TA 2 Flashcards
(140 cards)
1
Q
What is intraventricular hemorrhage?
A
Bleeding into the ventricles of the brain
2
Q
What factors affect the development of an IVH?
A
- Gestational age (23-32 weeks)
- Low birth weight (<1.5kg)
3
Q
What causes IVH?
A
Rupture of the germinal matrix
4
Q
What is the germinal matrix?
A
A vascular structure in the brain present from 20-36 weeks gestation that is prone to rupture due to lack of collagen fibres like in normal permanent vasculature.
5
Q
Where would an IVH most likely occur in a term neonate?
A
The lateral ventricles
6
Q
Where would an IVH most likely occur in a premature infant?
A
The germinal matrix
7
Q
What are some clinical factors that may affect cerebral blood flow?
A
Sepsis, PDA, systemic pressure changes, hyperglycemia, acidosis, etc.
8
Q
What might increase cerebral blood flow?
A
PDA, transfusion, volume expansion, hypercarbia
9
Q
What might decrease cerebral blood flow?
A
Sepsis, hypovolemia, hyperglycemia, hypocarbia
10
Q
What are the grades of IVH?
A
-Mild (Grade I)- limited to germinal matrix
-Moderate (Grade II)- germinal matrix bleed with blood in ventricles but no ventricle dilation
-Severe (Grade III)- same as Grade II but ventricles dilated
- Other (Grade IV)- dilated ventricles and bleed extends into the brain parenchyma
11
Q
What are common signs of bleeding in the germinal matrix?
A
Apnea, hypotension, decreased hematocrit, flaccidity, bulging fontanelles, tonic posturing
12
Q
What are the possible presentations of IVH?
A
- Asymptomatic
- Saltatory Syndrome (gradual deterioration)
- Catastrophic Deterioration (sudden change)
13
Q
How can we assess IVH?
A
Alertness, cranial nerve function ( suck and swallow, vision, pupil response), motor function, generalized hypotonia
14
Q
How can we prevent IVH?
A
Prolonging pregnancy if possible. Corticosteroids, antibiotics, delayed cord clamping
15
Q
What is one serious complication of IVH?
A
PHH- post hemorrhagic hydrocephalus. Caused by obstruction of CSF outflow impairment of CSF reabsorption of the brain
16
Q
What are some ways of managing IVH?
A
Avoid factors that create fluctuations in cerebral blood flow; avoid wide changes in BP, O2, pH; treat hyperbilirubinemia, drain shunts if necessary
17
Q
What is Bronchopulmonary Dysplasia?
A
A disorder of premature infants characterized by respiratory distress and impaired gas exchange.
18
Q
What is the pathogenesis of BPD?
A
Chronically recurring lung injury, with ongoing repair and healing of the injury
19
Q
What are some contributing factors of BPD?
A
PDA, fluid overload of VLBW infants, intrauterine nutritional deficiency, prematurity, inflammatory lung injury
20
Q
What are the direct causes of BPD?
A
Oxygen toxicity (causes thickening of the alveolar membrane), barotrauma, volutrauma
21
Q
Describe the clinical manifestations of BPD you would find on CXR.
A
Stage 1- reticulogranular pattern or RDS
Stage 2- coarse granular infiltrates that are dense enough to obscure cardia markings
Stage 3- Multiple cyst formation within the opaque lungs and visible cardiac borders
Stage 4- irregular cyst formation that alternates with areas of increased density
22
Q
What are some key features of BPD?
A
Alveolar hypoplasia, halt in development of terminal airways, alteration of pulmonary arteries ant their distribution.
23
Q
What are some cardiovascular changes caused by BPD?
A
Right ventricular hypertrophy, increased Rt ventricular systolic time intervals or left ventricular and septal wall thickening on echocardiogram
24
Q
How do we diagnose BPD?
A
- A chronic need for oxygen support
- Prolonged ventilatory support
- Chest radiographs
- Chronic changes in ABGs
25
What are some ways we can manage BPD?
Optimizing infant temperature from delivery to NICU, minimizing FiO2 to maintain safe oxygenation, and early optimization of ventilation
26
What is a major difference between neonatal and adult airways?
In adults the narrowest portion is the glottis, and in neonates the narrowest portion is the cricoid cartilage (below the glottis) making it more funnel shaped
27
What kind of laryngoscope blade do we use on neonates and why?
A miller blade to directly displace the epiglottis because it is big and floppy
28
What are some indications for intubating a neonate?
- Surfactant therapy, other med delivery
- Congenital anomalies (CDH)
- Apnea of prematurity
- Higher ventilating pressure requirements
- Access to lower airway for suctioning
- Ex-utero intrapartum treatment procedure (EXIT procedure) (baby remains attached to placenta before getting airway and is intubated during delivery to maintain placental blood flow and oxygenation)
29
What are some advantages and disadvantages of oral intubation?
Easier (no forceps required), better for VAP prevention. Baby cannot use pacifier
30
What are some advantages and disadvantages of nasal intubation?
More secure, baby is able to use pacifier to train suck and swallow reflex. More difficult and Macgill forceps required to direct the ETT into the glottis
31
Why do we use uncuffed tubes in neonates?
Narrow cricoid means there is very little leak in an appropriately sized tube. Chances of tracheal damage are higher with cuffed tubes especially on newborn and premature airways
32
How do we calculate ETT depth for neonates?
Weight in kg + 6 = ETT depth (ex 2kg = 8cm). Can also use nare to tragus length
33
Why do we use atropine when intubating neonates?
They have significant vasovagal responses so this prevents HR from dropping too much
34
What is a good position for intubating neonates?
Ear canal aligned with sternum. Can be achieved by placing a shoulder roll.
35
How do we tell if we have successfully intubated?
Visualizing tube going through cords, colorimetric CO2 detector, auscultation, chest rise, CXR to confirm placement
36
What differences are there between nasal and oral intubation?
Same steps but before laryngoscope is inserted advance the ETT through a nare until it is visible in the back of the oropharynx, then guide ETT through cords with macgill forceps
37
What is a neobar?
A method of securing and ETT tube for neonates that involves a little plastic arch that goes over the mouth and is secured on either side by sticky patches. Has stabilizer that ETT tube is taped directly to.
38
What are the normal ventilating parameters for a neonate? (RR, Vt, compliance, resistance)
40-60, 3.5-6 mls/kg but start at 5!! , 5-6, 25-30
39
What are some indications for mechanical ventilation in newborns?
Apnea, ventilatory failure, increased work of breathing, increasing oxygen requirements
40
What PIP should we set for newborns?
About 20 cmH2O
41
What PEEP should we start at for intubated neonates?
5-6
42
What Ti should we start at for intubated neonates?
0.3 s and be careful to have adequate slope to reach Vt (0.05s)
43
What should our flow trigger sensitivity be set at for intubated neonates?
0.5-1.5 lpm
44
What should we set our E-sense at for an intubated neonate?
20-40%
45
Why do we have leak in intubated neonates and how do we fix it?
Uncuffed ETT tube, acceptable unless >40% in which case we may have to size up due to baby growing. If we have leak but do not need to size up the tube we can increase the E-Sense so more breath is delivered before it is cycled
46
How do we set our vent alarms for neonates?
20% above and below, or whatever would make you concerned
47
What are the acceptable arterial PO2 values for premature and term infants?
<28 weeks: 45-64
28-40 weeks: 50-70
significantly lower values may be acceptable for infants with congenital heart defects
48
What are the acceptable arterial PCO2 values for neonates?
35-55 mmHg but may be highly variable with GA. Avoid <35 because of cerebral perfusion effects
49
What is a normal pH for a neonate?
7.3-7.4, but less in very fresh babies or premature (but still >7.25)
50
What is the normal SpO2 for a neonate?
Usually 88-92%
51
What is the normal SpO2 for a neonate with congenital heart defect?
70-80%
52
What is one of the first things we can do to fix oxygenation issues in an intubated neonate?
Suction
53
What can we do if an intubated neonate has low PCO2 but is not acidotic?
Decrease PIP and decrease respiratory rate
54
What can we do if an intubated neonate has low PO2 but is on high FiO2?
Increase PEEP, consider increasing PIP or Ti
55
Why do we extubate neonates quickly?
Decreases risk of VAP, able to put babies directly onto CPAP or BiPAP, reduces risk of damage to airways, allows for oral motor skill development
56
What is the general extubation procedure for neonates?
1. Check orders, weaned parameters, extubation criteria utilized for this patient
2. Consider extubation support
3. Prepare family
4. Prepare patient (position, suction, etc.)
5. Place patient on bagger to see if they will spontaneously breath
6. Pull ETT at peak inspiration
7. Assess how they are doing
8. Clean up!!
57
What is the main indicator of meconium aspiration syndrome?
Meconium stained fluid
58
Why is meconium passed in utero?
Baby is usually in distress
59
What GA does meconium aspiration syndrome usually affect?
Term or post-term infants
60
What might we see on the CXR of an infant with MAS?
Consolidation and haziness throughout
61
What criteria must be met for a MAS diagnosis?
Respiratory distress occurring in a meconium stained infant shortly after delivery, respiratory distress is not explained by any other cause, associated with the typical radiologic findings on CXR
62
What are some factors associated with increased risk of MAS?
Post-term pregnancy, preeclampsia, maternal htn, maternal diabetes, smoking, cardiovascular disease, fetal distress, oligohydramnios
63
If meconium is sterile, why does aspiration cause issues?
Obstructs the airway because it is thick and tarry; can cause air trapping as air is allowed in but not out, can also cause atelectasis. Also causes chemical pneumonitis which in turn causes poor V/Q matching, increasing pulmonary hypertension and starting inflammatory cascade.
64
What are some complications that arise as a result of MAS?
Barotrauma, PIE, BPD, increased pulmonary vascular resistance, increased ICP, IVH
65
What is the therapeutic range for high frequency jet ventilation?
240-420 BPM
66
What is the tidal volume for HFJV?
1-2mls/kg
67
How does a HFJV work?
Vent blows air through a pinch valve which opens and closes rapidly and jet is generated at the jet port adapter on the ETT. It de-couples oxygenation and ventilation and there may be two different vents set up so make sure to match FiO2s
68
What is one advantage HFJV has over oscillation?
We are able to achieve I:E ratios of 1:12 compared to 1:2 in oscillation so infants with MAS tend to do better on HFJV
69
How does HFJV flow through the lungs?
Double helical bi-directional flow; exhalation is passive and flows around the inhalation stream along the airway walls. This is very good for bringing up secretions
70
What are some major differences between dconventional ventilators and jet ventilators? (parameters)
Set PIP, Ti, and RR on jet ventilator; set PEEP, RR, PIP, Ti on conventional vent. Jet measures PIP, delta P, PEEP, MAP, Servo
71
What is servo?
The driving pressure required to regulate flow. Increased resistance and decreased compliance will generate lower servo pressure.
72
What are some advantages to HFJV?
Gentler, able to bypass holes in the airway due to flow pattern, minimizes risk of volutrauma and barotrauma
73
What are some indications for HFJV?
PIP >25, Vt <6mls/kg, airleak pathology, pulmonary hypoplasia, abdominal distension, ECMO being considered, extreme prematurity
74
When we combine two ventilators (jet and conventional) which vent controls what?
Jet ventilator controls ventilation, conventional controls oxygenation
75
How do we use servo pressure to evaluate our patient?
Trend is more important than the absolute number. Unexpected changes should be closely monitored. Decrease in servo pressure is a bad sign (increasing resistance and decreasing compliance)
76
How does jet ventilation affect our ability to suction?
Cannot be done conventionally, suction must be applied on the way down and up
77
What are the most common causes of pneumonia in neonates?
Group B strep!!!, E coli, cytomegalovirus, chlamydia
78
What is congenital pneumonia?
Associated with maternal bacterial or viral infections established during fetal life. Transplacental hematogenous. (herpes, varicella)
79
What are some risk factors for congenital pneumonia?
Eating undercooked meat, exposure to cat feces, CMV infection, disseminated HSV, varicella
80
What is early onset pneumonia?
Occurs in the first week of life. A result of pathogen exposure during delivery or intrauterine. Originates from contaminated amniotic fluid or premature rupture of membranes.
81
What is late onset pneumonia?
Occurs after the first week of life due to exposure to contaminated equipment, poor family/caregiver hand washing
82
What are some risk factors for late onset pneumonia?
Mechanical ventilation, prematurity, LBW, prolonged NICU stay, poor infection control
83
What causes PIE?
It is associated with lack of surfactant and is a problem for premature infants ( 23-32 weeks)
84
When does PIE occur?
In the first 24 hours after birth
85
What is PIE?
When air gets into the interstitial spaces surrounding the pulmonary vasculature
86
What part of the airway does PIE typically originate from?
Terminal bronchioles because they have less structure so they are more likely to stretch and shear
87
Describe the clinical manifestations of PIE?
Decreased lung compliance, tachypnea, retractions, barrel chest, worsening ABGs, cystic areas throughout lung parenchyma on CXR
88
What are 3 complications that can arise from PIE?
Pneumothorax, pneumomediastinum, subcutaneous emphysema
89
How do we manage PIE?
Administration of surfactant, maintaining good urine and cardiac outputs, ventilate with lower pressures, high frequency ventilation, giving dexamethasone (may reduce effects from inflammatory mediators)
90
How can we prevent PIE?
Early surfactant administration and antinatal steroids prior to delivery
91
What is the difference in exhalation between HFJV and HFOV?
HFOV uses active exhalation while HFJV uses passive
92
Describe Taylor Dispersion?
The enhanced diffusion of gases caused by the turbulence of gas flows reaching the small airways. Enhances simple molecular diffusion by superimposing convective flow, creating erratic formation of streams and eddies as the gas hits bifurcations in the lungs.
93
Describe Penduluft
Gas from fast filling alveolar units will empty into the slower filling units.
94
Why do we use HVOF?
More effective at recruiting and protecting acutely injured lungs, increases MAP while decreasing the shear forces associated with the cyclic opening of collapsed alveoli.
95
What are some indications for HFOV?
When conventional ventilation thresholds are met requiring toxic FiO2 levels, PIP >30-35 H2O, high PEEP, high MAP with failure of APRV or optimization of CMV
96
Describe Asymmetrical Velocity Profile?
Creates a "bullet shaped" flow where the center moves forwards and the periphery moves backwards. Improves ventilation as most of the outside is dead space anyways so it being pushed out while fresh air comes down the middle is good.
97
What does "attenuation" mean in regards to HFO?
The pressure at the end of the endotracheal tube dissipates, or attenuates, by the time it reaches the alveoli so HFO is very gentle.
98
What are some contraindications of HFO?
Cardiovascular instability (low BP), acute head injury (mindful if ICP), severe airflow obstruction (active exhalation may cause airway collapse)
99
Which HFO parameters are important for ventilation?
Amplitude and Hz
100
Which HFO parameters are important for Oxygenation?
MAP and FiO2
101
Where do we want our wiggle factor to when ventilating with HFO and what is a good starting amplitude to get there?
Umbilicus, 30
102
What is the difference between HFO and HFOVG?
HFOVG is volume guarantee and regulates the oscillatory volume (amplitude) which eliminates volume fluctuations from dynamic changes.
103
How do we increase CO2 clearance in HFO?
By increasing the Hz
104
How do we decrease CO2 clearance in HFO?
By decreasing the Hz
105
Where is nitric oxide naturally found?
Within vascular endothelial cells of lungs and upper airway
106
What are some indications for nitric oxide use?
Pulmonary hypertension, hypoxemia, ARDS, Right ventricular dysfunction, CHD, heart and lung transplants
107
What is the mechanism of action for NO?
It activates guanylate cyclase to increase cGMP levels. cGMP activates protein kinase that decreases free calcium. Lower levels of calcium cause smooth muscle relaxation = VASODILATION
108
Describe the pulmonary effects of inhaled NO.
It diffuses readily across the AC membrane so it causes vasodilation in areas of ventilation and perfusion without affecting poorly ventilated and/or perfused areas
109
How does iNO affect endogenous NO production?
It inhibits it by inhibiting NO synthase
110
What effects does NO have on coagulation?
It interferes with platelet and leukocyte function and limits platelet aggregation
111
Describe the overall response in the body caused by iNO?
Decreases pulmonary artery pressure, decreases peripheral vascular resistance, increases V/Q matching, increases oxygenation
112
What are some adverse effects of iNO?
Nitrogen Dioxide production (potent oxidant causes oxidative damage to airway and lung parenchyma), methemoglobinemia (decreases oxygen carrying capacity), Peroxynitrite (potent oxidant that destroys surfactant), rebound effect (severe hypoxemia after discontinuation of NO so must wean slowly), Acute pulmonary edema (increased pulmonary blood flow can overwhelm left heart)
113
What are some alternatives to NO?
Nitroglycerin, nitroprusside, dobutrex, sildenafil, prostacyclin
114
What is an esophageal fistula?
A condition where the esophagus ends into a pouch
115
What is the most common type of esophageal fistula?
The upper part of the esophagus ends in a pouch and the lower part connects to the trachea
116
What is a TE fistula typically associated with in utero?
Polyhydramnios
117
What are some symptoms of a TE fistula?
Accumulation of secretions in the mouth, repeated regurgitation of feedings, respiratory distress especially during feedings, barking cough
118
When is TE fistula typically diagnosed?
At the 20 week anatomy scan
119
What is the treatment for a TE fistula?
Baby kept at 45 degrees upright to prevent aspiration, repogle tube for continuous suction to remove oral secretions, NPO with IV nutrition, intubation if infant cannot maintain their own airway, corrective surgery
120
What is Robin Sequence?
Under developed jaw, obstruction of the upper airway due to the bulk of the tongue, cleft palate
121
What is the treatment for Robin Sequence?
Maintaining patent airway until mandible grows (6-12 months); sometimes requires a trach. Prone position to relieve obstruction, surgical repair
122
What is tracheomalacia?
A disorder of the trachea that causes it to be abnormally collapsible due to loss of structural integrity
123
What are some symptoms of tracheomalacia?
Noisy respirations, hoarse cry, inspiratory retractions severe enough to cause chest wall deformity in some cases, coordinating breathing and feeding problems, frequent infections, wheezes on auscultation
124
What is laryngomalacia?
Similar to tracheomalacia but affects larynx
125
What causes larygomalacia?
Abnormal integration of laryngeal nerves
126
What are some symptoms of larygomalacia?
Similar to tracheomalacia but will hear inspiratory stridor rather than biphasic noises
127
How do we diagnose laryngomalacia?
With flexible fiberoptic laryngoscopy and sometimes polysomnogram when associated with OSA
128
What is choanal atresia?
Choanae are the two openings in the posterior portion of the nasal cavity, directing flow into the nasopharynx. Choanal atresia occurs when the membrane that separates the nasal cavity from the nasopharynx during embryological development fails to disintegrate and blocks the passage of air
129
What are some symptoms of choanal atresia?
Immediate respiratory distress, issues latching and feeding, improvement with crying
130
How is choanal atresia treated?
OPA in the form of a soother with a hole (called a McGovern nipple), surgical removal of the membranes covering the choanae
131
Describe what a vascular ring is.
Double aortic arch or right aortic arch with ligamentum arteriosum form a ring which ends up causing major feeding and breathing problems. Corrected surgically.
132
What kind of shunt does PDA cause?
Left to right
133
How does prematurity affect a PDA?
The more premature the infant the greater the delay in closure of the PDA.
134
Where do we place the pulse ox on a patient suspected to have PDA?
One on right hand (preductal), one on left foot (post ductal). Results in a differeint of sats of 5-10%
135
What are the clinical manifestations of PDA?
CXR shows increased vascular markings if CHF develops, Echocardiology determines presence of PDA
136
What is PGE1 and what is it used for?
Alprostadil and it is a vasodilator. Given as a constant infusion for PDA to relax vascular smooth muscle
137
Why does PGE1 cause apneas?
May be related to the same pathways of the inflammatory release of PGE2 and interleukins that cause apneas with sepsis
138
What is transposition of the great arteries?
When the aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle
139
Describe transposition of the great arteries
Circulation is split into left and right. Right- deoxygenated blood circulates through the RA, RV,aorta, to systemic circulation and returns to the RA. Left circulation - oxygenated blood from pulmonary veins circulates in a continuous circuit through LA, LV, pulmonary circulation and back to LA
140
What is the treatment for transposition of the great vessels?
PGE1 to maintain PDA, intubation and ventilation to manage blood gas abnormalities, atrial septoplasty. Arterial switch (Jatene operation) literally just swap the arteries. Rastelli procedure if there is also a VSD as well that which will re-direct blood flow at the ventricular level. Conduit is attached from RV to PA and VSD is repaired allowing blood to flow only to the aorta
