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What are 3 consequences caused by a lack of surfactant? How does this apply to NRDS?

From this physiological principle, several consequences
1. In the absence of a substance to lower surface tension
forces, smaller alveoli collapse into larger ones;
2. Positive airway pressure applied during inspiration
infl ates such lungs to only small volumes with high
critical opening pressures, (PCO); and
3. Any open lung units are prone to premature collapse
toward very low lung volumes during expiration.

Much of what presents as neonatal RDS in a premature
infant follows as the predictable consequences of these principles,
and can initiate or synergize with defective or suboptimal
performances by other organ systems, including the heart.
FIGURE 39.1 Archival image of an unknown premature infant who was
receiving supplemental O2 therapy (at ambient PB) through a plastic hood
positioned over the head and neck. Note the extreme sternal concavity
associated with the child’s inspiratory eff orts.


What are some things that increase the risk of NRDS? Decrease it?

Increased Risk
Male gender
Caucasian race
Cesarean section
Maternal diabetes
Second-born twin
Family history of neonatal RDS

Decreased Risk
Fetal “stress”: Maternal hypertension, Placental insuffi ciency
Prenatal corticosteroids


Describe some physical exam findings in NRDS and why they occur.

Because patients with RDS move less air than normal with
each inspiratory effort, that is, VT is less, their respiratory frequency
f must increase to maintain ˙VE. This extra work of
breathing may eventually fatigue neonates, at which point
their Pao2 falls and Paco2 may rise. Episodic apnea is also
common in infants with RDS.

A patient with RDS refl exively attempts to overcome the
tendency for alveoli to collapse during expiration by partially
closing the glottis to create an air stent (see Chaps. 25
and 30). The increased PAW generated by expiring against a
partially closed glottis stabilizes alveoli. Then as the patient
opens the glottis to complete expiration and begin inspiration,
the increased PAW is suddenly released and causes an audible
grunt. Students may visit Web site
to hear a recording of grunting.

Chest Wall Retractions
Patients with RDS must generate more negative PIP to move
an equivalent volume of air into lungs that are less compliant
(see Fig. 5.2). A large negative PIP retracts inwardly the
unossifi ed chest wall during inspiration. While sternal and
thoracic retractions can be seen in many infants, they are particularly
prominent among premature ones whose chest walls
are excessively compliant (Fig. 39.1).

Nasal Flaring
The nares are prone to inward collapse during inspiration if
their patency is not maintained by contraction of the alea nares
muscles. The neonate with RDS attempts to minimize nasal
resistance to airfl ow during labored inspiration by refl exively
contracting these muscles and thus presents with the clinical
fi nding of nasal fl aring.


What lab findings lead to hypoxemia in NRDS? Explain how they occur. Do they cause an increase in PaCO2? Can they be treated with increased FiO2?

Pao2 and/or Sao2 fall in infants with RDS for the same reasons
that adults develop hypoxemia (Chaps. 8, 9, and 28). These
are summarized in Table 39.3, and as for ARDS can be categorized
by their responsiveness to only an increase in FIo2.
The neonate unable to maintain ˙VE due to fatigue, or whose
functional VD/VT increases due to parenchymal hypoplasia,
accumulates CO2 and increases Paco2. By Dalton’s law, Pao2
declines proportionally (Chaps. 1 and 9). Many babies with
RDS do not hypoventilate, but their hypoxemia can arise from
diffusion block. Such a block may be caused by delayed progression
to the alveolar stage (Chap. 2), yielding abnormally
thick alveolar septa at birth that impede gas exchange (Chaps. 2
and 9). Diffusion block can also occur from accumulated
proteinaceous material (hyaline membranes) within airways
and airspaces, representing in part sluffed epithelial cells of
the parenchyma (Chap. 26).
Perhaps an even greater contribution to neonatal hypoxemia
is made by ˙VA/Q ˙ mismatch, due to the perfusion of underdeveloped,
underventilated, or atelectatic alveoli (Chap. 8). Most
signifi cantly, each of these fi rst three causes of hypoxemia can
generally be treated by increasing the FIo2 and thus the PAo2
to the patient. The fourth cause of neonatal hypoxemia, that of
persistent right-to-left shunting cannot be overcome by providing
O2 alone. Oxygen will not be effectively delivered to
collapsed unventilated distal airways. If these distal airways
remain perfused, there will be an “intrapulmonary” right to
left shunt. Such a shunt cannot be overcome by increasing
the concentration of inspired oxygen. The alveoli must be
“recruited” into participation in gas exchange, for example,
by providing distending pressures to overcome their surface
tension forces, or providing surfactant to reduce their surface
tension forces, to overcome this intrapulmonary shunt.
In addition to such an intrapulmonary right to left shunt,
there are in newborn infants two important extrapulmonary
sites where shunting can occur. These are the foramen ovale
and the ductus arteriosus. A combination of factors in newborns
with RDS, including hypoxemia and acidemia, can
cause pulmonary vascular resistance to be elevated. If severe,
shunting from right to left across fetal channels can occur.
Treating this form of shunting depends upon lowering pulmonary
vascular resistance.
As mentioned previously, the infant with RDS must
breath rapidly to overcome a small functional VT. If this
response is insuffi cient, or if the infant tires, then Paco2 will
increase. Thus, hypoventilation can be an additional contributor
to the hypoxemia seen in infants with RDS. The resulting
respiratory acidosis (Chap. 17) will tend to increase pulmonary
vascular resistance and lead to increased right-to-left
shunting across fetal channels. In very severe cases, the Cao2
can become very low, systemic tissues may revert to anaerobic
metabolism and an additional metabolic (lactic) acidosis can
occur as well. It is this combination of problems that led to the
very high mortality and resistance to O2 therapy in the patient
group described earlier.


What can be seen radiographically in NRDS?

The diffuse alveolar instability and atelectasis of neonatal
RDS decreases TLC to an extent that may be apparent on the
AP chest x-ray. In addition, collapsed lung is radiographically
denser than normal, increasing the contrast between the
parenchyma and conducting airways on fi lm and making air
bronchograms easily visible (Fig. 39.3; see Fig. 15.8). The
contrast between open alveoli and those regions where collapse
or consolidation have occurred yield a dark graininess
against a lighter background on the chest fi lm, the so-called
“ground glass” appearance (compare with images in Chaps. 15,
24, and 28).


What are NRDS lungs like macroscopically? Microscopically?

Macroscopically, the lungs of an infant with neonatal RDS
appear smaller than normal. However, they are not hypoplastic
but rather underinfl ated. As expected, they have decreased
compliance, that is, they require more gas pressure to infl ate to
a similar volume, and show a sharply increased PCO compared
to normal term lungs. Thus the neonatal RDS lung is also
considered “stiff” like those of patients with ALI and ARDS
(Chap. 28). The lungs of the patient with RDS can be infl ated
at normal pressures, however, with fl uid rather than air, since
surface tension forces are no longer in play and the tissue elastic
recoil is normal (Chap. 5).
Microscopically the neonatal RDS lung often appears diffusely
atelectatic, but with microscopic areas of overinfl ation
that may be mistaken for emphysematous bullae (Chaps. 26
and 37). Under conventional staining with H&E, such lung
sections show both fl uid and proteinaceous debris that have leaked into the alveoli, comprising the hyaline membranes
(Fig. 39.4) of diffuse alveolar damage (DAD) that are also
seen in the lungs of some patients dying of ARDS (Chaps. 26
and 28).


Explain the various treatments that are used in NRDS, why they are used, and how they work.

Supplemental oxygen remains an important modality in treating
infants with RDS, as many of the contributors to hypoxemia
in this condition respond to oxygen. Much of the blood that is perfusing the lungs of an infant with RDS does not
encounter well-aerated alveoli for the reasons in Table 39.2.
This results in a range of ˙VA/ ˙Q mismatches 34 weeks’ gestation. Preventing preterm delivery is
most often attempted with tocolytic agents, medications that
block or slow intrauterine contractions.


What is the prognosis for NRDS?

For reasons only partially understood, the endogenous surfactant
system generally matures suffi ciently within 72 hours
of birth regardless of gestational age. Thereafter, additional
surfactant replacement is rarely necessary or benefi cial. However,
surfactant defi ciency is not the only abnormality of the
premature lung. Thus, very premature infants usually require
mechanical ventilatory support for a much longer period of
time, despite the presence of adequate surfactant in distalairways and alveoli. With currently available therapies, the
success rate for treating neonatal RDS is very high. Most of
the remaining morbidity and mortality in infants with RDS
relates to other complications of their prematurity, rather than
to surfactant defi ciency per se. Even with this caveat, the longterm
outcomes of the vast majority of U.S. infants born prematurely
are favorable, and continue to show improvement.
Survival rates are correspondingly lower in all settings where
maternal malnutrition, low socioeconomic status, and limited
access to prenatal and postnatal care continue to exert pronounced
negative effects.


Explain the rationale behind the theory about central chemoreceptors and the arcuate nucleus and SIDS.

Clinical correlations have been made between: (1) a diminished
arcuate nucleus and SIDS, as well as reduced muscarinic (acetylcholine),
kainate (glutamate), and lysergic acid (serotonin)
receptors in the brainstems of SIDS victims (Fig. 39.7, upper
panel); and (2) increased numbers of brainstem serotonergic
neurons in SIDS victims (Fig. 39.7, lower panel). However,
there is no proof that any of these correlations can explain SIDS type
disruptions in an infant’s cardiorespiratory behavior.


Explain generally how fetal reflexes could be related to SIDS.

Leiter and Böhm (2007) have suggested that neonates experience
changes in the balance between excitatory adult
refl exes that reduce SIDS risk and inhibitory fetal patterns
that increase the risk of SIDS. They hypothesize that in some
neonates, SIDS vulnerability is heightened and prolonged.
The primary responses of the fetus to ambient hypoxia are
bradycardia, reduced oxygen consumption, and redistribution
of blood fl ow to essential organs, since respirations are
not occurring in utero. Both the DR and the LCR induce bradycardia
and sympathetic activation, as well as apnea. Both
are considered conservative refl exes since a fetus can only respond to its environment, not change it. The rationale for
these responses during hypoxic situations is that the organism
must conserve its intrinsic oxygen stores for the two most
essential organs, the heart and the brain.


Explain specifically which fetal reflexes could be related to SIDS and how.

Stimulating the mucosa of the upper respiratory tract induces
several autonomic adjustments to prevent noxious gases, liquids,
or solids from entering the lungs. The DR is a collection
of refl exes induced by stimulation of the nasal mucosa that
naturally diving mammals utilize very effi ciently. It begins
with immediate apnea, an abrupt bradycardia, and selective
peripheral vasoconstriction. It is present in all mammals
including man, and is especially prominent in very young
infants (Fig. 39.8). A key feature in relation to SIDS is that
diving mammals do not breathe despite being hypercarbic
and hypoxemic, and similar cardiorespiratory responses can
be induced by nasal stimulation with CO2. Juvenile rats can
be trained to voluntarily submerge to traverse an underwater
maze. During their entire underwater excursion, these animals
show similar apnea, bradycardia, and increased systemic
blood pressure refl ecting abrupt peripheral vasoconstriction
that reduces blood fl ow to most tissues (Fig. 39.9).
The LCR is induced by stimulating the mucosa around
the glottis with water or acidic fl uid (eg, vomitus) that causes
cardiorespiratory responses similar to those initiated by the
DR (Fig. 39.10). Like the DR, the LCR is most prominent in
neonatal animals, is more prolonged in cases of hyperthermia,
and is greater in anesthetized humans.