Patent Ductus Arteriosus (PDA)
resistance, & potentially increased right ventricular
An acyanotic congenital heart defect, is an accessory
fetal vessel that connects the pulmonary artery to the
aorta or failure of the fetal ductus arteriosus (artery
connecting the aorta and the pulmonary artery) to close
within the first weeks of life or after several days of life
to babies born prematurely, incidence of 20 to 60 %.
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asymptomatic or may show signs of CHF.
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present.
Normal closure occurs between birth & 3 months.
If ductus arteriosus does not close after birth, it allows
blood to flow from the aorta (area of high pressure)
through the PDA & into the pulmonary artery (area of
low pressure).
With PDA, shunted blood returns to the left atrium, the
left ventricle, out the aorta, and back to the pulmonary
artery or repeats the cycle.
Born to mothers exposed to Rubella during pregnancy.
Hemodynamics:
Unoxygenated venous return through the SVC & IVC
enters the right atrium, proceeds to the right ventricle
via the tricuspid valve & into the pulmonary artery to be
delivered to the lungs for oxygenation. Oxygenated
blood from the lungs will empty into the pulmonary
veins & into the left atrium & left ventricle via the mitral
valve & proceeds to the aorta to be delivered to the
different parts of the body. But, because of the opening
between the aorta & the pulmonary artery (ductus
arteriosus), oxygenated blood is shunted back to the
pulmonary artery into the lungs for re-oxygenation.
REMEMBER: blood, or any liquid for that matter, will
always be shunted from an area of higher pressure to
an area of lower pressure). In other words, not all of the
oxygenated blood that should be delivered by the aorta
to the different parts of the body can be delivered
because some of it has gone back to the lungs because
of the defect. The effect of this altered circulation is
increased workload on the left side of the heart,
increased pulmonary vascular congestion & possibly
pressure & hypertrophy.
Assessment /Signs & Symptoms:
Patients may be asymptomatic or show signs of CHF.
1.
the left intra-clavicular area as the child ages.
2.
pulse are not palpable during the newborn period; if
they are, suspect PDA).
3.
4.
5. Growth & physical activity are limited
6. On ECG/ chest X-ray: left ventricular hypertrophy
7. Widened pulse pressure & bounding pulses result
from runoff of blood from aorta to the pulmonary
artery.
8. Continuous systolic early in life, diastolic, machinery
murmur auscultated at the 2 nd ICS, upper left sternal
border or out or under the left clavicle in older children.
9. If the defect is large enough, the flow to the lungs will
be significant & rales, congestion, increased work of
breathing, difficulty feeding, or failure to thrive occur.
Later, the left heart can become dilated. Confirmed by
an echocardiogram.
10. Risk for bacterial endocarditis & pulmonary vascular
obstructive disease in later life from chronic excessive
pulmonary blood flow.
Medical Management:
1.
inhibitor) has proved successful in closing a patent
ductus in premature infants & some newborns if
noted immediately after birth- a nonsteroidal anti-
inflammatory & prostaglandin inhibitor given in 3
separate doses IV.
2.
Lasix.
3. •
weight. the normal physiology of the heart & the
4. pathophysiology of the congenital heart defect with
heart dilation is noted from the extra blood flow – resultant complications.
PDA closure. •
the child & parents.
Surgical: •
from family.
1. Surgical division or Ligation of the Patent vessel via
left- sided thoracotomy incision does not require cardio •
pulmonary by-pass. •
Newer technique, visual- assisted thoracoscopic surgery •
(VATS), uses a thoracoscope & instruments placed congestion.
through 3 small incisions on the left side of the chest to
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place a clip on the ductus.
prostaglandin inhibitor & monitor side effects.
2. Rashkind umbrella procedure
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from family.
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congestion.
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prostaglandin inhibitor & monitor side effects.
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postoperative management.
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Non-surgical Treatment: postoperatively secondary to edema.
Use of coils to occlude the PDA in the catheterization •
laboratory is done in many centers antibiotics as necessary.
Prognosis: •
Without surgery, life expectancy is shortened because pulmonary complications.
of a common complication, bacterial endocarditis
(usually caused by streptococcus viridans).
Both procedures can be done at low risk with less than
1% mortality.

Nursing Implications:
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all children

OBSTRUCTION TO BLOOD FLOW
A. Coarctation of the Aorta (COA)- defects w/
obstruction to systemic blood flow.
Pathology /Defect- Narrowing of the lumen of the aorta
owing to a constricting band or there is
localized narrowing along the aorta (aortic arch), near
the insertion of the ductus arteriosus, resulting in
increased pressure proximal to the defect(head & upper
extremities) & decreased pressure distal to the
obstruction(body & lower extremities ,& aortic stenosis
& pulmonic stenosis are typical defects in this group. 4%
to 6% of all congenital defects, common in males than
in females.
Hemodynamics:
Unoxygenated blood from the SVC & IVC empties into
the right ventricle via the tricuspid valve to be delivered
to the lungs for oxygenation through the pulmonary
artery. Oxygenated blood from the lungs empties into
the pulmonary veins, proceeds to the left atrium & left
ventricle via the mitral valve to be delivered by the
aorta to the different parts of the body. BUT,
somewhere along the way, there is narrowing of the
aorta, so that the
oxygenated blood which is to be received by the
different parts of the body is very much diminished. In
view of this defect, COA is also known as obstructive
lesion of the heart. There is obstruction of pulmonary
blood flow & anatomic defect (atrial septal defect (VSD)
between the right & left sides of the heart. Because
blood has difficulty exiting the right side of the heart via
the pulmonary artery, pressure on the right side
increases, exceeding left-sided pressure. This allows
desaturated blood to shunt right to left, causing
desaturation in the left side of the heart & in systemic
circulation.
The effect of a narrowing within the aorta is increased
pressure proximal to the defect & decreased pressure
distal to it. In this preductal type of COA the lower half
of the body is supplied with blood by the right ventricle
through the ductus arteriosus. ,
In the post ductal type, right ventricular outflow cannot
maintain blood flow to the descending aorta. Therefore
collateral circulation develops during fetal life to
maintain flow from the ascending to the descending
aorta.
Signs & Symptoms:
1. Pathognomonic sign: Mild: absent brachial & femoral
pulses
2. Severe: headache, Vertigo, dizziness, fainting due
high BP
3. Leg cramps, fatigue, Epistaxis
4. Hypertension- Take BP in the right arm or either leg
with correct BP cuff. Pressures fairly equal w/ systolic
pressure in the lower extremity reading slightly higher
than in the upper extremity. If systolic pressure reading
in the right upper extremity is 10mm Hg higher than
that in the lower extremity, potential CoAo.
5. BP is higher in the upper extremities/ arm which may
lead to headaches & epistaxis, normally, BP in the legs is
higher 20-40 mm Hg higher than the arms because of
peripheral vascular resistance; the reverse is true in
COA (recall; BP is not usually taken in newborns unless
the doctor suspects COA
6. Lower extremities cool & with lower BP
7. If narrowing is significant, it can cause a systolic
murmur at the left sternal border & the left mid-
scapular area, increases resistance to the left ventricle
leading to left ventricular hypertension & hypertrophy.
8. If noted in infancy, more critical & can produce heart
failure. Within weeks of birth- require immediate
surgical intervention.
9. Assess for the presence of pulse equality in the upper
& lower extremities. Lying supine, right radial & femoral
pulses are palpated concurrently. Pulses should be felt
simultaneously without delay. No absence or weakness
in the femoral pulses w/ the radial or brachial pulse.
10. Impaired circulation in the lower extremities c.
a.
b.
11. Myocardial hypertrophy- usual response of the
heart when it pumps harder than usual because of an
obstruction.
12. Signs of CHF in infants- patient’s hemodynamic
condition deteriorates rapidly, & they are admitted to
the intensive care unit near death, usually severely
acidotic & hypotensive. Put on mechanical ventilation
before surgery.
13. aortic aneurysm or stroke

Management
Surgical Treatment:
1.
portion with end-to-end anastomosis of the aorta or
enlargement of the constricted section using a graft
of prosthetic material or a portion of the left
subclavian artery. Because this defect is outside the
heart or pericardium, cardiopulmonary by-pass is not
required & a thoracotomy incision is used.

Postoperative hypertension (greater than 160mmHg) is

treated with IV sodium nitroprusside or Amrinone,
followed by oral
Medications, such as captopril, hydralazine, & or
propranolol. Residual permanent hypertension after
repair of COA seem to be related to age & time of
repair.
To prevent both hypertension at rest & exercise,
elective surgery for COA is advised within the first 2
years of life. 5% -10% risk of recurrent narrowing in
patient who underwent surgical repair as infants
Percutaneous balloon angioplasty technique have
proved to be very effective in relieving residual
postoperative coarctation gradients.

Non-surgical
1.. Balloon Angioplasty/ stent
2. Use of prosthesis or graft
Prognosis
Less than 5% mortality in patients with isolated
coarctation; increased risk in infants with other complex
cardiac defects.

Nursing Implication:
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Address parents knowledge deficit
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from parents