09- Pulmonary Disorders Flashcards
Delivery room interventions for preterm infants
-Adding trained personnel
-Increase temps to 77 - 79 F
-Used warm pads and pre-warmed radiant warmer
-Place the newborn in re-closable, food-grade polyethylene bag
-Use a transport incubater when moving newborn
-Provide O2
Care for preterm infants
-Use pulse oximetry
-Provide noninvasive CPAP (4-6 cmH2O)
-Initiating PPV (20-25 cmH2O)-increase cautiously
-Once intubated, provide PEEP (2-5 cmH2O)
give surfactant early
-Handle baby gently
-Avoid Trendelenburg placement
-Avoid rapid infusion of fluid
Initial respiratory support for preterm infants
-Provide CPAP to help increase FRC and stability to alveoli
-Positive Pressure Ventilation- If spontaneous respiration and CPAP can’t provide adequate oxygenation.
-PIP 20-25 cmH2O.
-If intubated- provide PEEP at 2-5 cm H2O
-Surfactant if baby is <30
Why avoid excessive oxygen delivery to premature infants?
-Increases risk of brain injury (due to germinal matrix bursting d/t vasodilation)
-Increases risk of retinal damage and ROP
-Can cause permanent structural damage to Type I cells in alveoli (from too much O2)
Different Oxygen-delivery devices
-Traditional nasal cannula
-Heated high-flow nasal cannula
-Mask
-Oxygen hood
-Incubator
NCPAP
-Nasal continuous positive airway pressure. Can be given through nasal prongs and masks.
-Used to treat RDS
Benefits of NCPAP
-Alveolar and airway stabilization
-Decreased airway resistance
-Improve V/Q matching
-Decreased WOB
-Increased lung expansion
-Preservation of the pt’s natural surfactant
-Increased lung compliance
-Stabilization of the pt’s respiratory pattern
Indications to use NCPAP
-Increased WOB
-Inability to maintain a PaO2>50 with FiO2 <60 PaCO2 > 50 and pH > 7.25
-Infiltrated lung fields or atelectasis on CXR
Extubation from mechanical ventilation
NIPPV
-Noninvasive Positive Pressure Ventilation
-Adds a second level of pressure delivery at regular intervals to pt in an effort to improve success of NCPAP (Pressure support and IPAP)
- Creates higher mean airway pressure than NCPAP
Goals of Mechanical Ventilation
-Facilitates alveolar ventilation and CO2 removal
- pH 7.25-7.35 with PaCO2 45-55 mmHg
-Provides adequate tissue oxygenation
-Reduce EOB
-Support all spontaneous respiratory efforts
-Avoid pulmonary tissue injury (over distention)
-Minimize interference of PPV with cardiac circulation
Hyaline Membrane disease (HMD)
-First characterized in the early 20th century
-Thought to be a rare form of pneumonia
-Later became known as RDS
Respiratory Distress Syndrome (RDS)
-Characterized by severe impairment of respiratory function, caused by immaturity of the lungs, primarily due to the lack of surfactant
-Formerly known as HMD
Surfactant
-Stabilized the air-liquid interface of the alveoli and bronchioles and lowers surface tension
-Lower ST improves lung compliance, which decreases WOB
- Made and excreted by alveolar type II cells
-Appear at wGA 17-26
Symptoms of RDS
Abnormal breathing patterns, such as tachypnea or apnea
-Subternal and/or intercostal retractions
-Nasal Flaring
-Grunting (pursed lips)
-See-saw breathing pattern
-Hypoxemia
-Cyanosis
-Hypercarbia
-Respiratory acidosis
-Atelectasis
Apnea of prematurity (AOP)
-A sudden cessation of breathing that lasts for at least 20s or is accompanied by bradycardia or O2 desaturation in an infant younger than 37 wGA
Causes of apnea in premature infants
-Incorrect neural signaling
-Airway obstruction
What causes apnea of prematurity?
The physiological immaturity of the neurological and chemical receptor systems of the body that regulate respiration and respond to hypoxemia and hypercapnia
Difference between apnea and periodic breathing
-Periodic breathing is benign, abnormal, with cycles of hyperventilation followed by apneic pauses os <3 s
-Apnea- stops breathing for > 20 s
Three forms of AOP
-Central apnea
-Obstructive apnea
-Mixed apnea
Central apnea
-All neurologic
-Caused by a dysfunction of the nerve centers in the brainstem to send signals to the muscles of respiration, and no attempt at inspiration can be observed
Obstructive apnea
-Characterized by some attempt to ventilate, resulting in chest wall movement but without gas entry, usually caused by an upper-airway obstruction
Mixed apnea
-Consist of obstructed respiratory effort, usually following central pauses
-MOST COMMON
Pathophysiology of AOP
-Dysfunction of the respiratory-control system is the primary cause of the central apnea component of AOP
-Control of ventilation occurs at brainstem
-Central and peripheral chemoreceptors both play a role
Management and treatment of AOP
Methylxanthines- Stimulant medications, generally stimulating the central nervous system and cardiac muscles. Caffeine citrate is most commonly used
What do Methylxanthines do?
-Stimulates respiratory drive
-Increases diaphragmatic activity
-Increases minute ventilation
-Enhances chemoreceptor sensitivity to CO2
-Reduces periodic breathing
-Reduces hypoxic respiratory depression
-Increases metabolic rate
Increases oxygen consumption
-Stimulates diuresis
Other ways to manage and treat AOP
-Blood transfusion- May alleviate anemia
-Nasal Cannula- Works as a mild pressure in upper airway to prevent obstructive, and tactile stimulation in nares to prevent central apnea
-Noninvasive ventilation- NCPPAP and NIPPV
-Body positioning-Prone position to prevent tongue from obstructing upper airway
-Stimulation-can be tactile or kinesthetic
Course and Prognosis of AOP
-Resolution of apnea is a major developmental milestone
-Discharge depends on observation of apnea-free time period (3-8 days)
-Some infants can be sent home with caffeine citrate and provided with a home cardiorespiratory monitor
-Family education is essential (on discharge and basic life-skills)
-Long term outcomes have been challenging
Bronchopulmonary Dysplasia (BPD)
-Chronic lung disease, currently defined as the need for supplemental O2 for at least 28 days after birth, assessed at discharge or when the baby is close to his or her estimated full-term
When to asses for BPD
-For infants born <32 wGA: At 36 weeks post-menstrual age or discharge (whiechever comes first)
-For infants born >32 wGA: At >28 days but <56 days post-natal age or discharge home
Severity of BPD
-Mild: No supplemental oxygen requirement at time of evaluation
-Moderate: Need for FiO2 <0.30 and/or PPV or NCPAPA at time of evaluation
-Severe: Need for FiO2 >0.30 and/or PPV or NCPAPA at time of evaluation
Risk factors for new BPD (13)
<28 wGA
-Birth weight < 1000g
-Hypothermia at admission
-Hypotension at admission
-RDS
-Need for prolonged MV
-Hypercarbia (>50mmHg)
-Need for exogenous surfactant therapy
-Higher fluid therapy (washes out surfactant)
-Nosocomial infection
-More than two blood transfusion
-Chorioamnionitis
-Preeclampsia
Risk factors for severe BPD
-Acidosis at admission
-Surfactant therapy
-Nosocomial infections
-PDA (Patent ductus arteriosus)
-Oligohydramnios
-Apgas score < 6 at 5 minutes
Management and treatment of BPD
-Guaranteed prevention: Prevent premature birth
-Minimal O2 use
-Exogenous surfactant
Open lung ventilation and gentle ventilation
-Corticosteroids
-Caffeine citrate
-Mast cell stabilizers
-Vitamin A
-Inositol
-Antioxidants
-Inhales nitric oxide: increases gas exchange
-Treatment of pulmonary edema
-Fluid restriction
-Diuretics
-Bronchodilators
Course and prognosis of BPD
-Relatively unpredictable, and the course can vary widely
-Some exhibit some degree of obstructive lung disease that can persist into adolescence and young adulthood
-Usually have repeat hospitalizations, abnormal PF results, and the need for home supplemental oxygen
-About 40% of them will be sent with at home O2
-Frequent and recurrent respiratory symptoms and infections. May require special care and medications
-Poor neurodevelopmental outcomes (increase rate of cerebral palsy, developmental delays, and poor neuromotor outcomes at 6 months)
Economic impact of BPD
-A major impact on families’ daily lives after the neonatal period
-Home oxygen can impact the quality of life
-Incur greater costs for: prescriptions and respiratory-related care
Persistent Pulmonary Hypertension of the Newborn (PPHN)
-Syndrome with severe hypoxemia because PVR fails to decrease at birth.
-Lack of drop of PVR, causes flat of Foramen Ovale and ductus arteriosus to not close and some blood never passes through lungs
-This results in systemic hypoxemia and cyanosis
-Presents at birth or shortly after
-Characterized by a failure to establish adequate pulmonary and systemic oxygenation
-Without treatment, this can cause severe cardiac dysfunction, multiorgan dysfunction, and death
Preductal and postductal SpO2 in PPHN
-Preductal: Normal saturated blood. Taken from an area where arterial blood supply comes prior to the ductus arteriosus. Commonly in the right hand
-Postductal: O2 sat taken from area where arterial blood supply comes after the ductus arteriosus (skips lungs all together). Typically on lower limbs
-PPHN is suspected when the preductal SpO2 and postductal SpO2 show a greater than 10% difference
PPHN test
-Hyperoxia test: ABG is obtained on room air and 100% FiO2 and compared. PPHN is suspected when PaO2 >20 after 100%
-Echocardiogram: Needed to rule out congenital heart defects are cause of hypoxia. Can also document presence of shunts.
-Oxygenation index (OI): determines if we need ECMO. If OI>40 then ECMO is needed
Management and treatment of PPHN
-O2 therapy: PaO2 90-120mmHg
-Conventional mechanical ventilation (CMV)
-HFOV when CMV pressures or rates are too high
-Pulmonary vasodilators, iNO
-Maintain hematocrit at 35% to 45%
-ECMO for pts who are unresponsive to above therapeutic measures with an OI of >40
Nitric Oxide
-iNO selectively dilates the pulmonary vasculature adjacent to open lung units.
-Platelet inhibition
-Immune regulation
-Enzyme regulation
-Neurotransmission
-INITIAL DOSE: 20 PPM
-Can cause Hb to loose oxygen binding abilities
Meconium Aspiration syndrome (MAS)
-Respiratory distress occurring soon after delivery in a meconium-stained infant
-Primarily affects post-term infants or term infants under stress
Factors associated with increased risk of MAS
-Post term pregnancy >42 wGA
-Preeclampsia or eclampsia
-Maternal hypertension or diabetes
-Intrauterine growth retardation
-Abnormal biophysical profile
-Oligohydramnios
-Maternal heavy smoking or chronic respiratory or cardiovascular disease
-Abnormal fetal hear rate and nonreassuring fetal heart rate tracing
-Low 5-minute APGAR test
-Ethnicity
-Home birth
Development of MAS
-When amniotic fluid is stained with meconium, gasping or deep irregular respirations can result in aspiration
-Apiration of meconium may result in obstruction, chemical pneumonitis, atelectasis, and pulmonary hypertension
-Meconium inhibits surfactant function and is directly toxic to the pulmonary epithelium
-Meconium results in an inflammatory response. Lung becomes infiltrated with large numbers of white blood cells
Stages of airway obstruction due to MAS
-Partial: Allows some air into and out of lungs
-Ball-Valve obstruction: open during inspiration, but closed during exhalation. Causes air trapping
-Total obstruction: Inhalation and exhalation are not allowed, leads to atelectasis and hypoventilation.
Clinical manifestations of MAS
-Most infants with meconium asportation may present with no symptoms or be in respiratory failure at birth.
MAS symptoms
-Abnormal respiration rate (tachypnea, but fatigue)
-Increase respiratory effort
-Cyanosis
-Diminished breath sounds, rales, rhonchi, or wheezing
-Increased AP diameter of the chest
-Asymmetry of the chest
Management and treatment of MAS
-Nasal Cannula
-MV
-HFOV
-iNO
-ECMO
-Suction infant’s oral and nasal pharynx once head is delivered to prevent the additional aspiration
Intubating MAS baby
-Only intubate if infant is unresponsive immediately after birth (nonvigorous)
-Nonvigorous baby- depressed respiratory effort, poor muscle tone, and/or heart rate <100
-DO NOT intubate a vigorous baby. Suction mouth and nose with a bulb syringe
Transient Tachypnea of the newborn (TTN)
-Condition of term or near-term infants, characterized by mild respiratory distress during the first few hours of life
-Caused by failure to clear fetal lung fluid prior to delivery
-Resolves within 48-72 hours of life
-Looks a lot like pneumonia
Main risk factors of TTN
-Delivery via cesarean section
-Macrosomia
-Maternal asthma or diabetes
-Male gender
Clinical Manifestations of TTN
-respiratory distress within 6 hrs of birth
-Tachypnea: RR> 60 breaths/min
-Grunting
-Nasal flaring
-Retraction
Management and treatment of TTN
-O2 therapy: O2 bood or nasal cannula 90%-96%
-NCPAP of 4-6 cmH2O to resolve moderate distress
-Withholding enteral feeds
-Administration of IV fluids
-Administration of antibiotics. Because it might be pneumonia
-Use of thermoregulation
Atelectasis
-A collapsed or airless condition of the lung caused by decreased lung compliance, inadequate tidal volume, or airway obstruction.
Atelectotrauma
-Injury to the lung as a result of repeated collapse and re-expansion of alveoli. One of the major causes of lung injury in mechanically ventilated neonates.
-Pulling bandaid off analogy
Atelectasis causes
-Meconium obstruction in the terminal airways
-Lung compression from lung masses, tumors, or gastric contents
-Respiratory failure and hypoventilation due to very low lung compliance & surfactant deficiency
Clinical manifestations of atelectasis
-Grunting
-Cyanosis
-Tachypnea
-Nasal flaring
-Retractions
-Increased FiO2 requirement
-Decreasing VT
-Hypoxemia on ABG
-CXR will reveal increased opacity
Management and treatment of atelectasis
-Early extubation ad withdrawal of invasive MV
-Good airway clearance
-Frequent changes in patient positioning
-NCPAP to recruit collapsed alveoli gently
Pulmonary interstitial Edema (PIE)
-Dissection of air into the tissue of the lungs surrounding the pulmonary vasculature. An acute pulmonary complication seen most frequently in premature infants with RDS requiring mechanical ventilation
PIE
-Develops as a consequence of overdistension of the distal airways and alveoli
-Normally manifests as hypoxemia, hypercapnea, hypotension, and episodes of bradicardia
CXR of PIE
-Reveals cyst-like formation 1.00 - 4.0 mm in diameter; appear spongy
-Linear formation, irregular in form, are seen in the peripheral ling fields and perihilar areas
Management and treatment of PIE
-Best prevention: Minimizing overdistension of the lungs in RDS
-Minimizing pressure delivered to the lungs by: lowering PIP, PEEP, and TI, volume-targeted ventilation, avoiding auto-PEEP, and provideing HFJV
Pneumothorax
-A collection of air in the pleural cavity.
-Occurs when extra-alveolar air ruptures into the pleural space
Tension pneumothorax
-Occurs when each breath forces new air through the rupture, but it cannot escape through the route of entry
-An emergency the presents quickly and pt decompensate rapidly
Neonatal Risk Factors
-RDS
-MV
-Sepsis
Pneumonia
-Aspiration of meconium, blood, or amniotic fluid
-Congenital malformations
Clinical manifestations of pneumothorax
-Respiratory distress is the initial response to a less severe pneumothorax and includes tachypnea and retractions
-Definitive diagnosis of a pneumothorax is made with CXR
Tension pneumothorax symptoms
-Abrupt duskiness or cyanosis
-Hypotension
-Bradycardia
-Hypoventilation or apnea
-Decreased breath sounds on the affected side
-Decreased heart sounds
-Bulging of the affected hemithorax
-Mediastinal shift to the unaffected hemithorax
-Asymmetric chest wall movement
Clinical manifestations of pneumothorax
-If tension pneumothorax is suspected there is no time to wait for CXR
-Transillumination of the chest is the placement of a high-intensity light source on the thorax. The presence of a pneumothorax will cause the light to illuminate a large portion of the chest
Management and treatment of pneumothorax
-Small: resolves itself with observation
-Tension: Needle decompression immediately
——–19-, 20-, or 23-gauge IV or needle 20-cc syringe
-Chest tube for continuous suction -10 to -25 cmH2O
Pneumomediastinum
-Occurs when extra-alveolar air dissects through the lung interstitium and ruptures into the mediastinum.
Causes of pneumomediastinum
-Airway obstruction
-Mechanical ventilation
-Infections
-Obstructive lung disease
-Trauma
-Valsalva’s manuever
Clinical manifestations
-Tachypnea
-Bulging sternum
-Distant or crackly heart sounds
-Cyanosis
-Respiratory distress
-Subcutaneous emphysema
Diagnosis of pneumomediastinum
-CXR: free air in the mediastinal space, elevated thymus
-“spinnaker sail” sign
Treatment
-Not aggressive. If no other presence of other pulmonary leak
-Close observation and treatment of symptoms like cyanosis are enough support
Pneumopericardium
-Air within the pericardial sac
-Rare and life-threatening event
Tamponade
-Impairs the filling of the heart during diastole and impedes cardiac output
Signs and symptoms of Pneumopericardium
-Sudden Cyanosis
-Muffles or absent heart tones
-Arterial blood pressure decreases
-Peripheral pulses will disappear
-Bradycardia
-Hypoxia
-Pulseless electrical activity (PEA) will occur
CXR of Pneumopericardium
A broad, radiolucent halo will show completely surrounding the heart
Treatment of Pneumopericardium
-Close observation
-Antibiotics
-Support measures for hypotension
Treatment for a pt with tamponade
-Requires CPR
-Pericardiocentesis (procedure in which a needle is inserted into the pericardial sac to evacuate air emergently)
-Multiple pericardial taps may be necessary to sustain life
-Pericardial tube for continuous drainage until the air leak can heal
Retinopathy of prematurity (ROP)
-A complication of prematurity
-Occurs when the normal development of the retinal vessels in disrupted by premature delivery and the extrauterine environment
Factors associated with ROP
-Duration of mechanical ventilation
-Requirement for supplemental oxygen
-Several comorbidities of prematurity
Five stages of ROP
1- Characterized by incomplete blood vessel formation
2-Characterized by uncontrolled vasoproliferation and pathological neovascularization of the retina
3-Vascularization continues to proliferate
4-Begin partial and total retinal detachment - blindness
Safe practices of O2 delivery
-Minimizing abrupt change in FiO2
-Ensuring that prescriber orders for supplemental O2 include an accepatble SPO2
-Assessing a neonate for the cause of hypoxemia before increasing FIO2 levels
-Use of an air-oxygen blender
-Weaning off of oxygen ASAP as SPO2 rises about prescribed value
