PULMONARY ADAPTATION

Dr RAGHAVENDRA.

During fetal life the future air spaces are filled with unique liquid that is produced by epithelial lining of developing lung as a result of net transepithelial chloride and sodium flux.

This fetal lung fluid (FLF) plays a critical role in lung development by maintaining future air spaces in a distended state and also limits entry of amniotic fluid into the lungs.

This lung fluid is rich in chloride and potassium, lower in bicarbonate and has normal sodium concentration.

Foetal Lung Fluid

The clearance of lung fluid after birth is the result of multiple processes and only minimally due to the “thoracic squeeze” during passage through the birth canal.

labor is a powerful stimulus for the clearance of lung fluid, predominantly a process of active transport into the interstitium and drainage through the pulmonary circulation, with some fluid exiting through lymphatic drainage.

Clearance of Fluid at Birth

After birth there is active liquid absorption induced by epinephrine and is mediated by activation or opening of sodium channels on the apical surface of the pulmonary epithelium.

Other stimuli for FLF absorption,

-Oxygen -ADH, thyriod hormone. -Stretch of the epithelium -Somatostatin and glucagon -Nitic oxide.

Fetal and neonatal physiology-Fox and Polin Ch-82

The work required to expand inner respiratory surface is directly related to surface tension.

Surface-active material called surfactant at this interface in the alveoli provides surface-tension-lowering activity

Surfactant is stored within type II cells in large lipid-rich organelles called lamellar bodies.

Stretch, the mode of ventilation, and the labor process enhance surfactant secretion and extracellular surfactant pool sizes at birth.

surfactant

Breathing begins long before birth, in utero although of unknown purpose, because no gas exchange is involved.

it is regulated by carbon dioxide and oxygen concentration.

Fetal breathing is mostly continuous in early gestation (90 to 115 days) but becomes episodic in late gestation.

Fetal Breathing

Sufficient opening pressure must be generated across the lung to overcome

• the viscosity of the fluid in airways.• the forces of surface tension.• tissue resistance.

Pressure of 60 cm of h20 required to make FLF flow through airways with 1st inspiration.

The elastic recoil of the chest wall ,fluid content of the lung at birth facilitates lowering the opening pressure, and ensure air in lungs.

Mechanics of first post natal breath

According to Laplace equation

the pressure required to overcome surface tension is directly proportional to the surface tension and indirectly proportional to the radius of curvature .

• Radius is increased by FLF.

• Surface tension is decreased by surfactant.

first postnatal breath begins with no air volume in the lungs and no transpulmonary pressure gradient.

As the chest wall expands, the transpulmonary pressure increases until it overcomes the surface tension of small airways and alveoli.

At this point, actively inspired air begins to enter the lungs and, according to the Laplace equation, as the radius increases, the distending pressure required to open up those units decreases.

The creation of functional residual capacity (FRC) at the end of the first expiratory effort is essential for the normal pulmonary adaptation at birth.

FRC can only be created if pulmonary surfactant Is present allowing for stabilization of peripheral air spaces.

Functional residual capacity

The first few breaths facilitates clearance of fluid from the lungs and establish functional residual capacity.

Expiratory pressure, probably generated against a closed glottis, aids in clearing lung fluid and leads to a more even distribution of air throughout the lung.

The median time for onset of breathing is 10 secs stimulated by various intrinsic and extrinsic factors

Onset of breath

Occlusion of the umbilical cord .

Removal of respiratory inhibitory mechanisms including prostaglandins and adenosine.

Activation of cerebral nonadrenergic system .

Global stimulation of the forebrain respiratory drive.

Intrinsic factors

Switching on of genes encoding for neurotransmitters involved in respiratory control.

Activation of CO2 drive.

Activation of central chemoreceptor areas and peripheral chemoreceptor drive.

Cooling .

Painful stimuli such as flicking of feet.

Audiovisual ,proprioceptive and touch stimulus.

Extrinsic factors

The physiologic mechanism responsible for the establishment and inhibition of foetal breathing in continuous breathing at birth remains controversial.

Continuous breathing can be established in utero, by raising foetal PO2 and placental separation at birth.

hypothesized that placental factors especially PGE2, might be responsible for the inhibition of foetal breathing.

Continuous Breathing at Birth

Before birth PVR is higher than SVR that results in right to left shunting.

Clamping of the cord at birth stimulates peripheral and central chemoreceptor's, and in conjunction with tactile and thermal stimulation, results in increasing systemic blood pressure. .

At birth, PVR falls rapidly from 60mmHg to 30mmHg by 24hrs of age and pulmonary blood flow increases from 78ml/kg/min to 160ml/kg/min at 72hrs of life due to relief of hypoxia and lung expansion.

PVR VS SVR

Increase SVR, along with decrease PVR decreases the right to left shunt through the ductus arteriosus. Pao2 further stimulates functional closure of the ductus arteriosus.

Pulmonary artery blood flow increases, resulting in increased pulmonary venous return to the left atrium and increased pressure in the left atrium. exceeds right atrial pressure, the foramen ovale functionally closes.

Ductal closure

Respiratory gas exchange depends on alveolar-capillary membrane diffusion of respiratory gases which is a passive process .

The mean oxygen uptake is 7ml/kg/min at 15 seconds, 12ml/kg/min at 2 minutes and 8ml/kg/min by 5 minutes in healthy term infants.

Gaseous exchange at birth

Before birth the lung is filled with liquid to maintain future air spaces in a distended state.

Transition from fetal to newborn status is by loss of fetal lung fluid, secretion of surfactant,

establishment of FRC, decrease in PVR, increased systemic pressure, functional closure of two shunts and increase in pulmonary artery blood flow.

At birth the arterial saturation is about 60% at 1min increasing upto 85% at 5min of life.

SUMMARY

Polin , Fox, Abman. Fetal and neonatal physiology : 4th edition. Elsevier 2010; 885, 960-967, 907-911.

Avery s neonatology 6th edition Anne Greenough & Anthony D Miller. Neonatal

respiratory dissorders : 2nd edition . 2003; 9, 11-19, 26-34, 59-64

Richard J Martin, Avroy A Fanaroff, Michel C Walsh. Fanaroff & Martin’s Neonatal and Perinatal medicine: 9th edition 2009; 44, 1075, 1080-89

Christine A Gleason, Sherin U Devaskar. Avery’s diseases of newborn: 9th edition. 2012; 598-610

REFERENCES

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