patent ductus ateriosis pda muhammad syed md heart
TRANSCRIPT
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Patent Ductus AteriosisPDA
Muhammad Syed MD
Heart
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Low vascular resistance of the placenta
High vascular resistance of the fluid-filled fetal lung
Right-to-left shunts
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Two right-to-left shunts occur in the fetus• Foramen ovale — Blood shunted from the right
to left atrium • Ductus arteriosus — Blood shunted from the
pulmonary artery to the aorta
Ductus Arteriosus
ForamenOvale
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Two right-to-left shunts occur in the fetus
• Foramen ovale — Blood shunted from the right to left atrium
• Ductus arteriosus — Blood shunted from the pulmonary artery to the aorta
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TRANSITION AT DELIVERY
• Alveolar fluid clearance
• Lung expansion
• Circulatory changes
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Circulatory changes
• clamping of the umbilical cord, • rise in neonatal systemic blood pressure. • lung expansion reduces both pulmonary vascular
resistance and the pulmonary artery pressure.
• increased pulmonary arterial blood flow • raises pulmonary venous return to the left atrium and left
atrial pressure. • As the left atrial pressure increases and the right atrial
pressure falls, right-to-left shunting across the foramen ovale decreases.
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Patent Foramen Ovale
If the flap forms incompletely or does not completely seal close, then deoxygenated blood can pass from the right atrium to the left atrium. A patient with an open or patent foramen ovale will have a heart murmur. Unfortunately, this heart murmur maybe undetectable and the patient will exhibit no other obvious symptoms.
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If the ductus arteriosus remains open after birth and fails to close it is referred to as a patent ductus arteriosus.
Patent Ductus Arteriosus
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• PDA occurs commonly in premature infants, especially in those with respiratory distress syndrome
• Among very low birth weight (VLBW) infants (birth weight below 1500 g) PDA occurred in 30 percent
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Because of the large volume of blood flow, the ductus becomes a large vessel with a diameter similar to that of the descending aorta
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Patency of the ductus
Mainly on Low arterial oxygen content
Also is influenced by dilators,
• prostaglandins
• nitric oxide
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HYDROCORTISONE
Facilitates ductal constriction
Hydrocortisone treatment decreases the
sensitivity of the ductus to the dilating action
of PGE2
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CLOSURE
Constrictors (Increased O2)
PGE2, a vasodilator
Anatomic closure usually is complete within one to three months.
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Gestational age
In term infants, functional closure after birth
24 hours 50 %48 hours in 90 %72 hours in virtually all
In preterm infants, ductal closure can bedelayed and the ductus can reopen followingconstriction.
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Delayed closureOccurs especially when accompanying respiratory disease is present.
Severe respiratory distress syndrome; in ill infants less than 30 Wgestation, PDA persists on the fourth day in approximately 65 %
Two other factors may be important:
• Contractile capacity in ductal tissue is less in immature
• Ductus in preterm infants continues to dilate in response to PGE2 and NO, in contrast to term infants whose ductus loses responsiveness shortly after birth
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Reopening
• The histological changes following constriction of the ductus occur rapidly in term infants and prevent subsequent reopening.
• Reopening may occur because the effects of ductal constriction on events that lead to anatomic closure are influenced by immaturity.
• In one study, for example, constriction resulted in hypoxia, cell death, VEGF expression, endothelial proliferation, and intimal mound formation in the ductus of term but not preterm baboons
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Shunting of blood flow through a PDA in prematures is essentially all left-to-right
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Excessive flow through the pulmonary circulation
Pulmonary edema
Pulmonary hemorrhage
Bronchopulmonary dysplasia
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Systemic and cerebral blood flow effects
Preterm animals and infants with a PDA
increase their cardiac output. However,
postductal blood flow is reduced, which may
lead to organ dysfunction.
NEC
IVH
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CLINICAL FEATURES
• Machinery Murmur ( infraclavicular region and upper left sternal border)
• Prominent left ventricular impulse
• Bounding pulses,
• and widened pulse pressure (greater than 25 mmHg)
• "silent," especially in the first three days
(deterioration of respiratory status )
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Diagnosis
• ECHO
• A transductal diameter that exceeds 1.5 mm is the most commonly used definition of a significant PDA
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PDA closure indications
• Significant left-to-right shunt + symptomatic
• Evidence of left-sided volume overload (ie,
left atrial or ventricular enlargement),• reversible pulmonary arterial hypertension
• PDA closure is not recommended in patients with severe and irreversible PAH
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Small PDA Recommend closure of a small audible PDAeven in the absence of a significant L-to-Rright shunt
Silent PDA Never have hemodynamic consequencesRisk Of endocarditis
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Infants with a persistent PDA had a four-fold increased risk of death compared to infants who never had a significant PDA
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Management
• Supportive therapy — During evaluation and treatment, supportive measures are applied.
• A neutral thermal environment and adequate oxygenation minimize demands on left ventricular output.
• Positive end-expiratory pressure (PEEP) may improve gas exchange in infants with respiratory compromise.
• Maintaining the hematocrit at 35 to 40 percent may increase pulmonary vascular resistance and reduce the left-to-right shunt
• Not recommend routine use of furosemide or any other loop diuretic, which stimulates renal synthesis of PGE2.
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THERAPEUTIC INTERVENTIONS
Interventions for PDA closure include:
• Pharmacologic therapy, which is used exclusively in premature infants
• Surgical ligation
• Percutaneous catheter occlusion
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Pharmacologic therapy
Inhibitors of prostaglandin synthesis, such
as indomethacin and ibuprofen, are used as
the initial interventions for PDA closure in
preterm infants.
Indomethacin has proven to be ineffective in
term infants and older patients with a PDA.
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Thank you