Cardivascular problems in

the neonates

Iwona Maroszyńska

Polish Mother’s Health Centre

• Fetal circulation
• Congenital cardiac defect

– Critical heart malformation

• TGA
• TAPVR
• TA, PA, PS
• AS, CoA

– Treatment

• Prostaglandins
• Rashkind procedure

• Congestive heart failure

Fetal circulation

 The fetus is connected by the umbilical cord to

the placenta, the organ that develops and
implants in the mother's uterus during pregnancy

 Through the blood vessels in the umbilical cord,

the fetus receives all the necessary nutrition,
oxygen, and life support from the mother

 Waste products and carbon dioxide from the fetus

are sent back through the umbilical cord and
placenta to the mother's circulation to be
eliminated

Fetal circulation

• Blood from the mother enters the

fetus through the vein in the
umbilical cord. It goes to the liver
and splits into three branches. The
blood then reaches the inferior
vena cava

Inside the fetal heart:

 Blood enters the right atrium. Most of the blood

flows to the left side through a special fetal opening
between the left and right atria - foramen ovale

 Blood then passes into the left ventricle and then to

the aorta

 From the aorta, blood is sent to the head and upper

extremities

 After circulating there, the blood returns to the right

atrium of the heart through the superior vena cava

 About one-third of the blood entering the right

atrium does not flow through the foramen ovale,
but, instead, stays in the right side of the heart,
eventually flowing into the pulmonary artery

Fetal circulation

• Because the placenta does the work of

exchanging oxygen (O2) and carbon dioxide
(CO2) through the mother's circulation, the
fetal lungs are not used for breathing. Instead
of blood flowing to the lungs to pick up oxygen
and then flowing to the rest of the body, the
fetal circulation shunts (bypasses) most of the
blood away from the lungs through a
connecting blood vessel called the ductus
arteriosus

Fetal circulation

• Dependent on the mother’s circulation

• Gas exchange take place in the placenta
• Blood oxygenation

– Umbilical vein > Vena cava superior > Left

atrium > Left ventricle > Ascendens aorta (PaO2
20-22 mmHg, SaO2-90-95%) > Descendens
aorta (PaO2 16-18mmHg, SaO2-75-80%)

• Lung - extraction of the oxygen from the blood,

fluid production

Fetal circulation

• Low systemic vascular resistance because

of the placenta (low perfusion pressure,
high flow)

• High pulmonary vascular resistance

• Intracardiac and extracardiac bypass

system

• Tissue perfusion is determined by the local

vascular resistance

• Preload: RV > LV
• Afterload: RV > LV

Liver – the first organ that receives

oxygenated blood

The mixing of the oxygenated i

deoxygenated blood

Blood circulation after

birth:

• With the first breaths of air the baby takes at

birth, the fetal circulation changes. A larger
amount of blood is sent to the lungs to pick up
oxygen

 Because the ductus arteriosus (the normal

connection between the aorta and the
pulmonary arteria) is no longer needed, it
begins to wither and close of

 The circulation in the lungs increases and more

blood flows into the left atrium of the heart.
This increased pressure causes the foramen
ovale to close and blood circulates normally

PDA

40%

50%

40%

90%

10%

FO

10%

90%

50%

PDA

40%

40%

20%

80%

20%

FO

20%

80%

60%

PDA

120%

0%

100%

120%

FO

100%

100%

20%

120%

20 t.c.

38 t.c.

Postnat.

Catecholamines

• Contraction of the uterus

– Hypoxia
– Increased cardiac output

• Stimulation of the new-born baby
• Increase of the systemic vascular

resistance

• Preparing the lungs to the breathing

Newborn’s circulation

• Afterload of the left ventricle

50%

• Afterload of the right ventricle

Replacement of placenta by the lungs
Katecholamines

Decreased pulmonary vascular
resistance

Newborn’s circulation

• Preload of the left ventricle

• Preload of the right ventricle

75%

Increased venous return

Constans

Parturition

• Right ventricle

• Left ventricle

Newborn’s circulation

• CO double than that of the adult as

measured against unit of body weight

– Elevation of stroke volume
– Higher heart rate

• Fetal myocardium works at near peak

capacity (catecholamines realising)

– Maintaining of a greater passive tension
– Developing of a smaller active tension

Newborn’s circulation

• Reduced shortening velocity

– Larger ratio of non-contractile to contractile

components in the fetal myocardium

– Lower content of intercellular calcium

• Incomplete sympathetic innervation

– The reduced number of sympathetic nerves

fibres compares with normal numbers of
receptors

– Supersensitivity to catecholamines

SV

TSV

TDV

TSP

TDP

Pressure

Volume

Systole

Diastole

A

B

CO = F x SV
SV = TDV - TSV
TDV = SV + TSV
TSP = SBP

TSP/TSV

Newborn’s circulation

• At birth the lungs can inflate and perform

their true function meaning that the fetal
bypass systems are no longer required

 Umbilical vein - Constricts to form the

ligamentum teres, which extends from
the umbilicus to the liver. The
mesentery that surrounded the
umbilical vein becomes the falciform
ligament

 Ductus venosus - A sphincter in the

ductus venosus constricts so that all
blood entering the liver passes through
the hepatic sinusoids

• Foramen ovale - Due to aeration of

the lungs, pulmonary resistance
decreases and pulmonary blood flow
increases. The increase in
pulmonary blood flow causes the
pressure in the left atrium to raise
above that of the right which results
in the valve of the foramen ovale
being pushed against the septum
secundum. This closes the foramen
ovale and its vestige is known as the
fossa ovale

• Ductus arteriosus - The change

in the partial pressure of oxygen in
the blood once the lungs become
functional controls the constriction
of the ductus arteriosus. Closure of
the duct is usually complete soon
after birth and its remnant is known
as the ligamentum arteriosus

 Umbilical arteries - The intra-

abdominal portions of the umbilical
arteries constrict. Some parts remain
patent supplying the urinary bladder
and these are contained within the
lateral vesicle ligaments which are
vestiges of the mesentery
surrounding the umbilical arteries

Congenital cardiac defect

• The word congenital means 'inborn or

existing at birth.' The phrases congenital
heart defect and congenital heart disease
are often used to mean the same thing,
but the word defect is more accurate. It
means an abnormality, not a disease. The
defect was caused by the incorrect
development of the heart, or blood
vessels near the heart, before birth

Congenital cardiac defect

• Frequency - eight of every 1,000 infants

born alive. That is almost one percent of
live-born infants.

• Surgery helps many children whose

lives are endangered, or who are
severely afected by their heart
abnormality

What cause the congenital heart

defect?

• About ten percent of heart defects are

caused by specific genetic abnormalities

• These may result from:

– abnormal chromosomes, as in Down's

syndrome

– abnormal gene that is passed down

from one generation to the next, as in
Marfan syndrome

What cause the congenital heart

defect?

• For the remaining 90 percent, a poorly understood

combination of genetic predisposition and
environmental factors is thought to be responsible

• Some congenital heart defects result from

abnormalities in the mother's health during
pregnancy (diabetes or systemic lupus
erythematosus)

• Certain infections in the expectant mother may

also cause abnormalities. For example, rubella is a
significant risk of developing a heart defect
(approximately 35 percent)

What cause the congenital heart

defect?

• Certain drugs are felt to cause

developmental heart abnormalities. This
includes the mother's use of alcohol,
drugs, and seizure medications

What cause the congenital heart

defect?

• Parents with congenital heart defects are

more likely to have afected children than
are parents with normal hearts
(approximately ten percent versus one
percent)

• If one child in the family has a congenital

heart defect, the chance of having other
children with a heart defect is slightly
increased (four percent versus one percent)

10

90

60

40

60

40

0%

20%

40%

60%

80%

100%

First exam.

Symptoms (+)

Not

diagnosed

Symptoms (-)

Symptoms (+)

Not dignosed

Diagnosed

Died, symtoms<6week

• The time of greatest hazard to the

infant with congenital heart defect

• The time before admission to the

specialist centre

• Framework for the future

• Efficient stabilisation of the sick

child in the local hospital while

awaiting transfer

• 25% - not diagnosed before birth

• Mortality after switch operation -

1%

• Mortality before surgery - 4%

• A full sequential diagnosis is rarely

available during the initial phase of
the resuscitation

• Decision has to be based on

clinical findings

Critical heart diseases

• Cyanotic

– Pulmonary flow dependent on PDA

• Tricuspid atresia

• Pulmonary artesia

– TGA

– TAPVR

• Non-cyanotic

– Systemic flow dependent on PDA

• Aortic stenosis
• Coarctation of the aorta

• Congestive heart failure dur4ing fetal

live

– HLHS
– PS and AS (congestive heart failure)

RV

LV

RA

LA

Body

Lungs

TGA

• Complete transposition of the great arteries

(TOGA)

– The great arteries are reversed from their normal

connections

– The aorta, which normally comes of the left ventricle

and pumps red blood to the body, arises from the right
ventricle and pumps blue blood returning from the
body back to the body bypassing the lungs completely

– The pulmonary artery, which normally arises from the

right ventricle and pumps blue blood to the lungs,
arises from the left ventricle and sends red blood
returning from the lungs right back to the lungs

TGA

• The most common cyanotic

congenital heart disease (accounts
for 5 to 7% of all congenital heart
defects)

• It is more common in males
• Babies are usually normal birth

weight and size

TGA

• There are several other heart abnormalities

that may occur along with TGA

–

The most common associated problems are:

• ventricular septal defectt it can cause left ventricular

outflow tract obstruction

• coronary Artery Anomalies
• single ventricular morphology
• cardiac malposition

TGA

• For survival an atrial septal defect

and a patent ducts arteriosus is
necessary

RV

LV

RA

LA

Body

Lungs

RV RA

LA LV

LV

RA

LA

Body

Lungs

RV

LV

RA

LA

Body

Lungs

RV

LA

LV

RA

Obstructed systemic flow

• Diagnosis

– Systemic hypoperfusion
– Acidosis
– Hypotension
– Organ impairment
– CoA - femoral pulses weaker than the right

brachial pulse

• Treatment

– Optimise systemic oxygen delivery
– Prevent metabolic acidosis

RA

LA

Body

Lungs

RV

LV

RV

RA

LA LV

FiO

2

↑

MAP↓

Katecholamin
y

FiO2↓

MAP↑

Milrinon

Treatment of critical heart

diseases

• Prostaglandins

– Duct dependent

• Pulmonary flow (PA, TA)
• Systemic flow (CoA, AS, HLHS)

– Mixing of the blood (TAPVR, TGA)

• Rshkind procedure

– Restrictive FoA

Use of prostaglandins

• The risk of withholding

prostaglandins infusion depends on
the patient’s clinical condition

Cyanosed neonate

Noncyanosed neonate

Murmur

Abnormal puls

Prostaglandin infusion

Infant in extremis

Infant in good condition

+

+

Use of prostaglandins

• Ductal patency is vital for the survival

• Apnea secondary to prostaglandin

infusion - indication for intubation not to
reduce the dose and never to stop the
infusion

• Balance between the systemic and

pulmonary blood flow

Systemic, myocardial,

pulmonary circulation are in

parallel and constant

dynamic competition with

one another

Recommendations

• Prostaglandin infusion must be started at

a rate sufficient to maintain ductal
patency

• Ventilatory parameters should be

adjusted to manipulate the pulmonary
vascular resistance to avoid pulmonary
overcirculation, so as to maintain a
pulmonary to systemic blood flow ratio
about 1:1

Hypoxia

PEEP

Mean airway perssure

Pulmonary vasular resistance
Systemic saturation 75-85%

Hyperoxia
Respiratory alkalosis

Systemic vasular resistance
Systemic saturation 75-85%

PEEP
Mean airway perssure
Nitroprusside

Katecholamine

Recommendation

• Apply a modest PEEP - 4-6 cmH

2

O

• Ventilation with room air in the first

instance

• Adjusting inspiratory pressures, rate, tidal

volume to achieve an arterial CO

2

tension

50-60mmHg, systemic saturation 75-85%

• Avoiding respiratory alkalosis

Low cardiac output

• Reassess the baby to ensure that the

prostaglandin infusion is adequate and
intravascular volume is satisfactory

• Aneamia should be corrected
• Nitroprusside infusion- if the systemic

pressure is normal

• Low dose inotrope infusion may be benefit

in arresting the vicious cycle of metabolic
acidosis and worsening ventricular function

• High dose of katechlamine should

be avoided because they may
increase systemic vascular
resistance, forcing more blood into
lungs and worsening the
pulmonary to systemic blood flow
distribution

Lack of response to prostaglandin infusion

Obstructed total anomalous pulmonary venous return

Reduced pulmonary vascular resistance

Increased pulmonary flow

Congestive heart failure

Lack of response to prostaglandin infusion

Transposition of great arteries

with

Intact intraventricular septum

Restrictive atrial septum

Atrial septostomy

Diferential diagnosis

• Obstructed systemic circulation and sepsis

– Incidence of the two is about the same

– 22-47% of neonates with HLHS have non

cardiac murmur

– Neonate with severe sepsis may have

reduced peripheral pulses secondary to
low cardiac output

Persistence Pulmonary Hypertension

(PPH or PFC) and duct dependent

pulmonary flow

• 9% patients treated with ECMO have CHD
• RTG-oligaemic lungs
• NO test

– Improvement in CHD because of decreased

pulmonary vascular resistance

– Negative in PFC because of intracardiac right

to left shunt

• Prostaglandins

– Decreases pulmonary vascular resistance

• Indications for early ECMO

– Cyanosis
– CO

2

clearance is relatively easy to achieve

– Radiologically normal (or oligaemic) lungs

CHD and parenchymal lung

disease

• Obstructed TAPVR
• Unremarkable clinical cardiovascular

examination

• Clinically and radiologically

indistinguishable from diseases of lung
parenchyma (pneumonia, meconium
aspiration, early emphysema)

In utero diagnosis

• HLHS - mortality is similar after in-utero

and ex-utero diagnosis

• TGA - mortality after in-utero diagnosis

is lower than after ex-utero diagnosis

• Transfer in-utero and delivery in the

tertiary care centre

Transport

• The timing of transfer is determined by the

diagnosis and clinical condition of the
newborn

–

Stabilisation before transfer

–

Vascular access

–

Prostaglandin infusion

• The infant with the duct dependent lesion will

improve greatly once ductal patency has
been achieved with prostaglandin infusion

Transport

• Despite of prostaglandin infusion clinical

improvement and stability are not achieved

• Asses the infusion of prostaglandin and

venous access

• TGA with restrictive atrial septum and

TAPVR - stabilisation may not be possible
(prompt transfer to a cardiac centre)

Transport

• Indications for intubation

– Respiratory distress
– Sever metabolic acidosis
– Apnoea caused by prostaglandin infusion

• Mechanical ventilation should optimise

systemic myocardial and pulmonary
blood flow

SV

TSV

TDV

TSP

TDP

Pressure

Volume

Systole

Diastole

A

B

CO = F x SV
SV = TDV - TSV
TDV = SV + TSV
TSP = SBP

TSP/TSV

Newborn’s circulation

Congestive heart failure

• Failure to adequately perfuse the

capillary beds of various organs

• The loos of the possibility of

oxygenation transport to the organs

SV

TSV

TDV

TSP

TDP

Pressure

Volume

Contractility

Compliance

A

B

CO = F x SV
SV = TDV - TSV
TDV = SV + TSV
TSP = SBP

TSP/TSV

Isovolumetric
contraction

Ejection

filling

Isovolumetric

diastole

Relationship of pressure and volume

during contraction and diastole

SV

Pressure

Volume

Contraction

Diastole

A

B

A-1

B-1

Decreased contraction

Pressure

Volume

B

A

B-1

Decreased compliance

SV

Pressure

Volume

A

B

A-1

B-1

Change of the afterload

Pressure

Volume

B

A

B-1

Change the preload