screamAgitated / restless; grunts,

Moans 22 Incomprehensible sounds;grunts

No Response 11 No Response

< 2 Year BEST MOTOR RESPONSE > 2 Year< 2 Year BEST MOTOR RESPONSE > 2 Year< 2 Year BEST MOTOR RESPONSE > 2 Year

Spontaneous movements 6 Spontaneous movements

Localizes pain 5 Localizes pain

Withdraws from pain 4 Withdraws from pain

Abnormal flexion (decorticate) 3 Abnormal flexion (decorticate)

Abnormal extension (decerebrate) 2 Abnormal extension (decerebrate)

No response 1 No response

15Pediatric Reference

ACETAMINOPHEN

CLASSCLASSCLASSAnalgesicAnalgesicAnalgesic

ACTIONACTIONACTIONAlthough not fully elucidated, believed to inhibit the synthesis of prostaglandins in the central nervous system and work peripherally to block pain impulse generation; produces antipyresis from inhibition of hypothalamic heat-regulating center.

Although not fully elucidated, believed to inhibit the synthesis of prostaglandins in the central nervous system and work peripherally to block pain impulse generation; produces antipyresis from inhibition of hypothalamic heat-regulating center.

Although not fully elucidated, believed to inhibit the synthesis of prostaglandins in the central nervous system and work peripherally to block pain impulse generation; produces antipyresis from inhibition of hypothalamic heat-regulating center.

ONSET HALF-LIFE ELIMINATION

PEAK EFFECT

< 1 hour 2 hours (adults) 10-60 minutesMETABOLISMMETABOLISMMETABOLISM

At normal therapeutic dosages, primarily hepatic metabolism to sulfate and glucuronide conjugates, while a small amount is metabolized by CYP2E1 to a highly reactive intermediate, N-acetyl-p-benzoquinone imine (NAPQI), which is conjugated rapidly with glutathione and inactivated to nontoxic cysteine and mercapturic acid conjugates. At toxic doses (as little as 4 g daily) glutathione conjugation becomes insufficient to meet the metabolic demand causing an increase in NAPQI concentrations, which may cause hepatic cell necrosis. Oral administration is subject to first pass metabolism.



16

ADENOSINE

CLASSCLASSCLASSAntiarrhythmicAntiarrhythmicAntiarrhythmic

ACTIONACTIONACTIONSlows conduction time through the AV node, interrupting the re-entry pathways through the AV node, restoring normal sinus rhythm. Adenosine also causes coronary vasodilation and increases blood flow in normal coronary arteries with little to no increase in stenotic coronary arteries; thallium-201 uptake into the stenotic coronary arteries will be less than that of normal coronary arteries revealing areas of insufficient blood flow.

Slows conduction time through the AV node, interrupting the re-entry pathways through the AV node, restoring normal sinus rhythm. Adenosine also causes coronary vasodilation and increases blood flow in normal coronary arteries with little to no increase in stenotic coronary arteries; thallium-201 uptake into the stenotic coronary arteries will be less than that of normal coronary arteries revealing areas of insufficient blood flow.

Slows conduction time through the AV node, interrupting the re-entry pathways through the AV node, restoring normal sinus rhythm. Adenosine also causes coronary vasodilation and increases blood flow in normal coronary arteries with little to no increase in stenotic coronary arteries; thallium-201 uptake into the stenotic coronary arteries will be less than that of normal coronary arteries revealing areas of insufficient blood flow.


DURATION

Rapid < 10 seconds Very briefMETABOLISMMETABOLISMMETABOLISM

Blood and tissue to inosine then to adenosine monophosphate (AMP) and hypoxanthineBlood and tissue to inosine then to adenosine monophosphate (AMP) and hypoxanthineBlood and tissue to inosine then to adenosine monophosphate (AMP) and hypoxanthine

17

ASPIRIN (ACETYLSALICYLIC ACID)

CLASSCLASSCLASSPlatelet aggregation inhibitor, analgesic, antipyretic and anti-inflammatory.Platelet aggregation inhibitor, analgesic, antipyretic and anti-inflammatory.Platelet aggregation inhibitor, analgesic, antipyretic and anti-inflammatory.

ACTIONACTIONACTIONDecreases clotting by inactivating cycloxygenase, interfering with Thromboxane A2 production within the platelets. Thromboxane A2 also causes arteries to constrict. Reduces morbidity/mortality in adult patients with CP from MI.

Decreases clotting by inactivating cycloxygenase, interfering with Thromboxane A2 production within the platelets. Thromboxane A2 also causes arteries to constrict. Reduces morbidity/mortality in adult patients with CP from MI.

Decreases clotting by inactivating cycloxygenase, interfering with Thromboxane A2 production within the platelets. Thromboxane A2 also causes arteries to constrict. Reduces morbidity/mortality in adult patients with CP from MI.

ABSORPTION TIME TO PEAK DURATIONRapid 1-2 hours 4-6 hours

METABOLISMMETABOLISMMETABOLISMHydrolyzed to salicylate (active) by esterases in GI mucosa, red blood cells, synovial fluid, and blood; metabolism of salicylate occurs primarily by hepatic conjugation; metabolic pathways are saturable.

Hydrolyzed to salicylate (active) by esterases in GI mucosa, red blood cells, synovial fluid, and blood; metabolism of salicylate occurs primarily by hepatic conjugation; metabolic pathways are saturable.

Hydrolyzed to salicylate (active) by esterases in GI mucosa, red blood cells, synovial fluid, and blood; metabolism of salicylate occurs primarily by hepatic conjugation; metabolic pathways are saturable.COMMON NSAIDS (Not a complete list)OVER-THE-COUNTER

¬ Aspirin¬ Ibuprofen (Motrin IB, Advil,

Nuprin, Rufen)¬ Ketoprofen (Actron, Orudis KT)¬ Naproxen (Aleve)

PRESCRIPTION

¬ Ibuprofen (Motrin)¬ Indomethacin (Indocin) ¬ Tolmetin (Tolectin)¬ Ketoprofen (Orudis, Oruvail) ¬ Naproxen (Naprosyn, Anaprox)¬ Diclofenac (Voltaren, Cataflam,

Solaraze)

18

ATROPINE

CLASSCLASSParasympatholytic, anticholinergicParasympatholytic, anticholinergic

ACTIONACTIONBlocks the action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and the CNS; increases cardiac output, dries secretions. Atropine reverses the muscarinic effects of cholinergic poisoning. The primary goal in cholinergic poisonings is reversal of bronchorrhea and bronchoconstriction. Atropine has no effect on the nicotinic receptors responsible for muscle weakness, fasciculations, and paralysis.

Blocks the action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and the CNS; increases cardiac output, dries secretions. Atropine reverses the muscarinic effects of cholinergic poisoning. The primary goal in cholinergic poisonings is reversal of bronchorrhea and bronchoconstriction. Atropine has no effect on the nicotinic receptors responsible for muscle weakness, fasciculations, and paralysis.

ONSET HALF-LIFE ELIMINATIONRapid 2-3 hours

METABOLISMMETABOLISM

HepaticHepaticDISTRIBUTIONDISTRIBUTION

Widely throughout the body; crosses placenta; trace amounts enter breast milk; crosses blood-brain barrier.Widely throughout the body; crosses placenta; trace amounts enter breast milk; crosses blood-brain barrier.

19

DEXTROSE 50% IN WATER

CLASSCarbohydrate (Caloric Supplement)

ACTIONReplenishes blood glucose levels reversing hypoglycemia.

METABOLISM

Metabolized to carbon dioxide and water.

20

DIMENHYDRINATE (GRAVOL®)

CLASSCLASSCLASSAntiemetic, AntihistamineAntiemetic, AntihistamineAntiemetic, Antihistamine

ACTIONACTIONACTIONCompetes with histamine for H1-receptor sites on effector cells in the gastrointestinal tract, blood vessels, and respiratory tract; blocks chemoreceptor trigger zone, diminishes vestibular stimulation, and depresses labyrinthine function through its central anticholinergic activity.

Competes with histamine for H1-receptor sites on effector cells in the gastrointestinal tract, blood vessels, and respiratory tract; blocks chemoreceptor trigger zone, diminishes vestibular stimulation, and depresses labyrinthine function through its central anticholinergic activity.

Competes with histamine for H1-receptor sites on effector cells in the gastrointestinal tract, blood vessels, and respiratory tract; blocks chemoreceptor trigger zone, diminishes vestibular stimulation, and depresses labyrinthine function through its central anticholinergic activity.

ONSET PEAK EFFECT

DURATION

1-5 minutes (IV)15-30 minutes

(oral)

1-2 Hours 3-6 hour

21

DIPHENHYDRAMINE (BENADRYL®)

CLASSCLASSCLASSAntihistamineAntihistamineAntihistamine

ACTIONACTIONACTIONCompetes with histamine for H1-receptor sites on effector cells in the gastrointestinal tract, blood vessels, and respiratory tract; anticholinergic and sedative effects are also seen.

Competes with histamine for H1-receptor sites on effector cells in the gastrointestinal tract, blood vessels, and respiratory tract; anticholinergic and sedative effects are also seen.

Competes with histamine for H1-receptor sites on effector cells in the gastrointestinal tract, blood vessels, and respiratory tract; anticholinergic and sedative effects are also seen.

ONSET PEAK EFFECT DURATION1-5 minutes (IV)1-3 hours (oral)

1-2 hours (IV)2-4 hours (oral)

4-8 hours

HALF-LIFE ELIMINATIONHALF-LIFE ELIMINATIONHALF-LIFE ELIMINATION2-10 hours2-10 hours2-10 hours

22

DOPAMINE

CLASSCLASSCLASSSympathomimetic agentSympathomimetic agentSympathomimetic agent

ACTIONACTIONACTIONStimulates both adrenergic and dopaminergic receptors, lower doses are mainly dopaminergic stimulating and produce renal and mesenteric vasodilation, higher doses also are both dopaminergic and beta1-adrenergic stimulating and produce cardiac stimulation and renal vasodilation; large doses stimulate alpha-adrenergic receptors.

Stimulates both adrenergic and dopaminergic receptors, lower doses are mainly dopaminergic stimulating and produce renal and mesenteric vasodilation, higher doses also are both dopaminergic and beta1-adrenergic stimulating and produce cardiac stimulation and renal vasodilation; large doses stimulate alpha-adrenergic receptors.

Stimulates both adrenergic and dopaminergic receptors, lower doses are mainly dopaminergic stimulating and produce renal and mesenteric vasodilation, higher doses also are both dopaminergic and beta1-adrenergic stimulating and produce cardiac stimulation and renal vasodilation; large doses stimulate alpha-adrenergic receptors.


DURATION

5 minutes 2 minutes <10 minutesMETABOLISMMETABOLISMMETABOLISM

Renal, hepatic and plasma, 75% to inactive metabolites by monoamine oxidase and 25% to norepinephrine.Renal, hepatic and plasma, 75% to inactive metabolites by monoamine oxidase and 25% to norepinephrine.Renal, hepatic and plasma, 75% to inactive metabolites by monoamine oxidase and 25% to norepinephrine.

23

EPINEPHRINE

CLASSSympathomimetic agent

ACTIONStimulates alpha-, beta1-, and beta2-adrenergic receptors resulting in relaxation of smooth muscle of the bronchial tree, cardiac stimulation (increasing myocardial oxygen consumption), and dilation of skeletal muscle vasculature; small doses can cause vasodilation via beta2-vascular receptors; large doses may produce constriction of skeletal and vascular smooth muscle.

ONSET5-10 minutes (bronchodilation)

METABOLISM

Taken up into the adrenergic neuron and metabolized by monoamine oxidase and catechol-o-methyltransferase; circulating drug hepatically metabolized.

24

GLUCAGON

CLASSCLASSCLASSHyperglycemic agentHyperglycemic agentHyperglycemic agent

ACTIONACTIONACTIONStimulates adenylate cyclase to produce increased cyclic AMP, which promotes hepatic glycogenolysis and gluconeogenesis, causing a raise in blood glucose levels.

Stimulates adenylate cyclase to produce increased cyclic AMP, which promotes hepatic glycogenolysis and gluconeogenesis, causing a raise in blood glucose levels.

Stimulates adenylate cyclase to produce increased cyclic AMP, which promotes hepatic glycogenolysis and gluconeogenesis, causing a raise in blood glucose levels.


DURATION

30 minutes (IM) 8-18 minutes 60-90 minutes (SQ)

METABOLISMMETABOLISMMETABOLISM

Primarily hepatic, some inactivation occurring renally and I the plasma.Primarily hepatic, some inactivation occurring renally and I the plasma.Primarily hepatic, some inactivation occurring renally and I the plasma.

25

LIDOCAINE (XYLOCAINE)

CLASSCLASSClass Ib antiarrhythmicClass Ib antiarrhythmic

ACTIONACTIONSuppresses automaticity of conduction tissue, by increasing electrical stimulation threshold of ventricle, His-Purkinje system, and spontaneous depolarization of the ventricles during diastole by a direct action on the tissues; blocks both the initiation and conduction of nerve impulses by decreasing the neuronal membrane's permeability to sodium ions, which results in inhibition of depolarization with resultant blockade of conduction.

Suppresses automaticity of conduction tissue, by increasing electrical stimulation threshold of ventricle, His-Purkinje system, and spontaneous depolarization of the ventricles during diastole by a direct action on the tissues; blocks both the initiation and conduction of nerve impulses by decreasing the neuronal membrane's permeability to sodium ions, which results in inhibition of depolarization with resultant blockade of conduction.

ONSET DURATION45-90 seconds 10-20 minutes


90% Hepatic90% Hepatic

26

Xylometazoline (Baliminil)

CLASSCLASSSympathomimetic agentSympathomimetic agent

ACTIONACTIONXylometazoline nasal is a decongestant. A vasoconstrictor. The nasal formulation acts directly on the blood vessels in the nasal tissues. Constriction of the blood vessels in the nose and sinuses leads to a decrease in congestion.

Xylometazoline nasal is a decongestant. A vasoconstrictor. The nasal formulation acts directly on the blood vessels in the nasal tissues. Constriction of the blood vessels in the nose and sinuses leads to a decrease in congestion.

ONSET DURATIONRapid 10-20 minutes


90% Hepatic90% Hepatic

27

MIDAZOLAM (VERSED)

CLASSCLASSCLASSBenzodiazepine, CNS depressant, Sedative and AmnesicBenzodiazepine, CNS depressant, Sedative and AmnesicBenzodiazepine, CNS depressant, Sedative and Amnesic

ACTIONACTIONACTIONBinds to stereospecific benzodiazepine receptors on the postsynaptic GABA neuron at several sites within the central nervous system, including the limbic system, reticular formation. Enhancement of the inhibitory effect of GABA on neuronal excitability results by increased neuronal membrane permeability to chloride ions. This shift in chloride ions results in hyperpolarization (a less excitable state) and stabilization.

Binds to stereospecific benzodiazepine receptors on the postsynaptic GABA neuron at several sites within the central nervous system, including the limbic system, reticular formation. Enhancement of the inhibitory effect of GABA on neuronal excitability results by increased neuronal membrane permeability to chloride ions. This shift in chloride ions results in hyperpolarization (a less excitable state) and stabilization.

Binds to stereospecific benzodiazepine receptors on the postsynaptic GABA neuron at several sites within the central nervous system, including the limbic system, reticular formation. Enhancement of the inhibitory effect of GABA on neuronal excitability results by increased neuronal membrane permeability to chloride ions. This shift in chloride ions results in hyperpolarization (a less excitable state) and stabilization.

ONSET PEAK EFFECT DURATION15 minutes (IM)3-5 minutes (IV)4-8 minutes (IN)

0.5 – 1 hour 6 hours (IM)

18-41 minutes (IN)


Extensively hepaticExtensively hepaticExtensively hepaticHALF-LIFE ELIMINATIONHALF-LIFE ELIMINATIONHALF-LIFE ELIMINATION

2-6 hours2-6 hours2-6 hours

28

MORPHINE

CLASSCLASSCLASSOpioid analgesicOpioid analgesicOpioid analgesic

ACTIONACTIONACTIONBinds to opiate receptors in the CNS, causing inhibition of ascending pain pathways, altering the perception of and response to pain; produces generalized CNS depression.

Binds to opiate receptors in the CNS, causing inhibition of ascending pain pathways, altering the perception of and response to pain; produces generalized CNS depression.

Binds to opiate receptors in the CNS, causing inhibition of ascending pain pathways, altering the perception of and response to pain; produces generalized CNS depression.

ONSET PEAK EFFECT DURATION2-5 minutes (IV) 20 minutes (IV) 1 hour

HALF-LIFE ELIMINATIONHALF-LIFE ELIMINATIONHALF-LIFE ELIMINATION2-4 hours2-4 hours2-4 hours


HepaticHepaticHepatic

29

NALOXONE (NARCAN)

CLASSCLASSCLASSNarcotic AntagonistNarcotic AntagonistNarcotic Antagonist

ACTIONACTIONACTIONCompetitive narcotic antagonist. Displaces any narcotics bound to opiate receptor sites reversing their effects.Competitive narcotic antagonist. Displaces any narcotics bound to opiate receptor sites reversing their effects.Competitive narcotic antagonist. Displaces any narcotics bound to opiate receptor sites reversing their effects.


DURATION

2-5 minutes (IM)8-13 minutes

(IN)2 minutes (IV)

3-4 hours (neonates)

0.5-1.5 hours (adult)

30-120 minutes


Primarily hepaticPrimarily hepaticPrimarily hepaticDISTRIBUTIONDISTRIBUTIONDISTRIBUTION

Crosses placentaCrosses placentaCrosses placenta

30

NITROGLYCERIN

CLASSCLASSCoronary vasodilator, smooth muscle relaxant and an anti-anginal.Coronary vasodilator, smooth muscle relaxant and an anti-anginal.

ACTIONACTIONProduces a vasodilator effect on the peripheral veins and arteries with more prominent effects on the veins. Primarily reduces cardiac oxygen demand by decreasing preload (left ventricular end-diastolic pressure); may modestly reduce afterload; dilates coronary arteries and improves collateral flow to ischemic regions. In smooth muscle, nitric oxide activates guanylate cyclase which increases guanosine 3’5’ monophosphate (cGMP) leading to dephosphorylation of myosin light chains and smooth muscle relaxation.

Produces a vasodilator effect on the peripheral veins and arteries with more prominent effects on the veins. Primarily reduces cardiac oxygen demand by decreasing preload (left ventricular end-diastolic pressure); may modestly reduce afterload; dilates coronary arteries and improves collateral flow to ischemic regions. In smooth muscle, nitric oxide activates guanylate cyclase which increases guanosine 3’5’ monophosphate (cGMP) leading to dephosphorylation of myosin light chains and smooth muscle relaxation.

ONSET PEAK EFFECTS1-3 min.(sl sprays and sl tablet)

15-30 min. (topical)30 min.(transdermal)

5 min.(tablet)4-10 min.(sl spray)

60 min.(topical)120 min. (transdermal)

DURATIONDURATION25 min. (sl spray and sl tablet)

7 hours (topical)10-12 hours (transdermal)

25 min. (sl spray and sl tablet)7 hours (topical)

10-12 hours (transdermal)HALF-LIFEHALF-LIFE

1-4 minutes1-4 minutesMETABOLISMMETABOLISM

Extensive first-pass effect; metabolized hepatically to glycerol di- and mononitrate metabolites via liver reductase enzyme; subsequent metabolism to glycerol and organic nitrate; nonhepatic metabolism via red blood cells and vascular walls also occurs.

Extensive first-pass effect; metabolized hepatically to glycerol di- and mononitrate metabolites via liver reductase enzyme; subsequent metabolism to glycerol and organic nitrate; nonhepatic metabolism via red blood cells and vascular walls also occurs.

31

SALBUTAMOL (VENTOLIN)

CLASSCLASSCLASSSympathomimetic, Beta 2 agonistSympathomimetic, Beta 2 agonistSympathomimetic, Beta 2 agonist

ACTIONACTIONACTIONRelaxes bronchial smooth muscle by action on beta2-receptors with little effect on heart rate.Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on heart rate.Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on heart rate.


DURATION

10 minutes (nebulized/oral

inhalation)

3-8 hours (inhalation)

3-4 hours (nebulized/oral

inhalation)METABOLISMMETABOLISMMETABOLISM

Hepatic to an inactive sulfateHepatic to an inactive sulfateHepatic to an inactive sulfate

32

PCP Scope of PracticePerform the following skills:

Ø Semi-Automated External DefibrillationØ Manual defibrillation (when working with an ACP who has indicated that a shock

and its energy setting is to be delivered)Ø Intravenous monitoringØ Intravenous Access/Therapy for patients ≥ 2 years of age (if certified / authorized

in autonomous IV)Ø Volume (crystalloid) Replacement Therapy for patients ≥ 2 years of age (if

certified / authorized in autonomous IV)Ø Basic Airway managementØ Advanced Airway management with the King LTØ Oro-pharyngeal SuctioningØ Current CPR standards for Health-Care Providers Ø 3 lead monitoring and interpretationØ 12 and 15 lead acquisition and interpretationØ Administration of CPAPØ Preparation of ACP pre-loaded medicationsØ Assessments and Interpretation of findings ie chest sounds & txØ Capillary Blood Sampling & glucometer useØ Utilization/interpretation of SpO2

Administer the following medications:

Ø ASA (PO)Ø Dextrose: 50% solution (IV) (if certified / authorized in autonomous IV)Ø Dimenhydrinate (IV/IM) (IV only if certified / authorized in autonomous IV)Ø Diphenhydramine (IV/IM) (IV only if certified / authorized in autonomous IV)Ø Epinephrine 1:1000 (IM/Inhalation) Ø Glucagon (IM)Ø Nitroglycerin spray (SL)Ø Salbutamol MDI and nebulization (Inhalation)

By the following routes:

Ø Oral (PO)Ø Sublingual (SL)Ø Inhalation (nebulized or MDI)Ø Intramuscular (IM)Ø Intravenous (IV) (if certified / authorized in autonomous IV)

!

33

ACP Scope of PracticePerform the following skills:

Ø Manual DefibrillationØ Synchronized CardioversionØ Transcutaneous PacingØ Intravenous Access/TherapyØ Intraosseous Access/TherapyØ Volume (crystalloid) Replacement TherapyØ Advanced Airway management with the King LTØ Oral Endotracheal IntubationØ Nasal Tracheal IntubationØ Difficult Airway with lighted stylet / BougieØ Laryngoscopy Ø ETT (Deep) SuctioningØ FBAO Removal (Magill Forceps)Ø Needle Chest DecompressionØ 3 lead monitoring and interpretationØ 12 and 15 lead acquisition and interpretationØ Assessments and Interpretation of findings ie chest sounds & txØ Venous and Capillary Blood Sampling & glucometer useØ Utilization/interpretation of SpO2 and Endtidal CO2 monitoringØ Application of Continuous Positive Airway Pressure (CPAP)

Administer the following medications:Ø Atropine (IV/ETT)Ø ASA (PO)Ø Dextrose: 50%, 25% or 10% solutions (IV/IO)Ø Dimenhydrinate (IV/IM)Ø Diphenhydramine (IV/IM)Ø Dopamine (IV drip)Ø Epinephrine 1:1000 (IV/IM/IO/ETT/Inhalation) Ø Epinephrine 1:10,000 (IV/ETT)Ø Glucagon (IM)Ø Lidocaine injectable (IV/ETT) Ø Lidocaine topical (Inhalation)Ø Midazolam (IV/IM/IN/Buccal)Ø Morphine (IV)Ø Naloxone (IV/IM/IN/SC)Ø Nitroglycerin spray (SL)Ø Xylometazoline (Inhalation)Ø Salbutamol MDI (Inhalation)

!

34

By the following routes:Ø Intravenous (IV)Ø Endotracheal (ETT)Ø Oral (PO)Ø Sublingual (SL)Ø Subcutaneous (SC)Ø Buccal (BU)Ø Inhalation (nebulized or MDI)Ø Intraosseous (IO)Ø Intramuscular (IM)Ø Intranasal (IN)Ø Topical

35

Vital Signs Absent Patient

Here are some guidelines to help with the determination of the recognition of death and/or the termination of resuscitation when presented with a VSA:

1. Patient presenting as “Obviously Dead” a. Decapitation, transection, visible decomposition, putrefaction;

orb. Absence of vital signs and:

• A grossly charred body; or• An open head or torso wounds with gross outpouring of

cranial or visceral contents; or• Gross rigor mortis; or• Lividity

2. Patient without vital signs and the subject of a Ministry of Health and Long-Term Care Do Not Resuscitate Confirmation Form. Consider honoring the DNR Confirmation Form.

3. Patient without vital signs and the subject of a “legal looking’ document or the old DNR Medical Directive and Funeral Home Transfer Form, consider calling the BHP to receive termination of resuscitation order.

4. Patient without vital signs and the subject of the possible application of the TOR Medical Directive (Medical or Trauma). Consider calling the BHP for termination of resuscitation order. In the event that a physician on scene is willing to assume care and responsibility of the patient, provide assistance as possible within your scope of practice.

*Paramedics must carefully consider matters such as scene integrity, investigative issues, family concerns and disposition of body.

36

Death Notification Tips:

• Survivors are victims

• Non-verbal communication is important

o Eye contact without staring

o Same level as survivor

• Be aware of your appearance (take off PPE)

• Use a ‘D’ word such as ‘dead’ or has ‘died’

• Pauses and silence are okay!

• Avoid clichés

• Never try to talk the survivors out of their grief

• Be compassionate

• Be careful not to impose our personal religious beliefs

• Empower the survivors to take on their own grief and pain

o Give as much information as possible

o Listen to them and answer questions as best you can

37

Notes or stickers:

38

Notes or stickers:

39

Notes or stickers:

40

Notes or stickers:

41

42

Lbs Kg Lbs Kg10 5 125 5715 7 130 5920 9 135 6125 11 140 6430 14 145 6635 16 150 6840 18 155 7045 20 160 7350 23 165 7555 25 170 7760 27 175 7965 29 180 8270 32 185 8475 34 190 8680 36 195 8885 39 200 9190 41 205 9395 43 210 95

100 45 215 98105 48 220 100110 50 225 102115 52 230 104120 54 235 107

Pounds to Kilogram Conversion Chart

Documents

Pocket Reference Guide 2011 - Lakeridge Health · This pocket reference guide is to be used for reference ... Jaun Bothma Deepinder Brar Brenda Burns ... No signs of ﬂuid overload