Download - ACLS Module

Overview of ACLS Overview of ACLS PharmacologyPharmacology

and and Update on New ACLS Update on New ACLS

GuidelinesGuidelines

Krista Piekos, Pharm.D.Krista Piekos, Pharm.D.

Clinical Pharmacy Specialist - Critical CareClinical Pharmacy Specialist - Critical Care

Harper University Hospital Harper University Hospital

Adjunct Assistant ProfessorAdjunct Assistant Professor

Wayne State UniversityWayne State University

ObjectivesObjectives• Pharmacists should be able to identify: Pharmacists should be able to identify:

Why?Why? …we use an agent…we use an agent

When?When? …to use an agent…to use an agent

How?How? …to use an agent…to use an agent

What?What? ...to watch for ...to watch for • To familiarize the pharmacist with the ACLS To familiarize the pharmacist with the ACLS

algorithmsalgorithms• To help the pharmacist become To help the pharmacist become

comfortable with the crash cartcomfortable with the crash cart• To introduce the needless delivery systemTo introduce the needless delivery system

OutlineOutline

• Present conclusions of the International Present conclusions of the International Guidelines 2000 ACLS objectives with Guidelines 2000 ACLS objectives with 2003 updates2003 updates

• Classification of recommendationsClassification of recommendations• ACLS AlgorithmsACLS Algorithms• Pharmacology of agents used in Pharmacology of agents used in

algorithmsalgorithms• Overview of crash cart revisionsOverview of crash cart revisions• Overview of needless systemOverview of needless system

BackgroundBackground• In Seattle 43% of patients in VF survived In Seattle 43% of patients in VF survived

to hospital discharge if CPR w/in 4 min to hospital discharge if CPR w/in 4 min and defibrillation w/in 8 minand defibrillation w/in 8 min

• These figures are higher than national These figures are higher than national average - due to AED’s throughout publicaverage - due to AED’s throughout public

• Overall survival from CPR is poor 5-15%Overall survival from CPR is poor 5-15%• Survival for in-patient CPR to discharge Survival for in-patient CPR to discharge

is <10%is <10%

Guidelines 2000 for Guidelines 2000 for Cardiopulmonary Cardiopulmonary Resuscitation and Resuscitation and

Emergency Cardiovascular Emergency Cardiovascular CareCare

• 1st international consensus on 1st international consensus on resuscitation guidelinesresuscitation guidelines

• Experts from around the worldExperts from around the world• Identified issuesIdentified issues• Gathered scientific evidence; level (quality) of Gathered scientific evidence; level (quality) of

evidenceevidence• Integrate into a class of recommendationIntegrate into a class of recommendation

• Revised guidelinesRevised guidelines

Classification of Classification of Therapeutic InterventionsTherapeutic Interventions

Class I:Class I: definitely helpful, excellent definitely helpful, excellent Class II:Class II:

Class II a -probably helpful; Class II a -probably helpful; good to very good to very

goodgoodClass II b -possibly helpful; Class II b -possibly helpful;

fair fair to goodto good• Class Indeterminate:Class Indeterminate: insufficient insufficient

evidence; no harm, but no benefitevidence; no harm, but no benefit Class III:Class III: possibly harmful possibly harmful

New GoalsNew Goals

1.1.Early Defibrillation - Public Access Defibrillation (PAD)Early Defibrillation - Public Access Defibrillation (PAD)Probability of successful defibrillation and survival is negatively Probability of successful defibrillation and survival is negatively related to the time from onset of VF to delivery of first shockrelated to the time from onset of VF to delivery of first shock

““PAD has the potential to be the single greatest advance in the PAD has the potential to be the single greatest advance in the treatment of prehospital sudden cardiac death since the invention treatment of prehospital sudden cardiac death since the invention of CPR” of CPR” Circulation August 22, 2000Circulation August 22, 2000

2.2.Establishing a specific diagnosis by ECGEstablishing a specific diagnosis by ECG

3.3. Antiarrhythmic agents are just as likely to be Antiarrhythmic agents are just as likely to be proarrhythmic as they are antiarrhythmic.proarrhythmic as they are antiarrhythmic.

One, and only one antiarrhythmic should be used.One, and only one antiarrhythmic should be used.

Routes of Routes of AdministrationAdministration

IntravenousIntravenous• Preferred routePreferred route

Endotracheal Endotracheal · 2-2.5 X’s IV dose in 10ml volume2-2.5 X’s IV dose in 10ml volume· Each dose is followed by 10 ml NS flush down the ET tubeEach dose is followed by 10 ml NS flush down the ET tube· (Ex. epinephrine, atropine, lidocaine, diazepam, naloxone) (Ex. epinephrine, atropine, lidocaine, diazepam, naloxone) · Absorption occurs at alveolar capillary interfaceAbsorption occurs at alveolar capillary interface

Intraosseous (active bone marrow)Intraosseous (active bone marrow)· Pediatric patients without IV accessPediatric patients without IV access

Other: Sublingual, intracardiac, IM, SC (poor Other: Sublingual, intracardiac, IM, SC (poor absorption)absorption)

ACLS ACLS Algorithm Algorithm ApproachApproach

Universal AlgorithmUniversal Algorithm

EpinephrineEpinephrine

WHY?WHY? • Natural catecholamine with Natural catecholamine with and ß-adrenergic agonist and ß-adrenergic agonist

activityactivity• Results in: Results in:

flow to heart and brainflow to heart and brain SVR, SBP, DBPSVR, SBP, DBP electrical activity in the myocardium & automaticity (electrical activity in the myocardium & automaticity (

success with defibrillation)success with defibrillation)

• myocardial contraction (for refractory circulatory shock myocardial contraction (for refractory circulatory shock (CABG))(CABG))

increases myocardial oxygen requirementsincreases myocardial oxygen requirements

• Primary benefit: Primary benefit: -vasoconstriction-vasoconstriction• ß-adrenergic activity controversial b/c ß-adrenergic activity controversial b/c myocardial work myocardial work

WHEN?WHEN?• VF/VT, asystole, PEA, bradycardiasVF/VT, asystole, PEA, bradycardias

EpinephrineEpinephrine

HOW?HOW?• High dose versus standard dose?High dose versus standard dose?• Higher ROSC with high dose, but no change in survivalHigher ROSC with high dose, but no change in survival• High doses may exacerbate postresuscitation myocardial High doses may exacerbate postresuscitation myocardial

dysfunctiondysfunction

Recommendations:Recommendations:• Class I: 1 mg IV q 3 - 5 minClass I: 1 mg IV q 3 - 5 min• Class IIb: 2-5mg IVP q3-5min, or 1mg-3mg-5mg Class IIb: 2-5mg IVP q3-5min, or 1mg-3mg-5mg • Class Indeterminate: high-dose 0.1mg/kg IVP q3-5minClass Indeterminate: high-dose 0.1mg/kg IVP q3-5min• Infusion for Infusion for HR & HR & BP (IIb)BP (IIb)

• 1mg in 250ml NS or D5W - infuse @ 1-10 mcg/min1mg in 250ml NS or D5W - infuse @ 1-10 mcg/min

• ET Dose=2-2.5 times IV doseET Dose=2-2.5 times IV dose

What to watch for?What to watch for?• Tachycardia, hypertension, myocardial ischemia, acidosisTachycardia, hypertension, myocardial ischemia, acidosis

Incompatible with Ca, HCO3, aminophylline & PHY. Alkaline solutions cause auto-Incompatible with Ca, HCO3, aminophylline & PHY. Alkaline solutions cause auto-oxidation.oxidation.

VasopressinVasopressinWHEN?WHEN?

• Alternative to epinephrine for shock-refractory VT/VFAlternative to epinephrine for shock-refractory VT/VF

WHY?WHY?• Natural antidiuretic hormone Natural antidiuretic hormone

• Potent vasoconstrictor by stimulation of SM -VPotent vasoconstrictor by stimulation of SM -V11 receptors : receptors : BP & SVR; BP & SVR; CO, HR, myocardial O2 consumption and CO, HR, myocardial O2 consumption and

contractilitycontractility

• Does not Does not myocardial oxygen consumption myocardial oxygen consumption• Not affected by severe acidosisNot affected by severe acidosis• Class IIb for shock-refractory VFClass IIb for shock-refractory VF• Class Indeterminate for PEA, asystoleClass Indeterminate for PEA, asystole• Half life = 10-20 minutesHalf life = 10-20 minutes

Dose?Dose?• 40 Units IVP - one time only!!!40 Units IVP - one time only!!!

Why Vasopressin?Why Vasopressin? During CPR, plasma ADH levels are higher in patients During CPR, plasma ADH levels are higher in patients

with return of spontaneous circulation (ROSC)with return of spontaneous circulation (ROSC) During CPR patients may be severely acidoticDuring CPR patients may be severely acidotic Epinephrine compared to vasopressin pre-hospital CPR Epinephrine compared to vasopressin pre-hospital CPR

(20 patients/study group)(20 patients/study group) Multiple animal studies showing Multiple animal studies showing ROSC ROSC

EPI EPI (n=20)(n=20) VP VP (n=20)(n=20)

Survival to hospitalSurvival to hospital 35%35% 70% (p=0.06) 70% (p=0.06)

24 hour survival 24 hour survival 20%20% 60% (p=0.02) 60% (p=0.02)

Discharge alive Discharge alive 15% 40% 15% 40% (p=0.16)(p=0.16)

ILCOR Universal AlgorithmILCOR Universal Algorithm(International Liaison Committee on Resuscitation)(International Liaison Committee on Resuscitation)

Medication changes in 2000:Medication changes in 2000:• Emphasis on identification of all possible Emphasis on identification of all possible

stroke victims for IV fibrinolyticsstroke victims for IV fibrinolytics• Epinephrine has become Class IndeterminateEpinephrine has become Class Indeterminate• High-dose epinephrine no longer High-dose epinephrine no longer

recommendedrecommended• For shock-refractory VT/VF: Epinephrine 1 mg q 3-For shock-refractory VT/VF: Epinephrine 1 mg q 3-

5 min5 min

• Vasopressin 40 Units IVP one timeVasopressin 40 Units IVP one time • Epinephrine alone for non-VT/VFEpinephrine alone for non-VT/VF

Pulseless Ventricular Pulseless Ventricular Fibrillation Fibrillation

or Tachycardiaor Tachycardia

• In ACLS, always assume VF - most common In ACLS, always assume VF - most common • 85%-95% of survivors have VF85%-95% of survivors have VF• Survival dependant on early defibrillationSurvival dependant on early defibrillation• Medications indicated only after 3 failed shocksMedications indicated only after 3 failed shocks

VFib/Pulseless VT AlgorithmVFib/Pulseless VT Algorithm

““PPlease lease SShock-hock-SShock-hock-SShock, hock, EVEVerybody erybody SShock, hock, AAnd nd LLet's et's MMake ake PPatients atients BBetter” etter”

PPlease -lease - Precordial ThumpPrecordial Thump If pulse-less with no defibrillator If pulse-less with no defibrillator

SShock hock 200J*200J*

SShock hock 200-300J*200-300J*

SShock hock 360J* 360J* (*only consecutive, if persistent)(*only consecutive, if persistent)

EVEVerybody - erybody - Epinephrine Epinephrine 1 mg IV q3-5 min or 1 mg IV q3-5 min or VasopressinVasopressin 40 U IVP40 U IVP

If VF/PVT persists, "CONSIDER" antiarrhythmics and sodium bicarb. NOTE: always "max If VF/PVT persists, "CONSIDER" antiarrhythmics and sodium bicarb. NOTE: always "max out" one agent before proceeding to the next in order to limit pro-arrhythmic drug-drug out" one agent before proceeding to the next in order to limit pro-arrhythmic drug-drug interactionsinteractions

SShock hock 360J360J

AAnd - nd - AmiodaroneAmiodarone (First Choice) 300mg IV push. May repeat once at (First Choice) 300mg IV push. May repeat once at 150mg in 3-5 min. (max. cumulative dose: 2.2g IV/24hrs)150mg in 3-5 min. (max. cumulative dose: 2.2g IV/24hrs)

Drug-shock-drug-shock sequenceDrug-shock-drug-shock sequence (continued) (continued)

““PPlease lease SShock-hock-SShock-hock-SShock, hock, EVEVerybody erybody SShock, hock, AAnd nd LLet's et's MMake ake PPatients atients BBetter” etter”

LLet's - et's - LidocaineLidocaine 1.0-1.5 mg/kg IV. May repeat in 3-5 min (max=3 1.0-1.5 mg/kg IV. May repeat in 3-5 min (max=3 mg/kg)mg/kg)

MMakeake - - Magnesium SulfateMagnesium Sulfate 1-2 g slow IVP for suspected 1-2 g slow IVP for suspected Mg or TdP Mg or TdP

PPatientsatients- Procainamide- Procainamide 30 mg/min, or 100 mg IV q 5 min. for 30 mg/min, or 100 mg IV q 5 min. for refractory VF. (max. dose: 17 mg/kg)refractory VF. (max. dose: 17 mg/kg)NOTE: Besides having a pro-arrhythmic drug-drug interaction with amiodarone, procainamide is NOTE: Besides having a pro-arrhythmic drug-drug interaction with amiodarone, procainamide is

of limited value in an arrest situation due to a lengthy administration timeof limited value in an arrest situation due to a lengthy administration time

BBetter (consider buffers) - etter (consider buffers) - Bicarbonate Bicarbonate 1 mEq/kg IV for:1 mEq/kg IV for:• preexisting preexisting K+ K+• bicarb-responsive acidosisbicarb-responsive acidosis• some drug overdosessome drug overdoses• protracted code (intubated)protracted code (intubated)• ROSC after long code with effective ventilation.ROSC after long code with effective ventilation.

Drugs for VF/PVTDrugs for VF/PVT

• Epinephrine - Why? How? What?Epinephrine - Why? How? What?• Vasopressin - Why? How? What?Vasopressin - Why? How? What?• AmiodaroneAmiodarone• MagnesiumMagnesium• ProcainamideProcainamide• LidocaineLidocaine• BuffersBuffers

Classification of Classification of AntiarrhythmicsAntiarrhythmics

Class Drug Conduction Velocity Refractory Period Automaticity Ion Block

Ia QuinidineProcainamideDisopyramide

Sodium

Ib LidocaineMexiletineTocainide 0/

Sodium(fast on-off)

Ic FlecainidePropafenoneMoricizine 0

Sodium(slow on-off)

II Beta-Blockers Calcium

III AmiodaroneBretyliumSotalol 0 0

Potassium

IV VerapamilDiltiazem

Calcium

Drugs Used for Heart Rhythm Drugs Used for Heart Rhythm and Rateand Rate

AmiodaroneAmiodaroneWHY?WHY?

• Class III antiarrhythmic (characteristics of all classes)Class III antiarrhythmic (characteristics of all classes)• Na, K and Ca channel blocker & Na, K and Ca channel blocker & & & -adrenergic blocker-adrenergic blocker• Prolongs AP and RPProlongs AP and RP• Decreases AV conduction velocity & SN functionDecreases AV conduction velocity & SN function

New Recommendations (WHEN?):New Recommendations (WHEN?):• pulseless VT or VF (IIb)pulseless VT or VF (IIb)• hemodynamically stable VT (IIb), polymorphic VT (IIb), hemodynamically stable VT (IIb), polymorphic VT (IIb),

wide-complex tachycardia uncertain origin (IIb)wide-complex tachycardia uncertain origin (IIb)• refractory PSVT (preserved function, IIa; impaired function refractory PSVT (preserved function, IIa; impaired function

IIb)IIb)• atrial tachycardia (IIb)atrial tachycardia (IIb)• cardioversion of AF (IIa)cardioversion of AF (IIa)

AmiodaroneAmiodarone

HOW?HOW?• Cardiac arrest (PVT/VF) - 300mg IVP diluted Cardiac arrest (PVT/VF) - 300mg IVP diluted

in 20-30ml, may repeat with 150mg in 10 in 20-30ml, may repeat with 150mg in 10 minutes, or start infusion (max=2..2 g/24h)minutes, or start infusion (max=2..2 g/24h)

• Atrial & ventricular arrhythmias in impaired Atrial & ventricular arrhythmias in impaired hearts hearts

• 150mg IVP over 10 min150mg IVP over 10 min• May repeat q10-15 min, or start gtt 1mg/min x 6 May repeat q10-15 min, or start gtt 1mg/min x 6

hours, then 0.5mg/min x 18 hhours, then 0.5mg/min x 18 h

WHAT?WHAT?• Hypotension, bradycardia (slow rate, fluids)Hypotension, bradycardia (slow rate, fluids)

Why Amiodarone?Why Amiodarone?ARREST TrialARREST Trial

Objective: Objective:

Efficacy of IV amiodarone in out-of-hospital Efficacy of IV amiodarone in out-of-hospital cardiac arrest due to ventricular fibrillation or cardiac arrest due to ventricular fibrillation or pulseless ventricular tachycardiapulseless ventricular tachycardia

Endpoints:Endpoints:

Hospital admission with perfusing rhythmHospital admission with perfusing rhythm

Survival to dischargeSurvival to discharge

Functional neurologic status at discharge Functional neurologic status at discharge *Insufficiently powered to detect survival to discharge and *Insufficiently powered to detect survival to discharge and

functional neurologic status*functional neurologic status*

ARREST Trial: Amiodarone in the ARREST Trial: Amiodarone in the Resuscitation of Refractory Resuscitation of Refractory

Sustained Ventricular Sustained Ventricular TachyarrhythmiasTachyarrhythmias

• Prospective, randomized, DB, PC trialProspective, randomized, DB, PC trial• 504 patients, who failed >/= 3 shocks504 patients, who failed >/= 3 shocks• Randomized to placebo or 300mg IV amiodarone Randomized to placebo or 300mg IV amiodarone • Amiodarone Dosing: Amiodarone Dosing:

• 300mg diluted with 5% D5W to 20mL300mg diluted with 5% D5W to 20mL• Rapid IV bolusRapid IV bolus

• Found a statistically significant increase in the Found a statistically significant increase in the number of patients who arrived to hospital alive number of patients who arrived to hospital alive ((pp=0.03)=0.03)

• Consistent results regardless of presenting rhythm Consistent results regardless of presenting rhythm This is the only antiarrhythmic agent which has shown definitive benefit in This is the only antiarrhythmic agent which has shown definitive benefit in

cardiac arrest!cardiac arrest!

ARREST Trial - Subgroup ARREST Trial - Subgroup AnalysisAnalysis

0

10

20

30

40

50

60

70

% S

urv

ivin

g t

o

Adm

issio

n

Amiodarone Placebo


Magnesium SulfateMagnesium Sulfate

WHY?WHY? Magnesium deficiency causes arrhythmiasMagnesium deficiency causes arrhythmias

Facilitates ventricular repolarization by enhancing Facilitates ventricular repolarization by enhancing intracellular potassium flux, dilates coronary intracellular potassium flux, dilates coronary arteriesarteries

WHEN?WHEN? Suspected hypomagnesemia, pulseless VT/VF, Suspected hypomagnesemia, pulseless VT/VF, torsade de pointestorsade de pointes

HOW?HOW? Class IIa in suspected hypomagnesemia, TdP, andClass IIa in suspected hypomagnesemia, TdP, andClass IIb in VF/VT: 1 - 2gm slow IVP in 100ml Class IIb in VF/VT: 1 - 2gm slow IVP in 100ml

WHAT?WHAT? Hypotension at large dosesHypotension at large doses


ProcainamideProcainamide

WHY?WHY?• Suppresses both ventricular and atrial Suppresses both ventricular and atrial

arrhythmiasarrhythmias• Type Ia antiarrhythmic, affects fast Na+channels-Type Ia antiarrhythmic, affects fast Na+channels-

slowing conduction velocity, prolongs RP, and slowing conduction velocity, prolongs RP, and decreases automaticity decreases automaticity

• Phase IV depolarizationPhase IV depolarization

WHEN?WHEN?• Refractory/recurrent VF/VTRefractory/recurrent VF/VT• Control of rapid ventricular response (IIb)Control of rapid ventricular response (IIb)• Conversion SVT (AF/Fl) (IIa)Conversion SVT (AF/Fl) (IIa)


ProcainamideProcainamide

HOW?HOW? VF:VF: 20-30 mg/min slow infusion (max=17 mg/kg) 20-30 mg/min slow infusion (max=17 mg/kg)

AF with rapid vent. response:AF with rapid vent. response: 100 mg over 5 min 100 mg over 5 min then infuse@ 1 - 4 mg/minthen infuse@ 1 - 4 mg/min

1-2 gm/250ml D5W1-2 gm/250ml D5W

WHAT?WHAT? Stop infusion if patient hypotensive, widened QRS >50%, Stop infusion if patient hypotensive, widened QRS >50%, arrhythmia suppression, or dose=17mg/kgarrhythmia suppression, or dose=17mg/kg

Dose reduction in renal failureDose reduction in renal failure

SLE syndromeSLE syndrome

Levels: Levels: PA=4-12 µg/mlPA=4-12 µg/ml

NAPA=7-15 µg/ml (active metabolite-Class NAPA=7-15 µg/ml (active metabolite-Class III)III)

Drugs Used for Heart Rhythm Drugs Used for Heart Rhythm and Rateand RateLidocaineLidocaine

WHY?WHY?• Type IB antiarrhythmicType IB antiarrhythmic• Affects fast Na+ channels, shortens refractory periodAffects fast Na+ channels, shortens refractory period• Suppresses spontaneous depolarizationSuppresses spontaneous depolarization• Local anesthetic, increases fibrillation thresholdLocal anesthetic, increases fibrillation threshold• Suppresses ventricular ectopy post-MISuppresses ventricular ectopy post-MI• Without effecting myocardial contractility, BP or AV nodal conductionWithout effecting myocardial contractility, BP or AV nodal conduction

WHEN?WHEN?• SECOND-CHOICE agentSECOND-CHOICE agent• VT/VF refractory to electrical countershock and VT/VF refractory to electrical countershock and

epinephrineepinephrine (Indeterminate)(Indeterminate)• Control of PVC’s (Indeterminate)Control of PVC’s (Indeterminate)• Hemodynamically stable VT (IIb)Hemodynamically stable VT (IIb)

• Not for routine prophylaxis post-MI, however, accepted in high-risk Not for routine prophylaxis post-MI, however, accepted in high-risk patients patients (hypokalemia, myocardial ishchemia, LV dysfunction)(hypokalemia, myocardial ishchemia, LV dysfunction)

Drugs Used for Heart Rhythm Drugs Used for Heart Rhythm and Rateand RateLidocaineLidocaine

HOW?HOW? Class IIa: 1 - 1.5 mg/kg IVP q5 - 10 min Class IIa: 1 - 1.5 mg/kg IVP q5 - 10 min (max=3mg/kg)(max=3mg/kg)

Infusion (with pulse): 1 - 4 mg/min (if pulse is Infusion (with pulse): 1 - 4 mg/min (if pulse is regained)regained)

Therapeutic Levels: 1.5-6 µg/mlTherapeutic Levels: 1.5-6 µg/mlET Dose: 2-2.5 times IV doseET Dose: 2-2.5 times IV dosePreparation: Preparation: 1-2 gm/250 ml D5W or NS1-2 gm/250 ml D5W or NS

WHAT?WHAT? Hepatic metabolism, renal eliminationHepatic metabolism, renal eliminationBradycardia, cardiac arrest, seizuresBradycardia, cardiac arrest, seizuresLidocaine toxicity/neurotoxicity - twitching, LOC, Lidocaine toxicity/neurotoxicity - twitching, LOC,

seizures, seizures, coma coma Lidocaine levels persist in low CO statesLidocaine levels persist in low CO states

Drugs Used to Improve Cardiac Output and Drugs Used to Improve Cardiac Output and Blood PressureBlood Pressure

Sodium BicarbonateWHY?WHY? Enhances sodium shift intracellularly, buffersEnhances sodium shift intracellularly, buffers acidosis, acidosis,

decreases decreases toxicity of TCA’s, increasestoxicity of TCA’s, increases clearance of acidic clearance of acidic drugsdrugs

WHEN?WHEN? Class I - hyperkalemiaClass I - hyperkalemia

Class IIa - bicarbonate-responsive acidosis metabolic Class IIa - bicarbonate-responsive acidosis metabolic acidosis secondary to loss of bicarb (renal/GI); overdoses acidosis secondary to loss of bicarb (renal/GI); overdoses (TCAs, phenobarbital, aspirin)(TCAs, phenobarbital, aspirin)

Class IIb - protracted arrest in intubated patientsClass IIb - protracted arrest in intubated patients

Class III - hypoxic lactic acidosis Class III - hypoxic lactic acidosis

HOW?HOW? 1 mEq/kg IVP, 0.5mEq/kg q10 min prn1 mEq/kg IVP, 0.5mEq/kg q10 min prn

WHAT?WHAT? May worsen outcome if not intubated/ventilated. May worsen outcome if not intubated/ventilated. Metabolic alkalosis, decreased O2 delivery to tissues, Metabolic alkalosis, decreased O2 delivery to tissues,

hypokalemia, hypokalemia, CNS acidosis, hypernatremia, hyperosmolarityCNS acidosis, hypernatremia, hyperosmolarityIncompatible with calcium, epinephrine, atropine, norepinephrine, Incompatible with calcium, epinephrine, atropine, norepinephrine,

isoproterenolisoproterenol

SummarySummaryV.Fib and Pulseless V.TachV.Fib and Pulseless V.Tach

Changes:Changes:• Vasopressin addedVasopressin added - Class IIb 40 U IVP x 1 - Class IIb 40 U IVP x 1• EpinephrineEpinephrine - Class Indeterminate 1mg IVP q 3-5 - Class Indeterminate 1mg IVP q 3-5

minmin• Amiodarone addedAmiodarone added - Class IIb - Class IIb

• 300mg IVP (cardiac arrest dose). May repeat 150mg x 1300mg IVP (cardiac arrest dose). May repeat 150mg x 1

• Lidocaine - Class IndeterminateLidocaine - Class Indeterminate 1-1.5 mg/kg IVP q 1-1.5 mg/kg IVP q 3-5 min (Max = 3mg/kg)3-5 min (Max = 3mg/kg)

• ProcainamideProcainamide is acceptable but not recommended is acceptable but not recommended due to long administration times due to long administration times

• BretyliumBretylium fell off algorithm due manufacturing fell off algorithm due manufacturing problemsproblems

The Tachycardia The Tachycardia AlgorithmsAlgorithms

Major New Concepts:Major New Concepts:• Make a specific rhythm diagnosisMake a specific rhythm diagnosis• Identify patients with significantly Identify patients with significantly

impaired cardiac function (EF<40%, impaired cardiac function (EF<40%, overt HF)overt HF)

• Only use one antiarrhythmic, especially Only use one antiarrhythmic, especially in damaged heartsin damaged hearts

• Resulted in 3 new algorithmsResulted in 3 new algorithms

The Tachycardia Overview AlgorithmThe Tachycardia Overview Algorithm

Is the patient stable or unstable?Is the patient stable or unstable?

StableStable UnstableUnstable

Identify 1 of 4 types of tachycardiaIdentify 1 of 4 types of tachycardia Cardioversion Cardioversion

(premedicate)(premedicate)

VT, PSVT, VT, PSVT, 100J, 200J, 100J, 200J,

300J, 360J 300J, 360J

AF/AflutterAF/Aflutter

Narrow-complex Narrow-complex tachycardiatachycardia

Stable wide-complex Stable wide-complex tachycardiatachycardia

Stable monomorphic VTStable monomorphic VT

Tachycardia - Atrial Tachycardia - Atrial Fibrillation/FlutterFibrillation/Flutter

4 Clinical Features: 4 Clinical Features: • Unstable? Unstable? • Impaired cardiac function? Impaired cardiac function? • WPW? WPW? • Duration? <48h, or > 48h?Duration? <48h, or > 48h?

• Focus - treat unstable patients urgentlyFocus - treat unstable patients urgently• Control ventricular response Control ventricular response convert convert

anticoagulate anticoagulate

Atrial Atrial Fibrillation/FlutterFibrillation/Flutter

Conversion ConversionCondition Rate Control> 48h < 48h

EF > 40% CCB (I)-Blocker (I)

DC CardioversionAmiodarone (IIa)Ibutilide (IIa)Flecainide (IIa)Propafenone (IIa)Procainamide (IIa)

No DC CardioversionAnticoagulation x 3weeks, then CV, thenanticoagulation x 4 wkOR r/o clot by TEE,CV, then AC x 4 wk

EF < 40% Digoxin (IIb)Diltiazem (IIb)Amiodarone (IIb)

DC CardioversionORAmiodarone (IIb)

(See above)

WPW Preserved heartfxn:DC CardioversionAmiodarone(IIb)Flecainide (IIb)Procainamide (IIb)Propafenone (IIb)Sotalol (IIb)

ImpairedEF<40%:DC CardioversionAmiodarone(IIb)

DC CardioversionAmiodarone (IIb)Flecainide (IIb)Propafenone (IIb)Procainamide (IIb)Sotalol (IIb)

(See above)

Drugs Used in Afib/AFlutterDrugs Used in Afib/AFlutter

• Calcium channel blockersCalcium channel blockers• Beta-blockersBeta-blockers• DigoxinDigoxin• AmiodaroneAmiodarone• ProcainamideProcainamide• Flecainide Flecainide (IV form in ACLS -not available in (IV form in ACLS -not available in

US)US)• Propafenone Propafenone (IV form in ACLS -not available in (IV form in ACLS -not available in

US)US)• Sotalol Sotalol (IV form in ACLS -not available in US)(IV form in ACLS -not available in US)


Calcium Channel BlockersCalcium Channel Blockers

WHY?WHY? Blocks inward flow of Ca and Na, slows conduction,Blocks inward flow of Ca and Na, slows conduction, RP in AVN RP in AVN Terminate reentrant arrhythmias Terminate reentrant arrhythmias requiring AVN conductionrequiring AVN conduction Control ventricular Control ventricular response rate in AF/AFlresponse rate in AF/AFl Coronary Coronary vasodilationvasodilation

May exacerbate CHFMay exacerbate CHF

Verapamil:Verapamil: Negative inotrope & chronotrope (good anti-ischemic)Negative inotrope & chronotrope (good anti-ischemic)Class I for acute and preventative SVTClass I for acute and preventative SVT

Diltiazem:Diltiazem: Direct negative chronotropic effect, mild negative Direct negative chronotropic effect, mild negative inotropeinotrope

Highly effective in controlling ventricular response in Highly effective in controlling ventricular response in A FibA Fib

WHEN?WHEN? Control ventricular response rate in patients with AF/Fl, or Control ventricular response rate in patients with AF/Fl, or MATMAT

Verapamil: PSVT not requiring cardioversionVerapamil: PSVT not requiring cardioversion


Calcium Channel BlockersCalcium Channel BlockersHOW?HOW? Verapamil:Verapamil: 2.5 - 5 mg IVP, over 2 min 2.5 - 5 mg IVP, over 2 min

(max=30mg)(max=30mg)Inf @ 5-10 mg/hrInf @ 5-10 mg/hr

Diltiazem:Diltiazem: 0.25 mg/kg IVP, may repeat with 0.25 mg/kg IVP, may repeat with 0.35mg/kg in 15 min0.35mg/kg in 15 min

Infuse @ 5-15 mg/hrInfuse @ 5-15 mg/hr

WHAT?WHAT? Contraindicated in wide QRS complex tachycardias Contraindicated in wide QRS complex tachycardias and and ventricular tachycardias, exacerbation of CHF ventricular tachycardias, exacerbation of CHF inin patients patients with LV dysfunctionwith LV dysfunction

Transient decrease in BPTransient decrease in BPAvoid in sick sinus syndrome of AV block Avoid in sick sinus syndrome of AV block

(w/out pacer)(w/out pacer)May potentiate digoxin toxicity.May potentiate digoxin toxicity.Incompatible with bicarbonate, epinephrine, Incompatible with bicarbonate, epinephrine,

furosemidefurosemide


Beta - BlockersBeta - BlockersWHY?WHY? B-adrenergic blockade, slows conduction B-adrenergic blockade, slows conduction

and and increases refractory period in AV increases refractory period in AV nodenode

WHEN?WHEN? AMI (reduces rate of reinfarction), reduces AMI (reduces rate of reinfarction), reduces recurrent ischemia and incidence of VF in recurrent ischemia and incidence of VF in

post-post- MI patients, USAMI patients, USA

HOW?HOW? Atenolol:Atenolol: 2.5-5 mg IV over 5 min2.5-5 mg IV over 5 minMetoprolol:Metoprolol: 5 - 10 mg IVP q 5 min5 - 10 mg IVP q 5 minPropranolol:Propranolol: 0.1 mg/kg IV divided into 30.1 mg/kg IV divided into 3

doses @ 2 - 3 min intervalsdoses @ 2 - 3 min intervalsEsmolol:Esmolol: 500 mcg/kg over 1 min500 mcg/kg over 1 min

Inf @ 50 mcg/kg/minInf @ 50 mcg/kg/min

WHAT?WHAT? Hypotension, bradycardia, AV block, overt heart Hypotension, bradycardia, AV block, overt heart failure or severe failure or severe

bronchospasm/COPDbronchospasm/COPD

Stable Monomorphic Ventricular TachycardiaStable Monomorphic Ventricular Tachycardia

Medications: any one•Procainamide (IIA)•Sotalol (IIA)*•Amiodarone (IIB)•Lidocaine (IIB)

Amiodarone (IIB)•150 mg IV bolus over 10 min•may repeat 150mg q10-15min or start infusionORLidocaine (IIB)•0.5 to 0.75 mg/kg IV pushThen use•Synchronized cardioversion

NOTE!May go directly to cardioversion

Impaired LVImpaired LVEF<40% or EF<40% or CHFCHF

Preserved Preserved Cardiac Cardiac FunctionFunction

*Not yet available in the US.

Narrow-Complex Supraventricular Narrow-Complex Supraventricular TachycardiaTachycardia

• Vagal stimulationVagal stimulation• AdenosineAdenosine

• Junctional Junctional

• 1. EF > 40% - Amiodarone, B-blocker, CCB1. EF > 40% - Amiodarone, B-blocker, CCB• 2. EF <40%, CHF - Amiodarone2. EF <40%, CHF - Amiodarone

• PSVT PSVT • EF>40% - CCB, BB, digoxin, DC cardioversion EF>40% - CCB, BB, digoxin, DC cardioversion

(procainamide, amiodarone, sotalol)(procainamide, amiodarone, sotalol)• EF<40%, CHF - no DC cardioversion; digoxin, EF<40%, CHF - no DC cardioversion; digoxin,

amiodarone, diltiazemamiodarone, diltiazem

• MATMAT• EF>40% -No DC cardioversion; CCB, BB, amiodaroneEF>40% -No DC cardioversion; CCB, BB, amiodarone• EF<40% -No DC cardioversion; amiodaonre, diltiazemEF<40% -No DC cardioversion; amiodaonre, diltiazem

Wide-Complex TachycardiaWide-Complex Tachycardia• ““Wide” …. Prolonged QRS or QRST intervalWide” …. Prolonged QRS or QRST interval

• HR > 120 bpm (ex. VT, sinus tachycardia, HR > 120 bpm (ex. VT, sinus tachycardia, A.flutter)A.flutter)

• OLD - LidocaineOLD - Lidocaine• NEW - NEW -

• Establish diagnosis - 12-lead ECGEstablish diagnosis - 12-lead ECG• Adenosine if SVT- slows AV conduction. Short-lived Adenosine if SVT- slows AV conduction. Short-lived

hypotension hypotension • Amiodarone (IIa) normal LV functionAmiodarone (IIa) normal LV function• Amiodarone (IIb) impaired LV function Amiodarone (IIb) impaired LV function • Procainamide (IIa)- terminates SVT due to altering Procainamide (IIa)- terminates SVT due to altering

conduction across accessory pathwaysconduction across accessory pathways• Lidocaine if VTLidocaine if VT• Sotalol, propafenone, flecainideSotalol, propafenone, flecainide


AdenosineAdenosineWHY?WHY? Endogenous nucleoside, slows conduction through Endogenous nucleoside, slows conduction through

the the AV node and can interrupt AV nodal reentry AV node and can interrupt AV nodal reentry pathwayspathways

WHEN?WHEN? PSVT (half-life=10 sec)PSVT (half-life=10 sec)

If PSVT persists may want longer acting agent If PSVT persists may want longer acting agent (verapamil or diltiazem)(verapamil or diltiazem)

HOW?HOW? 6 mg rapid IV over 1 - 3 sec, followed by 20 ml 6 mg rapid IV over 1 - 3 sec, followed by 20 ml NS flush. May repeat in 1-2min with 12 mg NS flush. May repeat in 1-2min with 12 mg

dose.dose.

Max.=30 mgMax.=30 mg

WHAT?WHAT? Flushing, dyspnea, chest pain, post-conversion bradycardiaFlushing, dyspnea, chest pain, post-conversion bradycardia

Drug interaction with theophylline, dipyridamoleDrug interaction with theophylline, dipyridamole

Pulseless Electrical ActivityPulseless Electrical Activity• PEA… no pulse with + electrical activity (not PEA… no pulse with + electrical activity (not

VF/VT)VF/VT)• Reversible if underlying cause is reversed (5 H’s, 5 Reversible if underlying cause is reversed (5 H’s, 5

T’s)T’s)• Hypovolemia, hypoxia, hydrogen ion (acidosis), Hypovolemia, hypoxia, hydrogen ion (acidosis),

hyper/hypokalemia, hyper/hypothermiahyper/hypokalemia, hyper/hypothermia

• Tablets, tamponade, tension pneumothorax, thrombosis (ACS), Tablets, tamponade, tension pneumothorax, thrombosis (ACS), thrombosis (PE)thrombosis (PE)

InterventionIntervention Comments/DoseComments/Dose

ProblemProblem Search for the probable cause and intervene Search for the probable cause and intervene (HCO3)(HCO3)

EpinephrineEpinephrine 1 mg IV q3-5 min.1 mg IV q3-5 min.

AtropineAtropine With slow heart rate, 1 mg IV q3-5 min. With slow heart rate, 1 mg IV q3-5 min. (max. dose 0.04 mg/kg)(max. dose 0.04 mg/kg)

AtropineAtropineWHY?WHY? Anticholinergic/direct vagolyticAnticholinergic/direct vagolytic

Enhances sinus node automaticity and AVN Enhances sinus node automaticity and AVN conductionconduction

WHEN?WHEN? PEA, symptomatic sinus bradycardia, asystole, PEA, symptomatic sinus bradycardia, asystole,

HOW?HOW? Bradycardia: 0.5 -1 mg IV q3-5 minBradycardia: 0.5 -1 mg IV q3-5 min

Asystole: 1 mg IV q 3-5 min Asystole: 1 mg IV q 3-5 min

Max = 0.04 mg/kg or 3 mgMax = 0.04 mg/kg or 3 mgET Dose=1-2mg diluted in 10mlET Dose=1-2mg diluted in 10mlParadoxical bradycardia with insufficient dose (<0.5mg)Paradoxical bradycardia with insufficient dose (<0.5mg)

WHAT?WHAT? Tachycardia; 2nd or 3rd degree AV block (paradoxical Tachycardia; 2nd or 3rd degree AV block (paradoxical slowing may occur), MI (may worsen ischemia/HR)slowing may occur), MI (may worsen ischemia/HR)Incompatible with bicarbonate, epinephrine & norepinephrineIncompatible with bicarbonate, epinephrine & norepinephrine

BradycardiaBradycardia

““AAll ll PPatients atients DDeserve eserve EEmpathy”mpathy”(The sequence reflects interventions for increasingly severe bradycardia) (The sequence reflects interventions for increasingly severe bradycardia)

• Absolute (< 60 BPM) or relativeAbsolute (< 60 BPM) or relative• Serious signs and symptoms (CP, SOB, hypotension, mental Serious signs and symptoms (CP, SOB, hypotension, mental

status changes)status changes)

Mnemonic InterventionMnemonic Intervention Comments/DoseComments/Dose

AAllll AtropineAtropine 0.5-1.0 mg IVP q 3-5 min (max 0.03- 0.5-1.0 mg IVP q 3-5 min (max 0.03-0.04 mg/kg)0.04 mg/kg)

PPatientsatients PacingPacing Use Transcutaneous Pacing if Use Transcutaneous Pacing if severe S/Ssevere S/S

DDeserve eserve DopamineDopamine 5-20 µg/kg/min. 5-20 µg/kg/min.

EEmpathy mpathy EpinephrineEpinephrine 2-10 µg/min. 2-10 µg/min.

Medications for BradycardiaMedications for Bradycardia

• Atropine - Why? How?Atropine - Why? How?• DopamineDopamine• Epinephrine infusion Epinephrine infusion

•1mg/250 ml @ 1-4 mcg/min1mg/250 ml @ 1-4 mcg/min

Note: Lidocaine can be lethal if Note: Lidocaine can be lethal if HR is due to ventricular HR is due to ventricular escape rhythmescape rhythm

DopamineDopamine

WHY?WHY? NE precursorNE precursorStimulates DA, Stimulates DA, & & -adrenergic receptors -adrenergic receptors

(dose-related)(dose-related)Want Want -stimulation, for bradycardia-induced -stimulation, for bradycardia-induced

hypotensionhypotension

WHEN?WHEN? Hypotension/shockHypotension/shock

HOW?HOW? renal:renal: 2 - 5 mcg/kg/min 2 - 5 mcg/kg/mincardiac:cardiac: 5 - 10 mcg/kg/min ( 5 - 10 mcg/kg/min (BB11 & & alphaalpha))vascular: 10 - 20 mcg/kg/min (vascular: 10 - 20 mcg/kg/min (alphaalpha))

Preparation:Preparation: 400 mg/250 ml D5W or NS400 mg/250 ml D5W or NS

WHAT?WHAT? Tachycardia, tachyphylaxis, proarrhythmicTachycardia, tachyphylaxis, proarrhythmicIf requiring > 20mcg/kg/min consider adding If requiring > 20mcg/kg/min consider adding

NENE

ACLS AlgorithmsACLS AlgorithmsAsystoleAsystole

• Consider possible causes and treat accordingly Consider possible causes and treat accordingly (ex.hypoxemia, hyper/hypokalemia, acidosis)(ex.hypoxemia, hyper/hypokalemia, acidosis)Acronym “TEA”Acronym “TEA”

T T Transcutaneous Pacing (TCP)Transcutaneous Pacing (TCP) (Class IIb)(Class IIb) Only Only effective with early implementation along with effective with early implementation along with appropriate interventions and medicationsappropriate interventions and medications

E E EpinephrineEpinephrine 1 mg IV q3-5 min. 1 mg IV q3-5 min.

A A AtropineAtropine 1 mg IV q3-5 min. (max. dose 0.04 1 mg IV q3-5 min. (max. dose 0.04 mg/kg)mg/kg)

• Discourage shocking due to excess parasympathetic Discourage shocking due to excess parasympathetic dischargedischarge

• Consider Na Bicarbonate 1 mEq/kgConsider Na Bicarbonate 1 mEq/kg

Drugs Used for Drugs Used for Myocardial Ischemia/PainMyocardial Ischemia/Pain

• OxygenOxygen• NitroglycerinNitroglycerin• Morphine SulfateMorphine Sulfate

• AMI - Aspirin, thrombolytics, heparin, AMI - Aspirin, thrombolytics, heparin, lidocaine, beta-blockerslidocaine, beta-blockers

• Glycoprotein IIb/IIIa receptor antagonistsGlycoprotein IIb/IIIa receptor antagonists

Acute Myocardial InfarctionAcute Myocardial Infarction

• ““Call first, call fast, call 911”Call first, call fast, call 911”• Oxygen 4L/minOxygen 4L/min• NTG SL, paste or spray; if BP > 90 mm Hg, NTG SL, paste or spray; if BP > 90 mm Hg,

IV NTG IV NTG • Morphine IVMorphine IV• ASA PO (I)ASA PO (I)• Thrombolytics? (I) - within 6 hours of Thrombolytics? (I) - within 6 hours of

symptoms, (II) if > 6hrsymptoms, (II) if > 6hr• IV heparinIV heparin• B-B-blockersblockers• Magnesium (if Magnesium (if Mg) Mg)

OxygenOxygenWhy?Why?

• increases hemoglobin saturation, increases hemoglobin saturation, improves tissue oxygenationimproves tissue oxygenation

supply to ischemic tissues supply to ischemic tissues 16-17% oxygen from mouth-to-mouth 16-17% oxygen from mouth-to-mouth

When?When?• Must give supplemental oxygen in ACLSMust give supplemental oxygen in ACLS• Always for MIAlways for MI

How?How?• NC 4 L/min, intubation, etcNC 4 L/min, intubation, etc• Goal - Osat=97-98%Goal - Osat=97-98%• Confirm tube placementConfirm tube placement

Drugs Used for Myocardial Drugs Used for Myocardial Ischemia/PainIschemia/Pain

NitroglycerinNitroglycerinWHY?WHY?

• binds to receptors on vascular smooth binds to receptors on vascular smooth muscle - vasodilation (venous > arterial)muscle - vasodilation (venous > arterial)

venous BF to heart (preload) & O2 venous BF to heart (preload) & O2 consumptionconsumption

• dilates coronary arteries - dilates coronary arteries - myocardial blood myocardial blood supply supply

• antagonizes vasospasmantagonizes vasospasm• increases collateral flow to ischemic increases collateral flow to ischemic

myocardiummyocardium• inhibits infarct expansion inhibits infarct expansion • decreases paindecreases pain


NitroglycerinNitroglycerinWHEN?WHEN?

Ischemic CP; USA; pulmonary edema (when SBP>100); AMIIschemic CP; USA; pulmonary edema (when SBP>100); AMISL NTG -drug of choice for anginaSL NTG -drug of choice for anginaIV NTG - drug of choice for unstable angina or AMIIV NTG - drug of choice for unstable angina or AMICongestive heart failure with ischemiaCongestive heart failure with ischemia

HOW?HOW?IVIV: 10-20 mcg/min, increase by 5-10 mcg/min q5-10 min until desired : 10-20 mcg/min, increase by 5-10 mcg/min q5-10 min until desired effect or hemodynamic compromiseeffect or hemodynamic compromiseSLSL: 1 tablet (0.4mg) SL q5min times 3: 1 tablet (0.4mg) SL q5min times 3SpraySpray: 1 spray onto oral mucosa: 1 spray onto oral mucosaOintment 2%:Ointment 2%: 1-2 inches over 2-4 inch area 1-2 inches over 2-4 inch areaPatchesPatches: no role in acute therapy: no role in acute therapy


NitroglycerinNitroglycerinPreparation:Preparation: 50 mg/250 ml D5W or NS50 mg/250 ml D5W or NS

Must be in glass bottleMust be in glass bottle

Cautions:Cautions: • hypotension - treat with fluids, and rate hypotension - treat with fluids, and rate

reduction/eliminationreduction/elimination• bradycardia - vasovagal reflex to hypotensionbradycardia - vasovagal reflex to hypotension

• treat with fluids, rate reduction, atropinetreat with fluids, rate reduction, atropine• reflex tachycardia also a concernreflex tachycardia also a concern

• headache, dizziness - may be diminished by headache, dizziness - may be diminished by laying downlaying down

• patients develop tachyphylaxis to effects - patients develop tachyphylaxis to effects - promote nitrate-free periods, intermittent dosing promote nitrate-free periods, intermittent dosing and lowest-possible dosesand lowest-possible doses


Morphine SulfateMorphine SulfateWHY?WHY? (Pain can (Pain can catecholamines - catecholamines - BP, BP, HR, HR, O2 demands)O2 demands)

Opiate analgesic Opiate analgesic

pain, pain, preload and afterload, preload and afterload, SVR, SVR, anxiety anxiety

Relieves pulmonary congestion, Relieves pulmonary congestion, myocardial oxygen myocardial oxygen demanddemand

WHEN?WHEN?

Pain, pulmonary edema, BP > 90 mm HgPain, pulmonary edema, BP > 90 mm Hg

HOW?HOW?

1-3mg IVP (2-15 mg IVP q15-30 min prn)1-3mg IVP (2-15 mg IVP q15-30 min prn)

CAUTION?CAUTION?

Respiratory & CNS depression, bradycardia, hypotension, Respiratory & CNS depression, bradycardia, hypotension, N/VN/V

Drugs Used for Myocardial Drugs Used for Myocardial Ischemia/PainIschemia/Pain(Continued)(Continued)

• AspirinAspirin• HeparinHeparin• Thrombolytics - reteplase, Thrombolytics - reteplase,

alteplase, TNKalteplase, TNK• B BlockersB Blockers• MagnesiumMagnesium• Lidocaine - not for prophylaxisLidocaine - not for prophylaxis

Hypotension/Shock/Hypotension/Shock/Pulmonary EdemaPulmonary Edema

Identify Problem? Volume; Pump; Rate?Identify Problem? Volume; Pump; Rate?• Volume: Volume:

• fluids, blood, vasopressorsfluids, blood, vasopressors

• Pump: Pump: • s/s of shock - vasopressors; no s/s shock s/s of shock - vasopressors; no s/s shock

- dobutaminedobutamine BP (>100 mm Hg) - NTG, NitroprussideBP (>100 mm Hg) - NTG, Nitroprusside• pulmonary edema -furosemide pulmonary edema -furosemide

0.5-1mg/kg, morphine 1-3mg, NTG SL, 0.5-1mg/kg, morphine 1-3mg, NTG SL, oxygen/intubateoxygen/intubate

• Rate: see algorithmsRate: see algorithms

Drugs Used to Improve Cardiac Drugs Used to Improve Cardiac Output and Blood PressureOutput and Blood Pressure

NorepinephrineNorepinephrine

Action:Action: Alpha & ß-adrenergic stimulation, Alpha & ß-adrenergic stimulation, increases increases contractility and HR, contractility and HR, vasoconstriction, improves vasoconstriction, improves coronary blood flowcoronary blood flow

Indication:Indication: Shock refractory to fluid Shock refractory to fluid replacement, severe replacement, severe hypotensionhypotension

Dose:Dose: 0.5 - 1 mcg/min0.5 - 1 mcg/minrefractory shock = 8 - 30 mcg/minrefractory shock = 8 - 30 mcg/min

Preparation: Preparation: 4-8mg/250 ml D5W or NS4-8mg/250 ml D5W or NS

Caution:Caution: Hypertension, myocardial ischemia, cardiac Hypertension, myocardial ischemia, cardiac arrest, arrest, palpitationspalpitations


DobutamineDobutamine

Action:Action: B1- adrenergic activityB1- adrenergic activity

Indication:Indication: Inotrope in heart failure/hypotensionInotrope in heart failure/hypotension

Dose:Dose: 2 - 20 mcg/kg/min2 - 20 mcg/kg/min

Preparation: Preparation: 250 mg/250 ml D5W or NS250 mg/250 ml D5W or NS

Caution:Caution: tachyarrhythmias,worsens myocardial tachyarrhythmias,worsens myocardial ischemiaischemia


Inamrinone and MilrinoneInamrinone and Milrinone

Action:Action: Phosphodiesterase inhibitors, positive Phosphodiesterase inhibitors, positive inotropes and inotropes and vasodilatorvasodilator

Indication:Indication: Refractory heart failureRefractory heart failure

Dose:Dose: Inamrinone:Inamrinone: 750 mcg/kg over 2 - 3 min750 mcg/kg over 2 - 3 minInf @ 5 - 15 mcg/kg/minInf @ 5 - 15 mcg/kg/min

Milrinone:Milrinone: 50 mcg/kg over 10 min50 mcg/kg over 10 minInf @ 0.375 - 0.75 Inf @ 0.375 - 0.75

mcg/kg/minmcg/kg/min

Caution:Caution: Thrombocytopenia, worsens myocardial Thrombocytopenia, worsens myocardial ischemia, ischemia, SV and ventricular arrhythmiasSV and ventricular arrhythmias


IsoproterenolIsoproterenolWHY?WHY? Synthetic sympathomimetic amine Synthetic sympathomimetic amine

Pure B-adrenergic activity +inotropic& chronotropePure B-adrenergic activity +inotropic& chronotrope

HR/CO, contractility; HR/CO, contractility; MAP secondary vasodilation MAP secondary vasodilation

WHEN?WHEN? Symptomatic bradycardia Symptomatic bradycardia

Refractory torsades de pointesRefractory torsades de pointes

HOW? HOW? Class II - 2 - 10 mcg/minClass II - 2 - 10 mcg/min

Class III - higher dosesClass III - higher doses

Preparation: 1 mg/ 250 ml D5W or NSPreparation: 1 mg/ 250 ml D5W or NS

WHAT?WHAT? mycocardial O2 consumption & peripheral vasodilation mycocardial O2 consumption & peripheral vasodilation

Avoid in ischemic heart disease; arrhythmogenicAvoid in ischemic heart disease; arrhythmogenic


Sodium NitroprussideSodium Nitroprusside

Action:Action: Antihypertensive, peripheral vasodilator, Antihypertensive, peripheral vasodilator, reduces reduces afterload, increases CO and afterload, increases CO and relieves pulmonary relieves pulmonary congestioncongestion

Indication:Indication: Hypertension, AMI, CHFHypertension, AMI, CHF

Dose:Dose: 0.1 - 5 mcg/kg/min, and titrate up to 0.1 - 5 mcg/kg/min, and titrate up to 10mcg/kg/min10mcg/kg/min

Preparation:Preparation: 50 mg/250 ml D5W50 mg/250 ml D5W

Caution:Caution: Cyanide and thiocyanate toxicity, hypotensionCyanide and thiocyanate toxicity, hypotension

Summary of 2000 Summary of 2000 ChangesChanges

• NEW AGENTS - Amiodarone & VasopressinNEW AGENTS - Amiodarone & Vasopressin• Amiodarone (Class IIb) & Procainamide (Class IIb) - Amiodarone (Class IIb) & Procainamide (Class IIb) -

hemodynamically stable wide-complex tachycardia (esp. hemodynamically stable wide-complex tachycardia (esp. in poor cardiac fxn)in poor cardiac fxn)

• VT - amiodarone & sotalol (Class IIa)VT - amiodarone & sotalol (Class IIa)• Vasopressin (Class IIb) - alternative to epinephrineVasopressin (Class IIb) - alternative to epinephrine• Bretylium acceptable, but not recommendedBretylium acceptable, but not recommended• Lidocaine for VT/VF (Class Indeterminate) & Class III for Lidocaine for VT/VF (Class Indeterminate) & Class III for

prophylaxis of ventricular arrhythmias in AMIprophylaxis of ventricular arrhythmias in AMI• Magnesium (Class IIb) - Magnesium (Class IIb) - Mg or TdP Mg or TdP• High-dose epinephrine (Class Indeterminate)High-dose epinephrine (Class Indeterminate)• Fibrinolytics for AMI & StrokeFibrinolytics for AMI & Stroke

Crash Cart RevisionsCrash Cart RevisionsSummary of Changes:Summary of Changes:Additions:Additions: 5 amps of amiodarone 150mg/3ml (were 3)5 amps of amiodarone 150mg/3ml (were 3)

3 vials of vasopressin (20 Units/vial)3 vials of vasopressin (20 Units/vial)1 bag of premixed dopamine 400mg in 1 bag of premixed dopamine 400mg in

250ml250ml4 Na Bicarbonate syringes (were 3)4 Na Bicarbonate syringes (were 3)5 filter needles5 filter needles20 blunt cannulas20 blunt cannulas

Deletions:Deletions: 1 dopamine vial (new total=1)1 dopamine vial (new total=1)Remove 5 epinephrine syringes (new Remove 5 epinephrine syringes (new

total=10)total=10)Remove 1 lidocaine syringe (new total=2)Remove 1 lidocaine syringe (new total=2)Remove metoprolol Remove metoprolol

Needless System/CannulasNeedless System/Cannulas

Questions ?Questions ?