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Pulmonary Physiology of Neonatal ResuscitationTzong-Jin Wu, MD,* andWaldemar A. Carlo, MD† Objectives After completing this article, readers should be able to:
1. Describe the physiology of production and clearance of lung liquid.
2. Compare and contrast the initial breath in spontaneously breathing and asphyxiated
newborns.
3. Delineate the major respiratory reflexes involved in resuscitation.
4. List changes in pulmonary circulation at birth.
5. List possible deleterious effects of hyperoxia.
IntroductionThe most important part of the transition from intrauterine to extrauterine life is the
establishment of effective pulmonary gas exchange. Currently used techniques of resusci-tation, although usually successful, are based on few physiologic studies and have come
under critical review recently. This article reviews current understanding of pulmonary
physiology during transition and resuscitation, based primarily on experimental animal
studies, and relates it to clinical practices in neonatal resuscitation.
Lung Liquid in Neonatal TransitionThe switch from placental to pulmonary gas exchange at birth requires rapid removal of
lung liquid from the potential air space (Fig. 1)□ V . This process is much more complex than
simple mechanical compression of the chest at delivery that results in oral drainage of lung
liquid, and it is controlled primarily by ion transport across the airway and pulmonary
epithelium.
During fetal life, the lungs are filled with liquid, and normal growth of the lungsdepends in part on the balance between production and drainage of this fluid. The
pulmonary epithelium actively transports chloride into the lung lumen, generating an
osmotic gradient that causes liquid to flow from the microcirculation through the
interstitium into potential air spaces. In fetal lambs, the hourly production of lung liquid
increases from 2 mL/kg at midgestation to 5 mL/kg at term, and the total volume
increases from 4 to 6 mL/kg at midgestation to more than 20 mL/kg near term.
Secretion of lung liquid begins to decrease 2 to 3 days before spontaneous term or
preterm labor, resulting in a 15 mL/kg reduction in lung water. Labor decreases
extravascular lung water by 45%, with a further 38% reduction 6 hours after birth. At birth,
several factors drive fluid from the lung lumen into the interstitium. First, the lung
epithelium switches from a predominantly chloride-secreting membrane before birth to a
predominantly sodium-absorbing membrane after birth. The expression and function of the epithelial sodium channels at the apical membrane and Naϩ, K ϩ-ATPase at the
basolateral membrane increase at birth. The causes of these
changes are not clear but may be linked to alterations in the
hormonal milieu associated with delivery. Second, the lung
liquid contains almost no protein compared with 30 mg/mL
of protein in the interstitial fluid, resulting in an osmotic
pressure gradient. Third, inflation of the lungs with air
establishes transpulmonary pressure, decreases hydrostatic
pressure in the pulmonary circulation, and increases pulmo-
*Fellow Instructor.†Professor, Division of Neonatology, Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL.
Abbreviations
eNOS: endothelial nitric oxide synthase
FRC: functional residual capacity
PVR: pulmonary vascular resistance
Article neonatal resuscitation
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nary blood flow, which in turn increases effective vascular
surface area for fluid uptake. Under normal conditions,transepithelial liquid clearance requires 2 to 3 hours, and
drainage from the interstitium into the circulation is
complete by 6 hours. Most of the luminal fluid enters the
pulmonary microcirculation, but about 10% exits the
lungs through lymphatics. The process may be slower
with preterm birth, delivery by cesarean section without
prior labor, elevated lung microvascular pressure from
hypoxemia or left heart failure, and conditions of low
plasma protein concentration. Such circumstances often
result in delayed establishment of final lung volumes.
Initial BreathsIn spontaneously breathing term infants born vaginally,
the first breath generates a mean negative intrathoracic
pressure of 52.3Ϯ26.4 cm H2O during inspiration and a
mean positive pressure of 71.3Ϯ32.8 cm H2O during
expiration. The inspired volume averages 37.7Ϯ18.1
mL, with a functional residual capacity (FRC) of
15.1Ϯ7.9 mL. Babies delivered by cesarean section have
similar inspiratory pressure and volume but lower expi-
ratory pressure and develop FRC less frequently with the
first breath.
In contrast to spontaneously breathing newborns, an
opening pressure must be exceeded before lung expan-
sion occurs in asphyxiated infants. During resuscitation
of infants who never have breathed, the median pressure
on the first inflation to produce chest movement is 40 cm
H2O, and the median first inspiratory volume achieved is
8.6 mL/kg. An inflation pressure of 25 to 30 cm H2O
for 1 second achieves a tidal exchange of only 15 mL
compared with 40 mL in spontaneously breathing ba-
bies. Furthermore, FRC is not formed for several breaths
unless the baby exhibits a Head paradoxic reflex. By
maintaining the first inflation for up to 5 seconds, a tidal
volume similar to that seen in spontaneously breathing
babies could be delivered and an FRC could be formedconsistently. Thus, when resuscitating asphyxiated neo-
nates, lung volume similar to the first breath of sponta-
neously breathing babies can be accomplished either by
maintaining a pressure of 25 to 30 cm H2O for at least
3 seconds or by using higher pressure (up to 50 cm H2O)
for much shorter periods that is guided by chest wall
movement. Although physiologic studies have demon-
strated that lung inflation requires high or sustained
inflation pressures, clinical trials have not been per-
formed to validate this concept.
The amount of pressure needed to resuscitate preterm
babies remains controversial. In physiologic studies, in-
flation pressures of 27.3Ϯ4.8 cm H2O produced ade-
quate tidal exchange (ie, twice the anatomic dead space)in fewer than one third of preterm infants in the first
three breaths. Other data suggested the median pressure
to achieve chest wall movement was 22.8 (range, 14 to
30)cmH2O in infants younger than 36 weeks’ gestation
and could establish no correlation between the inflating
pressure and either birthweight or gestational age. In a
recent study of extremely low-birthweight infants, infla-
tion pressures of 20 to 25 cm H2O sustained for 15 sec-
onds followed by continuous positive airway pressure
seemed effective in establishing FRC and avoided unnec-
essary intubation. Further clinical trials of various strate-
gies to establish lung volumes and FRC in preterm
infants are needed to examine both short-term outcome
(oxygenation, ventilation, spontaneous breathing) and
long-term measures of severity of respiratory distress and
lung injury.
Respiratory ReflexesThe response of an infant to resuscitation is primarily a
product of physiologic reflexes. Infants are more vulner-
able to cardiopulmonary compromise because the auto-
nomic nervous system and the pulmonary mechanics are
immature. Without an understanding of the physiologic
reflexes, attempts at resuscitation actually may worsenapnea, bradycardia, and hypoxemia.
Laryngeal ReflexesChemical stimulation of the laryngeal receptors with
water, saline, or milk and mechanical stimulation with a
suction catheter induce bradycardia and apnea. The af-
ferent pathway from laryngeal chemoreceptors is the
superior laryngeal nerve, which transmits impulses to the
nucleus tractus solitarius and dorsal nucleus of the me-
dulla. The motor limb originates from the nucleus am-
biguus and nucleus retroambigualis in the medulla,
reaching the larynx via the recurrent laryngeal nerve.Sedation with reduced respiratory drive before stimula-
tion is associated with more prolonged apnea. Pre-
existing hypoxemia also enhances the laryngeal reflex.
Therefore, in asphyxiated infants, vigorous attempts to
suction the pharynx or intubate the larynx superimposed
on the effects of maternal sedation may lead to profound
apnea and bradycardia.
Carotid Body ReflexThe carotid bodies are peripheral chemoreceptors lo-
cated near the bifurcation of the common carotid arter-
ies. When stimulated by hypoxemia, they send afferent
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impulses via the glossopharyngeal nerve to the nucleus
tractus solitarius and then to the respiratory neurons inthe medulla. The efferent response includes hyperventi-
lation, vagal bradycardia, bronchoconstriction, dilation
of the upper airway, and alpha-adrenergic peripheral
vasoconstriction with increased blood pressure. The in-
crease in ventilation is enhanced by hypercapnia. How-
ever, newborns, especially preterm infants, respond to
hypoxia with an initial increase followed by a later de-
crease in ventilation with worsening hypoxemia, which
can lead to periodic breathing or apnea. On the other
hand, a single breath of 100% oxygen causes a decrease in
minute ventilation or even apnea in neonates during
quiet sleep, with preterm infants showing a greater re-
sponse. Stimulation of the laryngeal chemoreflex inhibits
the carotid body respiratory reflex and facilitates the
carotid body cardioinhibitory reflex, which may lead to
temporary cardiac arrest. Thus, the carotid body reflex in
the newborn can mediate apnea and bradycardia through
several pathways.
Respiratory Reflexes Arising from PulmonaryStretch ReceptorsHERING-BREUER REFLEX
Lung inflation stimulates stretch receptors located within
the smooth muscle of large and small airways, transmit-
ting afferent impulses via large myelinated fibers in the
vagus into the dorsal respiratory neurons, the apneustic
center, and the pneumotaxic center in the brainstem.
The reflex includes slowing of ventilatory frequency or
even apnea and bronchodilation. In addition, lung infla-
tions cause a decrease in vagal tone with an increase in
heart rate and vasoconstriction, which may reverse the
marked bradycardia and hypotension elicited by stimula-
tion of the laryngeal and carotid body reflexes. The
strength of the Hering-Breuer reflex is greater at 36°C
than at 24°C ambient temperature in newborn rats,
suggesting that newborns exposed to a warm environ-
ment are more susceptible to inhibitory inputs, andhyperthermia may predispose to respiratory depression.
PARADOXIC REFLEX OF HEAD
Lung inflation also can stimulate stretch receptors in the
lungs, followed by afferent transmission via the vagus,
causing very deep inspirations. This reflex is present as
early as 25 weeks of gestation, but generally persists only
in the first 5 days postnatally. It may be involved in the
sigh response to prevent atelectasis and in generating the
first breath of the newborn.
When a newborn is deprived of oxygen, respirations
cease after a few rapid breaths, and heart rate drops. This
primary apnea usually resolves with stimulation. How-
ever, if oxygen deprivation continues, the baby willdevelop several irregular gasping respirations followed
by a period of secondary apnea, which is associated with
significant bradycardia and hypotension (Fig. 2)□ V . This
secondary apnea cannot be relieved by stimulation alone;
it can be reversed only by positive-pressure ventilation.
Suctioning and attempts at intubation may stimulate
laryngeal reflexes and worsen the apnea, bradycardia,
hypotension, and hypoxemia. Face mask pressure and
cold air over the face can stimulate the trigeminal reflex,
also causing bradycardia. Adequate inflation of the lungs
is of utmost importance. Stimulation of the pulmonary
stretch receptors immediately mediates an increase in
heart rate and blood pressure, inhibits laryngeal and
carotid body reflexes, and induces the paradoxic reflex of
Head, with initiation of spontaneous respirations. Lung
inflation also gradually establishes FRC and improves
pulmonary blood flow and gas exchange.
Transition of Pulmonary Circulation at BirthDuring fetal life, pulmonary vascular resistance (PVR) is
high and pulmonary blood flow is low. Several potential
factors contribute to the high pulmonary vascular tone in
the fetus. Small pulmonary arteries are compressed by the
fluid-filled alveolar space. Low estrogen production and
low oxygen tension promote the synthesis of vasocon-
strictors such as endothelin-1 and inhibit the production
of vasodilators such as nitric oxide and prostacyclin.
Decreased concentrations of cyclic guanosine mono-
phosphate and cyclic adenosine monophosphate, which
are second messengers mediating vasorelaxation, also
potentiate the effects of vasoconstrictors.
In the fetus, most of the blood from the right side of
the heart flows through the ductus arteriosus into the
aorta (Fig. 3)□ V . At birth, clamping the umbilical vessels
removes the low-resistance placental circuit and increases
systemic blood pressure, while blood vessels in the lungs
relax. As a result, pulmonary blood flow increases imme-diately by 8- to 10-fold, and the flow through the ductus
arteriosus decreases (Fig. 4)□ V . The most important stim-
uli for increasing pulmonary blood flow are ventilation of
the lungs and an increase in oxygen tension. Intrauterine
ventilation of the fetal lamb without changing the arterial
tension of carbon dioxide or oxygen increases pulmonary
blood flow to about two thirds of that observed follow-
ing birth; breathing hyperbaric oxygen without ventilat-
ing the lungs increases pulmonary blood flow to levels
comparable to those after birth. The largest effects are
seen when ventilation and increases in arterial oxygen
tension occur simultaneously.
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The fall of PVR is due to mechanical and chemical
factors. Inflation of the lungs dilates and recruits thepulmonary circulation, resulting in a rapid fall in PVR
within the first 30 seconds. Establishment of gas-liquid
interphase and absorption of lung fluids also may con-
tribute. The basic mechanism by which increased oxy-
genation affects the pulmonary circulation is not well
understood, but it may be related to the release of various
vasodilators, which possibly account for the slower de-
cline of PVR over the subsequent 10 to 20 minutes.
Nitric oxide and arachidonic acid metabolites play an
essential role in inducing pulmonary vasodilatation at
birth. Expression of endothelial nitric oxide synthase
(eNOS) peaks during mid- to late gestation and de-
creases postnatally in rats and lambs. Rhythmic disten-
tion of the lung without changing oxygen tension in-
creases eNOS mRNA expression, and oxygen ventilation
further increases its mRNA and protein expression. In
addition, increased shear stress from increasing pulmo-
nary blood flow induces eNOS expression. Nitric oxide
also suppresses endothelin-1 synthesis, thus further con-
tributing to pulmonary vasodilatation.
Prostacyclin, formed by the action of cyclooxygenase
on arachidonic acid, increases dramatically during late
gestation and early postnatal life, accompanied by an
upregulation of cyclooxygenase expression. Prostacyclin
participates in reduction of PVR accompanying ventila-
tion, but not in response to oxygenation, and its effect is
more marked in the preterm than in the near-term fetus.
Prostaglandin D2 lowers pulmonary artery pressure in
the fetus and newborn during the first 2 to 3 days after
birth, but it is a primary vasoconstrictor in older animals.
It is possible that prostaglandin D2 also has a physiologic
role in producing vasodilatation at birth. Bradykinin is
released transiently from fetal lungs following ventilation
with oxygen. It increases prostacyclin production and
stimulates endothelial cells to release nitric oxide. Thus,
bradykinin also may have a physiologic role during tran-
sition.The normal pulmonary vascular transition at birth is
based on the complex structural and biochemical devel-
opment of the lungs. This process can be disrupted easily
by prematurity, intrauterine hypoxia, and parenchymal
lung disease. Adequate ventilation and oxygenation
through mechanical and humoral pathways are the most
important resuscitative measures for achieving normal
pulmonary circulation.
Oxygen: The More The Better?Hypoxia in the fetus leads to cessation of breathing
movement; hyperoxia initiates a continuous breathing
pattern. Therefore, supplemental oxygen may be thera-
peutic to initiate spontaneous respiration. However, hy-peroxia may turn off aortic chemoreceptors, leading to
hypotension, or it may turn off carotid chemoreceptors
and cause hypopnea. Hyperoxia may increase the work of
breathing, metabolic rate, and oxygen consumption, and
it has been shown to decrease cerebral blood flow in
preterm infants. Using 100% oxygen may lead to forma-
tion of more oxygen free radicals during the reperfusion/
reoxygenation period after ischemia/hypoxia, causing
more extensive tissue damage, especially in preterm in-
fants who have limited antioxidant defenses.
A series of experiments in piglets subjected to severe
neonatal hypoxia demonstrated that room air resuscita-
tion normalized blood pressure, acid-base variables, hy-
poxanthine in plasma and brain microdialysate, cerebral
blood flow, somatosensory evoked potentials, PVR, and
cerebral membrane Naϩ, K ϩ-ATPase activity as effi-
ciently as resuscitation with 100% oxygen. Brain mor-
phologic changes 4 days after the hypoxic insult were
similar in both groups of piglets. Two clinical trials
showed that resuscitation of asphyxiated newborns with
room air was as effective as 100% oxygen, and room
air-resuscitated infants seem to recover more quickly,
with earlier first breaths and higher Apgar scores.
Although biochemical evidence and preliminary clin-
ical evidence suggest the benefits of resuscitation with
lower oxygen concentrations, current clinical data are
insufficient to justify adopting this as routine practice.
Long-term neurodevelopmental effects are unknown,
and room air resuscitation may be inadequate in certain
circumstances. However, when 100% oxygen is not avail-
able, resuscitation can be initiated effectively with room
air. Furthermore, it seems prudent to use oxygen judi-
ciously and to avoid prolonged and unnecessarily high
concentrations.
Summary Although based primarily on experimental data, under-
standing of the complex physiologic changes involved in
transition at birth is increasing. These concepts are incor-
porated into the most recent recommendations for resus-
citation. Clearing fluid in the lungs, establishing ade-
quate lung expansion, and increasing pulmonary blood
flow are key factors in successful pulmonary gas ex-
change. In asphyxiated newborns, optimal lung inflation
and ventilation can increase heart rate and blood pressure
promptly via reflex mechanisms, and it can hasten lung
liquid clearance and decrease PVR, thereby improving
oxygenation. Oxygen should be used to correct hypox-
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emia, and prolonged hyperoxia should be avoided. Fur-
ther physiologic and clinical trials areneeded to refine thetechniques for establishing effective pulmonary gas ex-
change in infants who require resuscitation at birth.
ACKNOWLEDGMENT
Electronic assets (illustrations, photographs, videos, vir-
tual reality animations) were developed for the Neonatal
Resuscitation Program under the direction of Dana A.V.
Braner, MD, at the Media Lab of Doernbecher Chil-
dren’s Hospital, Portland, OR.
The quality of the electronic assets may vary, depend-
ing on the presentation format (CD-ROM versus Inter-net) and the system used for viewing.
Suggested Reading Aizad T, Bodani J, Cates D, Horvath L, Rigatto H. Effect of a single
breath of 100% oxygen on respiration in neonates during sleep.
J Appl Physiol . 1984;57:1531–1535
Angell-James JE, Daly MB. Some aspects of upper respiratory tract
reflexes. Acta Otolaryngol . 1975;79:242–252
Black SM, Johengen MJ, Ma ZD, Bristow J, Soifer SJ. Ventilation
and oxygenation induce endothelial nitric oxide synthase gene
expression in the lungs of fetal lambs. J Clin Invest . 1997;100:1448–1458
Bland RD. Formation of fetal lung liquid and its removal near birth.
In: Polin RA, Fox WW, eds. Fetal and Neonatal Physiology .
Philadelphia, Pa: WB Saunders Co; 1998:1047–1054
Bland RD, Nielson DW. Developmental changes in lung epithelial
ion transport and liquid movement. Annu Rev Physiol . 1992;
54:373–394
Brannon TS, North AJ, Wells LB, Shaul PW. Prostacyclin synthesis
in ovine pulmonary artery is developmentally regulated by
changes in cyclooxygenase-1 gene expression. J Clin Invest .
1994;93:2230–2235
Burchfield DJ. Physiology of resuscitation. In: Polin RA, Fox WW,
eds. Fetal and Neonatal Physiology . Philadelphia, Pa: WB Saun-
ders Co; 1998:1023–1031
Cummings JJ, Carlton DP, Poulain FR, Raj JU, Bland RD.
Hypoproteinemia slows lung liquid clearance in young lambs.
J Appl Physiol . 1993;74:153–160
Daly MD, Angell-James JE, Elsner R. Role of carotid body chemo-
receptors and their reflex interactions in bradycardia and cardiac
arrest. Lancet . 1979;1:764–767
Greenough A, Morley CJ, Davis JA. Respiratory reflexes in venti-
lated premature babies. Early Hum Dev . 1983;8:65–75
Halbower AC, Jones MD Jr. Physiologic reflexes and their impacton resuscitation of the newborn. Clin Perinatol . 1999;26:621–627
Halbower AC, Tuder RM, Franklin WA, Pollock JS, ForstermannU, Abman SH. Maturation-related changes in endothelial nitricoxide synthase immunolocalization in developing ovine lung.
Am J Physiol . 1994;267:585–591
Hird MF, Greenough A, Gamsu HR. Inflating pressures for effec-
tive resuscitation of preterm infants. Early Hum Dev . 1991;26:
69–72
Hoskyns EW, Milner AD, Boon AW, Vyas H, Hopkin IE. Endo-
tracheal resuscitation of preterm infants at birth. Arch Dis Child .
1987;62:663–666
Lakshminrusimha S, Steinhorn RH. Pulmonary vascular biology
during neonatal transition. Clin Perinatol . 1999;26:601–619
Leffler CW, Hessler JR, Green RS. Mechanism of stimulation of
pulmonary prostacyclin synthesis at birth. Prostaglandins . 1984;
28:877–887
Levitzky MG. The control of breathing. In: Pulmonary Physiology .
New York, NY: McGraw-Hill; 1999:189–215
Lindner W, Vobbeck S, Hummler H, Pohlandt F. Delivery room
management of extremely low birth weight infants: spontane-
ous breathing or intubation? Pediatrics. 1999;103:961–967
Mathew R. Development of the pulmonary circulation: metabolic
aspects. In: Polin RA, Fox WW, eds. Fetal and Neonatal Physi-
ology . Philadelphia, Pa: WB Saunders Co; 1998:924–929
Merazzi D, Mortola JP. Effects of changes in ambient temperature
on the Hering-Breuer reflex of the conscious newborn rat.
Pediatr Res . 1999;45:370–376
Milner AD. Resuscitation at birth. Eur J Pediatr . 1998;157:
524–527
Morin FC III, Egan EA. Pulmonary hemodynamics in fetal lambs
during development at normal and increased oxygen tension.
J Appl Physiol . 1992;73:213–218
Niermeyer S, Kattwinkel J, VanReempts P, et al. International
guidelines for neonatal resuscitation: an excerpt from the
Guidelines 2000 for Cardiopulmonary Resuscitation and Emer-
gency Cardiovascular Care: International Consensus on Sci-
ence. Pediatrics. 2000;106:e29 (http://www.pediatrics.org/
cgi/content/full/106/3/e29)
Overview and principles of resuscitation. In: Kattwinkel J, ed.
Textbook of Neonatal Resuscitation. 4th ed. Elk Grove Village,
Ill: American Academy of Pediatrics and American Heart Asso-
ciation; 2000:1–22
Raj JU, Bland RD. Lung luminal liquid clearance in newborn
lambs. Effect of pulmonary microvascular pressure elevation.
Am Rev Respir Dis . 1986;134:305–310
Ramji S, Ahuja S, Thirupuram S, Rootwelt T, Rooth G, Saugstad
OD. Resuscitation of asphyxic newborn infants with room air or
100% oxygen. Pediatr Res . 1993;34:809– 812
Rimell F, Goding GS Jr, Johnson K. Cholinergic agents in the
laryngeal chemoreflex model of sudden infant death syndrome.
Laryngoscope . 1993;103:623–630
Sladek M, Grogaard JB, Parker RA, Sundell HW. Prolongedhypoxemia enhances and acute hypoxemia attenuates laryngealreflex apnea in young lambs. Pediatr Res . 1993;34:813–820
Saugstad ID, Rootwelt T, Aalen O. Resuscitation of asphyxiatednewborn infants with room air or oxygen: an internationalcontrolled trial: the Resair 2 study. Pediatrics . 1998;102:e1(http://www.pediatrics.org/cgi/content/full/102/1/e1)
Teitel DF, Iwamoto HS, Rudolph AM. Changes in the pulmonary circulation during birth-related events. Pediatr Res . 1990;27:
372–378
Upton CJ, Milner AD. Endotracheal resuscitation of neonates
using a rebreathing bag. Arch Dis Child . 1991;66:39–42
Vyas H, Field D, Milner AD, Hopkin IE. Determinants of the first
neonatal resuscitation pulmonary physiology
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inspiratory volume and functional residual capacity at birth.Pediatr Pulmonol . 1986;2:189–193
Figure 1. Fluid replaced by air in alveoli with the first breaths
after birth. Reprinted with permission from Textbook of
Neonatal Resuscitation.
Figure 2. Heart rate and blood pressure changes during
primary and secondary apneas. Reprinted with permission
from Textbook of Neonatal Resuscitation.
Figure 3. The circulatory pattern before birth. Reprinted with
permission from Textbook of Neonatal Resuscitation.
Figure 4. The circulatory pattern after birth. Reprinted with
permission from Textbook of Neonatal Resuscitation.
NeoReviews Quiz
7. The switch from placental to pulmonary gas exchange at birth requires a rapid removal of lung liquid fromthe potential air spaces. Of the following, removal of lung liquid at birth is most likely to result from:
A. Chloride-secreting lung epithelium.B. Drainage into the lymphatics.C. Increased hydrostatic pressure in pulmonary circulation.D. Mechanical compression of the chest during delivery.E. Osmotic pressure gradient with interstitial fluid.
8. The goal of positive pressure ventilation during resuscitation of a newborn is to establish an adequate lungvolume, including functional residual capacity (FRC). Of the following, the most effective strategy forestablishing FRC is:
A. Continuous positive airway pressure of 4 cm H2
O.
B. Inflation pressure of 25 cm H2O.C. Inflation time of 5 seconds.D. Supplemental oxygen of 100%.E. Ventilation rate of 60 breaths/min.
9. The response of a newborn to resuscitation is primarily a product of several physiologic reflexes. Of thefollowing, the reflex most likely to result in increased ventilation frequency is:
A. Carotid body reflex.B. Hering-Breuer reflex.C. Laryngeal reflex.D. Paradoxic reflex of Head.E. Trigeminal reflex.
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