ACLS for the Clinical Pharmacist

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ACLS for the Clinical Pharmacist Krista A. Wahby, Pharm.D. Dale Tucker, RPh, MEd, BCPS June 2007

Objectives To review the importance of having a pharmacist attend codes To familiarize the pharmacist with the ACLS protocols To review routes of administration for medications used in code blue emergencies To introduce several common ECG rhythms To identify and discuss the most common drugs used by the ACLS algorithms

Why Involve Pharmacist? Improves outcomes in Code Blue Pharmacotherapy 2007. Apr 27(4);481-93. Pharmacotherapy 1999. 19(5);556-64. 64. Calculate drug doses Drug information Preparation of drugs Source of quick access for medications not on crash cart Assessment of patient s allergies and medication usage

Common Principles in New ACLS Guidelines - 2005 1. Early, effective bystander CPR 2. Early defibrillation - Public Access Defibrillation 3. Minimal interruptions in chest compressions 4. Establishing a specific diagnosis by ECG 5. Choose one antiarrhythmic agent One, and only one antiarrhythmic should be used. 6. If IV access is not established, Intraosseous cannulation is the first line alternative and endotracheal is an alternative.

Pharmacist Involvement Pharmacists should KNOW: How? Why? to use an agent we use an agent When? to use an agent What?...to watch for

How To Use the Medication?

Routes of Medications IV Push (IVP) Preferred route fast, convenient,+ bioavailability Peripheral flush w/ 20cc bolus and elevate arm for 10-20 seconds. Peak effect takes 1-21 2 minutes Central line should be placed (however, keep in mind it is a relative contraindication for thrombolytic therapy) V - vasopressin A amiodarone, atropine, adenosine L lidocaine E epinephrine

Intravenous Infusion Intravenous infusion Medications for continuous IV infusion only P procainamide I isoproterenol N norepinephrine D dopamine Central line preferred, however, peripheral OK in emergency

Intraosseous Administration When IV access not available Gives access to a noncollapsible venous access route Important when patients are in shock with peripheral vasoconstriction

Endotracheal Administration When IV access is not available Doses usually 2-2.52 2.5 times higher Absorption occurs at alveolar capillary interface Dilute drugs with 10ml 0.9% NaCl or Water to allow for adequate delivery (H2O preferred) L lidocaine (2-4 4 mg/kg) E epinephrine (2-2.5 2.5 mg) A atropine (2-3 3 mg) N naloxone (0.8-1.6 mg) V vasopressin (80-100 Units)

HOW? Medication Administration Do not interrupt chest compressions Time to maximum effect of drug may depend on the distance from the heart Administer 10-20ml NS after each drug administered (20ml if peripheral administration & elevate arm) Have medications labeled and ready in advance Best to give immediately after shock

WHEN To Use WHAT Medication?

Use of Algorithms Meant to treat broadest range of patients Memory aids Use wisely, not blindly Not meant to replace clinical judgment Where to find? American Heart Association Attached to crash cart Included in DMC Tier 2 policy acls.net on the web

Wave forms Check Rhythm ECG Rhythms healthcentral.org

ECG Rhythms Normal sinus rhythm healthcentral.org

ECG Rhythms Asystole Bradycardia healthcentral.org

ECG Rhythms Ventricular Tachycardia Ventricular Fibrillation healthcentral.org

ECG Rhythms Artifact (waveform interference) healthcentral.org

Cardiac Arrest Management 1. Pulseless Cardiac Arrest i.e. ASYSTOLE and PEA 2. VENTRICULAR FIBRILLATION and PULSELESS V.TACH

Pulseless Arrest Algorithm Minimize interruptions in chest compressions Limit pulse and rhythm checks Do not check pulse immediately after shock give 5 cycles, then check! Once advanced airway in place do not interrupt compressions

Asystole and Pulseless Electrical Activity (PEA) Asystole is a cardiac standstill PEA-pt has mechanical contractions but no pulse. Any rhythm possible Both are non-shockable rhythms Most do not survive Asystole means the patient s life has ended

Asystole & PEA Algorithm BLS Algorithm: Call for help, give CPR Give oxygen when available Attach monitor/defibrillator when available Check rhythm: shockable? YES or NO If NO and problem is asystole/pea Resume CPR immediately for 5 cycles Give vasopressor: Epinephrine or vasopressin Consider Atropine for asystole or slow PEA rate Give 5 cycles of CPR Check rhythm: shockable? If no:

Asystole and PEA Algorithm P E A Interventions Problem search via Differential Diagnosis table; treat accordingly. (PATCH 4MDs) Continue algorithm if indicated. Epinephrine 1 mg IVP/IO q3-5 5 min. OR Vasopressin 40 units IV/IO, once, in place of the first or second dose of epinephrine. Atropine 1 mg IVP/IO q3-5 5 minutes; 3mg maximum.

Problem Search: Differential Diagnosis PATCH(4) MDs Pulmonary embolism Acidosis Thrombolytics Bicarb./hyperventilation Tension pneumothorax Thoracostomy Cardiac tamponade Pericardiocentesis Hyperkalemia HCO3, CaCl,, Ins/Glc Glc,, HD, diuresis, kayexylate Hypokalemia Hypovolemia Hypoxia Myocardial infarct ACS protocol Avoid BB if cocaine Drugs Shivering

Basic Pharmacology Review

Vasoactive Receptor Effects α1 VASOCONSTRICTION of arteries and veins α2 Feedback and Vasoconstriction Decreases NE release β1 INOTROPE & CHRONOTROPE β2 VASODILATION (skin, kidneys, skeletal muscles, visceral and pulmonary arteries) and BRONCHODILATION

Vasopressor Therapy Increases SBP by increasing preload and ventricular filling pressure Enhance organ perfusion, increase cerebral and coronary perfusion pressures (increases success of defibrillation) Mostly via α 1 stimulation and V 1 stimulation List the Vasopressors: Epinephrine Vasopressin Norepinephrine Phenylephrine Dopamine

Inotropic Therapy Increase cardiac contractility and increase cardiac output (CO) Work via β1 1 stimulation and/or by increasing camp and Calcium influx List the Inotropes: Dobutamine Milrinone (or inamrinone) Digoxin Glucagon

Catecholamine Pharmacology Bind to β adrenoreceptor and stimulate Gs protein Stimulates adenylate cyclase, camp camp acts to INCREASE Ca INFLUX VASOCONSTRICTION, INOTROPY

E = Epinephrine 1mg IVP/IO every 3-53 5 minutes. GOAL Improve Perfusion to Essential Organs (Heart, Brain). Shifts blood centrally. MOA Alpha and Beta Adrenergic Agonist α1 Vasoconstriction. Increases BP; improves cerebral and coronary perfusion pressures β 1-2 - Stimulates the cardiac muscle increasing the strength of ventricular contraction. + inotrope and chronotrope. Does increase myocardial work

Epinephrine Side Effects Nervous system: anxiety, agitation Cardiovascular: dilated CM, LV dysfunction Psychiatric: disorientation, hallucinations Metabolic: acidosis, hypokalemia Renal: renal insufficiency Other: extravasation, skin necrosis

Vasopresssin Vasopressin 40 units IVP/IO x 1 (2 vials required. Each vial = 20 Units) May replace 1st or 2 nd dose of epinephrine Pharmacology: : Endogenous ADH Causes vasoconstriction at high doses by directly stimulating smooth muscle V 1 receptors Dilates cerebral blood vessels Coronary & renal vasoconstriction

Vasopressin Rationale Enhance organ perfusion Advantages over epinephrine? Longer half-life life (10-20 minutes) Not affected by acidosis Unique MOA - nonadrenergic Best outcomes in ASYSTOLE? Pharmacotherapy 2006;26(6):828-839

Vasopressin Side Effects GI: nausea, intestinal cramps Increased mesenteric vascular resistance Bronchial constriction Uterine contractions Extravasation - necrosis

A = Atropine 1mg IVP/IO every 3-53 5 minutes up to a maximum of 3 mg Excessive parasympathetic tone may play a role in stopping ventricular and supraventricular pacemaker activity Avoid if lack of cardiac activity has a clear explanation such as hypothermia

Atropine Pharmacology Competitive antagonist of acetylcholine Vagolytic action causes restoration of heart rate and blood pressure Reverses cholinergic-mediated decreases in: Heart rate Systemic vascular resistance Blood pressure

Atropine Side Effects Anticholinergic Confusion Blurred vision Dry mouth, skin, nose Constipation Urinary retention Lightheadedness

VF and PVT VF = ventricular fibrillation Fibrillary contractions of the ventricular muscle due to rapid repetitive excitation of myocardial fibers without coordinated contraction of the ventricle PVT = pulseless ventricular tachycardia An abnormally rapid ventricular rhythm with aberrant ventricular excitation most commonly associated with atrioventricular dissociation The patient has no pulse

ECG Rhythms Ventricular fibrillation healthcentral.org

ECG Rhythms Ventricular tachycardia healthcentral.org

VF/PVT Algorithm: SCREAM Give 1 shock Resume CPR immediately for 5 cycles Check rhythm: : Shockable? YES or NO? YES - Continue CPR while defibrillator is charging Give 1 shock Resume CPR immediately after the shock When IV/PO available give vasopressor (epinephrine( or vasopressin) during CPR before or after the shock Check rhythm: if shockable Continue CPR while defibrillator is charging Give 1 shock Resume CPR immediately after the shock Consider antiarrhythmic medications (amiodarone, lidocaine, magnesium): give during CPR before or after the shock After 5 cycles of CPR

Shock Manual biphasic Device specific Typically 120-200 200 J If unknown, use 200 J AED Device specific Monophasic 360 J

VF/PVT Algorithm: SCREAM S Shock 360J monophasic, 1 st and subsequent shocks. Shock every 2 minutes if indicated. C R CPR Rhythm After shock, immediately begin chest compressions followed by respirations for 2 minutes. Do not check rhythm or pulse. Rhythm check after 2 minutes of CPR (and after every 2 minutes of CPR thereafter) and shock again if indicated. Check pulse only if an organized or non-shockable rhythm is present Implement the Secondary ABCD Survey. Continue this algorithm if indicated. Give drugs during CPR before or after shocking. Minimize imize interruptions in chest compressions to < 10 seconds. Consider differential diagnosis.

VF/PVT Algorithm: SCREAM E Epinephrine 1mg IVP/IO q3-5 5 minutes or vasopressin 40 units IV/IO, once, in place of the 1 st or 2 nd dose of epinephrine. A M Antiarrhythmic Medications Consider antiarrhythmics: Any ny Legitimate Medication Amiodarone 300mg IVP/IO, may repeat once at 150mg in 3-53 5 minutes if VF/PVT persists or Lidocaine (if amiodarone unavailable) 1-1 1.5mg/kg IVP/IO, may repeat X2, q5-10 min at 0.5-0.75mg/kg 0.75mg/kg Max LD= 3mg/kg Magnesium Sulfate 1-22 gm IVP/IO diluted in 10m D5/W (5-20 min push) for torsades de pointes or suspected/known hypomagnesemia.

Amiodarone 300mg IVP/IO once, then consider additional 150mg IVP/IO once If pt is pulseless, give IVP, otherwise dilution with 20-30ml and a slower infusion results in less bradycardia, hypotension and phlebitis Infusion OK peripherally if < 2mg/ml Not for ET administration

Amiodarone MOA: Inhibits conduction through Sodium, Potassium and Calcium channels and α & β adrenergic blocking ability Inhibits adrenergic stimulation, prolongs the action potential and refractory period in myocardial tissue, and decreases AV conduction and sinus node function Based on ARREST and ALIVE Trials Side effects: hypotension, bradycardia, nausea, vomiting, tremor, dizziness, headache, phlebitis

Lidocaine 1-1.51.5 mg/kg first dose then 0.5-0.75mg/kg 0.75mg/kg IVP/IO q5-10 minutes Maximum of 3 doses or 3 mg/kg After return of ROSC infuse at 1-41 4 mg/min (50% reduction if cardiac or liver failure) Suppresses automaticity of conduction tissue and blocks both the initiation and conduction of nerve impulses Side effects: hypotension, headache, shivering

Magnesium 1-22 grams IVP/IO diluted in 10ml D5W over 5-205 minutes. If patient has pulse, can slow down infusion to 30-60 min INDICATION: torsades de pointes Low magnesium causes inhibition of conduction through K+ channels in heart prolongs AP and QT prolongation Side effects: flushing, somnolence, complete heart block, respiratory paralysis

Arrhythmia Management Bradycardia Tachycardia: SVT

Bradycardia Bradycardia: HR < 60 beats/minute or when the heart rate is slower than expected Signs and symptoms might include: Chest pain, shortness of breath Hypotension, pulmonary edema, congestive heart failure

ECG Rhythms Sinus bradycardia healthcentral.org

Bradycardia Algorithm: Pacing Always Ends Danger Maintain patient airway; assist breathing as needed Give oxygen Monitor ECG, blood pressure, oximetry Establish IV access Signs/symptoms of poor perfusion caused by the bradycardia? If yes: Prepare for transcutaneous pacing Consider atropine IV while awaiting pacer; if ineffective begin pacing Consider epinephrine or dopamine infusion while awaiting pacer or if pacing ineffective Prepare for transvenous pacing Treat contributing causes Consider expert consultation

Bradycardia Algorithm: Pacing Always Ends Danger Mnemonic Pacing Intervention TCP Note Immediately prepare for TCP with serious circulatory compromise due to bradycardia (especially high-degree blocks) or if atropine failed to increase rate Consider medications while pacing is readied. Always Ends Danger Atropine Epinephrine 2-10mcg/min Dopamine 2-10 mcg/kg/min First line drug, 0.5mg IV/IO q3-5 5 min (maximum 3mg) Second line drugs to consider if atropine and/or TCP are ineffective. Use with extreme caution

Transcutaneous Pacing Used to speed up a cardiac rhythm that is too slow If considered, start immediately To be effective, must be performed early and combined with drug therapy

Transcutaneous Pacing Apparatus

Atropine Atropine 0.5 mg IV while awaiting pacer 50% reduction in dose when compared with PEA algorithm May repeat to a total dose of 3 mg If ineffective, begin pacing

Epinephrine Consider epinephrine 2-102 mcg/min continuous infusion while awaiting pacer Use 1ml of the 1:1000 or 10 ml of the 1:10,000 in 500ml D5W Alternatively, 0.5 mg IVP boluses To avoid tachyarrhythmias Until continuous infusion available Until pacemaker available Or if pacing ineffective

Dopamine Or consider dopamine 2-102 mcg/kg/min infusion while awaiting pacer or if pacing ineffective MOA: Precursor of norepinephrine, stimulates heart through both alpha- and beta-adrenergic adrenergic receptors Increases both cardiac output and arterial perfusion pressure

Dopamine Side Effects Cardiovascular: ectopic heartbeats, tachycardia, vasoconstriction, hypotension, ventricular arrhythimas CNS: headache GI: nausea, vomiting Respiratory: dyspnea Other: Adrenal insufficiency

Tachycardia Algorithm Assess and support ABCs as needed Give oxygen Monitor ECG, blood pressure, oximetry Identify and treat reversible causes Symptoms persist and patient stable Establish IV access Obtain 12-lead ECG or rhythm strip Is QRS narrow or wide? Narrow QRS (<0.12 sec) with regular rhythm Narrow QRS (<0.12 sec) with regular rhythm

Tachycardia Algorithm (continued) Attempt vagal maneuvers Give adenosine 6mg rapid IVP If no conversion, give 12mg rapid IVP May repeat 12mg dose once Does rhythm convert? Note: Consider expert consultation Yes: Probable reentry SVT. Observe for recurrence. Treat recurrence with adenosine or diltiazem (Cardizem( Cardizem) ) or beta- blockers. or No: Possible atrial flutter, ectopic atrial tachycardia, or junctional tachycardia. Control rate with diltiazem (Cardizem)) or beta-blockers. blockers. Treat underlying cause. Consider expert consultation.

Tachycardia Algorithm Tachycardia is stable, narrow, and regular: Yes Yes 1-2-3, 1 think SVT, then V-A-C 1. Stable? 2. Narrow? 3. Regular? Yes: see question 2 Yes: see question 3 Yes: see mnemonic No: unstable = immediate electrical cardioversion No: wide = consult an expert with QRS 0.12 sec No: irregular = consult an expert www.acls.net

Tachycardia Algorithm Yes 1-2-3, 1 think SVT, then V-A-C Vagal maneuvers, if this fails Adenosine 6 mg rapid IVP (may repeat X2, q1-2 2 min at 12mg) Cardizem (diltiazem) managed by an expert if stable, narrow, regular tachyarrhythmia continues www.acls.net

Vagal Maneuvers Valsalva s maneuver A forcible exhalation effort against a closed glottis which results in an increase in intrathoracic pressure which interferes with venous return to the heart Carotid sinus massage Firm rotatory pressure applied to one side of the neck over the carotid sinus in a supine patient to cause vagal stimulation in order to slow or terminate tachycardia

Adenosine To convert SVT: 6 mg rapid IVP over 1-1 3sec followed by 20ml saline flush; if rate dose not convert in 1-21 2 min give 12mg IVP & repeat 12mg in 1-21 2 minutes again Larger doses required for patients with significant blood levels of theophylline, caffeine, or theobromine Reduce initial dose to 3 mg in patients taking dipyridamole or carbamazepine or those with transplanted hearts or if given by central venous access

Adenosine Slows conduction time through AV node, interrupts reentry pathways through AVN and restores NSR Side effects common but transient: flushing, dyspnea, chest pain

Diltiazem (Cardizem) Use if adenosine fails 15-20mg (0.25mg/kg) IVP over 2 min; if needed in 15 minutes give an IVP dose of 20-25mg 25mg (0.35mg/kg) Maintenance infusion dose is 5-15mg/hr5 Blocks conduction through the AV node Harmful if given to patients with atrial fibrillation or atrial flutter associated with known pre-excitation excitation such as Wolf- Parkinson-White

Cases: Rhythm: What is this? Algorithm? Drugs/Doses? Ventricular Fibrillation SCREAM Epi 1 mg q3-5min Amiodarone 300mg IVP, may repeat with 150mg

Cases: Rhythm: What is this? Algorithm? Drugs/Doses? Asystole PEA Epi 1 mg q3-5min (or vasopressin 40 Units IVP) Atropine 1mg q3-5 5 min to max dose = 3mg

Cases: Rhythm: What is this? Algorithm? Drugs/Doses? Bradycardia Pacing Always Ends Danger Atropine 0.5 mg q3-5min to max = 3mg Epi 2-102 mcg/min Dopamine 2-102 mcg/kg/min

Cases: Rhythm: What is this? Algorithm? Drugs/Doses? SVT Yes 1, 2, 3, then think VAC Adenosine 6mg IVP then 12mg IVP, then 12mg IVP Cardizem 15-20 mg IVP then 5-15 mg/hr

Other Code Situations Anaphylaxis: Epi 0.3-0.5 0.5 mg IV, steroids, ranitidine, diphenhydramine AFib: diltiazem, βb, digoxin, amiodarone, ibutilide Hyperkalemia: Insulin + D50; CaCl; Bicarb; albuterol, dialysis, kayexylate, furosemide Hypotension: Norepinephrine 5-205 mcg/min, Phenylephrine 20-180 mcg/min; Vasopressin 0.01-0.03 0.03 Units/min, Dopamine 10-20 mcg/kg/min

Other Code Situations Pulmonary Embolism: Massive PE with shock or hemodynamic instability should receive tpa 100mg IVPB over 2 hr Status Epilepticus: Lorazepam 0.1mg/kg IVP, Phenytoin 10-20 mg/kg IVPB or Fosphenytoin Prolonged Code: Systemic acidosis ensues NaBicarb may be appropriate

Induced Hypothermia Hypothermia for 24 hr Hypothermia After Cardiac Arrest (HACA) NEJM 2002;346:557-63 63 Ice packs, Artic Sun Protocol, Cooling blankets Requires continuous sedative and analgesic infusions, meperidine for shivering and avoidance of anticoagulation

Take Away Points Most frequently used medications Epinephrine: asystole, bradycardia, PEA, VF/PVT Atropine: asystole, bradycardia, PEA Vasopressin: asystole, PEA, VF/PVT

Take Away Points Medications IVPB only P - procainamide I - isoproterenol N - norepinephrine D - dopamine Medications IVP or IVPB V - vasopressin A amiodarone, adenosine, atropine L - lidocaine E - epinephrine Tracheal administration L lidocaine E epinephrine A atropine N naloxone V - vasopressin Doses usually 2-2.52 2.5 times those given IVP Follow each dose with 10 ml NS flush down tracheal tube if not diluted to that volume for administration

Supplemental Reading Cardiovascular complications of cocaine use. N Engl J Med 2001;345(5):351-358 358 Evolving role of vasopressin in the treatment of cardiac arrest. Pharmacotherapy 2006;26(6):828-839 839 Pharmacotherapy considerations in advanced cardiac life support. Pharmacotherapy 2006;26(12):1703-1729 1729