Cardiopulmonary Resuscitation Peizhi Huang Zhongshan Hospital Diagnosis of cardiac and respiratory arrest  Traditional methods :  1. Carotid pulse check by lay rescuers 2. Loss of consciousness 3. Pupil dilation 4. Respiratory arrest Guideline 2000 Elimination of the pulse check for lay rescuers Evaluate for signs of circulation in 10 seconds  breathing  ,  coughing , movement in response to  rescue breath  Assess for a pulse  Rate of false- positive(40%)  Results Pulseless  Pulse Mistakenly loss the saving opportunity Rate of false-negative (10 %) Results Pulse  Pulseless  Unnecessarily do CPR Electrocardiogram changes  of Cardiac arrest Ventricular fibrillation A flat line or only atrial wave  Pulseless Electrical Activity, PEA The chain of Survival Early access Early CPR Early Defibrillation Early advanced life support  * patient with Coma （immediately  do CPR ，not clear  obstructed airways at first ）Basic Life Support --- the first ABCD  Airway A  Breathing B  Circulation C  Defibrillation D Airway  Tilt the head backwards Lift the jaw Open the mouth Clearing obstructed airways from choking Subdiaphragmatic abdominal thrust (Heimlich maneuver)  Breathing  Mouth to mouth or mouth to nose Mouth to oropharyngeal tube Mouth to shield Mouth to mask(compressing the cricoid cartilage in order to decrease gastric distention and prevent gastric reflu) Bag-mask ventilation challenged endotracheal intubation –resuscitation’s “gold standard”Circulation  —external chest compression  High-frequency（100 compressions per min ）aortic pressure ↑myocardial perfusion pressure↑cardiac outputs ↑rise survival rate  Reduce interrupted compression ( compression –ventilation ratio simplified to 15:2) Compression-only CPR: unwilling or unable to perform mouth to mouth or cardiogenic cardiac arrest Circulation —Compression-only CPR  Research suggests: ①Survival rate with compression-only CPR in first 6~12 minutes is 40.8% ②Survival rate with chest compression add  artificial ventilation is 34.1% , because artificial  ventilation may be result in respiratory alkalosis. Mechanism of   external chest compression Chest pump - sequential increased and decreased pressure  in the thoracic cavity - valves maintaining forward direction of flow Cardiac pump -sequential filling and emptying of cardiac chambers -valves maintaining forward direction of flow Circulation  Thump version from 20-25 cm high to chest Cough Version in 10-15 second Intermittent abdominal compression-cardiopulmonary resuscitation （IAC-CPR) Activated compression-decompression （ACD-CPR) Phased －Chest and Abdominal ACD-CPR （Life-stick Resuscitation ）increase mean pressure ，coronary and cerebral perfusion pressure ，left ventricular and cerebral blood flow  Automated external defibrillator  --- AED  ①Ventricular fibrillation : may be used by 200J*3 times) or 200J 、200-300J 、300J ②If polymorphic ventricular tachycardia can not be clearly distinguished from ventricular fibrillation (VF),  treatment would refer to be as VF ③Atrial fibrillation :100-200J synchronized ④Atrial flutter or supraventricular tachycardia 50- 100J synchronized ⑤Ventricular tachycardia 100J synchronized Biphasic waveform defibrillation A compensated defibrillation for the second time in limited time Low-energy levels （150J correspond to  200-300J ）Reduce the myocardial injury Advanced Life Support --- the second ABCD  Endotracheal intubation (A) Mechanical ventilation and oxygen therapy (B) Intravenous injection (C) electrocardiogram and blood pressure monitoring, resuscitation drug , open chest cardiac compression (C) Differential diagnosis (D) Confirmation of  Endotracheal tube placement   Mark estimated depth Breath sounds by auscultation at 5 locus Thorax rise as inspiration increase of SaO2 Steam in canal of artificial ventilation device Use a specific technique or device to prevent tube dislodgment Mechanical ventilation  Low tidal volume 6-7ml/kg （400-600ml ）Hyper ventilation  High airway pressure and endogenous PEEP  Intracranial hypertension; High tidal volume Distension Too low tidal volume hypoxia and CO2 retention  Epinephrine EN --(1)  α-adrenergic receptor stimulating Peripheral  arterial vasoconstriction(not cerebral and coronary arterioles) mean arterial pressure↑myocardial and cerebral blood flow ↑Epinephrine EN --(2)  Recommended dosage : 1.0mg(0.01-0.02mg/kg ) iv every 3-5 minutes, then 1mg + GS 250ml iv gtt, 1μg/min→3-4μg/min, or 1mg 、3mg 、5mg iv Compared high dosage: 0. 1-0.2mg/kg High dosage (>0.2mg/kg) may be harmful  Endotracheal administration: NS 20ml + 2~2.5 time recommended dose Intracardiac injection: only in heart operation or  chest trauma Vasopressin  Act by direct stimulation of smooth muscle V1 receptors  vasoconstriction No increased myocardial oxygen consumption Half-life is 10 ~20 minute, longer than EN Applicable to VF or prolonged cardiac arrest, and with PEA （pulseless electrical activity ）or with asystole Effective in patients who remain in cardiac arrest after treatment with epinephrine Usage: 40IU iv Amiodarone(1)  Persistent VT or VF after defibrillation and epinephrine in cardiac arrest Hemodynamically stable VT polymorphic VT  wide-complex tachycardia Ventricular rate control of rapid atrial arrhythmias with impaired LV function when digitalis ineffective Amiodarone(2)  Initially 300mg iv diluted in 20-30 ml in cardiac arrest Initial dose of 150mg iv （over 10 min), followed by 1 mg/min infusion for 6 h, then 0.5mg/min Supplementary 150mg iv repeatedly for recurrent or resistant arrhythmias or hemodynamically unstable VT Maximum total dose: 2g ／24h adverse effects ：hypotension and bradycardia 	Magnesium sulfate  Torsades de pointes Arrhythmias caused by magnesium deficiency Loading dose :1 ～2g /50-100ml iv (over 5-60 minutes) Followed by an infusion of 0.5-1.0g/h  Sodium Bicarbonate （1 ）Only after the confirmed interventions are ineffective Preexisting metabolic acidosis, hyperkalemia, tricyclic or phenobarbitone overdose Protracted arrest or long resuscitative efforts Sodium Bicarbonate （2 ）Acid-base balance : chest compressions ROSC adequate alveolar ventilation and restoration of tissue perfusion CO2 more freely diffusible than HCO3 - into myocardial and cerebral cells intracellular acidosis Initial dosage ：5%NaHCO3 1mEq /kg iv gtt  ( 1ml≌0.6mEq ) Etiological factors  （5Hs ，5Ts) Optimal response  to resuscitation  Awake Responsive Breathing spontaneously restoration of spontaneous circulation (ROSC) Prolong Life Support  Postresuscitation care - Prevent and treatment SIRS and MODS organs function support Cerebral resuscitation  Postresuscitation syndrome Reperfusion failure Reperfusion injury Cerebral intoxication from ischemic metabolites Coagulopathy Postresuscitation syndrome --- 4 phases Cardiovascular dysfunction in the hours after ROSC in 24 hours SIRS leads to MODS over 1 to 3 days Serious infection occurs and the patient declines rapidly Death  Dopamine  A potent adrenergic receptor agonist and a strong peripheral dopamine receptor agonist. Effects are dose-dependent: 5 ～20μg ／min ／kg Low-dose (2 ~ 4 μg ／min ／kg) is no longer used for acute oliguric renal failure, because occasionally diuresis  no improve renal glomerular filtration rate. Middle dosage ：5~10μg ／min ／kg, positive inotropic effect High dosage ：10~20 μg ／min ／kg ，vasoconstriction Sodium Bicarbonate  immediately after ROSC  Guided by the partial pressure of CO 2 Cerebral resuscitation Maintain relative high blood pressure during CPR Hemodilution and mild hypothermia （32－34 ℃）for 12 h during CPR thrombolysis for ameliorate hypercoagulable state Antioxidant ，free radical scavenger Emergency hypothermia CPB Hyperbaric oxygen ：suitable for persistent vegetative state *  * Time is too longer Accurate rate  75 % Sensibitity  90% Specificity  60%  Hypovolemia  Hypoxia  Hydrogen ion (acidosis)  Hyperkalemia or Hypokalemia  Hyperthermia or Hypothermia  Tablets (drug)  Tamponade Tension Pneumothorax Thrombosis coronary Thrombosis pulmonary