om & g) PHILIPPINE HEART ASSOCIATION, INC. on “u=$”" PHILIPPINE COLLEGE OF CARDIOLOGY COUNCIL ON CARDIOPULMONARY RESUSCITATION — ILCOR Member: Resuscitation Council of Asia Affiliate of the International Liaison Committee on Resuscitation (ILCOR) MANUAL ON BASIC anpD ADVANCED CARDIAC LIFE SUPPORTFOREWORD When an adult has a sudden cardiac arrest, his or her survival immediate cardiopulmonary resuscitation (CPR) from someone life-saving technique. CPR techniques and interventions for both basi support (BLS and ACLS) are based on recommendations backed by Scientific evidence and general experts’ consensus The 2015 guidelines on CPR released by the American Heart Association (AHA) and the International Liaison Committee on Resuscitation (ILCOR), highlights some of the important updates and advances in the Management of sudden cardiac arrest that have evolved over the last century, including the major improvements observed in resuscitation techniques. The Philippine Heart Association (PHA) Council on CPR, a member of the Resuscitation Council of Asia, and affiliate of the ILCOR, calls on all CPR trainees, providers and educators to take note of the revisions, adopt the changes in clinical practice, and disseminate them to other CPR Providers. depends on i Gettin, Nearby. CPR ig 2 IC and advanced life The Council emphasizes that CPR is a skill that is learned and that needs regular evaluation and update. Knowledge and competency in BLS and ACLS deteriorate in as little as 3 to 6 months without practice or update. Continuous and frequent training and recertification is important. The recommended recertification period is every 2 years. This BLS and ACLS training handbook is intended as a guide for trainees during CPR courses conducted by the PHA Council on CPR. The trainee is advised to do further reading and refer to the 2015 AHA/ILCOR Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, published in the journal Circulation November 3,2015, volume 132(Issue 18, volume 2), pages S313 -S589, from which the recommendations are based on. The full journal article may be accessed at http://circ.ahajournals, org/content/132/18_suppl_2.toc or through the PHA website at www.philheart.org, EUROPEAN RESUSCITATION cOUNCHL ‘Finaing answers. For WjPHILIPPINE HEART ASSOCIATION, INC. PHILIPPINE COLLEGE OF CARDIOLOGY OFFICERS & BOARD OF DIRECTORS (2018-2019) Nannette R. Rey, MD President Aurelia G. Leus, MD Vice-President Mr. Romeo B. Cruz VP for Finance Atty. Darlene Marie B. Berberabe VP for External Affairs Orlando R. Bugarin, MD Secretary Gilbert C. Villela, MD Treasurer Jude Erric L. Cinco, MD Director Ronald E. Cuyco, MD Director Rodney M. Jimenez, MD Director Jorge A. Sison, MD Immediate Past President Gina Capili-Inciong Executive DirectorPHILIPPINE HEART ASSOCIATIN, INC. PHILIPPINE COLLEGE OF CARDIOLOGY COUNCIL ON CARDIOPULMONARY RESUSCITATION Full Member of the Resuscitation Council Of Asia, the Affliate Representative to the Internat ‘ais it Fah resentative tothe International Liaison Committee COUNCIL ON CARDIOPULMONARY RESUSCITATION (2017-2019) Chair: Francis N. Lavapie, MD Members: Jerelyn B. Adviento, MD Elmer Jasper B. Llanes, MD Marian N. Almajar, MD Elmer A. Linao, MD Gina D. Alemany, MD Adriano E. Magpali Jt, MD Ma, Magdalena S. Avelino, MD Muriel A. Morila, MD Raymund Paul C. Baello, MD Christopher Oliver P. Nazal, MD Crismelita Marifias-Baftez, MD Ma Gina A. Ogaco, MD Albert Hans P. Bautista, MD Annie U. Olarte, MD Raymond D. Bayaua, MD Ryan Nifo C. Padua, MD Max Geronimo T. Butardo, MD Ellen M Palomares, MD Katrina G. Castillo, MD Gretchen V, Parayno, MD Jude Erric L. Cinco, MD Eric S. Pascual, MD Chertamir C. Cruz-Rioveros, MD Elaine C. Payumo, MD Janice Lorie Tuazon-Cruz, MD Melco T. Perez, MD Alvin 0. De la Cruz, MD Jose Paolo A. Prado, MD Raymond A. De La Cruz, MD Percy Jun G, Prieto, MD Jeannica Kriselle L. De La Pefia, MD Elizabeth Gayle D. Ramos, MD Carlos F. De Las Llagas, MD Don Robespierre C. Reyes, MD Leah Divine M. De Las Llagas, MD Allan M. Romero, MD Aileen Cynthia F. De Lara, MD Michelangelo L. Sabas, MD Erwin M. Dolores, MD John Vincent T. Salvanera, MD Regidor_R. Encabo, MD Ma, Rosiete M. Samson, MD Rosalyn S. Enriquez, MD Jason S, Santos, MD Karen Gail A. Floren, MD Rodrigo C. Santos, MD Andrew T. Francisco, MD Joanne C. San Pedro, MD Ma. Victoria P. Garcia, MD Leah P. Sanglay, MD Mario Joselito D. Garcia, MD Karen Mae A. Sayson, MD Angelita G, Go, MD Luigi Pierre S. Segundo, MD Bernadette s. Halasan, MD Maria Carmelita A. Somera, MD Floydecielles L. Tuazon-Jasmin, MD Ma. Luz Joanna B. Soria, MD Gabriel B Jocson Ill, MD Richard Henry P. Tiongco I, MD Joyce S. Jumangit, MD Mark Denver A. Tiongson, MD Alex T. Junia, MD Eduardo L. Tin Hay, MD Gloria R. Lahoz, MD Anjanette Uy-Yumul, MD Regente |. Lapak, MD Ariel D. Valones, MD Victor L. Lazaro, MD Ma, Vanessa |, Yu, MD Rosie T. Lim, MD Immediate Past Chair: Orlando R. Bugarin, MD Advisers (Ex-officio): Marcellus Francis R. Ramirez, MD Raul E. Ramboyong, MD Roberto A. Raymundo, MD Clarissa M. Mendoza, MD Oscar P. Payawal Manual on Basic and Advanced Cardiac Life § Romeo A. Divinagracia, MD Ramoncito 8, Habaluyas, MD Leandro C. Bongosia, MD Petrarch B. Bravo, MD Marcelito L. Durante, MDXl XIL XII XIV. XV. XVI XVIL XVIIL XIX. Manual on Basic and Advanced Cardiac Life Support Table of Contents Sudden Cardiac Arrest and CPR Awareness The Chain of Survival Steps in Basic Life Support for Healthcare Providers... The New Step by Step Guide in CPR for Lay/Untrained Rescuers... The New Step by Step Guide in CPR for Trained Rescuers .... Algorithm Adult BLS Healthcare Providers .... Algorithm Pediatric BLS- Single Rescuer... Algorithm Pediatric BLS — 2 Rescuer Advanced Cardiac Life Support... Simple Approach to ECG Recognition of the Arrhythmias During the ACLS. Defibrillation .... Cardiac Drugs. Pulseless Cardiac Arrest Algorithm “Adult Cardiac Arrest” ... TachyCardia Algorithm... Bradycardia Algorithm... Post Cardiac Care Algorithm Acute Coronary Syndromes Algorithm... First Aid Ethics in Resuscitation...SUDDEN CARDIAC ARREST AND CPR AWARENESS BACKGROUND .¢ are the number 1 killer in our country, accounting for close to 20% of all causes Le an latest Department of Health statistics. of death according to the I Approximately half ofall deaths from cardiovascular disease occur as Sudden Cardiac Arrest diac arrest : ; Sudden cahappen at any time, to anyone, anywhere without warning ® most common mode of death in patients with coronary artery disease + although pre-existing heart disease is a common cause, it may strike people with no history of cardiac disease or cardiac symptoms. In sudden cardiac arrest or sudden cardiac death, the heart usually goes into a fatal arrhythmia called “Ventricular Fibrillation" (VF) wherein it suddenly goes into very irregular fast ineffective contractions, the heart stops beating, the victim loses consciousness, and if untreated, dies. Despite advances in Emergency Medical Systems and in the technology of resuscitation, sudden cardiac arrest remains a major public health problem. It is associated with low survival rate, and major long term severe mental impairment due to delays in cardiopulmonary resuscitation (CPR) and treatment. Majority of cardiac arrests occur outside the hospital- at home, in the workplace, in public institutions. + Almost 70 percent of out-of-hospital cardiac arrests occur at home and are witnessed by a family member and approximately 50% are unwitnessed. + Only 10.8% of Out-of Hospital Cardiac Arrest (OHCA) who have received CPR from (EMS) survive to hospital discharge . + _In-hospital cardiac arrest (IHCA) has a better outcome, with 22.3% to 25.5% of adults surviving to discharge Unfortunately, approximately less than 10 percent of sudden cardiac arrest victims survive because majority of those witnessing the arrest are people who do not know how to perform CPR or cardiopulmonary resuscitation is an emergency procedure used when someone's heart _ itis a simple inexpensive procedure that can be learned by anyone, and consists of 2 chnique using repetitive pressing to the chest and breathing into the person's ough oxygen and blood flowing to the brain 2dical skills and training is available for the ordinary person ter collapse, plus early advanced care fal rates for witnessed venticlar oeIf bystander CPR is not provided, a cardiac arrest victim's chances of survival fall 7 % to 10 % for every minute of delay until defibrillation.THE CHAIN OF SURVIVAL Sm EET aia tie See ed = . This is a concept which aims to improve the outcome for victims of cardiopulmonary arrest It involves a series of events which are interconnected to each other like the links of a chain. The 5 links in the Chain of Survival (Top figure) are described specifically as: (1) early access, (2) early CPR (3) early defibrillation, and (4) early ACLS., (5) Integrated post-cardiac arrest care, Based on the new 2015 AHA CPR/ECC Guidelines, they have recommended Separate Chains of Survival that identify the different pathways of care for patients who experienced Cardiac Arrest in the Hospital (IHCA) and Out of Hospital (OHCA) settings. (Left and right figures). The care for all post cardiac arrest patients (IHCA and OHCA) all converge in the hospital ICU setting. Patients who had an OHCA depend on their community for support where Lay rescuers ‘must recognize the arrest, call for help and initiate CPR and apply Public AED protocols until EMS arrives and patient ultimately transferred to Hospital. The patients who had IHCA depend ‘on a system of appropriate surveillance (e.g. rapid response or early warning system) to prevent cardiac arrest. All IHCA patients depend on a smooth multidisciplinary interaction among the department services and allied health providers including physicians, nurses, respiratory therapists and others. The First Link- Early Access * Awell-informed person - key in the early access link. Recognition of signs of heart attack and respiratory failure Call for help immediately if needed Activate the Emergency Medical System technique for cardiac & respiratory arrest s +/- Rescue breathingSTEPS IN BASIC LIFE SUPPORT FOR HEALTHCARE PROVIDERS IF YOU SEE A PERSON DROP DEAD, OR LOSE CONSCIOUSNESS, WITH PRESUMED SUDDEN CARDIAC ARREST, AREA Survey the scone. NON-RESPONSIVE, eetascreaeraeeeeses NO NORMAL BREATHING morewe mer | Geta Defibrillator! {1 he vitim Is unconscious, ‘rescuer calls for help. ‘Rescuer ACTIVATES the EMERGENCY MEDICAL cau FOR HELP: uence Emergency Services, Get AEDDefbrillatort Doctor a “PULSE CHECK |, = Palpate for Carotid Pulse within 10 seconds: = (atthe same time CHECK FOR BREATHING) + For trained healthcare providers only |) MOUTHTO MOUTH BREATHING and ~ \ y PULSE CHECK I * For trained healthcare providers only I + As short and quick as possible \ * Pulse check not more than 10 seconds * Ifunsure, proceed directly to CHEST | COMPRESSIONS| XN @)[ c- Compression (to assist CrrcuLatron) determining unconsciousness Le Ae calteg tor, Hand Location VV proceed immediately to do victim's chest ; - Place the heel of Cuest See EJ za Pc a ComPRESSIONS! @y i=. @® WEB tingers intertaced. a Give Chest Compressions at 100 - 120 per minute Compress breast bone 2:2.4 inches deep (5-6 cm) Compress at a rate of 100-120 per minute or more ® 30 Compressions Give * Compress breastbone 2 2.4 inches deep = (90 compressions should take 15-18 sec) ' Count aloud “1, 2.3, 4, 5.6,7,8,9,10,19,12,13,14,15,16,17,18,19, 20,21,22,23,24,25,26,27,28,20, and oNer’ Compress 30 times intially ‘Allow the chest to return to its normal position A-ATRWAY ene Nowy. lift method y it “Manual on Basic and Advanced Cardiac Life Su???Repeat cycles of 30 compressions Ge PULSE CHECK + RECHECK PULSE EVERY 2 MINUTES (equivalentto 5 cycles CPR) + Very brief pulse check - should take less than 10 seconds (atthe sametime |e«HELP ARRIVES. (Emergency Services, Ambulance, Doctor, AED) check for normal breathing) « Incase there is any doubt about the ce or absence of pulse, CONTINUE CHEST COMPRESSIONS *PERSON IS REVIVED. + For trained healthcare providers only a CONTINUE CPR @) If the victim is breathing Postion consists of rating the Ene here ha ee MEMORIZE THE STEPS! aoa aarti Beta Se ASST: + B~ Breathing: 2 breaths (| second/breath) ‘hest compressions 30 x ges 20: ggreereneion-venitetan, ‘Count 1-2-3- 1THE NEW STEP BY STEP GUIDE IN CPR FOR LAY / UNTRAINED RESCUERS: IF APATIENT/VICTIM SUDDENLY DROPS UNCONSCIOUS OR IS SEEN UNCONSCloys, do CPR ; 's safe to ‘esponsive, roll victim on his/her back. ddical services; call for an ambulance/doctor, Start chest compressions. Place the heel of your hand on the center of the victim's ches nd on top of the first with your fingers interlaced . aes sa eas eto tie chest at least 2 to 2.4 inches in oe Allow complete reooj after each compression. Compress continuously with both hands at a rate of 100-129) minute (Compress to the tune of Bee Gee's song “Stayin’ Alive.”) For lay or untrained rescuers, continue this Hands Only CPR - do continuous chest compressions until help arrives, an automated external defibrillator (AED) is available or the emergency personnel arrives, or the victim is revived back to life. Survey the scene to see if it Check victim's unresponsiveness. If unr Call for help; activate the emergency me: eo ie 2 THE NEW STEP BY STEP GUIDE IN CPR FOR TRAINED RESCUERS: IF APATIENT/VICTIM SUDDENLY DROPS UNCONSCIOUS OR IS SEEN UNCONSCIOus: - Survey the scene to see if it's safe to do CPR. . Check victim's unresponsiveness. If unresponsive, roll victim on his/her back. . Call for help; activate the emergency medical services; call for an ambulance/doctor. . Start chest compressions. Place the heel of your hand on the center of the victim's chest. Put your other hand on top of the first with your fingers interlaced. 5. Press down and compress the chest at least 2 to 2.4 inches in adults. Allow complete recoil after each compression. Compress 30 times with both hands at a rate of 100 - 120/minute or more (Compress to the tune of Bee Gee's song “Stayin’ Alive.”). .. After 30 compressions, you can now open the airway with a head tilt and chin lift. - Pinch to close the nose of the victim. Take a normal breath, cover the victim's mouth with yours to create an airtight seal, and then give two, one-second breaths as. you watch the chest rise. . Continue cycles of compressions and breaths — 30 compressions, two breaths - until help arrives, until an automated external defibrillator (AED) is available. until the victim is revived back to life, or until the emergency medical personnel takes over. eons No 2 does not have a barrier device for mouth to mouth, he may just do compression only, 0 Hands Only CPR: press hard and fast in the center of the chest by pressing down with two hands compressing the chest 2 to 2.4 inches at a fate of 100 — 120 per minute. pot Manual on Basic and Advanced Cardiac Life SUPBasic Life Support Sequence [step | Lay Rescuer Not Trained Lay Rescuer Trained Healthcare Provider 7 _| Ensure scene safety. Ensure scene safety. _| Ensure scene safety. Tp _| Check for response. Check for response. _| Check for response. Shout for nearby help and Shout for nearby help. ‘ activate the emergency Shout for nearby help/ Phone or ask pores (0 | response system (9-1-1, activate the resuscitation phone 9-1-1 (the phone | emergency response). If _ | team; can activate the 3 or caller with the phone someone responds, ensure | resuscitation team at this remains at the victim's that the phone is at the time or after checking side, with the phone on side of the victim if at all breathing and pulse speaker). possible. Check for no breathing or only gasping and check pulse (ideally simultaneously). Activation and retrieval of the AED/ ; emergency equipment by Follow the dispatchers | Check forno breathing or | either the lone healthcare 1 only gasping; if none, begin | © oy; instructions. Bee et etre. 4 | provider or by the second e * | person sent by the rescuer must occur no later than immediately after the check for no normal breathing and no pulse identifies, cardiac arrest. Look for no breathing ‘Answer the dispatcher’s _| Immediately begin 5 | oronly gasping, at the questions, and follow the | CPR, and use the AED/ direction of the dispatcher. | dispatcher's instructions. _| defibrillator when available. | rotowtnedspacners _|S9ndte second person | ven poise 2eton instructions. Swallable : CPR and use AED/ ; defibrillator. * AED indicates automated external defibrillator; and CPR, cardiopulmonary resuscitation. 13Cas One) ry Make sure the environment is safe for rescuers and victims TT Cou Excluding Newborns) Children (Age 1 Year to Puberty) Scene Safety = Check for responsiveness Recognition of ‘ pesrigasi No breathing or only gasping (ie, no normal brathing) No definite pulse felt within 10 seconds (Breathing and pulse check can be performed simultaneously in ess than 10 secondo) raeaion ef if you are alone with no Witnessed collapse emergency mobile phone, leave the victim Follow steps for adults and adolescents on the left response system | activate the emergency response system and get the Unwitnessed collapse ‘AED before beginning CPR Give 2 minutes of CPR Otherwise, send someone and | Leave the victim to activate the emergency response system and begin CPR immediately; use the get the AED ‘AED as soon as itis available Retum tothe child or infant and resume CPR; Use the AED as soon as itis available Compression- 1 or 2 rescuers Tach ventilation ratio 302 302 without advanced a 2ormore rescuers seit 182 Continuous compressions ata rate of 100-120/min Give 1 breath every 6 seconds (10 breaths/min) se 400-120imin ‘Atleast Zinches (5cm)" | Atleast one third AP diameter | Atleast one thd AP diameter of chest of chest ‘About 2 inches (5 om) About 1" inches (4 em) 2 hands or 1 hand (optional for 1 rescuer very small child) on the lower | 2 fingers in the center of the half of the breastbone (stemum) | chest, just below the nipple line 2 or more rescuers 2 thumb-encircing hands inthe center ofthe chest, ust belowjealthcare Provider ei cardieo Arrest Algorithm—2015 Update By this time in all scenarios, emergency response system or backup is activated, and AED and emergency equipment are retrieved or someone is retrieving them. 15BLS Healthcare Provider Pediatric Cardiac Arrest Algorithm for the Single Rescuer—2015 Update sna woe Victim is unresponsive. ‘Shout for nearby help. Activate emergency response system via mobile device ff appropriate). / Look for no breathing ‘breathing, has pulse he ‘or only gasping and check \\ has pulse pulse (si Is pulse definitely felt within 10 seconds? response system (f not already done). Return to victim No breathing or only gasping, no pulse Basic and Advanced Cardiac Life SupportBLS Healthcare Provider Pediatric Cardiac Arrest Algorithm for 2 or More Rescu lers—2015 Upd lateADVANCED CARDIAC LIFE SUPPORT ACLS includes sae Basic Life Support (BLS) The use of adjunctive equipment and special techniques for establishing and maintaining effective ventilation and circulation. Electrocardiographic (ECG) monitoring and arrhythmia recognition. Establishment and maintenance of intravenous (IV) access. Therapies for emergency treatment of patients with cardiac or respiratory arrests (including stabilization in the post arrest phase) and, Treatment for patients with suspected Acute Myocardial Infarction and stroke. ACLS includes the ability to perform these skills, and the knowledge, training, and judgment about when and how to use them. The Algorithm Approach to Emergency Cardiac Care (ECC) The following clinical recommendations apply to all treatment algorithms. First, treat the patient not the monitor. Algorithms for cardiac arrest presume that the condition under discussion continually persists, that the patient remains in cardiac arrest, and that CPR is always performed. Apply different interventions whenever appropriate indications exist. Adequate airway, ventilation, oxygenation, chest compressions, and defibrillation are more important than administration of medications and take precedence over initiating an intravenous line or injecting pharmacologic agents. Several medications (epinephrine, lidocaine, and atropine) can be administered via the endotracheal tube, but the dose must be 2 — 2.5 times the intravenous dose. (Use a catheter or suction tip which should be passed beyond the tip of the endotracheal tube. Dilute with water instead of NSS for endotracheal route. ) With a few exceptions, intravenous medications should always be administered rapidly, in bolus method. t each intravenous medication, give a 20-30 mi bolus of intravenous fluid and x ‘elevate the extremity. This will enhance delivery of drugs to the centralsIMPLE APPROACH TO ECG RECOGNITION OF THE AR RHYTHMIAS DURIN IG ACLS, inthe Systematic ECG Interpretation of the ACL: Regularity? Is it regular or irregular? S Rhythms Rate? Is it fast or slow or normal? Rhythm? Is it Sinus? Check the waveforms. Is there a P wave followed by a QRST? + Measure the Intervals: PR, QRS, QT steps i Is there a Rhythm abnormality? Correlate clinically. SINUS RHYTHM + Thereisa bpm P wave, followed by a QRS complex at a regular rhythm and rate of 60-100 SINUS BRADYCARDIA + There is re is a regular P wave followed by a regularly occurring QRST, but the rate is < 60 bpm SINUS TACHYCARDIA * There isa regu phere regular P wave followed by a regularly occurring QRST, but the rate is > 19iM: RDIA * Sinus bradycardia + Sinus pause + Escape rhythms: > Junctional rhythm > Idioventricular rhythm + Heart blocks > 1" degree AV block > 2m degree AV block + Mobitz | or Wenckebach + Mobitz II > 3" degree or complete AV block SINUS PAUSE (SINUS ARREST) * There is a P wave followed by a QRST, but at some point there is irregularity and slowing of the heart rate, and the ECG shows noP Renee aUaeat wave and no QRS. In other words, Pause JUNCTIONAL RHYTHM * This is an escape rhythm; Impulses come from the AV node Usually a regular slow heart rate, < 60 bpm (rate is usually between 40-50 bpm). QRS are narrow. There are no discernible P waves (actually the P waves are inverted or buried w/in QRS or follows the QRS) Junctional IDIOVENTRICULAR RHYTHM * Another escape rhythm; Impulse is ventricular in origin * Regular slow heart rate, < 40 bpm (usually between 20-40 bpm), wide QRS and no __ discernible P waves; QRS duration > 0.10 sec Idioventricular ek regular P wave, followed by a regular QRS complex, but the PR ) sec (75 small squares in the ECG strip) 4\ deg AV block and Advanced Cardiac Life SupportD DEGREE AV BLOCK MOBITZ | (WENCKEBACH) Progressive lengthening of the PR interval followed by wave NOT followed by a QRS) SECON! ¥ intermittent dropped beats (a P 2” deg AV block Mobitz | D DEGREE AV BLOCK MOBITZ II Fixed PR interval (NO progressive lengthening) w/ intermittent dropped beats SECON Important point: 2 degree AV block is ALWAYS IRREGULAR and usually presents with GROUP BEATING. 2:1 AV BLOCK + 2 Pwaves for every 1 QRS complex (every other P wave is blocked) —} 2:1 AV block HIGH GRADE AV BLOCK * Atrio-ventricular conduction ratio is 3:1 or higher * 3:4, 4:1, 5:1 AV block and anything higher is called High Grade AV block — : - - Heth tH I FEEEEEE] High grade AV block THIRD DEGREE AV BLOCK OR COMPLETE HEART BLOCK * No recognizable consistent or meaningful relationship between atrial and ventricular activity (there is ATRIO-VENTRICULAR DISSOCIATION) There are regularly occurring P waves, there are regularly occurring QRS complexes, but they are not related to each other (in other words, they are dissociated) QRS morphology is constant; QRS rate constant (15-60 beats/min); atrial rate is usually than Ventricular rate, but the atrial and ventricular rhythms are independent of ach other; ventricular rhythm is maintained by a junctional or idioventricular escaPe nythm or a ventricular pacemaker | Advanced Cardiac Life Support 2CHB Complete heart block with a ventricular escape rhythm Sinus tachycardia Supraventricular tachycardia Atrial fibrillation Atrial flutter Multifocal atrial tachycardia Ventricular tachycardia TACHYCARDIA — divided into Narrow complex and Wide complex Tachycardia Narrow QRS Complex Tachycardia Wide QRS Complex Tachycardia (QRS duration < 0.12 secs) (QRS duration >0.12 secs ) TACHYCARDIA Wide QRS SVTwith —_Proexclad AF Torsade vt aberrancy AF with aberrancy(ENTRICULAR TACHYCARDIA SUPRAVersylar narrow QRS complex tachycardia, usually with sudd vvth a rate of 150-250 beats/min len onset and termination, |. Nodiscerible P waves Se waves are generally buried in the QRS complex Ont ; prior to or just after the end of the QRS and esteee ae ranctiee: QRS complex that results in a pseudo-S or pseudo-r one svt ATRIAL FIBRILLATION rregularly irregular narrow complex tachycardia with no discernible P waves * Chaotic irregular atrial fibrillatory waves ATRIAL FLUTTER + Narrow complex tachycardia, regularity and rate depends on the degree of AV conduction ¢ sia rate = 220-360/min (P as flutter waves); Ventricular response usually 150-180 m * Look closely for your beautiful sawtooth flutter wavesMULTIFOCAL ATRIAL TACHYCARDIA + Impulses originate irregularly and rapidly at different points in the atrium + [regularly irregular narrow complex tachycardia with varying P wave, PR, PP and RR intervals, and 3 or more different P wave morphologies TS SEE pees SEE Ff = re sree i ee eed mat VENTRICULAR TACHYCARDIA + Atleast 3 consecutive PVC's + Rapid, bizarre, wide QRS complexes firing in succession at a rate of >100 bpm; usually no discernible P wave Fae ARREST RHYTHMS - there are only 4: ‘Asystole Pulseless electrical activity Ventricular fibrillation Pulseless VT LE The easiest rhythm to identify! There is no discernible electrical activity. ECG shows a - flat line. The patient is in CARDIAC ARREST! Asystole FIBRILLATION with coarse or fine chaotic undulations of the ECG baseline. There are and no true QRS complexes. The rate is indeterminate. The patient is in ARREST! I He Manual on Basic and Advanced Cardiac Life SupportLAR TACHYCARDIA PULSELESS Ve, wide ORS complexes fring in suocession at arate of 100 bom, but + Rap ant has NO PULSE and NO BLOOD PRESSURE. Patients also in CARDIAC ARREST! Treat as VF! Pack EA ANAM in PAE H LSELESS VENTRICU! pULSELESS ELECTRICAL ACTIVITY ECG shows an organized electrical activity (NOT VF or pulseless VT); either a narrow QRS or wide QRS rhythm; fast (>100 beats/min) or slow (<60 beats/min). «There is organized cardiac electrical impulses but no effective myocardial contraction is produced (also known as “electromechanical dissociation’); patient has ZERO blood pressure and ZERO heart rate, in other words, PATIENT IS IN CARDIAC ARREST! ECG of a patient with PEA- may show either bradycardia (commonly idioventricular or junctional) or tachycardia (other than VT) but the patient has NO pulse and is in cardiac arrest MISCELLANEOUS ACLS RHYTHMS WOLFF PARKINSON WHITE (WPW) ECG (PREEXCITATION) + ECG shows short PR interval (<0.12 secs), delta wave (upward slurring of the QRS complexes as indicated by arrows) and wide QRS complexes. These patients have an extra accessory pathway or bypass tract that may conduct impulses rapidly. They may present with supraventricular tachycardia (usual narrow QRS tachycardia) or with preexcited rapid atrial fibrillation which presents as irregular wide complex tachycardia (see below) and may be mistaken as VT or VF. In reality, such rapid preexcited AF may actually lead to VF and sudden death. ‘on Basic and Advanced Cardiac Life Support 25PREEXCITED RAPID ATRIAL FIBRILLATION * Rapid atrial fibrillation in a patient with WPW syndrome presents as wide complex tachycardia that may look like VF/VT. Just remember the acronym F-B-I: Fast-Broad- Irregular for preexcited tachycardia. Important point to remember: DO NOT GIVE digoxin or calcium channel blockers because these may convert the arrhythmia into VFI What to do: either IV procainamide, IV amiodarone, or Cardiovert the patient! Hh shalan M, A ann HTT nie Lilt i li Ky EMAKER RHYTHM ECG of a patient with an artificial pacemaker which is inserted for significant bradycardia. Tracing shows a sharp pacemaker potential or spike (as indicated by the _ arrows) followed by a wide QRS complex which indicate “capture” of the ventricle. = WPW AF Paced F occurring in patients with long QT interval. ECG shows also irregular ‘QRS complexes, hence also Fast-Broad-Irregular (F-B-l). But take complexes seem to change from a positive to a negative axis around a point). Torsade pointes means “twisting of the points”. TDPLOW THE SIMPLE ALGORITHM BELOW FOR EASY AND RAPID RECOGNITION OF THE ACLS RHYTHMS HR < 60 {stow Irregular P-QRS. Narrow QRS) Group beating + 4 + + Sinus : =j uncon] Idio- 3rd degree degree eee. } { ventricular) (_AV Block Cadet AV Block HR > 100 SVT MAT Tawi AFDEFIBRILLATION Defibrillation ‘oo + therapeutic use of electric current delivered in large amounts over very brief periods of time + temporarily “stuns” an irregularly beating heart and allows more coordinated contractile activity to resume. termination of VF for at least 5 seconds following the shock Rapid defibrillation is the major determinant of survival in cardiac arrest due to ventricular fibrillation (VF). Early defibrillation is critical for several reasons: 4. Ventricullar fibrillation (VF)- most frequent initial rhythm in sudden cardiac arrest (SCA) 2. Treatment of VF is electrical defibrillation 3. Probability of successful defibrillation diminishes rapidly overtime 4. VF tends to deteriorate to asystole within a few minutes 5. CPR prolongs VF, delays the onset of asystole, and extends the window of time during which defibrillation can occur. In witnessed arrest, defibrillation should be applied immediately after the onset of VF, i.e. before the heart becomes anoxic and acidotic, which would make successful defibrillation and resumption of cardiac activity less likely. ee is accomplished by passage of sufficient electric current (amperes) through the Current flows determined by the energy chosen (joules) and transthoracic impedance (ohms) a resistance to current flow. Factors that determine transthoracic impedance include: energy selected electrode size paddle-skin coupling material (gel/cream or saline-solution gauze) number and time interval of previous shocks phase of ventilation distance between electrodes (chest size) paddle electrode pressure. ELECTRODE POSITION Electrodes should be placed to maximize current flow through the myocardium, The standard placement is one electrode just to the upper part of the sternum below the clavicle and the other to the left of the nipple with the center of the electrode in the mid-axillary line NOneona should be taken that the electrodes are ‘separated and that paste or gel is not between the paddles on the chest. e, current may flow preferentially chest wall, “missing” the heart Manual on Basic and Advanced Cardiac Life SuppotENERGY REQUIREMENTS The recommended eneray for the first and succeeding defibrillation attempts is 360J monophasic or 200J biphasic. CPR should be continued immediately after defibrillation, for 2 minutes, followed by rhythm check. Biphasic waveform defibrillation with shocks of < 200J is safe and has equivalent or higher efficacy for termination of ventricular fibrillation (VF) compared with higher-energy monophasic — waveform shocks. SHOCK ENERGIES The optimal energy for first shock biphasic waveform defibrillation has not been determined + Biphasic: 120-200J (Class | LOE C) + If Manufacturer's recommendation not known: Use maximal dose (Class IIb) Monophasic: 360J PEDIATRIC + VF is uncommon in children + 2-4 Joules/kg is recommended SYNCHRONIZED CARDIOVERSION Synchronized cardioversion is delivery of electrical shock timed to the peak of the QRS complex, Synchronization of delivered energy reduces the possibility of induction of VF, which can occur when a shock impinges on the relative refractory period of the cardiac electrical activity. Thus, synchronization is recommended for unstable supraventricular tachycardia, atrial fibrillation, atrial flutter, and monomorphic ventricular tachycardia. ENERGIES FOR SYNCHRONIZED CARDIOVERSION + Atrial flutter and SVT (narrow regular) - 50 J to 100 J (monophasic or biphasic) + Atrial fibrillation (narrow irregular) - 120J to 200J (biphasic) OR 200J (monophasic) + Monomorphic VT (wide regular) — 100J Polymorphic VT (wide irregular) — defibrillation dose, NOT SYNCHRONIZED TECHNIQUE FOR EXTERNAL ELECTRICAL DEFIBRILLATION 1. Turn the main power switch on. Turn the synchronize switch of the defibrillator off. 2. Set the energy to be delivered at 360J (for adults) or equivalent biphasic waveform shock at 2004. 3. Lubricate the paddle with electrode gel. 4. Charge paddles. Someone should continue CPR while you are charging the defibrillator. 5. Interrupt chest compressions (preferably 10 seconds, maximally 20 seconds) for the defibrillation. Place one paddle just to the right of the upper sternum below the right clavicle, the other paddle just below and to the left of the left nipple as indicated in the paddles. 6. Apply firm pressure with paddles against the chest to reduce lung volume and electric resistance. 7. Confirm ECG diagnostic of VT or VF (Pulseless ventricular tachycardia or ventricular fibrillation) 8. Clear the area with no one touching the patient. Shout: “Iam going to shock the Patienton three! One I'm clear! Two you are clear! Three everybody clear!” Manual on Basic and Advanced Cardiac Life Support 299, Discharge the defibrillator by pushing the appropriate triggers on the paddles simultaneously. 10. After defibrillation, immediately continue CPR. : 11. Check rhythm after each 5 cycles (2mins) of CPR and proceed accordingly. (See VF/VT Algorithm) TO DO SYNCHRONIZED CARDIOVERSION, turn the “Synchronize” switch or “SYNC” ON and select the desired eneray for cardioversion. Continue with steps 3 to 9 above. When discharging, place the paddles on the chest longer, and firmly. IMPORTANT NOTES: * Pulseless VT is treated as VF Defib! * Unstable monomorphic (regular) VT with pulse synchronized cardioversion (100J, increase dose if no response to the 1*t shock) * Unstable polymorphic (irregular) VT w/ or w/o pulse- Defib! + Ifthere is any doubt if monomorphic or polymorphic VT in unstable patient, DO NOT DELAY shock delivery, provide high energy unsynchronized shocks (ie, defibrillation doses) CARDIAC DRUGS IMPORTANT PRINCIPLE: DURING A CARDIAC ARREST, DRUG INTERVENTION IS SECONDARY ONLY TO OTHER INTERVENTIONS. MOST IMPORTANT ASPECT IS STILL HIGH QUALITY CHEST COMPRESSIONS AND EARLY DEFIBRILLATION! Epinephrine * MOA- Increases SVR, BP, HR, Contractility, automaticity Increases blood flow to heart & brain, AV conduction velocity pueden effects can increase coronary & cerebral perfusion pressure during Beta-adrenergic effects may increase myocardial work & reduce subendocardial perfusion * No evidence to show that it improves survival * Dose: 1 mg IV bolus every 3-5 mins *Vasopressin already removed in Cardiac medication for Cardiac arrest based on latest 2015 guidelines Norepinephrine . * MOA -Naturally occurring potent vasoconstrictor and inotropic agent Usually induces renal and splanchnic vasoconstriction Indications: Severe hypotension (SBP < 70mmHg) Low total peripheral resistance Dose: - 0.1 — 0.5 mog/kg/min infusion Note: Not used for cardiac arrest Do not administer in same IV line as Na Bicarbonate = Catecholamine, alpha and beta-adrenergic receptor agonist and peripheral \ine receptor agonist ions: if ort Manual on Basic and Advanced Cardiac Life SupP*Hypotension (SBP 70-100mmHa) ‘Symptomatic significant bradycardia ‘After ROSC (Return of Spontaneous Circulation) Dose: - 2-20 meg/kg/min infusion, titrate to patient response 5 Note: Do not administer in same IV line as Na Bicarbonate Dobutamine ; MOA - synthetic sympathomimetic amine with positive inotropic action and minimal positive chronotropic activity at low doses (2.5 ug/kg per min), but moderate chronotropic activity at higher doses «Indication: Severe systolic heart failure (SBP 70-100mmHg) «Dose : 2-20 ug/kg/min Note: vasodilating activity precludes its use when a vasoconstrictor effect is required Do not administer in same IV line as Na Bicarbonate Buffers: Sodium Bicarbonate « Little data indicates that therapy with buffers improves outcome * Does not improve ability to defibrillate or improve survival rates in animals * Can compromise coronary perfusion pressure + May cause adverse effects due to extracellular alkalosis, including shifting the oxyhemoglobin saturation curve May induce hyperosmolality and hypernatremia Produce carbon dioxide May inactivate simultaneously administered catecholamine MOA : Reverses acidosis caused by global hypoperfusion Indications: Hyperkalemia Tricyclic or phenobarbital overdose Patients with pre-existing metabolic acidosis 2After a protracted arrest or long resuscitative efforts * Dose: 1 mEq/kg Diuretics: Furosemide * Potent diuretic * Direct venodilating effect in patients with acute pulmonary edema * Transient vasoconstrictor effect when heart failure is chronic * Onset of vascular effect is within 5 minutes * Dose: 0.5 ~ 1 mg/kg IV injected slowly Adenosine * MOA: Depresses AV node & sinus node activity * Half-life is < 5 seconds (degraded in the blood & periphery) * Indications: Should be used if SVT is suspected *Note : 2010 CPR Guideline with no 2015 update changes Recommended in the initial diagnosis & treatment of stable, undifferentiated regular, monomorphic wide-complex tachycardia * Dose: 6 mg rapid IV push in 2-3 seconds, followed by 20m! saline flush, raise the extremity for at least 30 seconds after push * Ifno response may give 2" dose: 12mg after 1-2 minutes.May give a 3" dose: 12 mq if still no response Manual on Basic and Advanced Cardiac Life Support 4 ti ee aacgiescinllCalcium Channel Blockers * MOA: Slow conduction & increase refractoriness in the AV node * May also control ventricular response rate in patients with AF, Flutter, or MAT * Systemic vasodilation * Negative Inotropic effect Verapamil * Indications: Effective in stable narrow complex PSVT Alternative drug after Adenosine * Contraindications Should not be given in patients with impaired ventricular function or heart failure Should not be given if hypotensive Dose: 2.5 — 5 mg IV given in 2 minutes. ‘Administered every 15 — 30 mins to a max of 20 mg + Indications: Class | in acute coronary syndromes To slow ventricular response (AF/ flutter, MAT) Also to convert SVT * Second line after adenosine * *Labetalol recommended for emergency anti-hypertensive therapy for hemorrhagic and acute ischemic stroke * Contraindications Hemodynamic instability 2Pand 3° AV block Asthma Cocaine-induced ACS * Labetalol Dose: 10 mg IV push (1-2mins), maybe repeated or doubled every 10 mins max dose 150mg OR same initial bolus then infusion at 2-8mg/min * Esmolol Dose: 0.5 mg/ kg loading dose 50 mcg/ kg per minute maintenance infusion > 2" bolus of 0.5 mg/kg infused in 1 minute repeated every 4 minutes for a total maximum of 300 meg/ kg per minute B-Adrenergic Blockers > Class | in acute coronary syndromes * Metoprolol Dose: 5 mg IV every 5 minute interval for total of 15 mg (IV form not available locally) Propranolol Dose: 0.1 mg/ kg IV every 2-3 minute interval (IV form not available locally) * Esmolol Dose: 0.5 mg/ kg loading dose 50 mcg/ kg per minute maintenance infusion ‘* 24 bolus of 0.5 mg/ kg infused in 1 minute repeated every 4 minutes for a total maximum of 300 mcg/ kg per minute Amiodarone e Class Ill anti-arrhythmic it MOA -Affects Na, K and Ca channels as well as alpha and beta adrenergic blocking properties Manual on Basic and Advanced Cardiac Life supperprolongs action potential duration, refractory period, decreases AV node conduction and sinus node function Indications: After defibrillation and epinephrine in cardiac arrest with persistent pulseless VT or VF, stable/unstable VT Ventricular rate control of rapid atrial arrhythmias in severely impaired LV function ‘Adjunct to electrical cardioversion in refractory PSVT's, atrial tachycardia & pharmacologic cardioversion of AF Side effects are hypotension and bradycardia Dose: VT with pulse - 150mg IV over 10mins followed by 1mg/min infusion for 6 hours, then 0.5mg/min Pulseless VT/VF — 300mg IV push then 150mg IV - 2" dose if needed after another cycle of CPR Lidocaine + Indications: vF/ pulseless VT that persist after defibrillation and administration of epinephrine Control of hemodynamically compromising PVC's Hemodynamically stable VT Alternative if Amiodarone unavailable ‘* Dose: Initial bolus of 1 — 1.5 mg/ kg IV. Additional bolus of 0.5 to 0.75mg/ kg can be given over 3 — 5 minutes for refractory VT/ VF. Narrow toxic-to-therapeutic range Routine use in AMI is not recommended No proven short-term or long-term efficacy in cardiac arrest CNS Toxicity: muscle twitching, slurred speech, resp. arrest, altered consciousness, seizures Magnesium + Effectively terminates torsades de pointes * Not effective in irregular/ polymorphic VT in patients with normal QT * Not recommended in cardiac arrest except when arrhythmias are suspected to be caused by magnesium deficiency * Dose: 1 —2 gm (8-16meqs) mixed in 50 ~ 100 ml DSW given over 15 to 60 mins. Followed by 0.5 to 1gm IV infusion © 1 to 2 gm diluted in 100 ml DSW administered over 1 — 2 mins in emergency situations Atropine * MOA: Parasympatholytic action: Accelerates rate of sinus node discharge Improves AV conduction Reverses cholinergic-mediated decreases in heart rate, systemic vascular resistance, & blood pressure * Indications : Symptomatic sinus bradycardia (Class !) AV block Nodal level Use with caution in AMI Should not be relied fully in Mobitz type I! block * Dose: 0.5 mg every 3 - 5 mins * total dose of 3 mg (0.04 mg/kg) results in full vagal blockade in humans Ifatropine is not effective, may give epinephrine infusion for symptomatic bradycardia as an alternative to pacing (see Bradycardia algorithm) Manual on Basic and Advanced Cardiac Life Support 33Epinephrine : it i D5 Wor normal Dose : 2-10 meg/min (1mg in 500cc of saline by continuous infusion) titrate to patient's response a BR creases SVR, BP, HR, Contractility, automaticity Increases blood flow to heart & brain, AV conduction velocity « Alpha-adrenergic effects can increase coronary & cerebral perfusion pressure during Dee: 2-10 meg/min (1mg in 500cc of D5 W or normal saline by continuous infusion) - titrate to patient's response e “Note: 2010 CPR guideline changes with no 2015 update changes If atropine is not effective, may give epinephrine infusion for symptomatic bradycardia as an alternative to pacing Digoxin ¢ MOA; enhances central and peripheral vagal tone, slows SA node discharge rate, shortens atrial refractoriness, and prolongs AV nodal refractoriness through ANS effect Indication: supraventricular arrhythmias (AF/flutter) Peak effect - after 1.5 - 3 hours Less effective than adenosine, verapamil, or beta blockers. Dose : Acute loading dose 0.5 to 1.0 mg IV or PO © 0,004 to 0.006mg/kg initially over 5 min. 0° Then 0.002 to 0.003mg/kg at 4-8hr interval. © Total of 0.008 to 0.012mg/kg divided to 8 to 16hrs Nitroglycerine * Decreases chest pain in ACS * Indication : ACS, CHF, Hypertensive urgency w/ ACS * MOA Increases venous dilation Decreases preload & 02 consumption Dilates Coronary Arteries Increases Collateral flow in MI Tolerance may develop IV bolus — 12.5 to 25 mcg (if no SL or spray given) Infusion — 10mcg/min titrate to effect Increase by 10 mcg /min every 3-5min until desired effect Max dose 200mcg/min Sublingual Tablet (0.3-0.4mg) 1 tab every 5min Spray — 1-2 sprays for 0.5—1sec every 5min, Max of 3 doses . . . ° . fie >diac Arrest Algorithm—2015 Update adult Ca «+ Push hard fat least 2 inches [B emp and fast (100-120/min) ‘and alow complete chest recoil + Minimize interruptions ia ‘compressions. “+ Avoid excessive vention. * Rotate compressor every 2 minutes, or eooner if fatigued + Hf no advanced airway, 30:2 compression-ventilation rato, + Quantitative wavetorm ‘capnography = Hf PEtCO, <10 mm Ha, attempt to Improve CPR quality. + intra-arterial pressure = Hf relaxation phase (dia- ‘stolie) pressure <20 mm Ha, attempt to improve CPR quality. Shock Energy for Befibriliation “Biphasic: Manufacturer | recommendation (@9, inital ‘dose of 120-200 Jj if unknown, use maximum avaiable. ‘Second and subsequent doses should be equivalent, and higher doses may be considered. ‘+ Monophasic: 260 J “+ Epinephrine IV/IO dose: ‘img every 3-5 minutes + Amiodarone W/O dose: Fist dose: 300 mg bots. Second | dose: 150 m3 erry ‘= Endotracheal intubation or supragiottic advanced airway '+ Wavetonm capnography or ‘capnomety to confirm and ‘monitor ET tube placement + Ones advanced airway in place, ‘ive 1 breath every 6 seconds (10 breathemin) with contnucus Chest compressions Return of Spontay retreat) + ise and blood pressure * Abrupt sustained increase in Petco, (ypically 240 mm Ha) ‘+ Spontaneous arterial pressure ‘waves wih intra-arterial monitoring + Hypovoiemia + Hypoxia + Yasogen on econ + Hypo-/hyperkalem + Hypothermia + Tension pneumothorax + Tamponade, cardiac * Toxine + Thrombosis, pulmonary + Thrombosis, coronary SE Ea pera arTACHYCARDIA ALGORITHM 1 ae Doses/Details ‘Assess appropriateness for clinical condition. Synchronized Heart rate typically > 150/min if tachyarrhythmia. Cardioversion om Initial recommended doses + Narrow regular: 50 J Identity and treat undertying cause Brecen, Daa tastaee, os 120-200 J biphasic o fain ole 200 J monophasic veces: (fhype ) + Wide regular: 100 J + Cartoc montero deity yt; monitor bod caer bm 2 pressure and oximetry (NOT synchronized) Adenosine WV Dose: First dose: 6 mg rapid IV push; follow with NSS flush’ ‘Second dose: 12 mg it Synchronized cardioversion ried + Acutely altered mental status? egal Antiarthythmic + Signs of shock? + Hfregular narrow complex, consider F ) infusions for Stable + Ischemic chest discomfort? seeks Wide-QRS Tachycardia Acute heart failure? Procainamide IV Dose: 20-50 mgimin until arnhythmia suppressed, hypotension ensues, QRS duration increases > 50%, or maximum dose 17 mgikg given. Maintenance infusion: 1-4 mgimin, Avoid if prolonged QT or CHE. + IV access and 12-lead ECG if available * Consider adenosine only if regular ‘and monomorphic + Consider antiarrhythmic infusion + Consider expert consultation ‘Amiodarone IV Dose: First dose: 150 mg over 10 minutes, Repeat as needed if VT recurs. paowed by maintenance * IV access and 12-lead ECG if are available + Adenosine (regular) Soto V Dose + B-Blocker or calcium channel 100 mg (1.5 mg/g) over ig B minutes + Consider expert consultation peak rose! OI Figure reprinted from 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care ‘Science, Circulation vol 122, no. 18, supplement 3 Manual on Basic and Advanced Cardiac Life SupportBRADYCARDIA ALGORITHM + Maintain patent airway; assist breathing as Adult Bradycardia (With Pulse) ‘Identify and treat underlying cause necessary Oxygen (if rypoxemic) + Cardiac monitor to identify rhythm; monitor blood pressure and oximetry IV access ‘24ead ECG i availabe; don't delay therapy Persistent bradyarrhythmia causing™ + Hypotension? + Acutely altered mental status? + Signs of shook? + Ischemic chest discomfort? ‘Acute hear failure? If atropine poet + Trascutaneous pacing OR + Dopamine infusion oR + Epinephrine infusion Consider: + Expert consultation + Transvenous pacing ‘Assess appropriateness for clinical condition Heart rate typically < 50/min if bradyarthythmia. DosesiDetails: ‘Atropine IV Dose: First dose: 0.5 mg bolus Repeat every 3-5 ‘minutes Maximum: 3mg Dopamine IV infusion: 2-10 megikg per minute, Epinephrine IV. Infusion: 2-10-meg per minute Figure reprinted from 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science, Circulation vol 122, no. 18, supplement 3 __ Manual on Basic and Advanced Cardiac Life Support 37POST-CARDIAC ARREST CARE ALGORITHM ‘Avoid excessive ventilation, Start at 10-12 breaths!min and titrate to target PeTco, of 35-40 mm Hg. When feasible, ttrate Fi, tominimum necessary to. achieve Seo, 224% * IV Bolus 4-2 Lnormal saline or lactated Ringer's. Ifinducing hypothermia, may se 4°C fd. Epinephrine IV Infusion 0.1-0.5 mogikg per minute (in 70-kg adult: 7-35 mcg er minute) Dopamine IV infusion 5-10 meg/kg per minute Norepinephrine IV Infusion 0.1.0.5 megikg per minute {in 70-kg adult: 7-35 meg per minute) Reversible Causes = Hypovolemia Hypoxia - Hydrogen ion (acidosis) = Hypotnyperkalemia - Hypothermia + Tension pneumothorax + Tamponede, cardiac + Toxins + Thrombosis, puimonary + Thrombosis, coronary Coronary rep {from 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care jon vol 122, no. 18, supplement 3 Manual on Basic and Advanced Cardiac Life SupportAGUIE CORONARY SYNDROMES ALGORIIHM ‘Symptoms suggestive of ischemia or infarction TEMS assessment and care and hospital preparation = Monit, support ABCS. Be prepared to provide CPR and deflation 1 Administer aspn and consider oxygen, niogiycern and merphine if needed * Obtain 124ead ECG, ST elevation * Noli receiving hospital with transmission or inlerpretaton; note time of onset and first medical contact + Nats hut mabe oe exes oer STEMI ‘Concurrent ED assessment (>10 minutes) Immediate ED general treatment + Check vlal signs; evaluate oxygen saturation + 02 sat < 94%, start oxygen at 4 Uiin, rato + Establish IV aocess + Aspirin 160 to 325 mq (not given by EMS) + Pecform tri, targeted history, physical exam + Nitroglyeerinsuiqual or spray + Reviewicomplete fiinayic checklist (Figue2): check | + Morphine IV discomfort rot relieved by nitrogycerin ‘contandcatons (Tale 6) + Obtain potable chest xray (>30 minutes) 4 Normal or non dlagnostic changes in ST segment orT wave suspicious ‘High-risk unsfabie angina! ‘non-ST-elevation ML WAMMSTEMM Consider admission to ED chest pain uni orto appropriate bed and fellow: + Serial cardiac markers (incucing oporin) + Repeat ECG! continous ST-segment monitosng + Consider non-invasive diagnos Troponin elevated orhigh-isk patient (Table 3,4 for tisk stratification). Consider early invasive strategy if + Refractory ischemic chest dscomfot + Recurentpersistent ST deviation + Ventricular tachycardia + Hemodynamic instability + Signs of heat faire Devens 1 or more: ‘Start adjunctive treatments as indicated (see tex) + Cinical igh-sk features += Nirogyoern * Heparin (UFH or LAW) + Dynamic ECG changes consistent + Consider PO p- blockers wih scheria + Consider: Clpidogre! Troponin elevates + Consider: Glycoprotein ila intibtor ‘Admit to monitored bed ‘Assess risk status (Tables 3,4) Continue ASA, Heparin and other therapes as indicat + ACE inhibitovARB + HG CoA reductase Innibitr (statin therapy) No at high risk cardlogy to ik say “Aonormal iagnast noninvasive maging or physoege, Tino evidence of chemi or infarction by] testing, ca dacharge wit follow ea ered from 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care oe, Circulation vol 122, no. 18, supplement 3 ». Basic and Advanced Cardiac Life Support