心肺复苏CPR教学课件英文

Cardiopulmonary Resuscitation(CPR)教学大纲要求掌握心跳骤停的诊断；掌握基础生命支持的内容和方法；掌握进一步生命支持的主要内容和方法；熟悉导致心跳骤停的常见原因；熟悉心脑后期生命支持的治疗原则；Vital Organ Function Oxygen Supply Sufficient Oxygenated BloodSufficient OxygenBloodGood circulationInsufficient or cease of Oxygen supplyVital organ ischemia or deathHypoxiaLow CBV or DesaturationCirculation problemVentilationAirwayHemorrhage or Hb abnormalCardiac PumphemodynamicsmicrocirculationDefinition of Cardiac Arrest-Clinical DeathMedical emergency with absent or inadequate contraction of the left ventricle of the heart that immediately causes bodywide circulatory failure.The signs and symptoms include loss of consciousness;rapid shallow breathing progressing to apnea(absence of breathing);profoundly low blood pressure(hypotension)with no pulses that can be felt over major arteries;and no heart sounds.Cardiac arrest is one of the greatest of all medical emergencies.Within several minutes,there is lack of oxygen(tissue hypoxia),leading to multiple organ injury.Unless cardiac arrest is quickly corrected,it is fatal.VentilationAirwayHemorrhage or Hb abnormalCardiac PumpHemodynamicsmicrocirculationCardiac Arrest Tissue HypoxiaBreathing Brain ischemiaVentilationAirwayHemorrhage or Hb abnormalHemodynamicsmicrocirculationCardiac Arrest HeartMI arrhythmiaHeart failurereflexSummery of Mechanisms of CAReduction of Coronary Blood FlowCritical Cardiac ArrhythmiaAbsent of inadequate Contraction of the Left VentricleSevere Reduction of Cardiac Return VolumeCardiac Arrest Brain ischemiaSigns of Cardiac ArrestUnconsciousDilated PupilsNo pulseBP o/oCyanosisNo BreathingNo bleedingNo SPO2 无脉性室速无脉性室速Pulseless VT室颤室颤VT无脉性电活动无脉性电活动Pulseless Electrical Activity心室停搏心室停搏AsystolePulseless VTVFPulseless Electrical ActivityAsystoleECG Patterns of Cardiac ArrestCardio-Pulmonary ResusitationAn emergency procedure in which the heart and lungs are made to work by manually compressing the chest overlying the heart and forcing air into the lungs.CPR is used to maintain circulation when the heart stops pumping,usually because of disease,drugs,or trauma.An emergency procedure consisting of external cardiac massage and artificial respiration;the first treatment for a person who has collapsed and has no pulse and has stopped breathing;attempts to restore circulation of the blood and prevent death or brain damage due to lack of oxygen The factors most related to poor outcome from cardiac arrestlong arrest time before CPR prolonged ventricular fibrillation without definitive therapy inadequate coronary and cerebral perfusion during cardiac massage.rapid application of closed chestcompression and early defibrillationlEarly AccesslEarly CPRlEarly DefibrillationlEarly Advanced CareChain of Survival for AdultsChain of Survival for ChildrenlPrevention of ArrestlEarly and Effective Bystander CPRlRapid Activation of the EMSlEarly Advanced Life SupportBasic Life Support(RABC)Objectives:to deliver oxygenated blood to vital organsnResponse(consciousness)nAirway Control nVentilation(Breathing)nChest Compression Help!Help!Help!Initial steps of CPRUnresponsive?Open airwayCheck breathing(10s)BreathingCheck Pulse(20 mm Hg during successful CPR)Earliest sign is a sudden increase in end-tidal CO2 to greater than 40 mm Hg,when spontaneous circulation resumes.no patient with an end-tidal CO2 10 mm Hg could be successfully resuscitated.not be useful for three to five minutes following bicarbonate administration.DefibrillationVentricular fibrillation is common in adults non-traumatic cardiac arrestEarlier defibrillation is important for survivalThe chances for survival decline 7-10%every minute lapseBe defibrillated at the earliest possible moment In hospital CA,defibrillation should be delivered in 3 minOut hospital CA,defibrillation better down in 5 minManagement of VTRapid defibrillation is keyMinutes:collapse to 1st shockIn Hospital DefibrillationA new study using data collected by NRCPR:6789 VF/VT patients in 369 hospitals Enrolled in NRCPR between Jan.1,2000,and July 31,2005.Defibrillation in 2 min：Survival rate to hospital discharge:39%Defibrillation more than 2 min:decreased to 22%.And Less likely to have no major neurological disabilityMechanisms of DefibrillationExternal current depolarize entire myocardium simultaneouslyEntire myocardium is in refractory phaseEctopic discharges of myocardium is not able to induce abnormal electro-activitiesSinus rhythm take control Energy for DefibrillationToo low will not provide successful cardiovertToo high may cause myocardium injuryUse unsynchronized defibrillation360J for monophasic damped sine(MDS)defibrillatorsStart with120-150J for biphasic,defibrillatorsGive 200 J for unknown defibrillatorsPosition of electropadAutomated external Defibrillator(AED)Commonly used by non-health workersCapable of electrocardiographic analysisRecognition of cardiac rhythm and VFDeliver biphasic shockDisadvantage for health worker is too slow to deliver a shockTips for DefibrillationMust put wet gauges(soaked with saline)or gels under the electropadsMust clear the people surrounded before giving the shockPerform CPR if defibrillator is not ready and continue CPR if shock is not successfulSummery of BLSA Airway:open the airwayB Breathing:positive-pressure ventilationC Circulation:Chest compressionD defibrillation:shock for VF/pulseless VTAdvanced Cardiac Life SupportA Airway:place airway deviceB Breathing:comfirmation airway deviceB Breathing:secure airway deviceB Breathing:effective oxygenationC Circulation:establish IV accessC Circulation:identify rhythmC Circulation:administer drugs for rhythm D differential diagnosis:identify reversible causesENDOTRACHEAL INTUBATION LARYNGEAL MASK AIRWAY(controversial in CPR)THE COMBITUBE VentilationIntubate the patients for airway protection and better oxygenationCardiac compression should not stop during intubation processVentilate manually or by ventilatorCardiac compression is not required to discontinue during lung inflationECG MonitoringConnect ECG monitors as soon as CPR startedFour common cardiac rhythms in CAlPulseless VTlVentricular fibrillationlAsystolelPulseless Electrical ActivityPharmacologic Agents for CPR1.Epinephrine Initial Dose:1mg IV(0.01 mg/kg,IV/IO for children)tracheal route:2-3times of IV dose diluted in 10ml salineSubsequent Doses(every 3-5 minutes)Repeat initial doseSubsequent Doses(every 3-5 minutes)May consider high-dose protocol;0.1 mg/kg,IVThe efficacy of epinephrine lies entirely in its-adrenergic propertiesepinephrine helps develop the critical coronary perfusion pressureHigh dose epinephrine has no improvement in survival to hospital discharge or neurological outcome,high dose epinephrine was used as rescue therapy.Epinephrine2.Vasopressin as an alternative to the first dose of epinephrine during ventricular fibrillation cardiac arrestdose:40 units IV,single dose,1 time onlyis a potent non-adrenergic vasoconstrictor,acting by stimulation of smooth muscle V1 receptors.half-life in the intact circulation is 10 to 20 minutes3.Amiodarone(胺碘酮）nBlock sodium,potassium,calcium,alpha-channels and beta-adrenergic receptorsnIndication:should be considered in CA due to VF or pulseless VT after third shock(refractory ventricular fibrillation).nDose:300mg IV Push,maintanace1mg/min for 6h,then 0.5mg/min,maximum daily dose of 2 gramsnCause hypotension and bradycardia when infused too rapidly4.LidocainenLidocaine:tends to reverse the reduction in VT threshold.nas second-line treatment for VF/VT after 3 unsuccessful shocks.nA starting dose of 1-1.5mg/kg.Repeat dose 0.5-0.75%within 5 to 10 min.Total dose should be lower than 300mg(200-300mg in an hour).nfollowed by a maintenance dose of 2mg/min.5 Bicarbonate best administered on the basis of blood-gas analysis.It is recommended in the presence of severe acidosis(arterial pH7.1,base excess-10).Dose:1moml/kg(1moml=0.6ml 5%NaHCO2)6.MagnesiumIndications:(1)Hypomagnesemia(2)Torsades de pointes even with normal serum levels of magnesiumDose:1-2g in 50-100ml 5%GS over 5-10min,followed by infusion 0.5-1g/hNot recommended in Cardiac arrest except when arrhythmia suspectedCardiac arrest Basic life support Attach defib/monitor Assess rhythm Pulse present?noPEA/AsystleCPR for 3 minAdrenaline 1mgDuring CPRlCorrect any reversible causeslConnect ECGlSet up IV accesslAdvanced airway control lGive adrenaline every 3 minlConsider alternative medicationsnoVF/VTDefibrillate X1CPR for 2minAdult protocolRescuers and health care providers must assume that all un-monitored adult cardiac arrests are due to VF/VT.Ventricular FibrillationandPulseless Ventricular Tachycardia The monitor shows:Probability of Survival Is Related to 2 Intervals:(1)Collapse to Defibrillation and(2)Collapse to CPRCollapse to start of CPR:1,5,10,15(min)Collapse to defibrillation interval(min)Probability of survival to hospital dischargeBackground:Defibrillation and Time Approximately 50%survival after 5 minutesSurvival reduced by 7%to 10%per minute(if no CPR)Rapid defibrillation is keyCPR prolongs VF,slows deterioration Minutes:collapse to 1st shockVF-Pulseless VT AlgorithmPulseless Electrical Activity(PEA)&AsystoleThe monitor shows:Sinus Tachycardia With No PulsePulseless Electrical ActivityPulseless Electrical Activity?Pulseless Electrical Activity?PEA?Asystole?PEA&AsystoleReversible Causes of PEA/AsystoleBradycardiaIdentify and treat possible causes:the 6 Hs and 5 TsAtropine dose for bradycardia is 0.5 mg with the maximum total dose at 3 mgPacing is used when the patient fails to respond to atropine or has a high-degree blockDosages for epinephrine:2-10g/min and dopamine 2-10 g/kg/min.Emergency Pacemaker Therapy-Transcutaneous cardiac pacing(TCP)Indications:to treat atropine-resistant symptomatic bradyarrhythmias Features:defibrillator model;disposable pacing electrodes positioned anterior-posterior manner.(negative on V2 electrocardiograph position,positive on the left posterior chest beneath the scapula and lateral to the spine Application:Current output is slowly increased until the pacing stimuli obtain electrical and mechanical captureTips:Patients may be sedated due to discomfort of skeletal muscle contractionTCP is a temporary measure,transvenous pacing or other definitive treatment should be initiated.BradycardiaBradycardiaTachycardiaSupraventricular Tachyarrhythmia include atrial flutter,atrial fibrillation,AV junctional tachycardia,multifocal atrial tachycardia,paroxysmal reentrant tachycardias 250/min180/minVentricular Tachyarrhythmia 280/minupotentially life-threatening uneed of urgent intervention uFind out the causes is very important(Hypoxia,hypercarbia,hypokalemia and/or hypomagnesemia,digitalis toxicity,and acid-base derangements TachycardiaPost-resuscitation therapy3/10 in hospital resuscitation survive the initial resuscitation procedures1.5/10 to be discharged1/10 survived for more than a yearMajority of them died of myocardial or central nervous system failureThis indicates the importance of post-resuscitation careFollowing resuscitation,all patients should be cared for on a special unitPOST-RESUSCITATION MYOCARDIAL DYSFUNCTIONnmyocardial dysfunction happens immediately after successful resuscitationn the most common causes of death Post-resuscitationnIncluding myocardial failure and ventricular arrhythmiacardiovascular post-resuscitation syndromeContractivity,LV peak systolic pressure ,LV diastolic pressureMyocardium complianceCOCI(up to 6hours)PCWPCardiac dysarrhythemia-multifocal run of premature ventricular contractions(PVCs)in commonMechanisms of post-resuscitation myocardial dysfunctionremains unclearseveral mechanisms have been proposedATP depletion(more likely to be due to impaired energy usage than to a reduction in the energy supply)Disturbance in Calcium homeostasis(During ischaemia,free radicals are released and the tissue pH is decreased by lactate production,degradation of high-energy phosphate and reduced removal of CO2.These result in reduced Na-Ca exchange with consequent cytosolic calcium overload.Oxygen free radicals decrease the calcium sensitivity of the contractile proteinsfree radicals is a major cause of reperfusioninjuryendothelin-1mediate a direct action on the myocardium results in diastolic myo-cardial dysfunctionglobal myocardial ischaemia increases the number of-adrenergic receptors in the cell surface.Prevention and treatment of post-resuscitation myocardial dysfunctionAffected by the severity and duration of the global myocardial ischaemiathe interval between circulatory arrest and the start of resuscitation e.orts(down time)and the efficacy of CPR Prevention:decreasing the down time and increasing the blood down flow to the myocardium during CPRlearly activation of the emergency medical system,l early initiation of basic CPR,learly defibrillation and learly advanced cardiac life supportManagement of post-resuscitation myocardial dysfunctiondetermining the cause of cardiac arrest,An assessment of hemodynamic function an identification of extracardiac factors that may affect vital organ function.Pharmacological interventions.Goals:improved myocardial systolic function with increases in stroke volume and reduction of ventricular filling pressurescontrol of arrhythmias.pharmacological agents:inotropic agents,specically dobutamine and phosphodiesterase inhibitors(amrinone)vasopressor agents,specically dopamine and norepinephrine;preload and afterload reducing agents,including nitroglycerin,nitroprusside,phosphodiesterase inhibitors and angiotensin-converting enzyme(ACE)Mechanical interventions.intra-aortic balloon pump is a reasonable option(The balloon is inated during diastole and deflated during systole,to favour increases in coronary blood flow and improve cardiac function)Partial cardiopulmonary bypassPOST-RESUSCITATION NEUROLOGICAL DYSFUNCTIONmaximal period of normothermic is 45 minutes(reversible to complete recovery of cerebral function and structure)1030%of long term survivors sufferfrom permanent brain damagePathophysiologyucalcium shiftsu brain tissue lactic acidosisuincreases of free fatty acids in the brainu osmolalityu extracellular concentrationof excitatory amino acidsComplete cerebral ischaemia Cause:Above occures within seconds,would return to normal if gain flow in 4-5minsecondary neuronal injury1.Perfusion failure that progresses through four stages:(i)multifocal no reflow which occurs immediately and may be readily overcome by normotensive or hyper-tensive reperfusion(ii)transient global reactive hyperaemia which lasts1530 minutes(iii)delayed,prolonged global and multifocal hypoperfusion that is evident from about 212 hours after arrest and is probably due to vasospasm,oedema and blood cell aggregates(iv)late resolution in which either global cerebral blood flow and cerebral O2 uptake are restored(as isconsciousness)or both remain low(with coma).secondary neuronal injury2.Reperfusion injury with chemical free radical and calcium-mediated cascades to cell necrosis3.Adverse cerebral effects of systemic extracerebral pathologies such as recurrent cardiac arrest,cardiopulmonary dysfunction,metabolic disturbances and formation of systemic toxins.4.Blood rheology disturbances or abnormalities due to stasis,including aggregates of polymorphonuclear leukocytes and macrophages that might obstruct capillaries,release free radicals and damage endothelia5.Post-arrest inflammatory process,which remains not well investigated in these settingsAssessment of neurological status and outcomeAssessment of brain stem reflexes is useful for predicting neurological outcome,especially pupillary light reactions which predict,when absent,persistent vegetative state in almost 100%Post-anoxic myoclonus,when generalized and robust,is associated with extensive brain damage and predicts poor outcomeGlasgow Coma Scale(GCS)Glasgow-Pittsburgh Coma Scale(A)Eye openingSpontaneous.4To speech.3To pain.2None.1(B)Best motor response(extremities of best side)Obeys.6Localizes.5Withdraws.4Abnormal flexion.3Extends.2None.1(C)Best verbal response(if patient intubate,give best estimate)Oriented.5Confused conversation.4Inappropriate words.3Incomprehensible sounds.2None.1 Total GCS(best GCS.15)(worst GCS.3)TreatmentGeneral brain-oriented life supportspecific cerebral resuscitation measuresGeneral brain-oriented life supportbasic requirements:Minimizing arrest time with earliest defibrillation and other advanced life support measures,and increasing blood flow to the brain during CPRepinephrine should be given early to increase perfusion pressures through the heart and brain.A spontaneous or induced hypertensive bout during or immediately after ROSC is associated with better cerebral outcome(SBP150-200mmHg)haematocrit level of 30%seems benefcialblood glucose levels at 100200 mg/dlmandatory general brain-orientated life measures(i)inducing a hypertensive bout during or immediately after ROSC,controlling normal pressure thereafter,(ii)avoiding hypoglycaemia or severe hyperglycaemia,(iii)controlling seizures and sedating with titrated benzodiazepine or barbiturate,(iv)controlling ventilation with normocapnia or slight hypocapnia with optional slight elevation of head.Specific cerebral resuscitation measures remain controversial although brain cooling seems to be promising