Cardiovascular problems Flashcards

1
Q

Why is a PDA more common in premature infants?

A

Smooth muscle in the wall of ductus is less responsive to high PaO2, thus less likely to constrict

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2
Q

Risk factors for PDA

A
  • Prematurity
  • Hypoxia
  • Acidosis
  • Increased pulmonary pressure/PVR
  • Systemic hypotension
  • Local release of prostaglandins
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3
Q

Why can a PDA be problematic from a physiological perspective?

A

Haemodynamically-significant PDA causes “ductal steal” - left-right shunting causes increased pulmonary blood flow and reduced systemic perfusion (with complications resulting from both of these)

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4
Q

Consequences of PDA

A

Effects of increased pulmonary blood flow:

  • Pulmonary oedema
  • Pulmonary haemorrhage
  • Bronchopulmonary dysplasia (4-5x risk in VLBW infants)

Effects of reduced systemic perfusion:

  • IVH (ischaemia-reperfusion injury)
  • NEC
  • Renal failure
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5
Q

Clinical manifestations of PDA

A
  • Hyperdyamic precordium, bounding pulses
  • Wide pulse pressure
  • Machine-like continuous or systolic murmur
  • Hepatomegaly
  • Increased O2 dependence and CO2 retention
  • renal failure
  • X-ray - cardiomegaly, incr pulmonary vascular markings
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6
Q

Approach to management of PDA

A

Controversial:

  1. Prophylactic treatment
  2. Closure of asymptomatic PDA
  3. Closure of only symptomatic PDA
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7
Q

Treatment options for PDA

A
  • Fluid restriction
  • Pharmacologic - COX inhibitors
  • Surgical ligation
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8
Q

What are the options for pharmacological closure of a PDA and what are their pros and cons?

A

All are COX inhibitors - inhibit prostaglandin production. Efficacy inversely proportional to GA and postnatal age.

  • Indomethacin 3/7 course - reduces risk of severe IVH, pulmonary haemorrhage, symptomatic PDA; no sig incr risk of NEC or spont perf
  • Ibuprofen - as effective as indocid but lower rates of oliguria, reduces mechanical vent, reduced rate of NEC; BUT does not reduce risk of IVH
  • Paracetamol - may be effective, less SEs
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9
Q

Contraindications to pharmacological treatment of PDA (indomethacin)

A
  • Thrombocytopenia <80
  • Active haemorrhage (incl severe IVH)
  • NEC
  • Incr creatinine >150 or oliguria <1
  • also avoid with concomitant use of hydrocortisone (incr risk of spont perf)
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10
Q

Indications for surgical ligation of PDA

A

failed pharmacological treatment or contraindications to COX inhibitors

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11
Q

Predisposing factors for PPHN

A
  • Birth asphyxia
  • MAS
  • Sepsis
  • RDS
  • Hypoglycaemia
  • Polycythaemia
  • Maternal use of NSAIDs (in utero DA constriction)
  • Maternal late trimester use of SSRIs
  • Pulmonary hypoplasia
    BUT often idiopathic
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12
Q

What is the pathophysiology of PPHN?

A

Increased neonatal PVR, due to:

  • Maladaptive from an acute injury (not demonstrating normal vasodilation in response to incr PaO2 after birth)
  • Result of incr pulmonary artery medial muscle thickness and extension of smooth muscle into normally non-muscular peripheral arterioles - result of chronic fetal hypoxia
  • Consequence of pulmonary hypoplasia
  • Obstructive - result of polycythaemia, TAPVR, or congenital diffuse developmental disorders of acing lung development
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