Advanced Cardiac Life Support. Basic Cardiac Life Support

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<ul><li> Slide 1 </li> <li> Advanced Cardiac Life Support </li> <li> Slide 2 </li> <li> Basic Cardiac Life Support </li> <li> Slide 3 </li> <li> Definitions of death Clinical death means that the heartbeat and breathing have stopped. This process is reversible. Biological death is permanent, cellular damage due to lack of oxygen, the brain cells are the most sensitive to the lack of oxygen. Brain damage occurs after 4 minute of cardio- respiratory arrest. </li> <li> Slide 4 </li> <li> CPR It is the simple procedures which prevent circulatory and/or respiratory arrest or insufficiency prompt intervention. These simple procedures include: Open and clear airway Mouth to mouth breathing (through a barrier) OR bag-mask ( Ambu-baging ) External cardiac compression </li> <li> Slide 5 </li> <li> Basic knowledge </li> <li> Slide 6 </li> <li> External cardiac compression give 25% of original Cardiac Output. It contract around 70 times/min, every contraction ejects 70 ml of blood, so minute Cardiac Output is around 5 L/min. ( at rest). Respiratory center is located in the brain which is stimulated by the level of the arterial carbon dioxide. Adult respiratory rate is about 12-15 times/min. Room air contain 21%O2 our expiration contain 16% O2 </li> <li> Slide 7 </li> <li> To start CPR The patient is Unresponsive Breathlessness Pulselessness </li> <li> Slide 8 </li> <li> Chain Of Survival ( Sequences of action linked together too tightly with no gap ) Activate code blue Start CPR until Defibrillator and team arrive Defibrillation if indicated Advanced cardiac life support actions to be followed i.e. intubation, IV line for fluids and drugs etc. </li> <li> Slide 9 </li> <li> Principles of Defibrillation Electric shock will terminate ventricular fibrillation by transmural current flow Entire myocardium is depolarised into refractoriness. The SA node, as the fastest pacemaker, may resume pacing function </li> <li> Slide 10 </li> <li> Safe Defibrillation To avoid accidental shocks to rescuer and patient injury Safe environment, away from pooled water or metal surface under patient or rescuer Apply conductive material Turn on defibrillator, select energy and charge defibrillator Proper electrode placement Apply firm pressure on electrodes </li> <li> Slide 11 </li> <li> Make sure no smearing of conductive gel Remove transdermal patches Keep paddles &gt;12 cm away from implanted cardiac pacemakers Make sure no personnel are directly in contact with the patient, clearing chant Ensure VF or pulseless VT Depress both discharge buttons simultaneously and deliver the electric shock </li> <li> Slide 12 </li> <li> Defibrillation Energy Adults 200J 200/300J 360J 360J thereafter (monophasic) Non-escalating 150J (biphasic) Children 2J/kg 2-4J/kg 4J/kg 4J/kg thereafter </li> <li> Slide 13 </li> <li> Some Determinants of Defibrillation Dose Chest impedance Electrode size and location Type of waveform Disease, drugs, metabolic state of the subject </li> <li> Slide 14 </li> <li> Factors Reducing Transthoracic Impedance Appropriate electrode size Coupling medium between electrodes and chest wall Repeated shocks Expiratory phase of respiration Electrode-chest wall contact pressure (&gt;10 kg) Post-cardiac surgery </li> <li> Slide 15 </li> <li> Electrode Size diameter of electrode impedance and defibrillation threshold In animals: 8 cm : 71% defib success 12.8 cm : 88% defib success Very large electrodes impedance, but in current density defibrillation success Inadequate contact with chest wall </li> <li> Slide 16 </li> <li> Coupling Medium Electrode paste (e.g. Redux paste) Electrode paste resulted in significantly lower impedance than the disposable defibrillation pads. No difference in defibrillation success. Beware of paste spread across the chest wall during CPR Disposable coupling pads (e.g. Defib-Pads) Adhesive pads </li> <li> Slide 17 </li> <li> Self-adhesive pads Advantages Prophylactic placement in high risk patients Less interference with external cardiac massage Incorrect coupling gel avoided Better operator safety Disadvantages Special connection Lack of firm pressure High impedance Hairy skin </li> <li> Slide 18 </li> <li> Electrode Position Proper polarity facilitates ECG interpretation. It does not affect success of defibrillation Three acceptable positions Sternal-apical Left-anterior-posterior Apical posterior </li> <li> Slide 19 </li> <li> Sternal-apical Below the outer right clavicle Cardiac apex </li> <li> Slide 20 </li> <li> Left-anterior-posterior Anterior apex just left of palpable cardiac apex Back inferior to the left scapula </li> <li> Slide 21 </li> <li> Apicalposterior Left ventricular apex Back inferior to the left scapula </li> <li> Slide 22 </li> <li> If VF Persists: Secure airway, ventilatory and circulatory support, IV access Appropriate medications to maintain myocardial and cerebral viability Detect and treat potentially reversible underlying causes Resume defibrillation attempts After each minute of CPR, or after each medication The best prospects for restoring a perfusing rhythm still remain with defibrillation </li> <li> Slide 23 </li> <li> Scope of ACLS Basic life support ECG monitoring, interpretation and arrhythmia recognition Advanced equipment and techniques for ventilation and circulation Therapies for respiratory or cardiac arrests Treatment of acute coronary syndromes Treatment with tPA for eligible stroke patients </li> <li> Slide 24 </li> <li> Scope of ACLS Basic life support ECG monitoring, interpretation and arrhythmia recognition Advanced equipment and techniques for ventilation and circulation Therapies for respiratory or cardiac arrests Treatment of acute coronary syndromes Treatment with tPA for eligible stroke patients </li> <li> Slide 25 </li> <li> International Guidelines 2005 Conference on Cardio-pulmonary Resuscitation and Emergency Cardiovascular Care </li> <li> Slide 26 </li> <li> The 3 Unequivocally Effective Interventions Basic cardiopulmonary resuscitation Oxygenation and ventilation of the lungs through a patent secure airway Defibrillation for ventricular fibrillation or pulseless ventricular tachycardia </li> <li> Slide 27 </li> <li> Advanced Equipment &amp; Techniques for Ventilation &amp; Circulation </li> <li> Slide 28 </li> <li> Airway Adjuncts Oropharyngeal airways Nasopharyngeal airways Laryngeal mask airway 64-100% success Combitube 69-100% success Cuffed oropharyngeal airways (COPA) Suction devices </li> <li> Slide 29 </li> <li> Combitube </li> <li> Slide 30 </li> <li> Endotracheal Intubation Optimal airway Secure and clear airway Protect airway No gastric inflation Drug Bronchial toilet Need 3 minutes of preoxygenation Ventilation should not be interrupted for &gt; 30 seconds Cricoid pressure Use of stylet or gum elastic bougie Confirm and secure tube position </li> <li> Slide 31 </li> <li> Breathing F i O 2 of 1.0 Manual resuscitators or ventilators 12-15 breaths/minute Tidal Volume 10-12 ml/kg, if intubated 6-7 ml/kg, if not unintubated </li> <li> Slide 32 </li> <li> Circulation Closed chest compression at 100/minute Open chest CPR should be restricted to operating theatre and selected instances of penetrating thoracic injury </li> <li> Slide 33 </li> <li> Specific Drug Therapy Meticulous, systematic review reveals that relevant, valid, and credible evidence to confirm a benefit due to these agents simply does NOT exist. </li> <li> Slide 34 </li> <li> Routes of Drug Administration Peripheral veins Central veins Tracheal Intraosseous Intracardiac </li> <li> Slide 35 </li> <li> Peripheral Venous Route Peak effect 1.5-3 min. after injection at antecubital fossa IV push 20 ml NS flush after drug injection circulation time by 40% Comparable to drug delivery through a central vein </li> <li> Slide 36 </li> <li> Central Venous Route Faster, higher peak concentration and more potent effect compared to peripheral injection Should be used if it is already in situ Inserting a central line is associated with problems of interrupting CPR, bleeding arterial puncture and air embolism </li> <li> Slide 37 </li> <li> Tracheal Route Second line route due to impaired absorption and unpredictable pharmacodynamics Need 2-3 times the IV dose, diluted to at least 10 ml in 0.9% NS Non-ionic drugs only: adrenalin, atropine, lignocaine and naloxone NEVER calcium or sodium bicarbonate </li> <li> Slide 38 </li> <li> Intracardiac Route NOT recommended May produce pneumothorax, injury to a coronary artery and prolonged interruption of cardiac massage. Inadvertent injection into the myocardium may produce intractable arrhythmias </li> <li> Slide 39 </li> <li> Drugs for Resuscitation Vasopressors Adrenaline Vasopressin Other Agents Atropine Buffer agents Calcium </li> <li> Slide 40 </li> <li> Adrenaline Adrenaline 1 mg (10 ml of 1:10,000 dilution) IV boluses every three minutes until pulse returns Short half life of 3-5 minutes -effect (vasoconstriction) aortic pressure to maintain myocardial and cerebral blood flow Cautions: solvent abuse, cocaine and other sympathomimetic drugs </li> <li> Slide 41 </li> <li> Vasopressin 40 U IV: powerful vasoconstriction V 1 receptors in smooth muscle Longer half-life of 10-20 minutes If there is no response 10-20 min. after 40 U of IV vasopressin, resume epinephrine 1 mg IV push every 3 to 5 minutes Used in VF/VT ? role in asystole or PEA </li> <li> Slide 42 </li> <li> Antiarrhythmic Drugs DrugFibrillation threshold Defibrillation threshold Proarrhythmo -genicity Quinidine++++++ Procainamide++0+ Flecainide++++++ Lignocaine++++ Bretylium++-+ Amiodarone++-0/+ Verapamil+++0 Diltiazem+++0 Nifedipine+00 Adrenergic agents -0+ Beta-blockers+++0 Sotolol+-+ </li> <li> Slide 43 </li> <li> Antiarrhythmic Drugs DrugFibrillation threshold Defibrillation threshold Proarrhythmo -genicity Quinidine++++++ Procainamide++0+ Flecainide++++++ Lignocaine++++ Bretylium++-+ Amiodarone++-0/+ Verapamil+++0 Diltiazem+++0 Nifedipine+00 Adrenergic agents -0+ Beta-blockers+++0 Sotolol+-+ </li> <li> Slide 44 </li> <li> Drugs for Persistent VF Amiodarone Class IIb Rapid infusion of 300 mg in 20-30 ml NS IV push (cardiac arrest dose) If VF/pulseless VT recurs, Supplementary doses of 150 mg IV by rapid infusion Followed by 1 mg/min for 6 hours and then 0.5 mg/min Maximum daily dose of 2 g </li> <li> Slide 45 </li> <li> Lignocaine Class indeterminate Initial bolus of 1.0-1.5 mg/kg Additional bolus of 0.5-0.75 mg/kg Maximum total of 3 mg/kg Maintenance infusion of 1-4 mg/min Magnesium sulphate 1-2 g diluted in 100 ml D5 over 1-2 minutes Class IIb in torsades de pointes or suspected hypomagnesaemia or severe refractory VF </li> <li> Slide 46 </li> <li> Atropine Good for haemodynamically significant bradycardia from high vagal tone, hypoxia or nodal ischaemia ? For asystole or PEA 1 mg up to 3 doses or single dose of 3 mg will produce a fully vagolytic effect </li> <li> Slide 47 </li> <li> Buffer Agents 8.4% sodium bicarbonate solution Initial dose of 1 mEq/kg Problems Left shift of Hb dissociation curve Paradoxical intracerebral acidosis High osmolality and Na load Inactivate simultaneously administered catecholamines </li> <li> Slide 48 </li> <li> Indications of NaHCO 3 Class I Preexisting hyperkalemia Pexisting bicarbonate-responsive acidosis Alkaline diuresis; overdose of tricyclic antidepressant, aspirin, etc. Class IIb Long arrest interval In intubated and ventilated patients On return of circulation Class III Hypercarbic acidosis </li> <li> Slide 49 </li> <li> Calcium Only used in hypocalcaemia, hyperkalaemia and calcium antagonist overdose 10% CaCl 2 at 2-4 mg/kg repeated as necessary at 10-minute intervals Worries regarding the role of Ca ++ in ischaemic cell damage during reperfusion to the heart and the brain </li> <li> Slide 50 </li> <li> Universal Advanced Life Support Algorithm </li> <li> Slide 51 </li> <li> The Universal Advanced Life Support Algorithm Two arrest rhythms VF/Pulseless VT Ventricular fibrillation Pulseless ventricular tachycardia Non-VF/VT Pulseless electrical activity Asystole </li> <li> Slide 52 </li> <li> VF / Pulseless VT VF: commonest primary arrest rhythm VF/VT: 85% to 95% of the survivors from cardiac arrest Pulseless VT deteriorates rapidly to VF and treatment is identical to that of VF </li> <li> Slide 53 </li> <li> Management of VF / Pulseless VT Electrical defibrillation is the most effective treatment for VF CPR unlikely to convert VF Speed of defibrillation is the major determinant of success of VF treatment Survival rates after VF arrest 7-10 %/min </li> <li> Slide 54 </li> <li> In-hospital Cardiac Arrest 1325 Resuscitation attempts using 1997 Guidelines Updated from: Gwinnutt C et al. Resuscitation 1998; 37: S64 VF/VTEMD/Asystole Number 422 (32%)903 (68%) ROSC 298 (71%)344 (38%) Survive discharge 179 (42%)58 (6%) </li> <li> Slide 55 </li> <li> Cardiac Arrest Time before Defibrillation Yakaitis et al. Crit Care Med 1982;8:157-163. </li> <li> Slide 56 </li> <li> Defibrillation Energy Balance between electrical injury and efficiency of defibrillation Damage related to the peak current, not the energy delivered </li> <li> Slide 57 </li> <li> Defibrillation Energy Weaver et al. N Engl J Med 1982;307:1101 </li> <li> Slide 58 </li> <li> Morbidity &amp; Mortality Dahl et al. Circulation 50:956. Ehsani et al. Am J Cardiol 37:12. Warner et al. Arch Pathol 99:55. </li> <li> Slide 59 </li> <li> Transthoracic Impedance 70-80 (range 15-143 ) impedance current Current-based defibrillation 30-40A MDS </li> <li> Slide 60 </li> <li> Defibrillation vs. Cardioversion Defibrillation Electric shock delivered without synchronization with ECG activity Used in VF or pulseless VT Synchronized Cardio- version Electric shock delivered with synchronization with R wave to avoid the R on T phenomenon Used in unstable tachyarrhytmias other than VF or pulseless VT </li> <li> Slide 61 </li> <li> Non- VF/VT Rhythms Universal Advanced Life Support Algorithm </li> <li> Slide 62 </li> <li> Non-VF/VT Rhythms Defibrillation is NOT indicated Prognosis much poorer than VF/VT Secure basic life support, airway, oxygen, ventilation, IV access Detect and treat potentially reversible conditions Consider: Atropine: 3 mg bolus given once or 1 mg bolus to a maximum of 3 mg Pacing if P waves are present </li> <li> Slide 63 </li> <li> Pulseless Electrical Activity (PEA) Absence or undetectable mechanical activity in the presence of coordinated electrical activity Includes Pseudo-EMD Idioventricular rhythms Ventricular escape rhythms Postdefibrillation idioventricular rhythms Bradyasystolic rhythms Rhythm of survival if a reversible cause of PEA is identified and treated appropriately </li> <li> Slide 64 </li> <li> Possible Underlying Reversible Causes Hs Hypovolemia Hypoxia Hydrogen ion (acidosis) Hyperkalemia/ hypokalemia/ metabolic disorders Hypothermia/ hyperthermia Ts Toxins/tablets (drug overdose) Tamponade, cardiac Tension pneumothorax Thrombosis, coronary Thrombosis, pulmo...</li></ul>