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Pediatric Respiratory. Scott T. Roethle MD January 13, 2009. Physiology. Neonates have weaker diaphragm and intercostal muscles, more pliable ribs, larger abd. Increased airway resistance. Requires more energy/work to breathe Lungs have low compliance, chest wall has high compliance.
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Pediatric Respiratory Scott T. Roethle MD January 13, 2009
Physiology • Neonates have weaker diaphragm and intercostal muscles, more pliable ribs, larger abd. Increased airway resistance. Requires more energy/work to breathe • Lungs have low compliance, chest wall has high compliance. • Chest wall collapse during inspiration. • Relatively low residual volume at expiration. • Neonates are obligate nose breathers • Hypoxic and hypercapnic respiratory drive is not very well developed in neonates.
Respiratory Distress Syndrome • Rare after 34wks gestation • Occurs 3x more frequently in C/S births than by vaginal • Other risks: maternal diabetes and perinatal asphyxia. Fetal hyperinsulinemia delays surfactant production. • Common cause of premie M&M, causing >50% of deaths in preterm neonates
RDS • Caused by deficiency in surfactant, resulting in alveolar collapse, inc pulm vasc resistance, R to L shunt, hypoxemia and metabolic acidosis • Type II pneumocytes produce surfactant • Inadequate surfactant production before 26wks • Maternal steroids (betamethasone or dexamethasone) for labor before 32 (or 34) weeks helps neonate produce sufactant • Immediate treatment with artificial surfactant greatly reduces mortality
Fetal lung maturity • Usually mature at 32-34wks • Testing by amniotic fluid L/S or S/A ratios • Lecithin to sphingomyelin ratio: • L/S > 2.2 is mature • Surfactant to albumin ratio: • S/A < 35 is immature; S/A > 55 mature • S/A 35 – 55 indeterminate
Bronchopulmonary Dysplasia • Chronic lung disease with continued oxygen requirement in neonate with h/o RDS, lung hypoplasia, recurrent aspiration, sepsis or PNA • Disease of small airways and lung parenchyma from any cause, as a consequence of oxygen therapy and mechanical ventilation and barotrauma
Bronchopulmonary Dysplasia • Risk factors associated with BPD are high FiO2, mech vent, infection and pneumonia, PDA, early fluid overload (first week) • Increased airway resistance, dec pulm compliance, V/Q mismatch, decrease PaO2, tachypnea, inc O2 consumption, increased pulmonary infections • Pulmonary htn and cor pulmonale can result from severe BPD • Often treated with continued oxygen and/or ventilation, bronchodilators, and lasix • Often shows improvement by age 5-8
Question 1 • A 1-month infant becomes hypoxemic faster during apnea than an adult. What is the primary reason? • A. FRC in an infant is half that of an adult • B. Metabolic rate in an infant is twice of an adult • C. Resting PaO2 in an infant is lower than an adult • D. The number of alveoli in an infant is 10% of adult • E. The Hgb dissociation curve in an infant is shifted to the right
Answer 1 • Correct Answer: B Oxygen consumption and metabolic rate in a 1 month infant are twice that of an adult • A: FRC in adult is 30 ml/kg. Infants are slightly reduced at 25-30 ml/kg. (Not ½). And not primary reason for desat. • C: PaO2 may be slightly lower in an infant, but this is not the primary cause of quicker desats. • D: Infants do have fewer alveoli (about 10% as many), but this is not the cause of quicker desats • E: Oxyhemoglobin dissociation curve is shifted to left in neonates due to HgbF.
Answer 1 • The higher ratio of minute ventilation to FRC in an infant is important cause of desats, but the FRC alone does not differ enough to be primary cause of this. • The increase metabolic rate and oxygen consumption is the primary cause.
Question 2 • Which of the following statements regarding O2 consumption in adult vs neonate is correct? • A. 7ml/kg per min adult, 3ml/kg per min neonate • B. 6ml/kg per min adult, 5ml/kg per min neonate • C. 10ml/kg per min adult, 4ml/kg per min neonate • D. 3ml/kg per min adult, 7ml/kg per min neonate • E. 5ml/kg per min adult, 5ml/kg per min neonate
Answer 2 • Correct Answer: • D. 3ml/kg per min adult, 7ml/kg per min neonate • O2 consumption in neonate is about 2 to 3 times that of an adult • Tidal volume (in ml/kg) is about the same, but respiratory rate is about 3x that of an adult
Question 3 • What level is the glottis in term neonates?
Answer 3 • In term neonate, glottis is at C4. In adult at C6. In preterm neonate can be at C3.
Question 4 • The ratio of minute ventilation to FRC in adults is approximately 1.5:1. What is it in neonates?
Answer 4 • 5:1 • TV is about the same in neonates and adults (ml/kg) • FRC is roughly the same (ml/kg) • RR is about 3 times greater in neonate • Thus MV is about 3 times greater in neonate • And ratio of MV : FRC is about 5:1
Question 5 • Which is true regarding post-op apnea? • A. Premature infants with congenital abnl are greatest risk • B. Spinal anesthesia may increase incidence of post-op apnea • C. 44 wk post-conception infant undergoing spinal anesthesia does not require prolonged post-op monitoring
Answer 5 • Correct: A • Highest risk of post-op apnea: premies, multiple cong abnl, h/o apnea and bradycardia, chronic lung dx • Etiology is multifactorial • Spinal without supplemental sedation decreases postop A&B • Guideline: monitor all infants <50 wks for at least 12 hrs postop (overnight), even if they had spinal anesthetic. (50-60wks is a bit of a gray area, but should also be monitored)
Question 6 • What is the goal PaO2 and sats to reduce risk of retinopathy of prematurity?
Answer 6 • Retinopathy of prematuriy is caused by oxygen toxicity and large variations in oxygenation • Goal PaO2 is 50-80mmHg • Goal sats is 90-95% (remember p90% = PaO2 of 60)
Question 7 • Congenital lobar emphysema • A. Most commonly affects right lower lobe • B. Usually presents with cardiovascular collapse due to mediastinal shift • C. Coexists with cong heart disease in about 15% of cases • D. Should be treated with assisted ventilation asap
Answer 7 • Answer: C • Cong lobar emphysema most commonly affects left upper lobe, but may involve whole lung. • Usually presents with progressive resp failure, but mediastinal shift and CV collapse can occur. • 15% have associated congenital heart defect • Minimize expansion of emphysema, maintain spont vent if possible until chest open, use low inspiratory pressures and avoid nitrous
Equations • PAO2 = FIO2(PB-47) - 1.2(PaCO2) • CaO2 = (SaO2 x Hb x 1.34) + .003(PaO2) • A-a gradient: usually 5-20 on room air, increases with age. Can be up to 100 on 100% oxygen
Random facts • Neonates have a relatively larger tongue, bigger occiput, long epiglottis, anterior and cephalad larynx, and short trachea and neck • Cricoid ring is narrowest portion of airway. • Only way neonate can increase cardiac output is by increasing HR. • Hypoxia causes bradycardia. • Immature baroreceptors decrease HR response to hypotension
Quicker anesthetic uptake due to higher MV:FRC ratio, greater cardiac output per kg, and more cardiac output goes to vessel rich organs (brain) • Weight: 12 mo; weight (kg) = 4 + (age in months/2) • Weight: 1–12 y; weight (kg) = 10 + [2 x (age in years)] • Blood volume: Premie: 90ml/kg. Neonate: 85ml/kg. Infant: 80ml/kg. Child: 75ml/kg. Adult: 65 (female)-70 (male) ml/kg.
Vital Signs • Median SBP = 90 mmHg + (2 x Age in years) • Minimum SBP = 70 mmHg + (2 x Age in years)