PERSISTENT

PULMONARY
HYPERTENSION OF THE
NEWBORN
( PPHN )

Nazardi Oyong
Subb perinatologi FK-UR / RSUD AA Pekanbaru

PPHN

Is a major clinical problem in the

neonatal intensive care unit.

Can contribute significantly to morbidity

and mortality in both term and preterm
infants.

Hypoxemic respiratory failure or PPHN

can place newborns at risk for death,
neurologic injury, and other morbidities.

Incidence is estimated at 0.2% of

liveborn term infants.

Fetal circulati adaption

Neonatal pulomonary
vasculature
Etiologi and mecanism
Treatment

1. Circulatory ADAPTATION

Fetus -

from 8 weeks until birth organs

mature to support external life

Fetal circulation

umbilical-placental circuit via umbilical cord

circulatory shunts to bypass
Liver
ductus venosus to inferior vena cava
Lungs
@ foramen ovale between right & left atria
@ ductus arteriosus connects pulmonary artery
to aorta

CIRCULATORY
ADAPTATION
Umbilical vein
Ductus venosus
Foramen Ovale
Ductus arteriosus
Pulmonary circ.
Systemic circ.
Umbilical artery

CIRCULATORY ADAPTATION
DUCTUS
VENOSU
S
BY PASS

CIRCULATORY ADAPTATION

BY PASS
II
FORAMEN
OVALE

CIRCULATORY ADAPTATION

BY PASS

PATENT
DUCTUS
ARTERIOSUS

III

CIRCULATORY ADAPTATION
FETAL CIRCULATION

High pulmonary resistance

Low resistance in systemic blood flow

RIGHT to LEFT shunt

Foramen Ovale
(Left arterial pressure low because returned lung blood is
low and right atrial pressure high due to large volume of
blood from placenta)
Ductus arteriosus
(High pulmonary resistance, Low fetal systemiv blood and
prostaglandin function)

CIRCULATORY ADAPTATION
NEONATAL CIRCULATION
H
H
H

Profound changes of circulation at birth

Increased pulmonary blood flow due to the drops
of pulmonary resistance - lung expansions.
Venous return from lung increase.

Left arterial press. is raised; Right

art.press.decrease
foramen ovale closed.

Systemic resistance higher than pulmonary

resistance
(24 hours) Prostaglandin function
Ductus close

Constrict umbilical arteries and placental blood

stops.

NEONATAL ADAPTATION

FETAL
CIRCULATIO
N

NEONATAL
CIRCULATIO
N

NEONATAL ADAPTATION
CIRCULATORY ADAPTATION
Fetus
Pulmonary
circulation

Newborn

Active, less
develop.

Active, increased
development

Foramen ovale

Open

Close

Ductus arteriosus
Botali

Open

Close

Ductus Venosus
Arantii

Open

Close

Active with low

resistance

Active with
increase
resistance

Systemic
circulation

Circulatory
ADAPTATION

NEONATAL
ADAPTATION
FETAL PULMONARY
DEVELOPMENT

Alveoli present : 25
weeks fill with lung fluids
Breathing movements:
Intermittently
Lung developments
Control of breathing
Fetus : gas exchange
placenta

NEONATAL
ADAPTATION
Temperature

Touch

Pain

Proprioceptive

FIRST
BREATH

Diafragm

Mechanical

Chemoreceptor

Neonatal Respiration
Irregular
Abdominal respiration

NEONATAL
ADAPTATION

PULMONARY ADAPTATION

CHAIN OF EVENTS AFTER FIRST

BREATH :
Converts fetal to adult circulation
Empties the lung fluids.
Begin pulmonary function.

THE NEWBORN
RESPIRATIONBEGI
N

PULMONARY ADAPTATION

FETUS

NEWBORN

Alveolus

Colaps

Develops

Pulmonary vessels

Non active

Active

Pulmonary
resistance

High

Decrease

Pulmonary blood

Low

Increase

Oxygen needs

Placenta

Lung

CO2 excretion

Placenta

Lung

PPHN

Persistent fetal circulation

Kombinasi :
High pressure in the pulmonary artery
Right to the left shunting from pulmonary
vascular bed
Structurally normal heart

Fetal circulati adaption

Neonatal pulomonary
vasculature
Etiologi and mecanism
Treatment

2. Neonatal pulomonary
vasculature

Sesnsitif to ; PaO2, PH, stress

Become hyperreaktive and constrict
Cause increase pressure
Neonatal heart cannot force blood flow to
the lung
Right to the left shunt ( for ovale & duct
arteriosus )
Infant become : hipoxemia, acidemia

The fetal pulmonary circulation undergoes

striking developmental . changes in vascular
growth, structure, and function.
-Because the placenta, not the lung, serves as
the organ of gas exchange, less than 10% of
the combined ventricular output is circulated
through the pulmonary vascular bed, and most
of the right ventricular output crosses the
ductus arteriosus to the aorta .

Despite increases in pulmonary

vascular
surface area, PVR (pulmonary
vascular resistance ) increases with
gestational
age when corrected for lung or
body weight,
suggesting that vascular tone
actually
increases during late gestation and

Pathways involved in maintaining high

pulmonary vascular tone in utero:
1) low oxygen tension
2) mediators such as endothelin-1 (ET-1) and leukotrienes.
3) basal production of vasodilator products : prostacyclin (PGI2) and
nitric oxide (NO) is relatively low
4) the fetal vasculature also has the interesting ability to oppose
vasodilation.

Normal Pulmonary Vascular Transition

The pulmonary vascular transition at

birth is characterized by :
1) rapid increase in pulmonary blood flow
2) reduction in PVR
3) clearance of lung liquid.

Central role in the pulmonary vascular

transition :
1. Pulmonary endothelial cells
2. NO
3. Arachidonic acid metabolites

At the time of birth, multiple

factors regulate these
pathways:
1. mechanical distention of the lung
2. a decrease in carbon dioxide tension
3. an increase in oxygen tension in the lungs.

Fetal circulati adaption

Neonatal pulomonary
vasculature
Etiologi and mecanism
Treatment

PPHN is categorized into:

1.

Parenchymal lung disease

(meconium aspiration syndrome,
respiratory distress syndrome,
sepsis)

2.

Idiopathic (or "black-lung")

3.

Pulmonary hypoplasia (as seen in

congenital diaphragmatic hernia).

Treatment of PPHN
1.Initial Therapies
-Treat metabolic derangements: correct acidosis, hypoglycemia,
hypocalcemia
-Optimize lung recruitment: mechanical ventilation, high-frequency
oscillatory ventilation, surfactant
-Optimize cardiac output and left ventricular function:
vasopressors, inotropic agents
2. Pulmonary Vasodilators
-Inhaled nitric oxide
3.Future Therapies
-Phosphodiesterase Inhibitors (sildenafil)
-Inhaled prostacyclin analogs (iloprost, prostacyclin)
-Recombinant superoxide dismutase

terimakasih