Pathophysiology

Precipitating Factors

-diabetes
Predisposing Factors -choronic HPN
-blood clotting disorder
-certain medications -alcohol
-smoking -anemia
-placenta previa
-drug toxicity -abruptio placenta
-alcohol -velamentous cord inserton

ANEMIA

Undeveloped villous

Constricting blood vessels

Decrease blood flow in the

placenta’s intervillous space

Diffusion of oxygen into

fetal capillaries

Fetal PO2/ Placental

nutrients

Bradycardia, Respiratory
Uteroplacental
Distress, IUGR
insufficiency

Maternal: Decreased
abdomen size/ Less fetal Decrease blood flow and Oxygen
movement to Fetal organs

HEART BRAIN MUSCULO-

LUNGS SKIN
SKELETAL
 The placenta plays an active role in fetal programming during intrauterine life,
and placental maturity, with fully mature villous tree and increased capillarization of
blood vessels. The placenta acts uniquely as both a channel of oxygen to the fetal
circulation and a significant consumer of oxygen to support its own metabolism and
competition. Amount of available oxygen is a critical factor in placental development and
development of placental blood vessels as well. However in cases in which maternal
oxygen supply is deficit such as in anemia, the normal functioning of the placenta is
altered. When there is decrease oxygen supply, the villous and other blood vessels in
the placenta cannot fully develop and function. For this reason, placental insufficiency
takes place which later on contributes to some abnormalities such as intrauterine
growth restriction (IUGR), respiratory distress and fetal late deceleration. This deficient
amount of oxygenated blood not only affects the placenta but also other systems of the
growing fetus.

The Lungs
LUNGS

hypoxia

Cessation of normal
fetal breathing

Inspiratory gasps

Aspiration of amniotic
fluid, epithelial
squames, meconium

Aphyxia

HMD

Death

In the studies of Dawes and coworkers (2015), it has shown that hypoxia rapidly
causes normal fetal breathing to cease. If hypoxia is prolonged the apnoeic phase is
followed by a period of inspiratory gasps. Unlike normal fetal breathing the gasping of
hypoxia causes considerable fluid movement and results in the aspiration of amniotic
fluid, epithelial squames and meconium deep into the lung acini down to the level of the
respiratory bronchioles and transitional ducts. There is evidence that some factor
associated with asphyxia predisposes to the later development of Hyaline Membrane
Disease (HMD). In the days when HMD was believed to be due to amniotic inhalation
the answer seemed quite simple as an intact amniotic sac would allow fluid to be
inhaled more readily (Snyder, 2015). Personally, I think it would be most useful to know
what happens to alveolar liquid formation and movement in severe hypoxia. It seems
possible that a change in alveolar wall permeability might occur, which would allow
reabsorption of lung liquid and its contained surfactant into the fetal circulation.

The Heart

hypoxia

Pulmonary Vascular
Resistance

Persistent Fetal Circulation

Pulmonary
vasoconstriction/
hypertension

Bradycardia

RV overload

Heart failure/death

Placental dysfunction creates hypoxia, increases pulmonary vascular resistance,

and can produce persistent fetal circulation (PFC), which is an expression of asphyxial
stress at birth. PFC is characterized by asphyxia, which causes pulmonary
vasoconstriction and pulmonary hypertension, leading to an overload of the right
ventricle and heart failure. In PFC there is a shunt from right to left because pulmonary
pressures are higher than systemic pressures. There is respiratory distress and
eventually heart failure and death unless the process can be reversed. The total
process involves uterine contraction constricting blood vessels in the wall of the uterus
which decreases blood flow through the intervillous space of the placenta, reducing
diffusion of oxygen into fetal capillaries causing decreased fetal PO2. When fetal PO2
decreases, chemoreceptors initiate an autonomic response in the fetus causing intense
vasoconstriction with increased blood pressure. The elevated blood pressure is
perceived by the baroreceptors which ultimately stimulate the parasympathetic system
to decrease the fetal heart rate, causing late deceleration.
The Skin (Integumentary)

hypoxia

Pulmonary Vascular
Resistance

Persistent Fetal Circulation

Pulmonary pressure

Shunt from right to left

(foramen ovale and ductus
level)

Cyanosis
(blue baby)

Cyanosis is a bluish purple appearance of the skin or mucous membranes

usually caused by an increased concentration of deoxygenated (unsaturated or
reduced) hemoglobin (Hgb). While occasionally a benign finding, as in a healthy
newborn with acrocyanosis or when observed in the lips and fingers of a child who has
been in the cold ocean, acute cyanosis often indicates a significant reduction in oxygen
concentration and may signify a life-threatening event. The presence or history of
cyanosis requires careful evaluation. 

In utero, the placenta oxygenates fetal blood. The deoxygenated fetal blood
bypasses the lungs due to high pulmonary vascular resistance (PVR) and travels via the
umbilical artery to the placenta, where it is oxygenated and returns to the fetus via the
umbilical vein. In placental insufficiency, there is abnormal communication between the
right and left sides of the heart or in between the systemic and pulmonary vessels
allowing deoxygenated systemic blood to bypass the lungs and return to the body.
The Brain

Chronic fetal hypoxia

Vasodilation in the
cerebral artery

Reduced total brain volume

and altered cortical volume
and structure, decreased
total number of cells and
myelination deficits,
neuronal migration deficits,
reduced dendritic
processes.

Increased risk for

impaired neurological
development

In developing fetus, sufficient blood supply is needed to support the metabolism,

development and functions of organs. The periods of prenatal development and early
postnatal life are extremely important for formation of brain structures which will be
involved in cognitive functions, including learning and memory, and shape life
experience and character of individuals. Chronic hypoxia increase risk of
neurodegenerative disorders in later life. Prenatal hypoxia also leads to a decrease in
brain adaptive potential and plasticity due to the disturbance in the process of formation
of new contacts between cells and propagation of neuronal stimuli, especially in the
cortex and hippocampus. The developing nervous system depends upon precise
regulation of oxygen levels. Hypoxia, the condition of low oxygen concentration, can
interrupt developmental sequences and cause a range of cellular and neuronal changes
and injuries. The roles and effects of hypoxia on the central nervous system (CNS) are
poorly characterized, even though hypoxia is simultaneously a normal component of
fetal development however severity of this condition leads to neurological impairment.
Work over the past decade has revealed that hypoxia causes specific disruptions in the
development of CNS connectivity, altering axon pathfinding and synapse development.
The Musculoskeletal
Decreased nutrient
supply

Decrease normal fetal

myogenesis

Decline in fetal
insulin-growth factor
2

Decrease amino acid

supply

Reduced rates of
myoblast
proliferation and
myofiber
hypertrophy

Reduction of skeletal
muscle mass

Intrauterine growth restriction (IUGR) caused by placental insufficiency is one of

the most common and complex problems in pregnancy, with no known cure. In
pregnancies affected by placental insufficiency, a poorly functioning placenta restricts
nutrient supply to the fetus and prevents normal fetal growth. Among other significant
deficits in organ development, the IUGR fetus characteristically has less lean body and
skeletal muscle mass due to decrease myogenesis associated with a decline in growth
factor which inhibits the proliferation of myblast and myofiber hypertrophy. If this
persistently happens, it will later on result to microsomic or SG (small fo gestational
age). This was also evident in our client since at 38 weeks and 5 days her fundic height
is only 31cm.