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2305 Neonatal Resuscitation > TA 2 > Flashcards

TA 2 Flashcards

1
Q

What is intraventricular hemorrhage?

A

Bleeding into the ventricles of the brain

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2
Q

What factors affect the development of an IVH?

A
  • Gestational age (23-32 weeks)
  • Low birth weight (<1.5kg)
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3
Q

What causes IVH?

A

Rupture of the germinal matrix

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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.

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5
Q

Where would an IVH most likely occur in a term neonate?

A

The lateral ventricles

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6
Q

Where would an IVH most likely occur in a premature infant?

A

The germinal matrix

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7
Q

What are some clinical factors that may affect cerebral blood flow?

A

Sepsis, PDA, systemic pressure changes, hyperglycemia, acidosis, etc.

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8
Q

What might increase cerebral blood flow?

A

PDA, transfusion, volume expansion, hypercarbia

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9
Q

What might decrease cerebral blood flow?

A

Sepsis, hypovolemia, hyperglycemia, hypocarbia

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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

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11
Q

What are common signs of bleeding in the germinal matrix?

A

Apnea, hypotension, decreased hematocrit, flaccidity, bulging fontanelles, tonic posturing

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12
Q

What are the possible presentations of IVH?

A
  • Asymptomatic
  • Saltatory Syndrome (gradual deterioration)
  • Catastrophic Deterioration (sudden change)
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13
Q

How can we assess IVH?

A

Alertness, cranial nerve function ( suck and swallow, vision, pupil response), motor function, generalized hypotonia

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14
Q

How can we prevent IVH?

A

Prolonging pregnancy if possible. Corticosteroids, antibiotics, delayed cord clamping

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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

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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

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17
Q

What is Bronchopulmonary Dysplasia?

A

A disorder of premature infants characterized by respiratory distress and impaired gas exchange.

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18
Q

What is the pathogenesis of BPD?

A

Chronically recurring lung injury, with ongoing repair and healing of the injury

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19
Q

What are some contributing factors of BPD?

A

PDA, fluid overload of VLBW infants, intrauterine nutritional deficiency, prematurity, inflammatory lung injury

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20
Q

What are the direct causes of BPD?

A

Oxygen toxicity (causes thickening of the alveolar membrane), barotrauma, volutrauma

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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

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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.

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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

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24
Q

How do we diagnose BPD?

A
  1. A chronic need for oxygen support
  2. Prolonged ventilatory support
  3. Chest radiographs
  4. Chronic changes in ABGs
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25
Q

What are some ways we can manage BPD?

A

Optimizing infant temperature from delivery to NICU, minimizing FiO2 to maintain safe oxygenation, and early optimization of ventilation

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26
Q

What is a major difference between neonatal and adult airways?

A

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

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27
Q

What kind of laryngoscope blade do we use on neonates and why?

A

A miller blade to directly displace the epiglottis because it is big and floppy

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28
Q

What are some indications for intubating a neonate?

A
  • 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)
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29
Q

What are some advantages and disadvantages of oral intubation?

A

Easier (no forceps required), better for VAP prevention. Baby cannot use pacifier

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30
Q

What are some advantages and disadvantages of nasal intubation?

A

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

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31
Q

Why do we use uncuffed tubes in neonates?

A

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

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32
Q

How do we calculate ETT depth for neonates?

A

Weight in kg + 6 = ETT depth (ex 2kg = 8cm). Can also use nare to tragus length

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33
Q

Why do we use atropine when intubating neonates?

A

They have significant vasovagal responses so this prevents HR from dropping too much

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34
Q

What is a good position for intubating neonates?

A

Ear canal aligned with sternum. Can be achieved by placing a shoulder roll.

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35
Q

How do we tell if we have successfully intubated?

A

Visualizing tube going through cords, colorimetric CO2 detector, auscultation, chest rise, CXR to confirm placement

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36
Q

What differences are there between nasal and oral intubation?

A

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

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37
Q

What is a neobar?

A

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.

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38
Q

What are the normal ventilating parameters for a neonate? (RR, Vt, compliance, resistance)

A

40-60, 3.5-6 mls/kg but start at 5!! , 5-6, 25-30

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39
Q

What are some indications for mechanical ventilation in newborns?

A

Apnea, ventilatory failure, increased work of breathing, increasing oxygen requirements

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40
Q

What PIP should we set for newborns?

A

About 20 cmH2O

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41
Q

What PEEP should we start at for intubated neonates?

A

5-6

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42
Q

What Ti should we start at for intubated neonates?

A

0.3 s and be careful to have adequate slope to reach Vt (0.05s)

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43
Q

What should our flow trigger sensitivity be set at for intubated neonates?

A

0.5-1.5 lpm

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44
Q

What should we set our E-sense at for an intubated neonate?

A

20-40%

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45
Q

Why do we have leak in intubated neonates and how do we fix it?

A

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

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46
Q

How do we set our vent alarms for neonates?

A

20% above and below, or whatever would make you concerned

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47
Q

What are the acceptable arterial PO2 values for premature and term infants?

A

<28 weeks: 45-64
28-40 weeks: 50-70
significantly lower values may be acceptable for infants with congenital heart defects

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48
Q

What are the acceptable arterial PCO2 values for neonates?

A

35-55 mmHg but may be highly variable with GA. Avoid <35 because of cerebral perfusion effects

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49
Q

What is a normal pH for a neonate?

A

7.3-7.4, but less in very fresh babies or premature (but still >7.25)

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50
Q

What is the normal SpO2 for a neonate?

A

Usually 88-92%

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51
Q

What is the normal SpO2 for a neonate with congenital heart defect?

A

70-80%

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52
Q

What is one of the first things we can do to fix oxygenation issues in an intubated neonate?

A

Suction

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53
Q

What can we do if an intubated neonate has low PCO2 but is not acidotic?

A

Decrease PIP and decrease respiratory rate

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54
Q

What can we do if an intubated neonate has low PO2 but is on high FiO2?

A

Increase PEEP, consider increasing PIP or Ti

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55
Q

Why do we extubate neonates quickly?

A

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

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56
Q

What is the general extubation procedure for neonates?

A
  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!!
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57
Q

What is the main indicator of meconium aspiration syndrome?

A

Meconium stained fluid

58
Q

Why is meconium passed in utero?

A

Baby is usually in distress

59
Q

What GA does meconium aspiration syndrome usually affect?

A

Term or post-term infants

60
Q

What might we see on the CXR of an infant with MAS?

A

Consolidation and haziness throughout

61
Q

What criteria must be met for a MAS diagnosis?

A

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
Q

What are some factors associated with increased risk of MAS?

A

Post-term pregnancy, preeclampsia, maternal htn, maternal diabetes, smoking, cardiovascular disease, fetal distress, oligohydramnios

63
Q

If meconium is sterile, why does aspiration cause issues?

A

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
Q

What are some complications that arise as a result of MAS?

A

Barotrauma, PIE, BPD, increased pulmonary vascular resistance, increased ICP, IVH

65
Q

What is the therapeutic range for high frequency jet ventilation?

A

240-420 BPM

66
Q

What is the tidal volume for HFJV?

A

1-2mls/kg

67
Q

How does a HFJV work?

A

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
Q

What is one advantage HFJV has over oscillation?

A

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
Q

How does HFJV flow through the lungs?

A

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
Q

What are some major differences between dconventional ventilators and jet ventilators? (parameters)

A

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
Q

What is servo?

A

The driving pressure required to regulate flow. Increased resistance and decreased compliance will generate lower servo pressure.

72
Q

What are some advantages to HFJV?

A

Gentler, able to bypass holes in the airway due to flow pattern, minimizes risk of volutrauma and barotrauma

73
Q

What are some indications for HFJV?

A

PIP >25, Vt <6mls/kg, airleak pathology, pulmonary hypoplasia, abdominal distension, ECMO being considered, extreme prematurity

74
Q

When we combine two ventilators (jet and conventional) which vent controls what?

A

Jet ventilator controls ventilation, conventional controls oxygenation

75
Q

How do we use servo pressure to evaluate our patient?

A

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
Q

How does jet ventilation affect our ability to suction?

A

Cannot be done conventionally, suction must be applied on the way down and up

77
Q

What are the most common causes of pneumonia in neonates?

A

Group B strep!!!, E coli, cytomegalovirus, chlamydia

78
Q

What is congenital pneumonia?

A

Associated with maternal bacterial or viral infections established during fetal life. Transplacental hematogenous. (herpes, varicella)

79
Q

What are some risk factors for congenital pneumonia?

A

Eating undercooked meat, exposure to cat feces, CMV infection, disseminated HSV, varicella

80
Q

What is early onset pneumonia?

A

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
Q

What is late onset pneumonia?

A

Occurs after the first week of life due to exposure to contaminated equipment, poor family/caregiver hand washing

82
Q

What are some risk factors for late onset pneumonia?

A

Mechanical ventilation, prematurity, LBW, prolonged NICU stay, poor infection control

83
Q

What causes PIE?

A

It is associated with lack of surfactant and is a problem for premature infants ( 23-32 weeks)

84
Q

When does PIE occur?

A

In the first 24 hours after birth

85
Q

What is PIE?

A

When air gets into the interstitial spaces surrounding the pulmonary vasculature

86
Q

What part of the airway does PIE typically originate from?

A

Terminal bronchioles because they have less structure so they are more likely to stretch and shear

87
Q

Describe the clinical manifestations of PIE?

A

Decreased lung compliance, tachypnea, retractions, barrel chest, worsening ABGs, cystic areas throughout lung parenchyma on CXR

88
Q

What are 3 complications that can arise from PIE?

A

Pneumothorax, pneumomediastinum, subcutaneous emphysema

89
Q

How do we manage PIE?

A

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
Q

How can we prevent PIE?

A

Early surfactant administration and antinatal steroids prior to delivery

91
Q

What is the difference in exhalation between HFJV and HFOV?

A

HFOV uses active exhalation while HFJV uses passive

92
Q

Describe Taylor Dispersion?

A

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
Q

Describe Penduluft

A

Gas from fast filling alveolar units will empty into the slower filling units.

94
Q

Why do we use HVOF?

A

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
Q

What are some indications for HFOV?

A

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
Q

Describe Asymmetrical Velocity Profile?

A

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
Q

What does “attenuation” mean in regards to HFO?

A

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
Q

What are some contraindications of HFO?

A

Cardiovascular instability (low BP), acute head injury (mindful if ICP), severe airflow obstruction (active exhalation may cause airway collapse)

99
Q

Which HFO parameters are important for ventilation?

A

Amplitude and Hz

100
Q

Which HFO parameters are important for Oxygenation?

A

MAP and FiO2

101
Q

Where do we want our wiggle factor to when ventilating with HFO and what is a good starting amplitude to get there?

A

Umbilicus, 30

102
Q

What is the difference between HFO and HFOVG?

A

HFOVG is volume guarantee and regulates the oscillatory volume (amplitude) which eliminates volume fluctuations from dynamic changes.

103
Q

How do we increase CO2 clearance in HFO?

A

By increasing the Hz

104
Q

How do we decrease CO2 clearance in HFO?

A

By decreasing the Hz

105
Q

Where is nitric oxide naturally found?

A

Within vascular endothelial cells of lungs and upper airway

106
Q

What are some indications for nitric oxide use?

A

Pulmonary hypertension, hypoxemia, ARDS, Right ventricular dysfunction, CHD, heart and lung transplants

107
Q

What is the mechanism of action for NO?

A

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
Q

Describe the pulmonary effects of inhaled NO.

A

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
Q

How does iNO affect endogenous NO production?

A

It inhibits it by inhibiting NO synthase

110
Q

What effects does NO have on coagulation?

A

It interferes with platelet and leukocyte function and limits platelet aggregation

111
Q

Describe the overall response in the body caused by iNO?

A

Decreases pulmonary artery pressure, decreases peripheral vascular resistance, increases V/Q matching, increases oxygenation

112
Q

What are some adverse effects of iNO?

A

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
Q

What are some alternatives to NO?

A

Nitroglycerin, nitroprusside, dobutrex, sildenafil, prostacyclin

114
Q

What is an esophageal fistula?

A

A condition where the esophagus ends into a pouch

115
Q

What is the most common type of esophageal fistula?

A

The upper part of the esophagus ends in a pouch and the lower part connects to the trachea

116
Q

What is a TE fistula typically associated with in utero?

A

Polyhydramnios

117
Q

What are some symptoms of a TE fistula?

A

Accumulation of secretions in the mouth, repeated regurgitation of feedings, respiratory distress especially during feedings, barking cough

118
Q

When is TE fistula typically diagnosed?

A

At the 20 week anatomy scan

119
Q

What is the treatment for a TE fistula?

A

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
Q

What is Robin Sequence?

A

Under developed jaw, obstruction of the upper airway due to the bulk of the tongue, cleft palate

121
Q

What is the treatment for Robin Sequence?

A

Maintaining patent airway until mandible grows (6-12 months); sometimes requires a trach. Prone position to relieve obstruction, surgical repair

122
Q

What is tracheomalacia?

A

A disorder of the trachea that causes it to be abnormally collapsible due to loss of structural integrity

123
Q

What are some symptoms of tracheomalacia?

A

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
Q

What is laryngomalacia?

A

Similar to tracheomalacia but affects larynx

125
Q

What causes larygomalacia?

A

Abnormal integration of laryngeal nerves

126
Q

What are some symptoms of larygomalacia?

A

Similar to tracheomalacia but will hear inspiratory stridor rather than biphasic noises

127
Q

How do we diagnose laryngomalacia?

A

With flexible fiberoptic laryngoscopy and sometimes polysomnogram when associated with OSA

128
Q

What is choanal atresia?

A

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
Q

What are some symptoms of choanal atresia?

A

Immediate respiratory distress, issues latching and feeding, improvement with crying

130
Q

How is choanal atresia treated?

A

OPA in the form of a soother with a hole (called a McGovern nipple), surgical removal of the membranes covering the choanae

131
Q

Describe what a vascular ring is.

A

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
Q

What kind of shunt does PDA cause?

A

Left to right

133
Q

How does prematurity affect a PDA?

A

The more premature the infant the greater the delay in closure of the PDA.

134
Q

Where do we place the pulse ox on a patient suspected to have PDA?

A

One on right hand (preductal), one on left foot (post ductal). Results in a differeint of sats of 5-10%

135
Q

What are the clinical manifestations of PDA?

A

CXR shows increased vascular markings if CHF develops, Echocardiology determines presence of PDA

136
Q

What is PGE1 and what is it used for?

A

Alprostadil and it is a vasodilator. Given as a constant infusion for PDA to relax vascular smooth muscle

137
Q

Why does PGE1 cause apneas?

A

May be related to the same pathways of the inflammatory release of PGE2 and interleukins that cause apneas with sepsis

138
Q

What is transposition of the great arteries?

A

When the aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle

139
Q

Describe transposition of the great arteries

A

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
Q

What is the treatment for transposition of the great vessels?

A

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

2305 Neonatal Resuscitation (15 decks)

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