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TRANSCRIPT
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Respiratory Care in the NICU
Cynthia Jensen, RNC-NIC, MS, CNS UCSF BCH Perinatal Outreach Program
June, 2018
Fetal Lung Development: Know the Stages
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http://basenat.u707.jussieu.fr/site_respirare/index.php?option=com_content&view=article&id=59&Itemid=30&lang=en&showall=1
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E = Embryonic
Copyright Satyan Lakshminrusimha used with permission
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Biochemical Lung Development
�Surfactant:
�Produced by Type II pneumocytes @ ~ 25-30 weeks
�Reduces surface-tension forces in alveoli to prevent collapse on expiration
�Chronic fetal stress will accelerate surfactant production
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Biochemical Lung Development
�Fetal lung fluids contribute to amniotic fluid
�Lung maturity can be tested by looking at phospholipids
�PG appears ~ 30 weeks + = Mature
�L/S ratios >2:1 = Mature except IDM
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Surfactant
�Exogenous types
• Beractant (Survanta)
• Poractant Alfa (Curosurf)
• Calfactant (Infasurf)
�Rescue vs Prophylactic treatment
�Administration
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Antenatal Steroids
�Antenatal steroids (Betamethasone) administered 48 hours prior to delivery
• Goal: To accelerate fetal lung maturity by increasing production of Type II pneumocytes
• Single course for women between 24 and 34* weeks gestation at risk for preterm delivery
• Reduces the incidence of RDS by 50% in infants < 31 weeks
• Decreases neonatal mortality by 30%
• Decreases incidence of IVH and NEC
• No adverse consequences identified
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Indications for Respiratory Support?
�Grunting, flaring, retracting, beyond transition �Apnea �Gasping, signs of exhaustion� Inadequate respiratory drive or signs of respiratory failure�Continued need for PPV, worsening apnea and bradycardia
�Rapidly increasing oxygen requirement�Hypercarbia and respiratory acidosis�Airway obstruction�Congenital anomalies�Bradycardia unresponsive to effective PPV
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Pulmonary Causes of Respiratory Distress
↑RR & ↑ CO2
TTN
Aspiration
Pulmonary Hemorrhage
Pneumonia
Respiratory Distress Syndrome
Airway Obstruction
Pneumothorax
Congenital Anomalies
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Non-Pulmonary Causes of Respiratory Distress
↑RR and ↓ CO2
Congenital Heart
Disease
Brain Disorders
Hemorrhage
Meningitis
Edema
Metabolic Acidosis
Shock
Inborn Errors
Oxygenation and Ventilation
�Hypoxia
�Hypoxemia
�Oxygen saturation
�Oxygen targeting
�Use of pulse oximeter
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Modes of Oxygenation and Ventilation
�Non-invasive • NC• HFNC• CPAP/SiPAP
�Conventional types• SIMV• AC• PS
�High Frequency�ECMO
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Blood Gas Refresher
What is normal?
�pH 7.35-7.45
�PaC02 35-45 mm Hg
�PaO2 50-80 mm Hg
�HCO3 22-26 mEq/L
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If the pH is normal the blood gas is COMPENSATED
Reflects the respiratory component
Reflects the metabolic component
Blood Gases: Acid Base Homeostasis
�Respiratory Acidosis pH CO2
�Respiratory Alkalosis pH CO2
�Metabolic Acidosis pH HCO3
�Metabolic Alkalosis pH HCO3
�Mixed Acidosis pH CO2 HCO3
�Lactate levels
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Let’s Practice
29 week, two hour old on HFNC, 40% O2, RR 80, HR 170, grunting, flaring, retracting
ABG drawn:
• pH 7.29
• PCo2 62
• HCo3 26
• Po2 40
�What type of blood gas is this?
�Next steps ?
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Continued
Baby was intubated, given surfactant, VS WNL, CXR ETT WNL, lungs expanded to T8 & follow up ABG:
• pH 7.49• Co2 27• HCO3 21• PaO2 295
�ABG type ?Was surfactant: A. Rescue? B. Prophylactic? �Next Steps ?
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The ABCs of Respiratory Pathophysiology
�Apnea of Prematurity
�BPD
�CDH
�Hypoplastic Lungs
�Meconium aspiration
�PPHN
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�Pneumothorax
�Pulmonary Hemorrhage
�RDS
�TTN
A is for Apnea
�Cessation of respirations for 15-20 seconds
�Common in preterm infants
�Primary versus Secondary Apnea
�Types:
• Central
• Obstructive
• Mixed
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Apnea: Causes
�Prematurity
�Sepsis, NEC
�Seizures, stroke
�Drugs (Maternal/Neonatal)
�Metabolic
�Polycythemia/Anemia
�GER
�Environmental
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Apnea: Management
�Avoid triggers & treat underlying cause
�Positioning
�Environmental
�Pharmacologic: Caffeine load and monitor levels
�Caffeine versus Theophylline
• Longer half life, wider therapeutic index and more reliable absorption
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The Infant on Caffeine Should Be Monitored for…
A. Hypocalcemia
B. Hypersomnolence
C. Feeding Intolerance
D. Temp Instability
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Central Apnea is Defined As?
A. Absence of airflow & respiratory effort
B. Absence of airflow with continued respiratory effort
C. Condition with both neurologic & obstructive components
D. Cyclic respirations 10-15 seconds followed by 5-10 seconds that occur 3 x in succession
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B is for BPD
Defined as: need for oxygen/respiratory support at 36 weeks CGA
�Causes include: lung injury from assisted ventilation and oxygen toxicity
�Prevention: Antenatal steroids, weaning respiratory support, surfactant, permissive hypercapnia, nutritional support, diuretics, steroids, RSV prevention
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Features of BPD
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Copyright Satyan Lakshminrusimha
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The Pulmonary Injury Sequence
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Increased Tidal Volume
Airway Stretch and
Dilation
Cellular Membrane
Injury
Edema
Loss of Surfactant
Increased Ventilation
and Oxygenation
Support
Copyright Satyan Lakshminrusimha
Congenital Diaphragmatic Hernia: Recognition
Signs & Symptoms• Flat or scaphoid abdomen• Respiratory distress• Shifted heart sounds• Bowel sounds in chest• S/S Pulmonary hypertension
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Copyright Satyan Lakshminrusimha
H is for: Hypoplastic Lungs
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Hypoplastic Lungs: Associated Conditions?
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M is for Meconium Aspiration
�Meconium is rarely present before 36 weeks
• Why?
�Most common with uteroplacentalinsufficiency
• Examples of uteroplacental insufficiency?
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Copyright Satyan Lakshminrusimha
P is for Persistent Pulmonary Hypertension of the Newborn (PPHN)
�Clinical syndrome characterized by:• Suprasystemic pulmonary arterial pressures.• Failure to transition.• Persistence of fetal circulation (R to L shunting).• Systemic hypoxemia.
�Assessment and diagnostic findings may include:• Cyanosis and respiratory distress with pre- and post-
ductal saturation differential.• Hyperdynamic precordium.• Elevated pulmonary pressures on echocardiogram.
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Copyright Satyan Lakshminrusimha
Etiology of PPHN: Types and Examples
�Maldevelopment : “Baby Noductus”‒Premature closure of PDA, exposure to NSAIDS‒Normal parenchyma, abnormal vasculature
�Maladaptive :“Baby McAspirate”‒Pulmonary vasoconstriction due to parenchymal
injury/disease‒MAS, RDS, Pneumonia
�Underdevelopment : “Baby Smallung”• Pulmonary hypoplasia ‒CDH‒Renal agenesis
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Maladaptive Associated Conditions
�Abnormal circulatory transition at delivery:
• Ineffective or delayed resuscitation, narcosis, hypothermia, hypoglycemia, hypocalcaemia, acidosis, hypoxia, myocardial dysfunction.
�Functional obstruction of the pulmonary vascular bed secondary to hyper viscosity and/or polycythemia.
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Underdevelopment Associated Conditions
�Congenital heart disease
�Pulmonary hypoplasia:
• CDH
• PROM
• Oligohydramnios
• Potter syndrome
• Cystic pulmonary adenomatoid malformation
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PPHN Treatment
�Supplemental oxygen�Treat acidosis�Pain and sedation tx�Treat underlying disease� Intubate, mechanical ventilation�Nitric oxide�Decompress the abdomen�Maintain systemic blood pressure� Inhaled NO�ECMO�Consider paralytics but not routine
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Inhaled Nitric Oxide
� iNO is a selective pulmonary vasodilator that does not effect systemic circulation
� Indications for use:• MAS• CDH• PPHN
�Contraindications:• Pulmonary hemorrhage• Heparin or anticoagulant therapy, thrombocytopenia• CHD with necessary R to L shunting.
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P is for Pneumonia
�Sign & Symptoms: Initially indistinguishable from RDS & Sepis
�Progressive: Apnea, shock like syndrome, PPHN
�CXR similar to RDS with possible pleural effusions (GBS), infiltrates
�Treatment
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Pneumonia Risk Factors
�Labor
�PROM >18 hours
�Maternal Fever/Chorioamnionitis
�Foul smelling amniotic fluid
�Fetal Tachycardia absent variability
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Pneumonia: Modes of Transmission
�Transplacental
�Amniotic
�Delivery
�Nosocomial
�Congenital
�Neonatal
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P is for Pulmonary Air Leaks
Recognition:• Tachypnea• Grunting, flaring and retracting• Cyanosis• Asymmetric chest wall movement
• Unequal breath sounds• Shifted or distant heart sounds• Acute desaturation• Hypotension
Copyright Satyan Lakshminrusimha. Used with permission
45Copyright Satyan Lakshminrusimha, used with permission
5/31/2018
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46Copyright Satyan Lakshminrusimha, used with permission
Air Leak Management
�Symptomatic Pneumothorax: Thoracentesis, Thoracostomy
�Pneumopericardium: Emergent treatment to remove air
�PIE: Minimize PIP, short I-time, HFOV, affected side down. High risk for BPD
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P is for Pulmonary Hemorrhage
The _______________ to _______________ shunting through the PDA results in Increased? Decreased? pulmonary blood flow in preterm infants and increases the risk for pulmonary hemorrhage
A. Right to left
B. Left to right
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R is for Respiratory Distress Syndrome (RDS)
�Most common cause of respiratory illness in preterm infants
� Incidence is inversely proportionate to gestational age�Most infants born <29 weeks gestation will have RDS related to:• Surfactant deficiency• Lack of lung development
�Small numbers of term infants will have RDS related to:• Damage to type II alveolar cells and/or altered enzyme
pathways• IDM, asphyxia, or MAS
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50 Copyright Satyan Lakshminrusimha, used with permission
Risk Factors for RDS
� Increased Risk:• Preterm birth.• Male sex.• IDM.• Asphyxia.• C-section without labor.• Caucasian race.• Chorioamnionitis /
Sepsis.• Hydrops.
�Decreased Risk:• Chronic uterine stress.• PPROM.• Maternal Hypertension.• IUGR / SGA.• Maternal drug use.• Tocolytic agents.
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RDS Clinical Findings
�Physical Exam:
• Tachypnea, grunting, flaring, retracting within minutes to hours of life
• Pallor, cyanosis
• Hypotension
• Decreased breath sounds
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RDS
�CXR:• Reduced lung volumes• Ground glass
appearance with areas of atelectasis and hyper-expansion
• Air bronchograms
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T is for Transient Tachypnea of the Newborn (TTN)�Delayed/Retained fetal lung fluid
�Term/LPI/C/S w/o Labor, precipitous delivery
�RDS, G,F, and tachypnea usually milder and resolves over 12/24/48 hours
�CXR diffuse haziness with clearing at the periphery with mild hyperinflation and fluid in the interlobar fissures
�ABG, Respiratory support, antibiotics if struggling
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Let’s talk about the V/Q
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Specific Respiratory Therapies
�Intubation
�Suctioning
�Surfactant Replacement Therapy
�Chest Tubes and Drainage Systems
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Indications for Intubation:
• Rapidly increasing oxygen requirement
• Worsening retractions and work of breathing
• Hypercarbia
• Respiratory acidosis
• Signs of exhaustion and impending respiratory failure
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Proper ETT Placement
� 1 cm above the carina, usually between T2-T3.
�Depth: 1-2-3 = 7-8-9 OR Weight + 6.
�DOCUMENT!
• ETT size.
• Centimeter marking at the lip.
• Tolerance of the procedure.
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Strategies to Prevent Lung Injury
�Avoid:
• Volutrauma (VG, VC modes).
• Oxygen toxicity (set O2 sat parameters)
• Hyperinflation (IMV, SIMV modes)
• Air leaks (PS, PC modes)
• Ventilator Acquired Pneumonia (Oral care and suctioning)
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Indications for ETT Suctioning
�Decreased oxygen saturation
�Coarse breath sounds
�Coughing and/or agitation
�Increased work of breathing
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Chest Tubes: Bubbling Scenarios
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Which of the Following is True for an Infant with a Chest Tube?
A. Repositioning should be minimized
B. Milking and stripping the tube are necessary to maintain patency
C. Continuous bubbling in the water seal chamber is an indication the tube is functioning properly
D. Tube patency, fluctuation and bubbling in the drainage chamber should be monitored and documented hourly
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References
� Finer, N. N., Rich, W., Halamek, L. P., & Leone, T. A. (2012). The delivery room of the future: The fetal and neonatal resuscitation and transition suite. Clinics in Perinatology, 39(4), 931-939.
� Kandraju, H., Murki, S., Subramanian, S., Gaddam, P., Deorari, A., & Kumar, P. (2013). Early routine versus late selective surfactant in preterm neonates with respiratory distress syndrome on nasal continuous positive airway pressure: A randomized controlled trial. Neonatology, 103(2), 148-154.
� Kumar, P., Denson, S. E., Mancuso, T. J., & Committee on Fetus and Newborn, Section on Anesthesiology and Pain Medicine. (2010). Premedication for nonemergency endotracheal intubation in the neonate. Pediatrics, 125(3), 608-615.
� Leone, T. A., Finer, N. N., & Rich, W. (2012). Delivery room respiratory management of the term and preterm infant. Clinics in Perinatology, 39(3), 431-440.
� Vaucher, Y. E., Peralta-Carcelen, M., Finer, N. N., Carlo, W. A., Gantz, M. G., Walsh, M. C., et al. (2012). Neurodevelopmental outcomes in the early CPAP and pulse oximetry trial. The New England Journal of Medicine, 367(26), 2495-2504.
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