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105 Cards in this Set
- Front
- Back
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How is RDS characterized? |
By severe impairment of respiratory function |
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What is RDS caused by? |
Immaturity of the lungs primarily due to lack of surfactant |
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What can be a result of RDS? |
Pulmonary hyaline membrane disease |
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Does RDS result in a decrease or increase in lung compliance? |
Decrease in lung compliance |
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What are the two other names for RDS? |
Hyaline membrane disease and infant respiratory distress syndrome |
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What are two etiology’s of RDS? |
Decreased surfactant and associated with prematurity |
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What is the L/S ratio for RDS? |
<2 |
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What are some clinical manifestations of RDS? |
Tachypnea, apnea (tired from Work of Breathing), cyanosis, edema, nasal flaring, grunting, retraction (0-50 secs), L/S ratio <2. |
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Name symptoms of RDS? |
Nasal flaring, grunting, see-saw breathing patterns, abnormal breathing patterns like apnea tachypnea, hypoxemia, hypercarbia, atelectasis, blood gas: respiratory acidosis, substernal and/or intercostal retractions. |
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What does X-ray of RDS show? |
Shows “ground glass,” “white out” appearance atelectasis. This often develops 6 to 12 hours after birth. Lab tests rule out infection as a cause of breathing problems. |
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What are treatments for RDS? |
Prevent premature birth, good prenatal care, a lab test can be done before delivery to check readiness of the baby’s lungs, corticosteroids may help speed up lung maturity, artificial surfactant, infants will be given warm and moist oxygen, mechanical ventilation with low pressure and high rate, continuous positive airway pressure (CPAP) may prevent the need for breathing machine in many babies, CPAP will provide alveolar stability and increase FRC for babies with surfactant deficiency. |
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What are complications with RDS? |
Long term complications may develop to: Too much oxygen, high pressures delivered to the lungs can cause pneumothorax, when RDS is worse can result in inflammation that causes lung or brain damage, periods when the brain or other organs didn’t get enough oxygen |
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What are the treatments for RDS? |
1. Beractant (survanta) 2. Calfactant (infasurf) 3. Poractant alfa (curosurf) 4. Colfosceril palmitate (exosurf) 5. Lucinactant (surfaxin) (59) |
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Name the dosage for the RDS medication? |
1. Beractant (survanta): 4 mL/kg 4 aliquots Repeat dosage: every 6 hours up to a maximum of 4 doses during the first 24 hours of life. 2. Calfactant (infasurf) Dosage: 3 mL/ kg in 2 aliquots. Repeat dosage: every 12 hours up to maximum of 3 doses. 3. Poractant alfa (curosurf) Dosage: 1st dose is 2.5 mL/ kg in 2 aliquots. The repeat dose 1.25 mL/ kg in 2 aliquots. Repeat dosage: every 12 hours up to a maximum of 3 doses. 4. Colfosceril palmitate (exosurf) Dosage: 5 mL/ kg in 2 aliquots. Repeat dosage: every 12 hours up to a maximum of 3 doses. 5. Lucinactant (surfaxin) (59) Dosage: 5.8 mL/ kg in 4 aliquots Repeat dosage: every 6 hours, up to a maximum of 4 doses. |
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What is apnea of prematurity? |
A sudden cessation of breathing that last at least 20 seconds or is accompanied by bradycardia or oxygen desaturation in an infant younger than 37 weeks gestation |
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What are causes of apnea in premature infants? |
Incorrect neural signaling and airway obstruction |
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What is AOP or apnea of prematurity caused by? |
Caused by physiological immaturity of the neurological and chemical receptor systems of the body that regulate respiration and respond to hypoxemia and hypercapnia. |
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What is AOP or apnea of prematurity caused by? |
Caused by physiological immaturity of the neurological and chemical receptor systems of the body that regulate respiration and respond to hypoxemia and hypercapnia. |
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What is periodic breathing? |
A benign abnormal form of breathing with cycles of hyperventilation followed by short apneic pauses of less than 3 seconds |
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How can AOP be classified? |
As central, obstructive, or mixed |
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What is central apnea caused by? |
Central apnea is caused by dysfunction of nerve centers in the brainstem to send signals to muscles of respiration and no attempt at inspiration can be observed |
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What is the primary role of the respiratory-control system? |
To regulate ventilation to supply the oxygen needs of the body and to remove carbon dioxide |
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What is the primary cause of central apnea? |
Dysfunction of respiratory control system |
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In central apnea what two chemoreceptors play a role? |
Central and peripheral chemoreceptors |
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In central apnea what two chemoreceptors play a role? |
Central and peripheral chemoreceptors |
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Control of ventilation occurs where? |
In the brainstem |
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What apnea is probably the most common type? |
Mixed apnea |
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What apnea is probably the most common type? |
Mixed apnea |
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How is obstructive apnea characterized? |
Characterized by some attempt to ventilate, resulting in chest wall movement but without gas entry, usually caused by an upper airway obstruction |
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What apnea is probably the most common type? |
Mixed apnea |
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How is obstructive apnea characterized? |
Characterized by some attempt to ventilate, resulting in chest wall movement but without gas entry, usually caused by an upper airway obstruction |
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How would you define mixed apnea? |
Consists of obstructive respiratory effects usually following central pauses and is probably the most common type of apnea |
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Apnea of prematurity is not a disease but an symptom of underlying causes, what are some underlying causes? |
Prematurity (all other causes should be excluded first), respiratory complications (RDS, congenital upper airways animalities, airway obstruction, hypoxia, pneumonia), cardiovascular ( patient ductus arteriosus, anemia, sepsis), CNS dysfunction ( trauma, seizures, meningitis, pharmacologic sedation, immaturity of respiratory centers, IVH), gastrointestinal (GERD, necrotizing enterocolitis), metabolic ( hypoglycemia, hypo or hypernatremia, hypocalcemia, hypo or hyperthermia), environmental ( temperature instability, vagal stimulation through suctioning or hyperinflation with feeding NG tube). |
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Apnea of prematurity is not a disease but an symptom of underlying causes, what are some underlying causes? |
Prematurity (all other causes should be excluded first), respiratory complications (RDS, congenital upper airways animalities, airway obstruction, hypoxia, pneumonia), cardiovascular ( patient ductus arteriosus, anemia, sepsis), CNS dysfunction ( trauma, seizures, meningitis, pharmacologic sedation, immaturity of respiratory centers, IVH), gastrointestinal (GERD, necrotizing enterocolitis), metabolic ( hypoglycemia, hypo or hypernatremia, hypocalcemia, hypo or hyperthermia), environmental ( temperature instability, vagal stimulation through suctioning or hyperinflation with feeding NG tube). |
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What is treatments for apnea of prematurity? |
Methylxanthines and caffeine citrate. |
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What is most commonly used to treat apnea of prematurity? |
Caffeine citrate |
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What is most commonly used to treat apnea of prematurity? |
Caffeine citrate |
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What are the causes of the treatment for apnea of prematurity? |
Stimulates respiratory drive, increases diaphragmatic activity, increases minute ventilation, increases chemoreceptor sensitivity to CO2, reduces periodic breathing, reduces hypoxia respiratory depression, increases metabolic rate, increases oxygen consumption, stimulates diuresis) |
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What is most commonly used to treat apnea of prematurity? |
Caffeine citrate |
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What are the causes of the treatment for apnea of prematurity? |
Stimulates respiratory drive, increases diaphragmatic activity, increases minute ventilation, increases chemoreceptor sensitivity to CO2, reduces periodic breathing, reduces hypoxia respiratory depression, increases metabolic rate, increases oxygen consumption, stimulates diuresis) |
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What is the treatment for apnea of prematurity? |
Blood transfusions: May alleviate anemia that can cause irregular breathing pattern in infants, nasal cannula: mild positive pressure in the upper airway to prevent obstructive apnea and tactile stimulation in the nares as a way to prevent central apnea, noninvasive ventilation: NCPAP and NIPPV which provides positive pressure that reduces likelihood of upper airway collapse, body positioning: prone positioning can improve thoraco- abdominal synchrony and stabilize the chest wall, stimulation: can be tactile kinesthetic. |
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What is bronchopulmonary dysplasia? |
A type of chronic lung disease currently defined as the need for supplemental oxygen for at least 28 days after birth assessed at discharge or when the baby is close to his or her estimated full term age. |
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What is bronchopulmonary dysplasia? |
A type of chronic lung disease currently defined as the need for supplemental oxygen for at least 28 days after birth assessed at discharge or when the baby is close to his or her estimated full term age. |
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What babies are at the greatest risk for respiratory distress syndrome? |
Premature infants born at gestational age 23 to 30 weeks |
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What is bronchopulmonary dysplasia? |
A type of chronic lung disease currently defined as the need for supplemental oxygen for at least 28 days after birth assessed at discharge or when the baby is close to his or her estimated full term age. |
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What babies are at the greatest risk for respiratory distress syndrome? |
Premature infants born at gestational age 23 to 30 weeks |
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What are the risk factors for development of new bronchopulmonary dysplasia? |
New BPD: gestational age less than 28 weeks, birth weight less than 1,000 grams, hypothermia and hypotension at admission, need for prolonged MV, hypercarbia the PaCO2 is greater than 50 mmHg, nosocomial infection, need for exogenous surfactant therapy, more than two blood transfusions, chorioamnionitis, preeclampsia |
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What is bronchopulmonary dysplasia? |
A type of chronic lung disease currently defined as the need for supplemental oxygen for at least 28 days after birth assessed at discharge or when the baby is close to his or her estimated full term age. |
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What babies are at the greatest risk for respiratory distress syndrome? |
Premature infants born at gestational age 23 to 30 weeks |
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What are the risk factors for development of new bronchopulmonary dysplasia? |
New BPD: gestational age less than 28 weeks, birth weight less than 1,000 grams, hypothermia and hypotension at admission, need for prolonged MV, hypercarbia the PaCO2 is greater than 50 mmHg, nosocomial infection, need for exogenous surfactant therapy, more than two blood transfusions, chorioamnionitis, preeclampsia |
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What are the risk factors for severe BPD? |
Acidosis at admission, surfactant therapy, nosocomial infections, oligohydramnios, Agar score less than 6 to 5 minutes |
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What are the clinical manifestations BPD? |
Rapid shallow breathing, sharp pulling of the chest below and between the ribs with each breath, grunting sounds, flaring of nostrils, episodes of cyanosis, miniature COPDers hypercarbia wean O2 slowly |
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What are the clinical manifestations BPD? |
Rapid shallow breathing, sharp pulling of the chest below and between the ribs with each breath, grunting sounds, flaring of nostrils, episodes of cyanosis, miniature COPDers hypercarbia wean O2 slowly |
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What is the first sign BPD for premature infants? |
Usually those more than 10 weeks early still need oxygen therapy by the time they reach their original due dates. |
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What are the clinical manifestations BPD? |
Rapid shallow breathing, sharp pulling of the chest below and between the ribs with each breath, grunting sounds, flaring of nostrils, episodes of cyanosis, miniature COPDers hypercarbia wean O2 slowly |
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What is the first sign BPD for premature infants? |
Usually those more than 10 weeks early still need oxygen therapy by the time they reach their original due dates. |
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What is mild BPD? |
No supplemental oxygen requirement at the time of evaluation |
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What is moderate BPD? |
FIO2 less than 30% and/or PPV or NCPAP at time of evaluation |
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What is moderate BPD? |
FIO2 less than 30% and/or PPV or NCPAP at time of evaluation |
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What is severe BPD? |
FIO2 greater than 30% and/or PPV or NCPAP at time of evaluation |
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What is moderate BPD? |
FIO2 less than 30% and/or PPV or NCPAP at time of evaluation |
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What is severe BPD? |
FIO2 greater than 30% and/or PPV or NCPAP at time of evaluation |
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What does the chest X-ray of a baby with BPD look like? |
Normally, the healthy air filled lungs appear black, in BPD the lungs become fibrotic with over simplified thickened alveoli, hyperinflated lung fields with linear interstitial opacities, patchy distribution of atelectasis and areas of hyperinflation |
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What is moderate BPD? |
FIO2 less than 30% and/or PPV or NCPAP at time of evaluation |
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What is severe BPD? |
FIO2 greater than 30% and/or PPV or NCPAP at time of evaluation |
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What does the chest X-ray of a baby with BPD look like? |
Normally, the healthy air filled lungs appear black, in BPD the lungs become fibrotic with over simplified thickened alveoli, hyperinflated lung fields with linear interstitial opacities, patchy distribution of atelectasis and areas of hyperinflation |
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What are complications of BPD? |
These babies are more at risk for influenza, RSV, pneumonia, pulmonary edema, and pulmonary hypertension. The risk for serious permanent complications is fairly small |
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What is the treatment for BPD? |
Use lowest FIO2 to maintain SpO2 greater than 88%, very slow wean off of O2( 1month to 1 years), CPT and bronchodilator therapy, keep of MV and CPAP, if MV needed try to extubate as soon as possible, treat PDA |
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What are preventative measures for BPD? |
Prevent premature birth, prenatal maternal steroid administration, use of post natal surfactant |
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Name 3 diseases of full term infants? |
Persistent Pulmonary Hypertension of the Newborn (PPHN), Meconium Aspiration Syndrome (MAS), and Transient Tachypnea of the Newborn (TTN) |
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Name 3 diseases of full term infants? |
Persistent Pulmonary Hypertension of the Newborn (PPHN), Meconium Aspiration Syndrome (MAS), and Transient Tachypnea of the Newborn (TTN) |
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What is persistent pulmonary hypertension of the Newborn or PPHN? |
A syndrome with severe hypoxemia and high pulmonary artery pressures that occurs when the pulmonary vascular pressure normally high in utero fails to decrease at birth |
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When does PPHN usually present itself? |
At birth or shortly after |
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How is PPHN characterized? |
By failure to establish adequate pulmonary and systematic oxygenation |
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How is PPHN characterized? |
By failure to establish adequate pulmonary and systematic oxygenation |
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What can happen if PPHN is untreated? |
Without treatment can cause severe cardiac dysfunction, multi organ dysfunction and death |
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What are diagnoses associated with pulmonary hypertension? |
MAS or Meconium Aspiration Syndrome, Asphyxia, Neonatal Respiratory Distress Syndrome, sepsis, pneumonia, congenital diaphragmatic hernia, pulmonary hypoplasia, total anomalous pulmonary venous return, hypoplastic left heart syndrome, left ventricular outflow tract obstruction |
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What is the most underlying diagnosis of PPHN? |
MAC or Meconium Aspiration Syndrome |
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Is PPHN a life threatening condition? |
Yes PPHN is a life threatening condition |
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What is another name for PPHN? |
Persistent Fetal Circulation (PFC) |
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In PPHN how is the baby’s body supply of oxygen decreased? |
Blood is forced away from the lungs due to the high blood pressure in the arteries that go to the lungs |
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In PPHN how is the baby’s body supply of oxygen decreased? |
Blood is forced away from the lungs due to the high blood pressure in the arteries that go to the lungs |
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What will cause PVR to increase? |
Hypoxia, hypercarbia, and acidosis |
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When do signs and symptoms of PPHN usually appear? |
Usually appear at birth or shortly after (12- 24 hours after birth) |
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What are clinical manifestations of PPHN? |
Cyanosis, respiratory distress: (tachypnea, retractions, grunting), the CXR may be normal with idiopathic PPHN or there may be mild to moderate parenchymal disease, prominent vascular markings (pulmonary congestion), cardiomegaly |
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What are clinical manifestations of PPHN? |
Cyanosis, respiratory distress: (tachypnea, retractions, grunting), the CXR may be normal with idiopathic PPHN or there may be mild to moderate parenchymal disease, prominent vascular markings (pulmonary congestion), cardiomegaly |
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What is the hypoxic/cyanotic FIO2 % in PPHN? |
The FIO2 is greater than 60% |
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What is the PaO2 in PPHN? |
PaO2< 100 mmHg on 100% FIO2, low blood oxygen levels even after giving oxygen |
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What is the PaO2 in PPHN? |
PaO2< 100 mmHg on 100% FIO2, low blood oxygen levels even after giving oxygen |
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Is blood pressure low or high in PPHN? |
Low |
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Is urine output increased or decreased in PPHN? |
Decreased |
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How is PPHN diagnosed? |
Pre (R) and Post (L) ductal SpO2 to detect R to L shunt. A greater than 10% difference suggests pulmonary hypertension. A trans thoracic endocardiogram: acute diagnosis, rule out congenital heart defects |
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What are the objectives in management and treatment for PPHN? |
The objectives in managing PPHN is to fix the underlying disease, maintain adequate systemically blood pressure, maintain optimal delivery of oxygen to the tissues, decrease PVR, minimize ventilatory induced lung injury, normalize pH |
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How to treat mild PPHN? |
Supplement O2 therapy, maintain preductal PaO2 of 90 to 120 mmHg |
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How to treat mild PPHN? |
Supplement O2 therapy, maintain preductal PaO2 of 90 to 120 mmHg |
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How to treat significant PPHN? |
Sedation and analgesia, intubation and mechanical ventilation (CMV or HFOV), Inotropes, pulmonary vasodilators like inhaled nitric oxide, sildenafil, and prostacyclin, and ECMO( Extracorporeal membrane oxygenation) the oxygen index should be greater than 40. The oxygen index is equal to = Paw x FiO2 x 100/ PaO2 |
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What is the patient selection criteria for ECMO or Extracorporeal Membrane Oxygenation? |
Oxygen index greater than 40, no major cardiac defects, reversible lung disease, gestational age greater than 33 weeks, mechanical ventilation less than 14 days, no major intraventricular hemorrhage, no significant coagulopathy or bleeding complications |
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What does meconium mean? |
Meconium is a baby’s first bowl movement and it usually occurs shortly after delivery |
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What is Meconium Aspiration Syndrome? |
MAS is defined as respiratory distress occurring soon after delivery in a meconium-stained infant. MAS is a disease primarily affecting term and post-term infants |
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What is Meconium Aspiration Syndrome? |
MAS is defined as respiratory distress occurring soon after delivery in a meconium-stained infant. MAS is a disease primarily affecting term and post-term infants |
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What three obstructions can MAS be and what does each mean? |
Partial obstruction: allows some passage of air in and out of alveolar space Ball-valve obstruction: open during inspiration closes during expiration causing air trapping Total obstruction: will not allow for inhalation or exhalation causes atelectasis and hypo ventilation |
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What is Meconium Aspiration Syndrome? |
MAS is defined as respiratory distress occurring soon after delivery in a meconium-stained infant. MAS is a disease primarily affecting term and post-term infants |
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What three obstructions can MAS be and what does each mean? |
Partial obstruction: allows some passage of air in and out of alveolar space Ball-valve obstruction: open during inspiration closes during expiration causing air trapping Total obstruction: will not allow for inhalation or exhalation causes atelectasis and hypo ventilation |
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What does the X-ray of MAS look like? |
Large ropey and strand like density. Patchy infiltrates or irregular streaky, linear densities |
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Clinical manifestations of MAS? |
Abnormal breathing patterns, increased respiratory effort (grunting, nasal flaring, retractions), abnormal lung sounds, cyanosis, hypoxemia, respiratory acidosis |
