Overview of ACLS Pharmacology and Update on New ACLS Guidelines

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Presentation transcript:

Overview of ACLS Pharmacology and Update on New ACLS Guidelines 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 AED’s throughout public Overall survival from CPR is poor 5-15% Survival for in-patient CPR to discharge is <10%

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

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

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 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)

ACLS Algorithm Approach

Universal Algorithm *NOTE: if no response to vasopressin, wait 10-20 minutes before administering epinephrine

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

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.

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!!!

Survival to hospital 35% 70% (p=0.06) Discharge alive 15% 40% (p=0.16) 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)

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

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

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 Vasopressin 40 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)

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 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.

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

Classification of Antiarrhythmics

Drugs Used for Heart Rhythm and Rate Amiodarone 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)

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)

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*

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!

ARREST Trial - Subgroup Analysis

Drugs Used for Heart Rhythm and Rate Magnesium 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

Drugs Used for Heart Rhythm and Rate Procainamide 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)

Drugs Used for Heart Rhythm and Rate Procainamide 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)

Drugs Used for Heart Rhythm and Rate Lidocaine 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)

Drugs Used for Heart Rhythm and Rate Lidocaine 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

Drugs Used to Improve Cardiac Output and Blood Pressure Sodium 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

Summary V.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 *Note: if no response to vasopressin, wait 10-20 minutes before administering epinephrine

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

The Tachycardia Overview Algorithm Is the patient stable or unstable? Stable Unstable 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

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

Atrial Fibrillation/Flutter

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)

Drugs Used for Heart Rhythm and Rate Calcium 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

Drugs Used for Heart Rhythm and Rate Calcium 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

Drugs Used for Heart Rhythm and Rate Beta - 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

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.

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

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

Drugs Used for Heart Rhythm and Rate Adenosine 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

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)

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

“All Patients Deserve Empathy” 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.

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

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

ACLS Algorithms Asystole 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

Drugs Used for Myocardial Ischemia/Pain Oxygen Nitroglycerin Morphine Sulfate AMI - Aspirin, thrombolytics, heparin, lidocaine, beta-blockers Glycoprotein IIb/IIIa receptor antagonists

Acute Myocardial Infarction “Call first, call fast, call 911” Oxygen 4L/min NTG SL, paste or spray; if BP > 90 mm Hg, IV NTG Morphine IV ASA PO (I) Thrombolytics? (I) - within 6 hours of symptoms, (II) if > 6hr IV heparin B-blockers Magnesium (if  Mg)

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

Drugs Used for Myocardial Ischemia/Pain Nitroglycerin WHY? 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

Drugs Used for Myocardial Ischemia/Pain Nitroglycerin WHEN? Ischemic CP; USA; pulmonary edema (when SBP>100); AMI SL NTG -drug of choice for angina IV NTG - drug of choice for unstable angina or AMI Congestive heart failure with ischemia 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

Drugs Used for Myocardial Ischemia/Pain Nitroglycerin Preparation: 50 mg/250 ml D5W or NS Must be in glass bottle 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

Drugs Used for Myocardial Ischemia/Pain Morphine Sulfate WHY? (Pain can  catecholamines - BP, HR, O2 demands) Opiate analgesic  pain,  preload and afterload,  SVR,  anxiety Relieves pulmonary congestion,  myocardial oxygen demand WHEN? Pain, pulmonary edema, BP > 90 mm Hg HOW? 1-3mg IVP (2-15 mg IVP q15-30 min prn) CAUTION? Respiratory & CNS depression, bradycardia, hypotension, N/V

Drugs Used for Myocardial Ischemia/Pain (Continued) Aspirin Heparin Thrombolytics - reteplase, alteplase, TNK 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 Rate: see algorithms

Drugs Used to Improve Cardiac Output and Blood Pressure Norepinephrine Action: Alpha & ß-adrenergic stimulation, increases contractility and HR, vasoconstriction, improves coronary blood flow Indication: Shock refractory to fluid replacement, severe hypotension Dose: 0.5 - 1 mcg/min refractory shock = 8 - 30 mcg/min Preparation: 4-8mg/250 ml D5W or NS Caution: Hypertension, myocardial ischemia, cardiac arrest, palpitations

Drugs Used to Improve Cardiac Output and Blood Pressure Dobutamine Action: B1- adrenergic activity Indication: Inotrope in heart failure/hypotension Dose: 2 - 20 mcg/kg/min Preparation: 250 mg/250 ml D5W or NS Caution: tachyarrhythmias,worsens myocardial ischemia

Drugs Used to Improve Cardiac Output and Blood Pressure Inamrinone and Milrinone Action: Phosphodiesterase inhibitors, positive inotropes and vasodilator Indication: Refractory heart failure Dose: Inamrinone: 750 mcg/kg over 2 - 3 min Inf @ 5 - 15 mcg/kg/min Milrinone: 50 mcg/kg over 10 min Inf @ 0.375 - 0.75 mcg/kg/min Caution: Thrombocytopenia, worsens myocardial ischemia, SV and ventricular arrhythmias Amrinone NOW CALLED inamrinone

Drugs Used for Heart Rhythm and Rate Isoproterenol WHY? Synthetic sympathomimetic amine Pure B-adrenergic activity +inotropic& chronotrope  HR/CO, contractility;  MAP secondary vasodilation WHEN? Symptomatic bradycardia Refractory torsades de pointes HOW? Class II - 2 - 10 mcg/min Class III - higher doses Preparation: 1 mg/ 250 ml D5W or NS WHAT?  mycocardial O2 consumption & peripheral vasodilation Avoid in ischemic heart disease; arrhythmogenic

Drugs Used to Improve Cardiac Output and Blood Pressure Sodium Nitroprusside Action: Antihypertensive, peripheral vasodilator, reduces afterload, increases CO and relieves pulmonary congestion Indication: Hypertension, AMI, CHF Dose: 0.1 - 5 mcg/kg/min, and titrate up to 10mcg/kg/min Preparation: 50 mg/250 ml D5W Caution: Cyanide and thiocyanate toxicity, hypotension

Summary of 2000 Changes NEW AGENTS - Amiodarone & Vasopressin Amiodarone (Class IIb) & Procainamide (Class IIb) - hemodynamically stable wide-complex tachycardia (esp. in poor cardiac fxn) VT - amiodarone & sotalol (Class IIa) Vasopressin (Class IIb) - alternative to epinephrine Bretylium acceptable, but not recommended Lidocaine for VT/VF (Class Indeterminate) & Class III for prophylaxis of ventricular arrhythmias in AMI Magnesium (Class IIb) -  Mg or TdP High-dose epinephrine (Class Indeterminate) Fibrinolytics for AMI & Stroke

Crash Cart Revisions Summary of Changes: Additions: 5 amps of amiodarone 150mg/3ml (were 3) 3 vials of vasopressin (20 Units/vial) 1 bag of premixed dopamine 400mg in 250ml 4 Na Bicarbonate syringes (were 3) 5 filter needles 20 blunt cannulas Deletions: 1 dopamine vial (new total=1) Remove 5 epinephrine syringes (new total=10) Remove 1 lidocaine syringe (new total=2) Remove metoprolol

Needless System/Cannulas

Questions ?