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MCN568 > RESPIRATORY > Flashcards

RESPIRATORY Flashcards

Fanaroff 11th; chapters 62,63,64,65,66,67,68,69,70,38,37

1
Q

most effective treatment for RDS in neonatology

A

antenatal corticosteroids and postnatal surfactant

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2
Q

lung structural development “stages”

A

embryonic, pseudoglandular, canalicular, saccular and alveolar;

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3
Q

embryonic period

A

lobar airway 37 days
segmental airway 42 days
subsegmental bronchi 48 days
mesenchyme

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4
Q

pseudoglandular stage

A

5-18 weeks; airway branching is complete;

cuboidal cells filled with glycogen; major components of lungs are completed

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5
Q

in what stage airway, arteries and veins have developed?

A

18 weeks, pseudoglandular stage

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6
Q

canalicular stage

A

16-25 weeks; transformation of the previable lung to the potentially viable lung that can exchange gas
3 major events:
-appearance of acinus(berry-like clustering oof cells at the distal ends of respiratory brioncholes)
-epithelial differentiation (development of the air-blood barrier)
-start of the surfactant synthesis (recognizable type II cells)

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7
Q

what is the first critical step for the development of the future gas exchange surface?

A

saccular branching (acinus: 6 branching generations of respiratory brioncholes, alveolar ducts, and alveoli)

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8
Q

saccular stage

A

24 weeks to term; terminal sac is developing respiratory bronchiole (alveolar duct) to about 32 weeks(initiation of alveolarization)
type I pneumocytes: modulate gas exchange
type II pneumocytes: synthesis and secretion of surfactant

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9
Q

when is the most rapid rate of accumulation of the alveoli?

A

32 weeks till first months after delivery

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10
Q

factors that delay/interfere with alveolarization?

A 
mechanical ventilation
antenatal and postnatal glucocorticoids
pro-inflammatory mediators
chorioamninitis
hyperoxia or hypoxia
poor nutrition
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11
Q

factors that stimulate alveolarization?

A

vit A(retinoids) and thyroxin

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12
Q

stages of branching

A

airway branching, saccular branching, alveolarization

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13
Q

number of distal structures

A

24 weeks: 65000

adult: 500 million

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14
Q

fetal lung fluid

A

high chloride; bicarb and protein low;

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15
Q

what can completely stop fetal lung fluid production?

A

epinephrine IV

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16
Q

delay clearance of fetal lung fluid can cause what?

A

transient respiratory difficulties

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17
Q

what causes secondary pulmonary hypoplasia?

A

restricted lung growth (mass, effusion, external compression)
renal agenesis (potter syndrome) and prolonged oligohydramnios
congenital diaphragmatic hernia
absence of fetal breathing

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18
Q

pulmonary sequestrations

A

portion of the lungs that are in isolation from neighboring lung tissue and with no communication th the bronchial tree

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19
Q

alveolar macrophages

A

immune cells; functions: immune surveillance, phagocytosis, antigen presentation, interaction with adaptive immune cells, surfactant homeostasis; fetus normally do NOT have macrophages; they populate in lungs with an onset of breathing; *chorioamnionitis can mature and stimulate macrophages prior the delivery

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20
Q

surfactant composition

A

70-80% phospholipids (60% are saturated) , 8% protein, 10% neutral lipids

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21
Q

what is measured for fetal lung maturity?

A

AF Phosphatidylglyceroid

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22
Q

4 proteins in surfactant

A

SP-A (innate host defense protein); not used for RDS
SP-B (surface absorption of lipids and low surface tension on surface area compression); lack of SP-B lethal respiratory failure
SP-C only in type II cells; similar to SP-B
SP-D similar to SP-A; used in surfactant for ventilator mediated inflammation

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23
Q

surfactant synthesis and secretion

A

type II cells;

synthesis: ?
secretion: stimulated by adenosine triphosphate mechanical stretch (distention or hyperinflation)

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24
Q

what is primary cause of RDS?

A

surfactant deficiency

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25
Q

surfactant pool sizes

A

long delay between synthesis and secretion balanced by slow catabolism and clearance: this is favorable for surfactant treatment strategies

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26
Q

alveolar life cycle of surfactant

A

lamellar bodies “unravel” tubular myelin …?

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27
Q

physiologic effects of surfactant in the preterm lung

A 
alveolar stability (prevent from collapsing, and keep interstitial fluid from entering the alveolus, normalize size)
pressure-volume curves (increases maximal volume at max pressure, increase in lung volume increase gas exchange, stabilization of the lung on deflation
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28
Q

Lung maturation

A

surfactant appearance, induced lung maturation, glucocorticoids, intrauterine infections
defined by lack of RDS generally, present after 35 weeks of normal gestation

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29
Q

surfactant appearance test

A

L/S ration lecithin to sphingomyelin

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30
Q

fetal stress, fetal growth restriction or preeclampsia induce lung maturation

A

FALSE

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31
Q

fetal exposure to inflammation may have short time benefits of decreasing RDS

A

TRUE

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32
Q

corticosteroids and lung maturation

A

induce lung maturation by increasing the surface area for gas exchange; decrease pulmonary edema; induce surfactant synthesis; improve response to postnatal surfactant;

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33
Q

other use of maternal corticosteroids

A

PDA, IVH, NEC, increase kidney function and postnatal BP

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34
Q

clinical observations

A

respiratory rate, retractions, nasal flaring, grunting, cyanosis

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35
Q

work of breathing components

A

elastic and resistive

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36
Q

elastic component

A

work required to stretch the lungs and chest wall during a tidal inspiration

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37
Q

resistive component

A

work required to overcome friction caused by lung tissue movement and gas flow through the airways

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38
Q

respiratory rate

A

TV 6-7ml/kg; 40-60 bpm

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39
Q

retractions

A

substernal, subcostal, intercostal; caused by negative intrapleural pressure generated by the contraction of the diaphragm and other respiratory muscles and the mechanical properties of the lung and chest wall
suggest low lung compliance, obstruction or atelectatis

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40
Q

what increases retractions?

A

RDS (lung stiffness); airway obstruction, misplacement of ETT, pneumothorax, atelectasis

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41
Q

grunting definition

A

neonates attempt to close (adduct) their vocal cords during the initial phase of expiration, holding gas in the lungs and producing an elevated transpulmonary pressure in the absence of airflow. The elevated pressure and corresponding increased lung volume result in the enhancement of the ventilation-perfusion ratio (V̇/Q̇). During the last part of the expiratory phase, gas is expelled from the lungs against partially closed vocal cords, causing an audible grunt
compensatory mechanism to maintain FRC and maximize pO2 (partial pressure of oxygen)

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42
Q

central cyanosis

A

check tounge and oral mucosa; desaturated hemoglobin

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43
Q

assessing pulmonary function

A

pulse oximetry and blood gas

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44
Q

pressure of alveolar oxygen

A

PaO2

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45
Q

optimal gas exchange

A

appropriate matching of the alveolar gas with the mixed venous blood

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46
Q

mixed venous blood composition and volume include what?

A

arterial blood gas content, cardiac output, oxygen consumption, and carbon dioxide production

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47
Q

what does the quantity of oxygen bound to hemoglobin depends on?

A

PaO2 and oxygen dissociation curve

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48
Q

arterial oxygen content

A

CaO2; sum of hemoglobin bound and dissolved oxygen

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49
Q

indexes used to estimate the degree of oxygen derangement

A
  1. arterial-alveolar oxygen tension ratio
  2. alveolar-arterial oxygen tension gradient mmHg
  3. oxygen ration mmHg
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50
Q

oxygenation index

A

OI

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51
Q

pulse oximetry

A

measures the amount of hemoglobin molecules that is bound with oxygen

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52
Q

ideal oxygen saturation

A

currently UNKNOWN; AAP guideline recommendation 90-95%

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53
Q

hyperoxia test

A

differentiate between primary lung disease and congenital heart disease with right-to-left shunting

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54
Q

hyperoxia-hyperventilation test

A

distinguish between structural congenital heart disease and PPHN (both have right to left shunting)

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55
Q

preductal

A

right hand

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56
Q

postductal

A

left hand/ or any foot

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57
Q

respiratory physiologic measurements

A

airflow (pneumotachometer), lung volume, pressure

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58
Q

functional residual capacity FRC

A

the volume of gas in the lungs that is in direct communication with the airways at the end of expiration; oxygen storage compartment; volume of gas left in the lung after a normal expiration

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59
Q

thoracic gas volume

A

total volume of gas in the thorax at the end of expiration

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60
Q

tidal volume

A

volume of gas in and out of the lungs in a single breath

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61
Q

pressure

A

transpulmonary vs transrespiratory

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62
Q

respiratory mechanics

A

compliance, resistance, time constant, forced expiratory maneuvers, forced oscillation technique, work of breathing

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63
Q

lung compliance

A

measure of elasticity; reciprocal: elestance

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64
Q

resistance

A

measure of the friction encountered by gas flowing through the nasopharynx, trachea, and bronchi and by tissue moving against tissue. reciprocal: conductance

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65
Q

equation of motion

A

relationship between pressure, flow, volume, and the elastic, resistive, and inertial components of the respiratory system

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66
Q

time constant

A

duration (expressed in seconds) necessary for a step (e.g., pressure or volume) change to partially equilibrate throughout the lungs; resistance * compliance

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67
Q

work of breathing

A

a measure of the energy expended in inflating the lungs and moving the chest wall

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68
Q

goal of respiratory support

A

optimize oxygenation and CO2 elimination with the lowest possible ventilator settings to minimize lung injury

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69
Q

RDS pathologic diagnosis

A

surfactant deficiency; risk factors: GA and low BW; predominant factors: elective deliveries, maternal DM and perinatal hypoxia-ischemia; white boys ;)

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70
Q

RDS pathophysiology

A

diffuse atelectasis; impaired or delay surfactant synthesis and secretion

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71
Q

is RDS genetic?

A

too rare to determine

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72
Q

RDS radiographic findings

A

diffuse reticulogranular pattern, giving the classic ground-glass appearance in both lung fields with superimposed air bronchograms

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73
Q

RDS clinical presentation

A

grunting, retractions, nasal flaring, cyanosis, increased oxygen requirement

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74
Q

RDS RX

A

positive pressure ventilation, surfactant therapy, inhaled NO, assessment of blood gas(pulse oximetry, noninvasive carbone dioxide monitoring-capnography; arterial sampling), acid-base therapy, CV management, ABX

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75
Q

positive pressure ventilation

A

invasive: via an endotracheal tube utilize a time-cycled, pressure-limited mode, or volume-controlled mode with synchronized ventilated breaths; jet, oscillator, and conventional
noninvasive: CPAP, Noninvasive positive-pressure ventilation (NIPPV) increases tidal and minute volumes, improves lung recruitment, decreases work of breathing, may reduce apnea of prematurity, and may reduce the need for mechanical ventilation

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76
Q

benefits of CPAP

A

maintenance of a constant airway opening pressure, establishment, and maintenance of functional residual capacity, reduction of pharyngeal or laryngeal obstruction, improvement of oxygenation, and release of surfactant stores
reduces barotrauma, volutrauma, airway damage, and risk of secondary infections, and enhances mucociliary transport.

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77
Q

surfactant therapy

A

4 types approved for use in the US; bovine, porcine and synthetic mix of SP-B and SP-C protein; no proven adverse effects; INSURE technique (INtubate, SURfactant, Extubate)

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78
Q

inhaled Nitric Oxide therapy (iNO)

A

for preterm infants at risk for developing BPD or in RDS that is complicated by pulmonary hypertension

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79
Q

pulse oximetry

A

Continuous noninvasive measurement of arterial hemoglobin oxygen saturation

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80
Q

UAC placement

A

high T6-T8 (above aortic bifurcation); low L3-L4

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81
Q

complication of UAC

A

blanching or cyanosis of part or all of a distal extremity or the buttock area, resulting either from vasospasm or a thrombotic or embolic incident
use heparin to avoid thrombi
flushing can cause retrograde blood flow and transient elevated BP
increase in bloodstream infection (ideal not more than 3 days)
Allen test for radial artery line to establish the presence of adequate collateral circulation to the fingers

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82
Q

acid-base therapy

A

use of sodium bicarbonate has adverse effects and not recommended

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83
Q

CV management of the RDS

A

decreased perfusion can be caused by lactic acidemia or metabolic acidosis (monitor BP via A-line), use of pressors and monitor cortisol levels
PDA complications

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84
Q

what can happen after surfactant administration to the CV system

A

unrecognized overdistension of the lungs by excessive mechanical ventilation support can decrease systemic venous return to the heart and result in a decrease in cardiac output. Xray will show: squeezed-heart silhouette and flattened diaphragm are found,
vital signs, peripheral pulses, capillary refill, and urine output as surrogate markers of adequate cardiac output.

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85
Q

ABX in RDS

A

pneumonia indistinguishable from RDS on x-ray

Penicillin combined with an aminoglycoside is recommended for 48h until blood culture results are back

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86
Q

what is the major contributor to long injury?

A

mechanical ventilation

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87
Q

noninvasive respiratory support modalities

A

single level pressure support: CPAP, HFNC
bilevel: BiPAP, SiPAP
nasal NIPPV

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88
Q

CPAP in RDS

A

prevent collapse of alveoli at end-expiration, maintaining some degree of alveolar inflation; helps maintain functional residual capacity and to facilitate gas exchange; useful in treating apnea of prematurity

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89
Q

CDP continous distending pressure

A

can be provided by CPAP and PEEP

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90
Q

clinical indications of CPAP

A 
delivery room resuscitation
RDS
post-extubation support
apnea
mild upper airway obstruction
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91
Q

types of CPAP

A

flow driven
bubble CPAP
ventilator-derived CPAP

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92
Q

HFNC

A

1-8 L/min; issues with sizing and leaks(no baseline pressure); use: after birth, post-extubation, apnea

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93
Q

noninvasive nasal ventilation

A

PEEP, PIP, RR, inspiratory time can be manipulated

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94
Q

CPAP complications

A 
nasal trauma
lung overinflation
increase or air leaks
can increase intrathoracic pressure and decrease venous return and cardiac output
to high cause carbone dioxide retention
gastric distention (OG)
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95
Q

indication for assisted ventilation

A

absolute:
failure to initiate or sustain spontaneous breathing
persistent bradycardia
major airway or pulmonary malformations (diaphragmatic hernia, severe hydrops
sudden respiratory or cardiac collapse with As and Bs (not responding to mask ventilation or pulmonary hemorhage)
Relative: “50-50 rule”
likelihood of subsequent respiratory failure
surfactant administration
impaired gas exchange
worsening As
need to maintain airway patency
need to control carbon dioxide elimination
medication-induced respiratory depression (magnesium, anesthetics, analgesics)
sepsis, MAS, PPHN

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96
Q

General Principles of Assisted Ventilation

A

oxygenation
ventilation
time constant

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97
Q

PEEP/ positive end expiration pressure

A

baseline pressure, the lowest level to which airway pressure falls; PEEP increases mean airway pressure (mean Paw)

98
Q

PIP/ peak inspiratory pressure

A

driving pressure, increases mean Paw; establishes the upper limit of the amplitude

99
Q

determinants of oxygenation in Assisted Ventilation

A 
fraction of inspired oxygen
mean airway pressure
PEEP
PIP
inspiratory time
frequency
gas flow rate
100
Q

determinants of ventilation in Assisted Ventilation

A 
tidal volume
amplitude PIP-PEEP
frequency
minute volume: conventional (freq*TV) high-freq (freq*TV square)
expiratory time (I:E ratio)
101
Q

ventilation

A

carbon dioxide removal; tidal volume (TV) and frequency

102
Q

tidal volume TV

A

amplitude of mechanical breath: the difference between PIP and PEEP

103
Q

amplitude too high, newborn will do what?

A

infant’s hypercapnic drive will be abolished, and the baby will “ride” the ventilator rate

104
Q

amplitude too low, newborn will do what?

A

baby will compensate by increasing the spontaneous breathing rate

105
Q

time constant

A

the time required to allow pressure and volume equilibration in the lungs; product of compliance and resistance

106
Q

conventional mechanical ventilator vs high frequency

A

CMV delivers physiological tidal volumes HFV delivers TV that is less than physiologic dead space

107
Q

CMV types

A 
ventilatory modalities (control the type of ventilation)
ventilatory modes (determine the breath type)
108
Q

control variables (ventilatory modalities)

A

time, pressure, volume, only one can be controlled

109
Q

phase variables (ventilatory modes)

A

trigger, limit, cycle, PEEP

110
Q

modes of ventilation

A

intermittent mandatory ventilation IMV: set rate, supported by PEEP
synchronized intermittent mandatory ventilation SIMV, supported by PEEP
assist/control A/C set minimal breath rate
pressure support ventilation PSV

111
Q

starting TV reference

A

4-6ml/kg preterm; 5-8ml/kg term

112
Q

starting PEEP reference

A

4-6 cm h2o

113
Q

when infant is ready to wean?

A

improved gas exchange and pulmonary mechanics, more spontaneous breathing

114
Q

what is most common reason for failure to wean

A

failure to wean

115
Q

what is the best way to wean

A

change one parameter at the time (does NOT apply to HFOV), reduce the most harmful one first

116
Q

what is the best predictive value of positive extubation

A

attention to spontaneous breathing

117
Q

High Frequency Ventilation HFV

A

delivered gas volumes are less than the anatomic dead space and are provided to a patient at a very rapid rate; carbon monoxide is a product of frequency, set amplitude lower than CMV, shorter inspiratory time (less barotrauma); higher PEEP than CMV; does NOT mimic spontaneous breaths; airway resistance (not long compliance) is the major determinant of gas distribution
JET
OSCILLATOR

118
Q

JET in what conditions?

A

active inspiration, passive exhalation; 360-450bpm

“air leaks”, pulmonary interstitial emphysema, E/T artesia or fistulas

119
Q

HFOV in what conditions?

A

active inspiration, active exhalation; 8-15Hz (480-900bmp); best to deliver iNO;

120
Q

monitoring ventilated infants

A
  1. clinical evaluation
  2. assessment of gas exchange
  3. chest imagining
  4. pulmonary functions and mechanics testing
  5. extrapulmonary monitoring (ECHO)
121
Q

oxygenation depends on what?

A

ventilation-perfusion matching

122
Q

movement of CO2 depends on what?

A

alveolar ventilation

123
Q

base deficit

A

product of metabolic acidosis; 3-5mEq/L health infant; 5-10 should be ok

124
Q

complications od assisted ventilation

A

airway:
UPPER: trauma, abnormal dentition, esophageal perforation, nasal septal injury, acquired palatal groove
TRACHEA: mucosal metaplasma, subglottic cysts, tracheal enlargement, vocal cord paralysis, subglottis stenosis, necrotizing tracheobronchitis
LUNGS: VAP, air leaks, ventilator-induced lung injury, BPD

125
Q

air leaks examples

A

pneumomediastinum (nitrogen washout?)
pneumothorax
pulmonary interstitial emphysema (PIE)
pneumopericardium (air from pleural space or mediastinum enters pericardial sac)
pneumoperitoneum (rupture or perforation of abdominal viscus

126
Q

pneumothorax ventilator causes?

A

high inspiratory pressure and unevenly distributed ventilation
certain diseases: MAS, CF, pulmonary hypoplasia
clinical S&S:
ASYMPTOMATIC: none, just xray
Deterioration in labs or bedside monitoring findings
Acute clinical deterioration

127
Q

tension pneumotorax clinical evaluation

A

agitation and worsening respiratory distress
diminished or absent breath sound sounds on affected side
contralateral shift of heart sounds at the PMI
mixed acidosis and hypoxemia on CBG
transillumination: increased light on involved side

128
Q

tension pneumothorax RX

A

thoracentesis (needle aspiration)

thoracostomy (chest tube)

129
Q

PIE pulmonary interstitial emphysema

A

most compliant portion of the terminal airway ruptures, gas leaks into interstitial space
xray: fine linear or radial radiolucencies

130
Q

pneumopericardium/cardiac tamponade

A

air completely encircling the heart

131
Q

pulmonary injury sequence in VILI

A

barotrauma (too much pressure)
volutrauma ( too much gas, overdistention)
atelectrauma (repetitive opening and closing of lung units)
biotrauma (infection, inflammation, stress)
rheotrauma (inappropriate flow)

132
Q

Bronchopulmonary Dysplasia BPD

A

chronic respiratory insufficiency
supplemental oxygen requirements
abnormal xray at 36 weeks GA
caused by: excessive TV

133
Q

right to left shunting

A

high pulmonary resistance (early RDS, MAS)

134
Q

left to right shunting

A

high systemic vascular resistance

135
Q

nonpulmonary etiologies of respiratory distress

A

thermal instability, circulatory problems, cardiac diseases, neuromuscular diseases, sepsis, anemia, polycythemia, methemoglobinemia

136
Q

agenesis

A

total absence of pulmonary parenchyma, supporting vasculature and bronchi; antenatal US: mediastinal shift without diaphragmatic hernia

137
Q

pulmonary hypoplasia

A

result of deficient or incomplete development of the lung parenchyma leading to decreased number of distal airways, alveoli, and associated pulmonary vessels
primary
secondary: oligohydramnios (renal malformation, prolonged AF leak, placental abnormalities, IUGR
space-occupying lesion (hernia)
cystic lung disease
cardiac malformations (cardiomegaly)
absence ob abnormal diaphragmatic activity

138
Q

congenital diaphragmatic hernia

A

(CDH) results from a developmental defect during the formation of the diaphragm that permits abdominal contents to herniate into the thoracic cavity

139
Q

CDH types

A 
posterolateral (Bochdalek) most common
anterior (Morgagni)
central
1 in 2000-3000 live births
more common on L side
140
Q

CDH clinical presentation

A

severy respiratory distress, cyanosis, scaphoid abdomen, absence of breath sounds
xray: bowel loops in chest cavity, OG tube in thorax

141
Q

CDH management

A

ECMO criteria
gentle ventilation and permissive hypercapnia HFOV, low PIP
preductal sat above 85%, postductal dont matter
CO2 less or equal to 65, pH at least 7.25
dont use iNO
delay surgical therapy until stable and improvement of PPHN

142
Q

CDH long term complications

A

pulmonary
GERD
hypoxemia: developmental delay
scoliosis

143
Q

Alveolar Capillary Dysplasia

A

fatal; hypoxemia and PPHN not responding to treatment in first 48 hours

144
Q

congenital pulmonary lymphangiectasia

A

CPL, dilation of lymphatic vessels in multiple areas of the lungs
intractable respiratory failure, cyanosis, and hypoxia associated with bilateral chylothoraces in the first few hours of life
nonimmune hydrops
xray: hyperinflation of the lung with bilateral interstitial infiltrates and bilateral pleural effusions
DX: lung biopsy: increased fibrous tissue with dilation of cystic lymphatic spaces and collapsed alveoli
poor prognosis if symptomatic early

145
Q

chylothorax

A

accumulation of lymphatic fluid (chyle) in the pleural cavity
xray: pleural effusion, compression of the lung on the affected side, and displacement of the heart to the opposite side
DX: analysis of pleural fluid
RX: supportive, spontaneous resolution within 4-6 weeks

146
Q

Congenital Cystic Pulmonary Malformations

A

congenital pulmonary airway malformations
bronchopulmonary sequestration
bronchogenic cyst
congenital lobar emphysema

147
Q

congenital pulmonary airway malformations

A

(CPAM) constitutes multiple different hamartomatous lesions arising from the abnormal branching of the immature bronchial tree
4 types

148
Q

bronchopulmonary sequestration

A 
(BPSs) are microscopic cystic masses of nonfunctioning lung tissue thought to arise from the primitive foregut. Usually not connected to the main airway, and their blood supply arises from the systemic circulation intralobar sequestration (ILS)
extralobar sequestration (ELS)
149
Q

bronchogenic cyst

A

single cyst lined by respiratory epithelium and covered with elements of the tracheobronchial tree, including cartilage and smooth muscle
treatment: complete surgical excision

150
Q

congenital lobar emphysema

A

postnatal overdistension of one or more segments or lobes of the lung

151
Q

Pulmonary Arteriovenous Malformation

A

malformations are direct communications between the smaller pulmonary arteries and veins, allowing blood to bypass the capillary system

152
Q

meconium

A

comprised of desquamated fetal intestinal cells, bile acids, minerals, and enzymes, including alpha1 antitrypsin and phospholipase A2, as well as swallowed amniotic fluid, lanugo, skin cells, and vernix caseosa

153
Q

MAS mechanisms

A

complete or partial obstruction of airways, inflammation, complement activation and cytokine production, inhibition of surfactant synthesis and function, apoptosis of epithelial cells, and increased pulmonary vascular resistance

154
Q

typical MAS infant

A

postmaturity, with evidence of weight loss; cracked, peeling skin; and long nails, together with heavy staining of nails, skin, and umbilical cord with a yellowish pigment
barrel chest
rales
xray: coarse, irregular pulmonary densities with areas of diminished aeration or consolidation

155
Q

MAS suctioning

A

amnioinfusion: not recommended
intrapartum: not recommended
routine intubation and suctioning: not recommended

156
Q

MAS NICU

A 
supportive respiratory and CV care
ABX
HFOV
surfactant lavage
complicated by PPHN, iNO should be considered
157
Q

neonatal pneumonia

A

early: 3-7 days, aspiration of infected amniotic fluid, ruptures membranes, birth canal bacteria; Group B Streptococcus (GBS), herpes simplex and other TORCH, candidal infections
late: VAP, hospital-acquired; viral can take longer to develop because of the virus incubation period

xray: nonspecific, but persist for weeks

158
Q

neonatal pneumonia RX

A

broad spectrum ABX till culture comes back

early: amp and gent
late: vanco and gent or nafcillin and gent

159
Q

Transient Tachypnea of the Newborn

A

TTN from pulmonary edema secondary to inadequate or delayed clearance of fetal alveolar fluid
48-72 hours
risk factors: premature or elective cesarean delivery without labor, large birth weight, maternal diabetes, maternal asthma, twin pregnancy, and male gender
transient nature of this disease
no specific RX
wheezing syndrome early in life

160
Q

pulmonary hemorrhage

A

defined as a gush of blood through an endotracheal tube in intubated neonates associated with a worsening clinical picture, requiring increased ventilatory support and blood product transfusion
before 72 hours of life, median 40 hours
risk factors:extreme prematurity, surfactant administration, patent ductus arteriosus (PDA) with left-to-right shunting, multiple birth, and male gender

161
Q

pulmonary hemorrhage patho

A

pathophysiology of pulmonary hemorrhage is believed to be secondary to a sudden decrease in pulmonary vascular resistance, causing increased left-to-right shunting and pulmonary vascular engorgement, pulmonary edema, and ultimately, rupture of pulmonary capillaries

162
Q

pulmonary hemorrhage treatment

A 
increase in PEEP (stops bleeding)
avoid suctioning
epinephrine: not sure
blood products
exogenous surfactant administration
prophylactic indomethacin
163
Q

Pulmonary Air Leak Syndromes

A 
pneumothorax
pneumomediastinum
pulmonary interstitial emphysema
pneumopericardium
pneumoperitoneum
subcutaneous emphysema
164
Q

rib cage abnormalities

A 
asphyxiating thoracic dystrophy (Jeune syndrome)
thanatophoric dysplasia
achondrogenesis
homozygous achondroplasia
osteogenesis imperfecta (severe form)
Ellis-van Creveld syndrome (chondroectodermal dysplasia)
hypophosphatasia
spondylothoracic dysplasia
rib-gap syndrome
165
Q

Phrenic Nerve Injury

A

Phrenic nerve injury with paralysis of the diaphragm is an unusual cause of respiratory distress
C3 to C5

166
Q

breathing activity fetus

A

11 weeks

167
Q

neonatal respiratory activity

A

irregular with spontaneous changes alternating between eupnea, apnea, periodic breathing, and tachypnea

168
Q

laryngeal chemoreflex

A

reflex-induced apnea

response to instilling saline in the oropharynx

169
Q

Hering-Breuer reflex

A

Stimulation of pulmonary stretch receptors through increasing lung volume causes shortening of inspiratory time, prolongation of expiratory time, or both
prevents long overdistention on CPAP

170
Q

breathing neurotransmitters

A

adenosine, GABA, prostaglandins, endorphins, and serotonin(SIDS)

171
Q

apnea

A

the cessation of breathing for greater than 15-20 seconds. Shorter events (<15 seconds) may also be identified as apnea if accompanied by oxygen desaturation and bradycardia

172
Q

apnea types

A

central, obstructive, mixed

173
Q

ABD definition

A

defined as >10 seconds if accompanied by bradycardia (HR <100 beats/minute) and desaturation (SpO2 <80%)

174
Q

apnea clinical association

A

sepsis
intracranial hemorrhage, hypoxic-ischemic encephalopathy, and brain malformations
NEC
RSV
anemia
hypoglycemia, hypocalcemia and electrolyte imbalances, temperature instability, and metabolic acidosis
opiates, benzodiazepines, magnesium sulfate, and prostaglandin

175
Q

ALTE vs BRUE

A

apparent life-threatening event(old definition) vs Brief Resolved Unexplained Events(new terminology)

176
Q

apnea treatment

A

HFNC
Methylxanthines: aminophylline
theophylline and caffeine
Xanthine

177
Q

nasal and nasopharyngeal lesions

A 
Pyriform Aperture Stenosis
Nasolacrimal Duct Cysts
Choanal Atresia
Congenital Nasal Masses
Nasopharyngeal Teratoma
Mucosal Obstruction
Continuous Positive Airway Pressure Trauma
178
Q

Oral and Oropharyngeal Lesions

A

micrognathia, glossoptosis, and posterior tongue displacement and subsequent airway obstruction
Pierre Robin sequence, Treacher Collins syndrome, Goldenhar syndrome, Crouzon disease, Down syndrome
Lymphatic Malformations
Oral Cavity Cysts

179
Q

Laryngeal Lesions

A 
Laryngomalacia (stridor)
Bifid or Absent Epiglottis
Laryngeal Cysts
Vocal Cord Paralysis
Laryngeal Web
Congenital Subglottic Stenosis
Subglottic Hemangioma
Laryngeal Cleft
Congenital high airway obstruction syndrome (CHAOS)
Intubation Trauma
180
Q

Bronchopulmonary dysplasia

A

the most important respiratory complication of preterm birth, and it is associated with long-term respiratory morbidities

181
Q

NIH BPD definition

A

severity-based definition of BPD into three categories based on the duration and level of oxygen therapy required:
mild
moderate
severe

182
Q

BPD pathogenesis

A

injury to developing lung secondary to prolonged mechanical ventilation with high airway pressures and inspired oxygen concentration

183
Q

BPD pathogenic factors

A

prematurity
pre- and postnatal infections
mechanical trauma from positive pressure ventilation
oxygen toxicity
pulmonary edema secondary to increased pulmonary blood flow from patent ductus arteriosus (PDA) acts on the immature alveolar and vascular structure of the immature lung

184
Q

BPD pulmonary functions

A

low compliance, low to normal functional residual capacity (FRC), and high airway resistance
fibrosis, edema, overdistention, and collapse of lung parenchyma
increased work of breathing that contributes to the hypoventilation and hypercapnia
minute ventilation increased
CO2 retention
hypoxemia and require supplemental oxygen to maintain acceptable oxygenation levels

185
Q

does surfactant reduce BPD

A

no

186
Q

what can reduce BPD?

A

steroids NO
less invasive ventilation MAYBE/individualized
volume-targeted ventilation
targets in oxygen saturation (low YES, but cause NEC)
postnatal systemic corticosteroids YES, has side effects
inhaled steroide YES, but side effects
caffeine YES
vit. A YES
iNO ?

187
Q

postnatal systemic corticosteroids

A

decrease bronchospasm

188
Q

management of established BPD

A 
respiratory support
bronchodilator therapy
corticosteroids therapy
management of pulmonary hypertension
fluid management
nutrition
infection prevention
189
Q

ECMO

A

Extracorporeal membrane oxygenation

190
Q

ECMO definition

A

cardiopulmonary bypass support for term and late preterm infants with severe, life threatening, hypoxic respiratory failure. Affected infants present within the first 2 weeks of life, and the majority of these also have persistent pulmonary hypertension of the neonate

allowing the lung to rest and recover until pulmonary arterial pressures decline and blood flow to the lung is restored

191
Q

iNO inhaled Nitric Oxide

A

a noninvasive inhalational therapy that can elicit selective pulmonary vasodilation

192
Q

PPHN persistent pulmonary hypertension of the neonate

A

pulmonary vascular resistance approaches or exceeds systemic vascular resistance, offering significant impedance to pulmonary blood flow

193
Q

PPHN desaturated blood

A

Desaturated blood returning to the right heart is shunted to the systemic circulation (following the path of least resistance) across one or both persistent fetal channels, the patent ductus arteriosus (PDA) and the foramen ovale, resulting in marked cyanosis

194
Q

what diagnosis will benefit from surfactant?

A

MAS, RDS, or pneumonia

195
Q

what diagnosis will NOT benefit from surfactant?

A

CDH and HRF, nor in infants with isolated PPHN

196
Q

ECMO types

A

venoarterial (VA) bypass

venovenous (VV) bypass

197
Q

oxygenation on ECMO

A

varying blood flow through the ECMO circuit. The higher the volume of cardiac output diverted through the membrane lung, the better the oxygen delivery from the ECMO circuit

198
Q

blood flow in ECMO

A

80-100ml/kg; weaning at 10-20ml/kg
no pressors and vasodilators needed
mild sedation

199
Q

ECMO anticoagulation

A

Systemic anticoagulation therapy with unfractionated heparin: Activated clotting times (ACTs), antifactor Xa assays or Thromboelastography (TEG)
Bivalrudin if heparin can NOT be used because of HIT

200
Q

ECMO ventilator support

A

“lung rest” on CMV rate 10; PEEP(use higher), PIP

maintain FRC and to allow for continued pulmonary toilet

201
Q

advantage of VV ECMO

A

avoidance of carotid artery cannulation, bot NO cardiac support provided to the infant

202
Q

ECMO criteria

A

Gestational age of 34 weeks or older
Normal cranial ultrasound or stable grade I or II intraventricular hemorrhage
Absence of complex congenital heart disease
Less than 10-14 days of mechanical ventilation
Reversible lung disease, including congenital diaphragmatic hernia
Failure of maximum medical therapy
No lethal congenital anomalies or evidence of irreversible brain damage

203
Q

ECMO oxygenation criteria

A 
Oxygenation Index (OI): OI = (MAP × FiO2 × 100)/PaO2
The usual criterion is OI of 35-60 for 0.5-6 hours.

Alveolar-Arterial Oxygen (Aado2) Gradient (at Sea Level)
AaDO2 = FiO2 (P − 47) − PaO2 − PaCO2 (FiO2 + (1 − FiO2)/R)
Usual criterion is AaDO2 > 605-620 mm Hg for 4-12 hours.

Partial Pressure of Arterial Oxygen
Usual criterion is PaO2 < 60 mm Hg for 2-12 hours.

Acidosis and Shock
Usual criterion is pH < 7.25 for longer than 2 hours or with hypotension

204
Q

what exam needs to be done before ECMO

A

ECHO to R/O serious congenital heart disease

205
Q

potent vasodilators

A

tolazoline, nitroprusside, prostoglandin E and prostoglandin D

206
Q

Nitric Oxide NO

A

inhaled NO decrease pulmonary vascular resistance and improve pulmonary blood flow without compromising systemic blood pressure or worsening V/Q mismatch

207
Q

NO life

A

short-life (seconds) dose 5-20ppm

208
Q

testing for NO toxicity

A

methemoglobin

209
Q

treatment alternative to iNO

A

Revatio (Sildenafil PDE5)-long-term not recommended

Milrinone

210
Q

tidal volume

A

amount fo gas moved during one normal inspiration and expiration

211
Q

Functional Residual Capacity FRC

A

volume of gas left in the lung after a normal expiration

212
Q

residual volume

A

minimum lung volume possible-air left in lung after max expiration

213
Q

vital capacity

A

maximum amount of air that can be moved

214
Q

total lung capacity

A

total amount of volume present in lung

215
Q

minute volume

A

combination of tidal volume and respiratory rate

216
Q

anatomic dead space

A

part of airway where NO gas exchange occurs

217
Q

physiological deas space

A

alveoli that is ventilated but under or not perfused

218
Q

V/Q ratio

A

balance between ventilation (airflow at the alveoli) and perfusion (blood flow entering the lungs)

219
Q

V/Q mismatch

A

lungs are ventilated but not perfused
or lungs are perfused but not ventilated
leads to hypoxemia and hypercarbia

220
Q

lung development is completed by what age?

A

16-18 years of age

221
Q

asphyxia symptoms

A

progressive hypoxia, hypercarbia, acidosis

222
Q

side effects of Prostoglandin E

A

apnea or respiratory depression

223
Q

side effect of methylxanthine

A

gastroesophageal reflux

224
Q

anatomic dead space

A

conducting airway

225
Q

wasted ventilation

A

the amount of ventilation that does NOT participate in gas exchange

226
Q

oxyhemoglobin dissociation curve

A

a relation between dissolved oxygen and the affinity for oxygen by the hemoglobin molecule

227
Q

oxyhemoglobin curve shifts to the right

A

caused by decrease in pH

228
Q

oxyhemoglobin dissociation curve shifts to the left

A

caused by increase in pH

229
Q

chronic hypoxia caused what electrolyte imbalance

A

decreased chloride

230
Q

respiratory distress may lead to what?

A

hypoglycemia

231
Q

false reading on pulse oximetry is due to what?

A

phototherapy

232
Q

PEEP may cause an increase in what?

A

PVR pulmonary vascular resistance

233
Q

increased PEEP cause what?

A

barotrauma

234
Q

what factor increases PVR

A

sepsis

235
Q

side effect of surfactant

A

pulmonary hemorrhage

236
Q

normal ABG values

A

pH (between 7.35 - 7.45);
CO2 (between 35 - 45 mmHg);
HCO3 (22-26 mEq/L)

237
Q

“sigh: setting in HFV

A

decrease microatelectasis and recruit alveoli

238
Q

how antenatal steroids work?

A

accelerate the rate of glycogen depletion

results in thinning the intra-alveolar septa and increases the size of the alveoli.

239
Q

burned out xray

A

over exposed xray

240
Q

intrauterine pass of meconium theory include what?

A

maternal HTN

MCN568 (11 decks)

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