Pulmonary Physiology of Neonatal Reanimation

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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

NeoReviews Vol.2 No.2 February 2001 e45



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

neonatal resuscitation pulmonary physiology

e46 NeoReviews Vol.2 No.2 February 2001



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.





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-





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.

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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.



Pulmonary Physiology of Neonatal Reanimation

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