 Pulmonary surfactants are a complex of

specific lipids, proteins and carbohydrates

secreted by type II alveolar epithelial cells.

 The complex is amphiphilic (i.e. it contains

both hydrophobic and hydrophilic groups),
making it ideal agent to decrease surface
tension at the air– liquid interface in the
alveoli .
 The primary function of the lipid component of
surfactant is to lower surface tension in the
alveoli at the air–liquid interface.

 surface tension is the result of forces of

attraction (pressure difference) between
molecules at a surface.

 This is related Laplace’s formula: P=2T/R where

P is the pressure difference, 2T is the surface
tension and r is the radius of the sphere
NORMAL ALVEOLI WITHOUT SURFACTANT
 Enhance macrophage activity

 Enhance mucociliary clearence

 Reduces inflammation
 Development starts from foregut as a bud at
3-4 weeks

 At the end of 16 weeks of gestation tracheo

bronchial tree is complete

 Lamellar bodies and surfactant proteins can

be detected by 24 weeks in type 2 alveolar
cells.
 Surfactant is synthesised from endoplasmic
reticulum and golgi bodies from type 2 alveolar
cells

 Stored in lamellar bodies and transported by

exocytosis

 The surfactant proteins and phospholoipids

assemble into a tubular myelin

 When the surfactant is subjected to high

pressure and low lung volume desorption of
surfactant lipid occurs.
 DPPC is the primary surface-active molecule at
the air– fluid interface in the alveoli.

 DPPC is palmitic acid, which is fully saturated

(hydrogenated).

 Saturation of the acyl chain enables the

molecule to form ordered monolayers
andconfers the ability to be compressed firmly

 (during expiration, a property essential to

decrease surface tension at low lung volumes).
 Between 5-10% of surfactant consists of
proteins .Currently 4 types of non serum
proteins are identified.
1.SP-A
2.SP-B
3.SP-C
4.SP-D
 It is synthesised from two genes in humans,
SFTPA1 and SFTPA2, on the long arm of
chromosome 10

 SP-A binds specifically and avidly to DPPC,

suggesting a key role in surfactant
homeostasis .

Deficiency results in impairment of host

defense mechanism,infections like mycoplasma
,h,.influenza and pseudomonas
 SP-B is a 79-amino acid hydrophobic
polypeptide synthesised by the SFTPB gene
on chromosome 2, and always remains
associated with surfactant phospholipids. Its
oligomeric form consists of dimers and
tetramers

 It helps in interfacial film stability.

 Deficiency results in severe RDS.

 SP-C is the most hydrophobic protein in
surfactant, consisting of 35aa synthesised by
the SFTPC gene on chromosome 8 . The
nuclear magnetic resonance structure of SP-C
suggests it is a transmembrane protein,
which can span a fluid DPPC bilayer .

 Unprocessesd accumulation proSPC results in

ILD in neonates/idiopathic pulmonary
fibrosis.
 SP-D is a 43-kDa collectin synthesised by the
SFTPD gene on the long arm of chromosome
10, in close proximity to the SP-A genes.

 Deficiency results in infection with respiratory

syncitial virus and influenza A virus.
 Deficiency of protease involved in processing
SP –B results in ILD

Deficiency of napsin A ,a protease of SP A

Results in accumulation of unfolded proteins
Which activates apoptotic pathways in
endoplasmic reticulum.
 PREMATURITY

SURFACTANT DEFICIENCY AND IMMATURE

LUNG.

V/Q MISMATCH AND HYPOVENTILATION

HYPOXEMIA AND HYPERCAPNEA

RESPIRATORY ACIDOSIS
 PULMONARY VASOCONSTRICTION

IMPAIRED ENDOTHELIAL AND EPITHELIAL

INTEGRITY

PROTEINACEOUS EXUDATE

RESPIRATORY DISTRESSS SYNDROME

WHICH ON CHRONICITY CAUSES BRONCHO

PULMONARY DYSPLASIA
 AARC CLINICAL PRACTICE GUIDELINE 2013

 PREMATURE INFANTS <32 weeksor low birth

weight < 1.3kg

 Lecithin /spingomyelin ratio<2:1

 Who require mechanical ventilation secondary

to respiratory failure
 Fio2>0.40

 Clinical and radiological evidence of RDS

 Treatment of respiratory syncitial virus

induced respiratory failure may shorten the
duration of mechanical ventilation

 Post operative development of ARDS

following cardiac surgery reduces the icu and
hospital stay.
 Presence of congenital anomalies which is
incompatible with life

 Congenital diaphragmatic hernia

 Active pulmonary haemorrhage.

 INSURE
intubation
surfactant
extubation

This technique features early surfactant

replacement therapy with prompt extubation
 Pharyngeal instilation before first birth ( only
animal studies)

 Laryngeal mask airway administration 0nly

when ETT intubation skills are lacking.

 Broncho alveolar lavage in treatment of MAS

 OBSTRUCTIVE LUNG DISEASES :
airway inflammation

activation of alveolar macrophages

release of proteolytic enzymes and

inflammatory mediators.
 mutaTion of GMCSF Granulocyte macrophage
colony stimulating factor

defective clearence of surfactant by macrophage

impaired formation of tubular myelin and

increased amount of surfactant
 The content of SP-A SP-B AND SP-C are
increased in BAL

 ALTERATION in constituent lipids and fail to

Aggregate properly.

 Secondary PAP is associated with

haematological disorders ,toxic inhalations
without anti GMCSF antibodies
 Whole lung lavage

 GM-CSF supplemental therapy

 Rituximab and plasma pherisis

 Sarcoidosis ,ILD ,idiopathic pulmonary
fibrosis and hypersensitivity pneumonitis

 Mutations in SP-B SP-C and ABC 3 .

 Total phospholipid content decrease in case

of IPF

 IN chronic lung diseases like cystic fibrosis

inflammation induces lipolysis of surfactants
 Within a week of known clinical insult

 Bilateral opacities not fully explained by

effusions lobar collapse or nodules

 Origin of edema: respiratory failure not fully

explained by cardiac failure or fluid overload
to exclude hydrostatic edema
 Mild: PF ratio 200</300
 Moderate : PF ratio 100</200
 Severe :PF< 100
with PEEP>/5