呼吸衰竭和急性呼吸窘迫综合征英文课件

UTHSCSA Pediatric Resident Curriculum for the PICU,RESPIRATORY FAILURE & ARDS,RESPIRATORY FAILURE,Inability of the pulmonary system to meet the metabolic demands of the body through adequate gas exchange. Two types of respiratory failure: Hypoxemic Hypercarbic Each can be further divided into acute and chronic. Both types of respiratory failure can be present in the same patient.,CENTRAL ETIOLOGIES,Trauma: head injury, asphyxiation, hemorrhage Infection: meningitis, encephalitis Tumors Drugs: narcotics, sedatives Neonatal apnea Severe hypoxemia or hypercarbia Increased ICP from any of the above causes,OBSTRUCTIVE ETIOLOGIES,Upper Airway Anatomic: choanal atresia, tracheomalacia, tonsillar hypertrophy, laryngeal web, vascular rings, vocal cord paralysis, macroglossia Aspiration: mucus, foreign body, vomitus Infection: epiglottitis, abscesses, laryngotracheitis Tumors: hemangioma, cystic hygroma, papilloma, Laryngpospasm,Lower Airway Anatomic: bronchomalacia, lobar emphysema Aspiration: FB, mucus, meconium, vomitus Infection: pneumonia, pertussis, bronchiolitis, CF Tumors: teratoma, bronchogenic cyst Bronchospasm,RESTRICTIVE ETIOLOGIES,Lung Parenchyma Anatomic: agenesis, cyst, pulmonary sequestration Atelectasis Hyaline membrane disease ARDS Infection: pneumonia, bronchiectasis, pleural effusion, Pneumocystis carinii Air leak: pneumothorax Misc: hemorrhage, edema, pneumonitis, fibrosis,Chest Wall Muscular: diaphragmatic hernia, myasthenia gravis, muscular dystrophy, botulism Skeletal: hemivertebrae, absent ribs, fused ribs, scoliosis Misc: distended abdomen, flail chest, obesity,HYPOXEMIA,V/Q mismatch Most common reason. Blood perfuses non-ventilated lung. Seen in atelectasis, pneumonia, bronchiectasis Global hypoventilation: apnea Right-to-left shunt Intracardiac lesions, e.g., tetralogy of Fallot Incomplete diffusion Oxygen must diffuse across increased distance secondary to interstitial edema, fibrosis, or hyaline membrane. Low inspired FiO2: high altitude,HYPERCARBIA,Pump Failure Reduced central drive: apnea, metabolic alkalosis, drugs, brainstem injury, hypoxia Muscle fatigue: muscular dystrophy Increased pulmonary workload: decreased compliance, increased obstruction Increased CO2 production: fever, seizure, malignant hyperthermia Increased dead space: V/Q mismatch (ventilation of non-perfused lung),PHYSICAL EXAM,Tachypnea Dyspnea Retractions Nasal flaring Grunting Diaphoresis Tachycardia Hypertension,Altered mental status Confusion Agitation Restlessness Somnolence Cyanosis (need 5mg/dl of unoxygenated blood),CXR FINDINGS,CXR may be normal if problem is with upper airway Can see hyperinflation, atelectasis, infiltrate, cardiomegaly Additional studies may be needed, e.g., chest CT, barium swallow, echocardiogram,BLOOD GAS,For any age patient, breathing room air, respiratory failure is defined as arterial pCO2 50mm Hg or arterial pO2 60mm Hg. If the patient is hyperventilating, a normal pCO2 is disturbing. The above definition assumes the absence of an anatomic shunt. Chronic hypercarbic respiratory failure will often have a normal pH because of compensatory metabolic alkalosis.,MANAGEMENT,REMEMBER PALS Airway Breathing Circulation,AIRWAY,Repositioning Position of comfort Jaw thrust/chin lift Oral airway Unconscious patients only Nasal trumpet Nasal or mask CPAP Bag-mask ventilation Use during preparation for intubation Tracheal intubation,BREATHING,Decrease respiratory workload -agonists Decadron or steroids Antibiotics CPAP Supplemental O2 Nasal cannula Closed face mask Non-rebreather Counteract drug effects Bag-mask ventilation Mechanical ventilation,CIRCULATION,Suppress anaerobic metabolism and acidosis Correct anemia to improve oxygen delivery Ensure adequate cardiac output Inotropes: oxygen, vasopressors Fluid boluses,ARDS,A patient must meet all of the following: Acute onset of respiratory symptoms CXR with bilateral infiltrates No evidence of left heart failure PaO2/FiO2 200mm Hg (regardless of PEEP) American-European Consensus Conference on ARDS (Am J Resp Crit Care Med 149:818, 1994) The following are implied: Previously normal lungs Decreased lung compliance Increased shunting Hypoxemic respiratory failure,ETIOLOGY,ARDS represents about 3% of PICU admissions. Numerous precipitating events: Trauma Pneumonia Burns Sepsis Drowning Shock,PATHOPHYSIOLOGY,Acute Injury Latent Period Early Exudative Phase Cellular Proliferative Phase Fibrotic Proliferative Phase,Royall and Levin J Peds 112:169-180; 335-347, 1988,PATHOLOGY OF ARDS,Green arrows point to hyaline membrane Blue arrows point to type II pneumocytes and alveolar macrophages,MANAGEMENT,Meticulous supportive care is the mainstay of therapy Prevent secondary lung injury Ensure adequate cardiac output Limit secondary infections Drugs Good nutrition,VENTILATOR STRATEGIES The hallmark of ARDS is heterogeneous lung.,Limit Barotrauma Keep PIP 7.20,Limit O2 Toxicity Give enough PEEP to lower FiO2 to 90%. PEEP E) ventilation.,CARDIAC OUTPUT,Keep cardiac output 4.5 L/min/m2. Keep O2 delivery 600 ml O2/min/m2. Keep Hct 30%, higher if signs of heart failure. Use inotropes to augment cardiac output. Ensure adequate preload.,LIMIT SECONDARY INFECTIONS,Wash your hands. Use the gut as soon as possible for nutrition and meds. Discontinue indwelling catheters as soon as possible. Have high index of suspicion. Treat infections early, but tailor antibiotics to culture results.,DRUGS,Diuretics: a dry lung is a good lung. Inotropes Steroids: 2mg/kg/day begun after a week into the course may be of benefit, otherwise dont use. Pulmonary vasodilators (nitric oxide, prost