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Krista Piekos, Pharm.D. Clinical Pharmacy Specialist - Critical Care Harper University Hospital Adjunct Assistant Professor Wayne State University
Objectives
Pharmacists should be able to identify: Why? we use an agent When? to use an agent How? to use an agent What? ...to watch for To familiarize the pharmacist with the ACLS algorithms To help the pharmacist become comfortable with the crash cart To introduce the needless delivery system
Outline
Present conclusions of the International Guidelines 2000 ACLS objectives with 2003 updates Classification of recommendations ACLS Algorithms Pharmacology of agents used in algorithms Overview of crash cart revisions Overview of needless system
Background
In Seattle 43% of patients in VF survived to hospital discharge if CPR w/in 4 min and defibrillation w/in 8 min These figures are higher than national average - due to AEDs throughout public Overall survival from CPR is poor 5-15% Survival for in-patient CPR to discharge is <10%
1st international consensus on resuscitation guidelines Experts from around the world
Identified issues Gathered scientific evidence; level (quality) of evidence Integrate into a class of recommendation
Revised guidelines
New Goals
1. Early Defibrillation - Public Access Defibrillation (PAD)
Probability of successful defibrillation and survival is negatively related to the time from onset of VF to delivery of first shock PAD has the potential to be the single greatest advance in the treatment of prehospital sudden cardiac death since the invention of CPR
Circulation August 22, 2000
2. Establishing a specific diagnosis by ECG 3. Antiarrhythmic agents are just as likely to be proarrhythmic as they are antiarrhythmic. One, and only one antiarrhythmic should be used.
Routes of Administration
Intravenous Preferred route Endotracheal
2-2.5 Xs IV dose in 10ml volume Each dose is followed by 10 ml NS flush down the ET tube (Ex. epinephrine, atropine, lidocaine, diazepam, naloxone) Absorption occurs at alveolar capillary interface
Intraosseous (active bone marrow) Pediatric patients without IV access Other: Sublingual, intracardiac, IM, SC (poor absorption)
Universal Algorithm
Epinephrine
WHY?
Natural catecholamine with and -adrenergic agonist activity
Results in:
flow to heart and brain SVR, SBP, DBP electrical activity in the myocardium & automaticity ( success with defibrillation) myocardial contraction (for refractory circulatory shock (CABG)) increases myocardial oxygen requirements
Primary benefit: -vasoconstriction -adrenergic activity controversial b/c myocardial work WHEN? VF/VT, asystole, PEA, bradycardias
Epinephrine
HOW? High dose versus standard dose? Higher ROSC with high dose, but no change in survival High doses may exacerbate postresuscitation myocardial dysfunction Recommendations:
Class I: 1 mg IV q 3 - 5 min Class IIb: 2-5mg IVP q3-5min, or 1mg-3mg-5mg Class Indeterminate: high-dose 0.1mg/kg IVP q3-5min Infusion for HR & BP (IIb)
1mg in 250ml NS or D5W - infuse @ 1-10 mcg/min
Vasopressin
WHEN? Alternative to epinephrine for shock-refractory VT/VF WHY? Natural antidiuretic hormone Potent vasoconstrictor by stimulation of SM -V1 receptors :
BP & SVR; CO, HR, myocardial O2 consumption and contractility
Does not myocardial oxygen consumption Not affected by severe acidosis Class IIb for shock-refractory VF Class Indeterminate for PEA, asystole Half life = 10-20 minutes Dose? 40 Units IVP - one time only!!!
Why Vasopressin?
During CPR, plasma ADH levels are higher in patients with return of spontaneous circulation (ROSC) During CPR patients may be severely acidotic Epinephrine compared to vasopressin pre-hospital CPR (20 patients/study group) Multiple animal studies showing ROSC EPI (n=20) VP (n=20)
85%-95% of survivors have VF Survival dependant on early defibrillation Medications indicated only after 3 failed shocks
VFib/Pulseless VT Algorithm
Please Shock-Shock-Shock, EVerybody Shock, And Let's Make Patients Better Please - Precordial Thump If pulse-less with no defibrillator Shock 200J* Shock 200-300J* Shock 360J* (*only consecutive, if persistent)
Shock 360J
And - Amiodarone (First Choice) 300mg IV push. May repeat once at 150mg in 3-5 min. (max. cumulative dose: 2.2g IV/24hrs)
Drug-shock-drug-shock sequence
(continued)
Please Shock-Shock-Shock, EVerybody Shock, And Let's Make Patients Better Let's - Lidocaine 1.0-1.5 mg/kg IV. May repeat in 3-5 min (max=3 mg/kg) Make - Magnesium Sulfate 1-2 g slow IVP for suspected Mg or TdP Patients- Procainamide 30 mg/min, or 100 mg IV q 5 min. for refractory VF. (max. dose: 17 mg/kg)
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 time
Amiodarone
Magnesium Procainamide Lidocaine Buffers
Classification of Antiarrhythmics
Class Ia Drug Quinidine Procainamide Disopyramide Lidocaine Mexiletine Tocainide Flecainide Propafenone Moricizine Beta-Blockers Amiodarone Bretylium Sotalol Verapamil Diltiazem Conduction Velocity Refractory Period Automaticity Ion Block Sodium
Ib
0/ 0
Ic
II III
0
Calcium
IV
New Recommendations (WHEN?): pulseless VT or VF (IIb) hemodynamically stable VT (IIb), polymorphic VT (IIb), wide-complex tachycardia uncertain origin (IIb) refractory PSVT (preserved function, IIa; impaired function IIb) atrial tachycardia (IIb) cardioversion of AF (IIa)
Amiodarone
HOW? Cardiac arrest (PVT/VF) - 300mg IVP diluted in 2030ml, may repeat with 150mg in 10 minutes, or start infusion (max=2..2 g/24h) Atrial & ventricular arrhythmias in impaired hearts
150mg IVP over 10 min May repeat q10-15 min, or start gtt 1mg/min x 6 hours, then 0.5mg/min x 18 h
Why Amiodarone?
ARREST Trial
Objective: Efficacy of IV amiodarone in out-of-hospital cardiac arrest due to ventricular fibrillation or pulseless ventricular tachycardia Endpoints: Hospital admission with perfusing rhythm Survival to discharge Functional neurologic status at discharge
*Insufficiently powered to detect survival to discharge and functional neurologic status*
Rapid IV bolus
patients who arrived to hospital alive (p=0.03) Consistent results regardless of presenting rhythm
This is the only antiarrhythmic agent which has shown definitive benefit in cardiac arrest!
% Surviving to Admission
60 50 40 30 20 10 0
All Patients VF Asystol e or PEA ROSC No ROSC
WHEN?
HOW?
Class IIa in suspected hypomagnesemia, TdP, and Class IIb in VF/VT: 1 - 2gm slow IVP in 100ml Hypotension at large doses
WHAT?
Suppresses both ventricular and atrial arrhythmias Type Ia antiarrhythmic, affects fast Na+channels-slowing conduction velocity, prolongs RP, and decreases automaticity Phase IV depolarization
Refractory/recurrent VF/VT Control of rapid ventricular response (IIb) Conversion SVT (AF/Fl) (IIa)
WHEN?
WHAT?
Stop infusion if patient hypotensive, widened QRS >50%, arrhythmia suppression, or dose=17mg/kg Dose reduction in renal failure SLE syndrome Levels: PA=4-12 g/ml NAPA=7-15 g/ml (active metabolite-Class III)
Type IB antiarrhythmic Affects fast Na+ channels, shortens refractory period Suppresses spontaneous depolarization Local anesthetic, increases fibrillation threshold Suppresses ventricular ectopy post-MI
Without effecting myocardial contractility, BP or AV nodal conduction
WHEN?
SECOND-CHOICE agent VT/VF refractory to electrical countershock and epinephrine
Not for routine prophylaxis post-MI, however, accepted in high-risk patients (hypokalemia, myocardial ishchemia, LV dysfunction)
WHAT?
Drugs Used to Improve Cardiac Output and Blood Pressure Sodium Bicarbonate
WHY?
Enhances sodium shift intracellularly, buffers acidosis, decreases toxicity of TCAs, increases clearance of acidic drugs Class I - hyperkalemia Class IIa - bicarbonate-responsive acidosis metabolic acidosis secondary to loss of bicarb (renal/GI); overdoses (TCAs, phenobarbital, aspirin) Class IIb - protracted arrest in intubated patients Class III - hypoxic lactic acidosis 1 mEq/kg IVP, 0.5mEq/kg q10 min prn
WHEN?
HOW?
WHAT?
May worsen outcome if not intubated/ventilated. Metabolic alkalosis, decreased O2 delivery to tissues, hypokalemia, CNS acidosis, hypernatremia, hyperosmolarity
Incompatible with calcium, epinephrine, atropine, norepinephrine, isoproterenol
Lidocaine - Class Indeterminate 1-1.5 mg/kg IVP q 3-5 min (Max = 3mg/kg) Procainamide is acceptable but not recommended due to long administration times Bretylium fell off algorithm due manufacturing problems
Stable
Identify 1 of 4 types of tachycardia
Unstable
Cardioversion
(premedicate)
AF/Aflutter Narrow-complex tachycardia Stable wide-complex tachycardia Stable monomorphic VT VT, PSVT, 100J, 200J, 300J, 360J
Atrial Fibrillation/Flutter
Condition EF > 40% Rate Control CCB (I) -Blocker (I) Conversion > 48h DC Cardioversion Amiodarone (IIa) Ibutilide (IIa) Flecainide (IIa) Propafenone (IIa) Procainamide (IIa) DC Cardioversion OR Amiodarone (IIb) Impaired EF<40%: DC Cardioversion Amiodarone(IIb) DC Cardioversion Amiodarone (IIb) Flecainide (IIb) Propafenone (IIb) Procainamide (IIb) Sotalol (IIb) Conversion < 48h No DC Cardioversion Anticoagulation x 3 weeks, then CV, then anticoagulation x 4 wk OR r/o clot by TEE, CV, then AC x 4 wk (See above)
EF < 40%
Digoxin (IIb) Diltiazem (IIb) Amiodarone (IIb) Preserved heart fxn: DC Cardioversion Amiodarone(IIb) Flecainide (IIb) Procainamide (IIb) Propafenone (IIb) Sotalol (IIb)
WPW
(See above)
Verapamil:
Diltiazem:
WHEN?
Diltiazem:
WHAT?
Contraindicated in wide QRS complex tachycardias and ventricular tachycardias, exacerbation of CHF in patients with LV dysfunction Transient decrease in BP Avoid in sick sinus syndrome of AV block (w/out pacer)
May potentiate digoxin toxicity.
HOW?
Medications: any one Procainamide (IIA) Sotalol (IIA)* Amiodarone (IIB) Lidocaine (IIB)
*Not yet available in the US.
Amiodarone (IIB) 150 mg IV bolus over 10 min may repeat 150mg q10-15min or start infusion OR Lidocaine (IIB) 0.5 to 0.75 mg/kg IV push Then use Synchronized cardioversion
PSVT
EF>40% - CCB, BB, digoxin, DC cardioversion (procainamide, amiodarone, sotalol) EF<40%, CHF - no DC cardioversion; digoxin, amiodarone, diltiazem
MAT
EF>40% -No DC cardioversion; CCB, BB, amiodarone EF<40% -No DC cardioversion; amiodaonre, diltiazem
Wide-Complex Tachycardia
Wide . Prolonged QRS or QRST interval
HR > 120 bpm (ex. VT, sinus tachycardia, A.flutter) OLD - Lidocaine NEW Establish diagnosis - 12-lead ECG Adenosine if SVT- slows AV conduction. Short-lived hypotension Amiodarone (IIa) normal LV function Amiodarone (IIb) impaired LV function Procainamide (IIa)- terminates SVT due to altering conduction across accessory pathways Lidocaine if VT Sotalol, propafenone, flecainide
WHEN?
HOW?
WHAT?
Intervention
Problem Epinephrine
Comments/Dose
Search for the probable cause and intervene (HCO3) 1 mg IV q3-5 min.
Atropine
With slow heart rate, 1 mg IV q3-5 min. (max. dose 0.04 mg/kg)
Atropine
WHY? Anticholinergic/direct vagolytic Enhances sinus node automaticity and AVN conduction PEA, symptomatic sinus bradycardia, asystole, Bradycardia: 0.5 -1 mg IV q3-5 min Asystole: 1 mg IV q 3-5 min Max = 0.04 mg/kg or 3 mg ET Dose=1-2mg diluted in 10ml
Paradoxical bradycardia with insufficient dose (<0.5mg)
WHEN? HOW?
WHAT?
Tachycardia; 2nd or 3rd degree AV block (paradoxical slowing may occur), MI (may worsen ischemia/HR)
Incompatible with bicarbonate, epinephrine & norepinephrine
Bradycardia
All Patients Deserve Empathy
(The sequence reflects interventions for increasingly severe bradycardia)
Absolute (< 60 BPM) or relative Serious signs and symptoms (CP, SOB, hypotension, mental status changes)
Intervention Comments/Dose
Mnemonic
All mg/kg)
Patients
Atropine
Pacing
Deserve
Empathy
Dopamine
Epinephrine
5-20 g/kg/min.
2-10 g/min.
Dopamine
WHY? related) hypotension WHEN? NE precursor Stimulates DA, & -adrenergic receptors (doseWant -stimulation, for bradycardia-induced Hypotension/shock
HOW?
renal: 2 - 5 mcg/kg/min cardiac: 5 - 10 mcg/kg/min (B1 & alpha) vascular: 10 - 20 mcg/kg/min (alpha)
400 mg/250 ml D5W or NS Tachycardia, tachyphylaxis, proarrhythmic If requiring > 20mcg/kg/min consider adding NE
Preparation: WHAT?
A mg/kg)
AMI - Aspirin, thrombolytics, heparin, lidocaine, beta-blockers Glycoprotein IIb/IIIa receptor antagonists
Oxygen
Why? increases hemoglobin saturation, improves tissue oxygenation supply to ischemic tissues 16-17% oxygen from mouth-to-mouth When? Must give supplemental oxygen in ACLS Always for MI How? NC 4 L/min, intubation, etc Goal - Osat=97-98% Confirm tube placement
binds to receptors on vascular smooth muscle vasodilation (venous > arterial) venous BF to heart (preload) & O2 consumption dilates coronary arteries - myocardial blood supply antagonizes vasospasm increases collateral flow to ischemic myocardium inhibits infarct expansion decreases pain
HOW?
IV: 10-20 mcg/min, increase by 5-10 mcg/min q5-10 min until desired effect or hemodynamic compromise SL: 1 tablet (0.4mg) SL q5min times 3 Spray: 1 spray onto oral mucosa Ointment 2%: 1-2 inches over 2-4 inch area Patches: no role in acute therapy
Cautions:
hypotension - treat with fluids, and rate reduction/elimination bradycardia - vasovagal reflex to hypotension treat with fluids, rate reduction, atropine reflex tachycardia also a concern headache, dizziness - may be diminished by laying down patients develop tachyphylaxis to effects - promote nitrate-free periods, intermittent dosing and lowest-possible doses
B Blockers
Magnesium Lidocaine - not for prophylaxis
Hypotension/Shock/Pulmonary Edema
Identify Problem? Volume; Pump; Rate? Volume:
fluids, blood, vasopressors
Pump:
s/s of shock - vasopressors; no s/s shock -
dobutamine BP (>100 mm Hg) - NTG, Nitroprusside pulmonary edema -furosemide 0.5-1mg/kg, morphine 1-3mg, NTG SL, oxygen/intubate
Indication:
Dose:
Preparation: Caution:
Indication:
Dose:
Inamrinone:
Milrinone:
750 mcg/kg over 2 - 3 min Inf @ 5 - 15 mcg/kg/min 50 mcg/kg over 10 min Inf @ 0.375 - 0.75 mcg/kg/min
Caution:
Needless System/Cannulas
Questions ?