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CARDIOPULMONARY RESUSCITATION Dr A. Anvaripour Cardiac Anesthesiologist History of resuscitation back to 1966 Standards for the performance of CPR Most recent recommendations Guidelines 2005 New guidelines has undergone comprehensive evidencebased evaluation BASIC LIFE SUPPORT Early recognition of medical emergencies Emergency response system (e.g., dialing 911 in the United States) BLS assessments : Airway, breathing, and circulation performed without equipment BLS interventions: breathing/Heimlich maneuver/application- use of an automated external defibrillator (AED)/CPR GOAL supporting the circulation until restoration of spontaneous circulation occurs after SCA FOR THOSE PERFORMING BLS INTERVENTIONS Importance of prompt initiation and expert these skills cannot be overemphasized performance of Antegrade systemic arterial blood flow continues after cardiac arrest until the pressure gradient between the aorta and right heart structures reach equilibrium Similar process occurs during cardiac arrest with antegrade pulmonary blood flow between the pulmonary artery and the left atrium Arterial-venous pressure gradients dissipate left heart becomes less filled/the right heart becomes more filled/venous capacitance vessels become increasingly distended CORONARY PERFUSION AND CEREBRAL BLOOD FLOW STOP When arterial and venous pressure equilibrates (approximately 5 minutes after cardiac arrest) CPR is performed until return of spontaneous circulation occurs CPR is far less efficient than the native circulation , it can provide coronary circulation and cerebral blood flow sufficient to afford full recovery in many case Push hard and push fast chest compressions performed at a rate of 100/min until generate a palpable carotid or femoral pulse are considered ideal. CHEST COMPRESSIONS Must not frequently interrupted CURRENT RECOMMENDATIONS Placing increased emphasis on limiting interruptions in chest compressions single- and two-person CPR compression-ventilation ratios of 30 : 2 “ CARDIAC PUMP MECHANISM ” Blood is ejected Actual compression heart between the sternum and the vertebral column Reduction in left and right ventricular volume Closure of the tricuspid and mitral valves Ejection of blood into the arterial system COUGH CPR Forceful coughing sustain consciousness during ventricular fibrillation (VF) 100 seconds Coughingarterial pressure pulseopens the aortic valve THORACIC PUMP MECHANISM Increases in intrathoracic pressure generate forward blood flow cardiac pump and thoracic pump mechanisms exist during resuscitation Systemic, coronary, and cerebral blood flow during CPR is dependent on effective chest compressions Modest increases in intrathoracic pressure will impair return of venous blood reducing the chance of spontaneous circulation Cardiac output during effective CPR: 25% 30% oxygen content in the lungs at the time of cardiac arrest usually sufficient for maintaining an acceptable arterial oxygen content during the first several minutes of CPR RESULT Breaths are less important than initiating chest compressions immediately after the onset of SCA MONITORING DURING CPR palpation of the carotid or femoral observation of pupillary size Initial pupillary size and changes during CPR are of some prognostic value 1978, Kalenda described the use of capnography as a guide to the effectiveness of external chest compressions Rapid decrease in PETCO2 with the onset of arrest Immediate increase with resuscitation Noninvasive guide to advanced life support interventions during CPR Severe reductions in pulmonary blood flow acute failure of delivery of O2 to the lungs very low PETCO2 External chest compression & ventilaitonPETCO2 increased to 1.9% ± 0.3%, After successful defibrillation and 12 minutes of CPR PETCO2 immediate increase to 4.9% ± 0.3% RESULT Close correlation was found between changes in cardiac output and PETCO2 MAJOR DETERMINANTS OF P ETCO 2 CO2 production Alveolar ventilation Pulmonary blood flow. BREATHING Breathing is indicated for a nontracheally intubated cardiac arrest two 1-second breaths are delivered after the 30th compression Provide only enough force and volume to cause chest rise Excessive ventilation gastric inflation With tracheal tube 8 to 10 breaths per minute independent of chest compressions SCISSORS MANEUVER “SNIFF“ POSITION MACINTOSH LARYNGOSCOPE IN POSITION SCHEMATIC VIEW OF THE GLOTTIC OPENING DURING DIRECT LARYNGOSCOPY SUPRAVENTRICULAR TACHYARRHYTHMIA Atrial flutter Atrial fibrillation AV junctional tachycardia Multifocal atrial tachycardia Paroxysmal reentrant tachycardia HEMODYNAMIC COMPROMISE Paroxysmal supraventricular tachycardia (PSVT) Atrial fibrillation (or flutter) with rapid ventricular rates Multifocal atrial tachycardia PSVT PSVT With hemodynamic deterioration cardioversion 100 to 200 J if a monophasic defibrillator 100 to 120 J with a biphasic defibrilator PSVT Energy can be increased as needed if is resistant to therapy the arrhythmia HEMODYNAMICALLY STABLE PSVT vagal maneuvers (Valsalva ) before initiating pharmacologic interventions terminate about 20% to 25% Adenosine (very effective in terminating PSVT) ADENOSIN slows sinoatrial and AV nodal conduction prolongs refractoriness diagnostic usefulness with uncertain origin AFTER INJECTION OF 6 MG ADENOSIN short half-life (<5 seconds) and short lived side effects Flushing Dyspnea chest pain tachyarrhythmia may recur another drug necessitate the use of VERAPAMIL PSVT does not respond to adenosine or if it recurs contraindicated in WPW syndrome AF/AF Rate-related hemodynamic compromise cardioversion 100 to 200 J with monophasic 100 J to 120 J with biphasic Escalation of energy doses for the second and subsequent doses is indicated AF/AF hemodynamically stable patients pharmacologic Ibutilide most rapid onset in restoring sinus rhythm Prolongs the action potential dration / effective refractory 1 mg given over a 10-minute second dose can be administered 10 minutes after the first, if necessary Conversion to sinus rhythm is more frequent with atrial flutter than with atrial fibrillation (63% versus 31%) IBUTILIDE SIDE EFFECTS Prolongation of the QT interval PVT (polymorphic v tach) OPTIONS FOR THE TREATMENT OF SUPRAVENTRICULAR ARRHYTHMIAS DRUGS Diltiazem Verapamil β-blocking medications Procainamide Amiodaron MULTIFOCAL (MULTIFORM) ATRIAL TACHYCARDIA Often misdiagnosed as atrial fibrillation Increased automaticity in multiple atrial foci At least three morphologically different P waves in the same lead with ventricular rate more rapid than 100/min occurring in patients with COPD, especially during exacerbations, and ICU management MAT OCCUR COPD, especially during exacerbations Hypokalemia Catecholamine administration Acute myocardial ischemia TREATMENT underlying conditions Digitalization Cardioversion Calcium channel blockers β-adrenergic blockers Amiodarone VENTRICULAR BRADYARRHYTHMIA Urgent treatment is complete heart block Atropine can be tried Choice is external or transvenous pacing as soon as possible VENTRICULAR TACHYARRHYTHMIA VT life-threatening and sometimes pre-arrest arrhythmias Urgent intervention VT ETIOLOGY Hypoxemia Hypercapnia Hypokalemia Hypomagnesemia Digitalis toxicity Acid-base derangements Stable and ventricular function preserved Amiodaron Procainamide and cardioversion AMIODARON 150 mg / 100 cc over a 10-minute period Loading infusion of 1 mg/min for 6 hours and then a 0.5- mg/min maintenance infusion over an 18-hour period, may be effective MAJOR ADVERSE EFFECTS OF AMIODARONE Hypotension Bradycardia can be prevented by slowing the rate of infusion Unsatable patients, systemic hypotension, pulmonary edema clinical or electrocardiographic signs of acute myocardial ischemia or infarction Monophasic energy doses of 360 j Biphasic 120 j ATYPICAL VT (TWISTING POINTS) CHARACTERISTIC long-short initiating sequence This arrhythmia occurred in a patient after resuscitation from cardiac arrest TREATMENT Underlying correction ( esp. Hypokalemia) Pace Magnesium sulfate Without prolonged QT interval similar to VT MANAGEMENT OF CARDIAC ARREST Pulseless Ventricular Tachycardia or Ventricular Fibrillation Most treatable arrhythmia In the hospital and out of the hospital Long-term survival DEFINITIVE INTERVENTION Rapid Defibrillation TERMINATION OF VF Amount of energy available from a defibrillator Resistance to flow of current GUIDELINES Self-adhesive defibrillation pads Defibrillation should occur at the end of expiration to minimize impedance Momophasic 360 J Biphasic 150-200 J insufficient evidence that escalation of energy is superior to nonescalating energy shocks in terminating recurrent VF Witness arrested Unwitnes arrested Defebrilator Chest compression VF recurs after successful conversion defibrillation should be repeated IF THE DEFIBRILLATOR IS IMMEDIATELY AVAILABLE Delay Enditracheal Intubation No response to 1st Defebrilator 5 cycle CPR 30/2 second defibrillatory shock pharmacologic interventions should accompany the resuscitative efforts CURRENTLY, ONLY TWO MEDICATIONS Epinephrin Vasopressin EPINEPHRIN 1 mg (1 : 10,000 solution) Every 3 to 5 minutes From tracheobronchial tree2-2.5 times IV routs Large doses of epinephrine (up to 0.2 mg/kg) VASOPRESSIN Beneficial effects on perfusion of vital organs during cardiac arrest High level of plasma concentration in stress situation Muscle V1 receptors muscle constriction in the presence of severe acidosis maintain coronary perfusion Alternative to one dose of epinephrine during refractory VF One-time dose of 40 units intravenously or intraosseously VF PERSISTS Amiodarone (preferred antiarrhythmic agent) Lidocaine AMIODARON Initial amiodarone dose of 300 mg IV Can be followed by a single dose of 150 mg AMIODARONE IN OUTOF-HOSPITAL RESUSCITATION OF REFRACTORY SUSTAINED VENTRICULAR TACHYCARDIA (ARREST Out-of-hospital cardiac arrest Persistent VF Three attempts at defibrillation 1 mg of intravenous epinephrine 300 mg Amiodartone ALIVE STUDY demonstrated that amiodarone was superior to lidocaine in terminating persistent VF in the outof-hospital setting SODIUM BICARBONATE cardiac arrest that does not respond Preexisting metabolic acidosis Severe metabolic acidosis documented during CPR Overdoses of tricyclic antidepressants Hyperkalemia INJECTED DRUGS initial drug injection from IV rout fluid bolus to propel typically require 1 to 2 minutes to resum central circulation Two minutes of CPR should be performed after drug administration & before defebrilation Intraosseous cannulation Central circulation FLUIDS Normal saline Lactated Ringer glucose-containing solutions not recommended PULSELESS ELECTRICAL ACTIVITY Hypovolemia Hypoxia Acidosis Hypo/Hyperkalemia Tamponade Tension pnemothorax Coronary thrombosis Pulmonary thrombosis PEA TREATMENT Epinephrin 1 mg IV push Q 3-5 min repeated Atropin 1 mg ( if rate of PEA is slow) Q3-5 min repeared , total dose 0.04 mg/kg CPCR Cardiopulmonary cerebral rescucitation POST CARDIAC ARREST INDUCED HYPOTHERMIA HYPOTHERMIA Intracellular PH increased significantly ischemic tolerance Cerebral o2 consumption in profound hypothermia decreased CBF/CMRO2 = 75/1 normothermia = 20/1 METHODS Systemic ( Blanket) Topical (Ice application on head ) CONTRAVERSIES Systemic hypothermia + topical hypothermia Q10 predict safe time of arrest # 15 min /20 degree of c. 30 – 45 min Brain Tolerated Therapeutic Hypothermia 32 – 34 d of c. Induced with External cooling 12 – 24 hours After Resuscitation Appears decreased neurological outcome in VF arrested patient DHCA Nasopharyngeal Temp 11- 14 max safe duration 30 min Nasopharyngeal Temp 12.5 99.5% Electrocortical silence OUTCOME AFTER IN HOSPITAL RESUSCITATION Discharge survival rates 8-21 % Average survival rate of approximately 14% Intraoperative cardiac arrest survival 38%( Retrospective) Primary cardiac event was presumed to be causative in 50% LIMIT SURVIVAL VARIABLES Age Duration longer than 30 min Sepsis Cancer Pre- arrest hypotension Renal failure Unwitnessed arrest MAJOR DETERMINANT Age AGE ALONE SHOULD NOT PRECLUDE PATIENTS FROM RECEIVING CPR UNWARRANTED CPR Sepsis or cancer in an elderly patient Unwitnessed bradyarrhythmic arrested