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UTHSCSA Pediatric Resident Curriculum for the PICU

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

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UTHSCSA Pediatric Resident Curriculum for the PICU

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  1. UTHSCSA Pediatric Resident Curriculum for the PICU RESPIRATORY FAILURE & ARDS

  2. 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.

  3. 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

  4. 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 OBSTRUCTIVE ETIOLOGIES

  5. 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 RESTRICTIVE ETIOLOGIES

  6. 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

  7. 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)

  8. Tachypnea Dyspnea Retractions Nasal flaring Grunting Diaphoresis Tachycardia Hypertension Altered mental status Confusion Agitation Restlessness Somnolence Cyanosis (need 5mg/dl of unoxygenated blood) PHYSICAL EXAM

  9. 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

  10. 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.

  11. MANAGEMENT • REMEMBER PALS • Airway • Breathing • Circulation

  12. 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

  13. 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

  14. CIRCULATION • Suppress anaerobic metabolism and acidosis • Correct anemia to improve oxygen delivery • Ensure adequate cardiac output • Inotropes: oxygen, vasopressors • Fluid boluses

  15. 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

  16. ETIOLOGY • ARDS represents about 3% of PICU admissions. • Numerous precipitating events: • Trauma • Pneumonia • Burns • Sepsis • Drowning • Shock

  17. PATHOPHYSIOLOGY • Acute Injury • Latent Period • Early Exudative Phase • Cellular Proliferative Phase • Fibrotic Proliferative Phase

  18. Royall and Levin J Peds 112:169-180; 335-347, 1988

  19. PATHOLOGY OF ARDS Green arrows point to hyaline membrane Blue arrows point to type II pneumocytes and alveolar macrophages

  20. MANAGEMENT • Meticulous supportive care is the mainstay of therapy • Prevent secondary lung injury • Ensure adequate cardiac output • Limit secondary infections • Drugs • Good nutrition

  21. Limit Barotrauma Keep PIP <35 cm H2O Use pressure-control ventilation Use TV of 6-10cc/kg Keep rate <30 bpm Permissive hypercapnia Use bicarb or THAM to keep pH >7.20 Limit O2 Toxicity Give enough PEEP to lower FiO2 to <60% while maintaining O2 >90%. PEEP <15 cm H2O shouldn’t decrease cardiac output. Increase mean airway pressure with inverse ratio (I>E) ventilation. VENTILATOR STRATEGIESThe hallmark of ARDS is heterogeneous lung.

  22. 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.

  23. 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.

  24. 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 don’t use. • Pulmonary vasodilators (nitric oxide, prostaglandins, nitroprusside): of little benefit. NO may be of benefit in some patients. • Surfactant replacement: probably no benefit • NSAIDs: no clinical benefit

  25. 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 baseline. • Begin enteral feeds as soon as is safe. • “Pulmonary” formulas probably of little benefit.

  26. MORTALITY/MORBIDITY • Published mortality is 50% in children. • Pulmonary failure accounts for only 15% of the deaths. • Lung function usually returns to normal within 18 months after leaving the hospital.

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