心肺复苏cpr教学课件（英文）摘要

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 Blood Sufficient Oxygen Blood Good circulation Insufficient or cease of Oxygen supply Vital organ ischemia or death Hypoxia Low CBV or Desaturation Circulation problem Ventilation Airway Hemorrhage or Hb abnormal Cardiac Pump hemodynamics microcirculation DEFINITION OF CARDIAC ARREST -CLINICAL DEATH Medical 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. Ventilation Airway Hemorrhage or Hb abnormal Cardiac Pump Hemodynamics microcirculation Cardiac Arrest Tissue Hypoxia Breathing Brain ischemia Ventilation Airway Hemorrhage or Hb abnormal Hemodynamics microcirculation Cardiac Arrest HeartMI arrhythmia Heart failure reflex SUMMERY OF MECHANISMS OF CA Reduction of Coronary Blood Flow Critical Cardiac Arrhythmia Absent of inadequate Contraction of the Left Ventricle Severe Reduction of Cardiac Return Volume Cardiac Arrest Brain ischemia Signs of Cardiac Arrest Unconscious Dilated Pupils No pulse BP o/o Cyanosis No Breathing No bleedingNo SPO2 无脉性室速 Pulseless VT 室颤 VT 无脉性电活动 Pulseless Electrical Activity 心室停搏 Asystole Pulseless VT VF Pulseless Electrical Activity Asystole ECG Patterns of Cardiac Arrest CARDIO-PULMONARY RESUSITATION An 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 arrest long arrest time before CPR prolonged ventricular fibrillation without definitive therapy inadequate coronary and cerebral perfusion during cardiac massage. rapid application of closed chest compression and early defibrillation lEarly Access lEarly CPR lEarly Defibrillation lEarly Advanced Care Chain of Survival for Adults Chain of Survival for Children lPrevention of Arrest lEarly and Effective Bystander CPR lRapid Activation of the EMS lEarly Advanced Life Support BASIC LIFE SUPPORT (RABC) Objectives: to deliver oxygenated blood to vital organs nResponse (consciousness) nAirway Control nVentilation (Breathing) nChest Compression Help! Help ! Help! INITIAL STEPS OF CPR Unresponsive? Open airway Check breathing (10s) Breathing Check 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. DEFIBRILLATION Ventricular fibrillation is common in adults non- traumatic cardiac arrest Earlier defibrillation is important for survival The chances for survival decline 7-10% every minute lapse Be defibrillated at the earliest possible moment In hospital CA, defibrillation should be delivered in 3 min Out hospital CA, defibrillation better down in 5 min MANAGEMENT OF VT Rapid defibrillation is key Minutes: collapse to 1st shock IN HOSPITAL DEFIBRILLATION A 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 disability MECHANISMS OF DEFIBRILLATION External current depolarize entire myocardium simultaneously Entire myocardium is in refractory phase Ectopic discharges of myocardium is not able to induce abnormal electro-activities Sinus rhythm take control ENERGY FOR DEFIBRILLATION Too low will not provide successful cardiovert Too high may cause myocardium injury Use unsynchronized defibrillation 360J for monophasic damped sine (MDS) defibrillators Start with120- 150J for biphasic, defibrillators Give 200 J for unknown defibrillators POSITION OF ELECTROPAD AUTOMATED EXTERNAL DEFIBRILLATOR (AED) Commonly used by non-health workers Capable of electrocardiographic analysis Recognition of cardiac rhythm and VF Deliver biphasic shock Disadvantage for health worker is too slow to deliver a shock TIPS FOR DEFIBRILLATION Must put wet gauges (soaked with saline) or gels under the electropads Must clear the people surrounded before giving the shock Perform CPR if defibrillator is not ready and continue CPR if shock is not successful SUMMERY OF BLS A Airway: open the airway B Breathing: positive-pressure ventilation C Circulation: Chest compression D defibrillation: shock for VF/pulseless VT ADVANCED CARDIAC LIFE SUPPORT A Airway: place airway device B Breathing: comfirmation airway device B Breathing: secure airway device B Breathing: effective oxygenation C Circulation: establish IV access C Circulation: identify rhythm C Circulation: administer drugs for rhythm D differential diagnosis: identify reversible causes ENDOTRACHEAL INTUBATION LARYNGEAL MASK AIRWAY(CONTROVERSIAL IN CPR) THE COMBITUBE VENTILATION Intubate the patients for airway protection and better oxygenation Cardiac compression should not stop during intubation process Ventilate manually or by ventilator Cardiac compression is not required to discontinue during lung inflation ECG MONITORING Connect ECG monitors as soon as CPR started Four common cardiac rhythms in CA lPulseless VT lVentricular fibrillation lAsystole lPulseless Electrical Activity PHARMACOLOGIC AGENTS FOR CPR 1. Epinephrine Initial Dose: 1mg IV(0.01 mg/kg, IV/IO for children) tracheal route : 2-3times of IV dose diluted in 10ml saline Subsequent Doses (every 3-5 minutes)Repeat initial dose Subsequent Doses (every 3-5 minutes) May consider high-dose protocol; 0.1 mg/kg, IV The efficacy of epinephrine lies entirely in its- adrenergic properties epinephrine helps develop the critical coronary perfusion pressure High dose epinephrine has no improvement in survival to hospital discharge or neurological outcome, high dose epinephrine was used as rescue therapy. Epinephrine 2. Vasopressin as an alternative to the first dose of epinephrine during ventricular fibrillation cardiac arrest dose : 40 units IV, single dose, 1 time only is a potent non-adrenergic vasoconstrictor, acting by stimulation of smooth muscle V1 receptors. half-life in the intact circulation is 10 to 20 minutes 3. AMIODARONE (胺碘酮） nBlock sodium, potassium, calcium, alpha- channels and beta-adrenergic receptors nIndication: 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 grams nCause hypotension and bradycardia when infused too rapidly 4. LIDOCAINE nLidocaine: 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. MAGNESIUM Indications: (1) Hypomagnesemia (2) Torsades de pointes even with normal serum levels of magnesium Dose: 1-2g in 50-100ml 5% GS over 5-10min, followed by infusion 0.5-1g/h Not recommended in Cardiac arrest except when arrhythmia suspected Cardiac arrest Basic life support Attach defib/monitor Assess rhythm Pulse present? no PEA/Asystle CPR for 3 min Adrenaline 1mg During CPR lCorrect any reversible causes lConnect ECG lSet up IV access lAdvanced airway control lGive adrenaline every 3 min lConsider alternative medications no VF/VT Defibrillate X1 CPR for 2min Adult protocol Rescuers and health care providers must assume that all un-monitored adult cardiac arrests are due to VF/VT. VENTRICULAR FIBRILLATION AND PULSELESS VENTRICULAR TACHYCARDIA THE MONITOR SHOWS: PROBABILITY OF SURVIVAL IS RELATED TO 2 INTERVALS: (1) COLLAPSE TO DEFIBRILLATION AND (2) COLLAPSE TO CPR Collapse to start of CPR: 1, 5, 10, 15 (min) Collapse to defibrillation interval (min) Probability of survival to hospital discharge BACKGROUND: DEFIBRILLATION AND TIME Approximately 50% survival after 5 minutes Survival reduced by 7% to 10% per minute (if no CPR) Rapid defibrillation is key CPR prolongs VF, slows deterioration Minutes: collapse to 1st shock VF-PULSELESS VT ALGORITHM PULSELESS ELECTRICAL ACTIVITY (PEA) 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 capture Tips: Patients may be sedated due to discomfort of skeletal muscle contraction TCP is a temporary measure, transvenous pacing or other definitive treatment should be initiated. BRADYCARDIA BRADYCARDIA TACHYCARDIA SUPRAVENTRICULAR TACHYARRHYTHMIA include atrial flutter, atrial fibrillation, AV junctional tachycardia, multifocal atrial tachycardia, paroxysmal reentrant tachycardias 250/min 180/min VENTRICULAR TACHYARRHYTHMIA 280/min upotentially 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 TACHYCARDIA POST-RESUSCITATION THERAPY 3/10 in hospital resuscitation survive the initial resuscitation procedures 1.5/10 to be discharged 1/10 survived for more than a year Majority of them died of myocardial or central nervous system failure This indicates the importance of post-resuscitation care Following resuscitation, all patients should be cared for on a special unit POST-RESUSCITATION MYOCARDIAL DYSFUNCTION nmyocardial dysfunction happens immediately after successful resuscitation n the most common causes of death Post-resuscitation nIncluding myocardial failure and ventricular arrhythmia CARDIOVASCULAR POST-RESUSCITATION SYNDROME Contractivity , LV peak systolic pressure ,LV diastolic pressure Myocardium compliance CO CI(up to 6hours) PCWP Cardiac dysarrhythemia-multifocal run of premature ventricular contractions (PVCs) in common MECHANISMS OF POST-RESUSCITATION MYOCARDIAL DYSFUNCTION remains unclear several mechanisms have been proposed ATP 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 proteins free radicals is a major cause of reperfusion injury endothelin-1mediate a direct action on the myocardium results in diastolic myo-cardial dysfunction global myocardial ischaemia increases the number of -adrenergic receptors in the cell surface. PREVENTION AND TREATMENT OF POST- RESUSCITATION MYOCARDIAL DYSFUNCTION Affected by the severity and duration of the global myocardial ischaemia the 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 CPR learly activation of the emergency medical system, l early initiation of basic CPR, learly defibrillation and learly advanced cardiac life support MANAGEMENT OF POST-RESUSCITATION MYOCARDIAL DYSFUNCTION determining 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 pressures control 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 bypass POST-RESUSCITATION NEUROLOGICAL DYSFUNCTION maximal period of normothermic is 45 minutes (reversible to complete recovery of cerebral function and structure) 1030% of long term survivors suffer from permanent brain damage PATHOPHYSIOLOGY ucalcium shifts u brain tissue lactic acidosis uincreases of free fatty acids in the brain u osmolality u extracellular concentration of excitatory amino acids Complete cerebral ischaemia Cause: Above occures within seconds, would return to normal if gain flow in 4-5min SECONDARY NEURONAL INJURY 1. 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 is consciousness) or both remain low (with coma). SECONDARY NEURONAL INJURY 2. Reperfusion injury with chemical free radical and calcium- mediated cascades to cell necrosis 3. 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 endothelia 5. Post-arrest inflammatory process, which remains not well investigated in these settings ASSESSMENT OF NEUROLOGICAL STATUS AND OUTCOME Assessment of brain stem reflexes is useful for predicting neurological outcome, especially pupillary light reactions which predict,when absent, persistent