resp_ardsslides - UTHSCSA Pediatric Resident Curriculum for...

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Unformatted text preview: UTHSCSA Pediatric Resident Curriculum for the PICU UTHSCSA Pediatric Resident Curriculum for the PICU RESPIRATORY FAILURE RESPIRATORY & ARDS ARDS RESPIRATORY FAILURE RESPIRATORY Inability of the pulmonary system to meet the metabolic Inability demands of the body through adequate gas exchange. demands 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 Both patient. patient. CENTRAL ETIOLOGIES CENTRAL 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 OBSTRUCTIVE Upper Airway Anatomic: choanal atresia, Anatomic: tracheomalacia, tonsillar hypertrophy, laryngeal web, vascular rings, vocal cord paralysis, macroglossia paralysis, Aspiration: mucus, foreign Aspiration: body, vomitus body, Infection: epiglottitis, Infection: abscesses, laryngotracheitis abscesses, Tumors: hemangioma, cystic Tumors: hygroma, papilloma, Laryngpospasm Lower Airway Anatomic: bronchomalacia, Anatomic: lobar emphysema lobar Aspiration: FB, mucus, Aspiration: meconium, vomitus meconium, Infection: pneumonia, Infection: pertussis, bronchiolitis, CF pertussis, Tumors: teratoma, Tumors: bronchogenic cyst bronchogenic Bronchospasm RESTRICTIVE ETIOLOGIES RESTRICTIVE Lung Parenchyma Anatomic: agenesis, cyst, Anatomic: pulmonary sequestration pulmonary Atelectasis Hyaline membrane disease ARDS Infection: pneumonia, Infection: bronchiectasis, pleural effusion, Pneumocystis carinii carinii Air leak: pneumothorax Misc: hemorrhage, edema, Misc: pneumonitis, fibrosis pneumonitis, Chest Wall Muscular: diaphragmatic Muscular: hernia, myasthenia gravis, muscular dystrophy, botulism botulism Skeletal: hemivertebrae, Skeletal: absent ribs, fused ribs, scoliosis scoliosis Misc: distended abdomen, Misc: flail chest, obesity flail HYPOXEMIA HYPOXEMIA V/Q mismatch Most common reason. Blood perfuses non-ventilated Most lung. Seen in atelectasis, pneumonia, bronchiectasis lung. Global hypoventilation: apnea Right-to-left shunt Intracardiac lesions, e.g., tetralogy of Fallot Incomplete diffusion Oxygen must diffuse across increased distance secondary Oxygen to interstitial edema, fibrosis, or hyaline membrane. to Low inspired FiO2: high altitude high HYPERCARBIA HYPERCARBIA Pump Failure Reduced central drive: apnea, metabolic alkalosis, drugs, Reduced brainstem injury, hypoxia brainstem Muscle fatigue: muscular dystrophy Increased pulmonary workload: decreased compliance, Increased increased obstruction increased Increased CO2 production: fever, seizure, malignant hyperthermia hyperthermia Increased dead space: V/Q mismatch (ventilation of non-perfused lung) non-perfused PHYSICAL EXAM PHYSICAL Tachypnea Dyspnea Retractions Nasal flaring Grunting Diaphoresis Tachycardia Hypertension Altered mental status Confusion Agitation Restlessness Somnolence Cyanosis (need 5mg/dl Cyanosis of unoxygenated blood) of CXR FINDINGS CXR CXR may be normal if problem is with upper airway Can see hyperinflation, atelectasis, infiltrate, Can cardiomegaly cardiomegaly Additional studies may be needed, e.g., chest CT, Additional barium swallow, echocardiogram barium BLOOD GAS BLOOD For any age patient, breathing room air, respiratory For failure is defined as arterial pCO2 > 50mm Hg or failure arterial pO2 < 60mm Hg. arterial If the patient is hyperventilating, a normal pCO2 is disturbing. disturbing. The above definition assumes the absence of an The anatomic shunt. anatomic Chronic hypercarbic respiratory failure will often Chronic have a normal pH because of compensatory metabolic alkalosis. metabolic MANAGEMENT MANAGEMENT REMEMBER PALS Airway Breathing Circulation AIRWAY 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 BREATHING Decrease respiratory workload ß-agonists Decadron or steroids Antibiotics CPAP Supplemental O2 Nasal cannula Closed face mask Non-rebreather Counteract drug effects Bag-mask ventilation Mechanical ventilation CIRCULATION CIRCULATION Suppress anaerobic metabolism and acidosis Correct anemia to improve oxygen delivery Ensure adequate cardiac output Inotropes: oxygen, vasopressors Fluid boluses ARDS ARDS A patient must meet all of the following: patient Acute onset of respiratory symptoms CXR with bilateral infiltrates No evidence of left heart failure PaO2/FiO2 < 200mm Hg (regardless of PEEP) 3 American-European Consensus Conference on ARDS (Am J Resp American-European Crit Care Med 149:818, 1994) Crit The following are implied: Previously normal lungs Decreased lung compliance Increased shunting Hypoxemic respiratory failure ETIOLOGY ETIOLOGY ARDS represents about 3% of PICU admissions. Numerous precipitating events: Trauma Pneumonia Burns Sepsis Drowning Shock PATHOPHYSIOLOGY 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 PATHOLOGY Green arrows point to hyaline membrane Blue arrows point to type II pneumocytes and alveolar macrophages MANAGEMENT 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 VENTILATOR The hallmark of ARDS is heterogeneous lung. Limit Barotrauma Keep PIP <35 cm H2O Use pressure-control Use ventilation ventilation Use TV of 6-10cc/kg Keep rate <30 bpm Permissive hypercapnia Use bicarb or THAM to Use keep pH >7.20 keep Limit O2 Toxicity Give enough PEEP to Give lower FiO2 to <60% while lower maintaining O2 >90%. maintaining PEEP <15 cm H2O shouldn’t decrease cardiac output. cardiac Increase mean airway Increase pressure with inverse ratio (I>E) ventilation. ratio CARDIAC OUTPUT CARDIAC 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 LIMIT Wash your hands. Use the gut as soon as possible for nutrition and Use meds. meds. Discontinue indwelling catheters as soon as Discontinue possible. possible. Have high index of suspicion. Treat infections early, but tailor antibiotics to culture Treat results. results. DRUGS DRUGS Diuretics: a dry lung is a good lung. Inotropes Steroids: 2mg/kg/day begun after a week into the Steroids: course may be of benefit, otherwise don’t use. course Pulmonary vasodilators (nitric oxide, prostaglandins, Pulmonary nitroprusside): of little benefit. NO may be of benefit in some patients. in Surfactant replacement: probably no benefit NSAIDs: no clinical benefit NUTRITION NUTRITION Ensure adequate calories as soon as possible: 50-60kcal/kg/day in infants 35-45kcal/kg/day in older children. After day 4, increase calories by 25-50% above After baseline. baseline. Begin enteral feeds as soon as is safe. “Pulmonary” formulas probably of little benefit. MORTALITY/MORBIDITY MORTALITY/MORBIDITY Published mortality is 50% in children. Pulmonary failure accounts for only 15% of the Pulmonary deaths. Lung function usually returns to normal within 18 Lung months after leaving the hospital. months ...
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This note was uploaded on 12/24/2011 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

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