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Overview of ACLS Pharmacology and Update on New ACLS Guidelines
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Overview of ACLS Pharmacology and Update on New ACLS Guidelines

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  1. Overview of ACLS Pharmacologyand Update on New ACLS Guidelines Krista Piekos, Pharm.D. Clinical Pharmacy Specialist - Critical Care Harper University Hospital Adjunct Assistant Professor Wayne State University

  2. 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

  3. 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

  4. 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 AED’s throughout public • Overall survival from CPR is poor 5-15% • Survival for in-patient CPR to discharge is <10%

  5. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care • 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

  6. Classification of Therapeutic Interventions • Class I: definitely helpful, excellent • Class II: Class II a -probably helpful; good to very good Class II b -possibly helpful; fair to good • Class Indeterminate: insufficient evidence; no harm, but no benefit • Class III: possibly harmful

  7. 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.

  8. Routes of Administration Intravenous • Preferred route Endotracheal • 2-2.5 X’s 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)

  9. ACLS Algorithm Approach

  10. Universal Algorithm

  11. Epinephrine WHY? • Natural catecholamine with  and ß-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 • ß-adrenergic activity controversial b/c  myocardial work WHEN? • VF/VT, asystole, PEA, bradycardias

  12. 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 • ET Dose=2-2.5 times IV dose What to watch for? • Tachycardia, hypertension, myocardial ischemia, acidosis Incompatible with Ca, HCO3, aminophylline & PHY. Alkaline solutions cause auto-oxidation.

  13. 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!!!

  14. 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) Survival to hospital 35% 70% (p=0.06) 24 hour survival 20% 60% (p=0.02) Discharge alive 15% 40% (p=0.16)

  15. ILCOR Universal Algorithm(International Liaison Committee on Resuscitation) Medication changes in 2000: • Emphasis on identification of all possible stroke victims for IV fibrinolytics • Epinephrine has become Class Indeterminate • High-dose epinephrine no longer recommended • For shock-refractory VT/VF: Epinephrine 1 mg q 3-5 min • Vasopressin 40 Units IVP one time • Epinephrine alone for non-VT/VF

  16. Pulseless Ventricular Fibrillation or Tachycardia • In ACLS, always assume VF - most common • 85%-95% of survivors have VF • Survival dependant on early defibrillation • Medications indicated only after 3 failed shocks

  17. 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) EVerybody - Epinephrine 1 mg IV q3-5 min or Vasopressin40 U IVP 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 interactions 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)

  18. 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 Sulfate1-2 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 Better (consider buffers) - Bicarbonate 1 mEq/kg IV for: • preexisting  K+ • bicarb-responsive acidosis • some drug overdoses • protracted code (intubated) • ROSC after long code with effective ventilation.

  19. Drugs for VF/PVT • Epinephrine - Why? How? What? • Vasopressin - Why? How? What? • Amiodarone • Magnesium • Procainamide • Lidocaine • Buffers

  20. Classification of Antiarrhythmics

  21. Drugs Used for Heart Rhythm and RateAmiodarone WHY? • Class III antiarrhythmic (characteristics of all classes) • Na, K and Ca channel blocker &  & -adrenergic blocker • Prolongs AP and RP • Decreases AV conduction velocity & SN function 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)

  22. Amiodarone HOW? • Cardiac arrest (PVT/VF) - 300mg IVP diluted in 20-30ml, 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 WHAT? • Hypotension, bradycardia (slow rate, fluids)

  23. 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*

  24. ARREST Trial: Amiodarone in the Resuscitation of Refractory Sustained Ventricular Tachyarrhythmias • Prospective, randomized, DB, PC trial • 504 patients, who failed >/= 3 shocks • Randomized to placebo or 300mg IV amiodarone • Amiodarone Dosing: • 300mg diluted with 5% D5W to 20mL • Rapid IV bolus • Found a statistically significant increase in the number of 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!

  25. ARREST Trial - Subgroup Analysis

  26. Drugs Used for Heart Rhythm and RateMagnesium Sulfate WHY? Magnesium deficiency causes arrhythmias Facilitates ventricular repolarization by enhancing intracellular potassium flux, dilates coronary arteries WHEN? Suspected hypomagnesemia, pulseless VT/VF, torsade de pointes HOW? Class IIa in suspected hypomagnesemia, TdP, and Class IIb in VF/VT: 1 - 2gm slow IVP in 100ml WHAT? Hypotension at large doses

  27. Drugs Used for Heart Rhythm and RateProcainamide WHY? • Suppresses both ventricular and atrial arrhythmias • Type Ia antiarrhythmic, affects fast Na+channels-slowing conduction velocity, prolongs RP, and decreases automaticity • Phase IV depolarization WHEN? • Refractory/recurrent VF/VT • Control of rapid ventricular response (IIb) • Conversion SVT (AF/Fl) (IIa)

  28. Drugs Used for Heart Rhythm and RateProcainamide HOW?VF: 20-30 mg/min slow infusion (max=17 mg/kg) AF with rapid vent. response: 100 mg over 5 min then infuse@ 1 - 4 mg/min 1-2 gm/250ml D5W 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 µg/ml NAPA=7-15 µg/ml (active metabolite-Class III)

  29. Drugs Used for Heart Rhythm and RateLidocaine WHY? • 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 (Indeterminate) • Control of PVC’s (Indeterminate) • Hemodynamically stable VT (IIb) • Not for routine prophylaxis post-MI, however, accepted in high-risk patients (hypokalemia, myocardial ishchemia, LV dysfunction)

  30. Drugs Used for Heart Rhythm and RateLidocaine HOW? Class IIa: 1 - 1.5 mg/kg IVP q5 - 10 min (max=3mg/kg) Infusion (with pulse): 1 - 4 mg/min (if pulse is regained) Therapeutic Levels: 1.5-6 µg/ml ET Dose: 2-2.5 times IV dose Preparation: 1-2 gm/250 ml D5W or NS WHAT? Hepatic metabolism, renal elimination Bradycardia, cardiac arrest, seizures Lidocaine toxicity/neurotoxicity - twitching, LOC, seizures, coma Lidocaine levels persist in low CO states

  31. Drugs Used to Improve Cardiac Output and Blood PressureSodium Bicarbonate WHY?Enhances sodium shift intracellularly, buffers acidosis, decreases toxicity of TCA’s, increases clearance of acidic drugs WHEN?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 HOW? 1 mEq/kg IVP, 0.5mEq/kg q10 min prn 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

  32. SummaryV.Fib and Pulseless V.Tach Changes: • Vasopressin added - Class IIb 40 U IVP x 1 • Epinephrine - Class Indeterminate 1mg IVP q 3-5 min • Amiodarone added - Class IIb • 300mg IVP (cardiac arrest dose). May repeat 150mg x 1 • 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

  33. The Tachycardia Algorithms Major New Concepts: • Make a specific rhythm diagnosis • Identify patients with significantly impaired cardiac function (EF<40%, overt HF) • Only use one antiarrhythmic, especially in damaged hearts • Resulted in 3 new algorithms

  34. The Tachycardia Overview Algorithm Is the patient stable or unstable? StableUnstable Identify 1 of 4 types of tachycardia Cardioversion (premedicate) VT, PSVT, 100J, 200J, 300J, 360J AF/Aflutter Narrow-complex tachycardia Stable wide-complex tachycardia Stable monomorphic VT

  35. Tachycardia - Atrial Fibrillation/Flutter 4 Clinical Features: • Unstable? • Impaired cardiac function? • WPW? • Duration? <48h, or > 48h? • Focus - treat unstable patients urgently • Control ventricular response  convert  anticoagulate

  36. Atrial Fibrillation/Flutter

  37. Drugs Used in Afib/AFlutter • Calcium channel blockers • Beta-blockers • Digoxin • Amiodarone • Procainamide • Flecainide (IV form in ACLS -not available in US) • Propafenone (IV form in ACLS -not available in US) • Sotalol (IV form in ACLS -not available in US)

  38. Drugs Used for Heart Rhythm and RateCalcium Channel Blockers WHY? Blocks inward flow of Ca and Na, slows conduction, RP in AVN Terminate reentrant arrhythmias requiring AVN conduction Control ventricular response rate in AF/AFl Coronary vasodilation May exacerbate CHF Verapamil: Negative inotrope & chronotrope (good anti-ischemic) Class I for acute and preventative SVT Diltiazem: Direct negative chronotropic effect, mild negative inotrope Highly effective in controlling ventricular response in A Fib WHEN? Control ventricular response rate in patients with AF/Fl, or MAT Verapamil: PSVT not requiring cardioversion

  39. Drugs Used for Heart Rhythm and RateCalcium Channel Blockers HOW? Verapamil: 2.5 - 5 mg IVP, over 2 min (max=30mg) Inf @ 5-10 mg/hr Diltiazem: 0.25 mg/kg IVP, may repeat with 0.35mg/kg in 15 min Infuse @ 5-15 mg/hr 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. Incompatible with bicarbonate, epinephrine, furosemide

  40. Drugs Used for Heart Rhythm and RateBeta - Blockers WHY? B-adrenergic blockade, slows conduction and increases refractory period in AV node WHEN? AMI (reduces rate of reinfarction), reduces recurrent ischemia and incidence of VF in post- MI patients, USA HOW? Atenolol: 2.5-5 mg IV over 5 min Metoprolol: 5 - 10 mg IVP q 5 min Propranolol: 0.1 mg/kg IV divided into 3 doses @ 2 - 3 min intervals Esmolol: 500 mcg/kg over 1 min Inf @ 50 mcg/kg/min WHAT? Hypotension, bradycardia, AV block, overt heart failure or severe bronchospasm/COPD

  41. Stable Monomorphic Ventricular Tachycardia Impaired LV EF<40% or CHF Preserved Cardiac Function NOTE! May go directly to cardioversion • 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 • Medications: any one • Procainamide (IIA) • Sotalol (IIA)* • Amiodarone (IIB) • Lidocaine (IIB) *Not yet available in the US.

  42. Narrow-Complex Supraventricular Tachycardia • Vagal stimulation • Adenosine • Junctional • 1. EF > 40% - Amiodarone, B-blocker, CCB • 2. EF <40%, CHF - Amiodarone • 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

  43. 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

  44. Drugs Used for Heart Rhythm and RateAdenosine WHY? Endogenous nucleoside, slows conduction through the AV node and can interrupt AV nodal reentry pathways WHEN? PSVT (half-life=10 sec) If PSVT persists may want longer acting agent (verapamil or diltiazem) HOW? 6 mg rapid IV over 1 - 3 sec, followed by 20 ml NS flush. May repeat in 1-2min with 12 mg dose. Max.=30 mg WHAT? Flushing, dyspnea, chest pain, post-conversion bradycardia Drug interaction with theophylline, dipyridamole

  45. Pulseless Electrical Activity • PEA… no pulse with + electrical activity (not VF/VT) • Reversible if underlying cause is reversed (5 H’s, 5 T’s) • Hypovolemia, hypoxia, hydrogen ion (acidosis), hyper/hypokalemia, hyper/hypothermia • Tablets, tamponade, tension pneumothorax, thrombosis (ACS), thrombosis (PE) Intervention Comments/Dose Problem Search for the probable cause and intervene (HCO3) Epinephrine 1 mg IV q3-5 min. Atropine With slow heart rate, 1 mg IV q3-5 min. (max. dose 0.04 mg/kg)

  46. Atropine WHY? Anticholinergic/direct vagolytic Enhances sinus node automaticity and AVN conduction WHEN? PEA, symptomatic sinus bradycardia, asystole, HOW? 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) WHAT? Tachycardia; 2nd or 3rd degree AV block (paradoxical slowing may occur), MI (may worsen ischemia/HR) Incompatible with bicarbonate, epinephrine & norepinephrine

  47. 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) Mnemonic Intervention Comments/Dose All Atropine 0.5-1.0 mg IVP q 3-5 min (max 0.03-0.04 mg/kg) Patients Pacing Use Transcutaneous Pacing if severe S/S Deserve Dopamine 5-20 µg/kg/min. Empathy Epinephrine 2-10 µg/min.

  48. Medications for Bradycardia • Atropine - Why? How? • Dopamine • Epinephrine infusion • 1mg/250 ml @ 1-4 mcg/min Note: Lidocaine can be lethal if  HR is due to ventricular escape rhythm

  49. Dopamine WHY? NE precursor Stimulates DA,  & -adrenergic receptors (dose-related) Want  -stimulation, for bradycardia-induced hypotension WHEN? Hypotension/shock HOW? renal: 2 - 5 mcg/kg/min cardiac: 5 - 10 mcg/kg/min (B1 & alpha) vascular: 10 - 20 mcg/kg/min (alpha) Preparation: 400 mg/250 ml D5W or NS WHAT? Tachycardia, tachyphylaxis, proarrhythmic If requiring > 20mcg/kg/min consider adding NE

  50. ACLS AlgorithmsAsystole • Consider possible causes and treat accordingly (ex.hypoxemia, hyper/hypokalemia, acidosis) Acronym “TEA” T Transcutaneous Pacing (TCP)(Class IIb) Only effective with early implementation along with appropriate interventions and medications E Epinephrine 1 mg IV q3-5 min. A Atropine 1 mg IV q3-5 min. (max. dose 0.04 mg/kg) • Discourage shocking due to excess parasympathetic discharge • Consider Na Bicarbonate 1 mEq/kg