Overview of ACLS Pharmacology and Update on New ACLS Guidelines

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 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!!! 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) Survival to hospital 24 hour survival Discharge alive 35% 20% 15% VP (n=20) 70% 60% 40% (p=0.06) (p=0.02) (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 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 Sodium (fast on-off) Sodium (slow on-off) Calcium Potassium Ic II III 0 0 Calcium IV 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 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 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 Amiodarone 70 Placebo % Surviving to Admission 60 50 40 30 20 10 0 All Patients VF Asystol e or PEA ROSC No ROSC 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 Suspected hypomagnesemia, pulseless VT/VF, torsade de pointes 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? 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 Refractory/recurrent VF/VT Control of rapid ventricular response (IIb) Conversion SVT (AF/Fl) (IIa) WHEN? • • • 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 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) WHAT? 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 Hepatic metabolism, renal elimination Bradycardia, cardiac arrest, seizures Lidocaine toxicity/neurotoxicity - twitching, LOC, seizures, coma Lidocaine levels persist in low CO states WHAT? 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 1 mEq/kg IVP, 0.5mEq/kg q10 min prn 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 HOW? WHAT? 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 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 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 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 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) 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 Negative inotrope & chronotrope (good anti-ischemic) Class I for acute and preventative SVT Direct negative chronotropic effect, mild negative inotrope Highly effective in controlling ventricular response in A Fib Control ventricular response rate in patients with AF/Fl, or MAT Verapamil: PSVT not requiring cardioversion Verapamil: Diltiazem: WHEN? 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 0.25 mg/kg IVP, may repeat with 0.35mg/kg in 15 min Infuse @ 5-15 mg/hr 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. 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 postMI patients, USA Atenolol: Metoprolol: Propranolol: Esmolol: 2.5-5 mg IV over 5 min 5 - 10 mg IVP q 5 min 0.1 mg/kg IV divided into 3 doses @ 2 - 3 min intervals 500 mcg/kg over 1 min Inf @ 50 mcg/kg/min HOW? WHAT? Hypotension, bradycardia, AV block, overt heart failure or severe bronchospasm/COPD Stable Monomorphic Ventricular Tachycardia Preserved Cardiac Function NOTE! May go directly to cardioversion Impaired LV EF<40% or CHF 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 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 PSVT (half-life=10 sec) If PSVT persists may want longer acting agent (verapamil or diltiazem) WHEN? 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 Flushing, dyspnea, chest pain, post-conversion bradycardia Drug interaction with theophylline, dipyridamole WHAT? 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 Epinephrine Atropine Search for the probable cause and intervene (HCO3) 1 mg IV q3-5 min. 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? HOW? 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) 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 Atropine Pacing Dopamine Comments/Dose 0.5-1.0 mg IVP q 3-5 min (max 0.03-0.04 Use Transcutaneous Pacing if severe S/S 5-20 µg/kg/min. Mnemonic All mg/kg) Patients Deserve 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? related) hypotension WHEN? HOW? NE precursor Stimulates DA,  & -adrenergic receptors (dose- Want  -stimulation, for bradycardia-induced Hypotension/shock 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? ACLS Algorithms Asystole • Consider possible causes and treat accordingly (ex.hypoxemia, hyper/hypokalemia, acidosis) Acronym “TEA” Transcutaneous Pacing (TCP) (Class IIb) Only effective with early implementation along with appropriate interventions and medications E A mg/kg) Epinephrine 1 mg IV q3-5 min. Atropine 1 mg IV q3-5 min. (max. dose 0.04 T • 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 Shock refractory to fluid replacement, severe hypotension 0.5 - 1 mcg/min refractory shock = 8 - 30 mcg/min 4-8mg/250 ml D5W or NS Hypertension, myocardial ischemia, cardiac arrest, palpitations Indication: Dose: Preparation: Caution: Drugs Used to Improve Cardiac Output and Blood Pressure Dobutamine Action: Indication: Dose: Preparation: Caution: B1- adrenergic activity Inotrope in heart failure/hypotension 2 - 20 mcg/kg/min 250 mg/250 ml D5W or NS tachyarrhythmias,worsens myocardial ischemia Drugs Used to Improve Cardiac Output and Blood Pressure Inamrinone and Milrinone Action: Phosphodiesterase inhibitors, positive inotropes and vasodilator Refractory heart failure 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 Indication: Dose: Caution: Thrombocytopenia, worsens myocardial ischemia, SV and ventricular arrhythmias 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 Hypertension, AMI, CHF Indication: Dose: Preparation: 0.1 - 5 mcg/kg/min, and titrate up to 10mcg/kg/min 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 ?