Patent ductus arteriosus pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Priyamvada Singh, M.B.B.S. [2], Cafer Zorkun, M.D., Ph.D. [3], Assistant Editor-In-Chief: Kristin Feeney, B.S. [4]

Overview

The pathophysiological consequences depend on the size of the defect and the pulmonary vascular resistance.[1]

Pathophysiology

Small-Sized PDA

Medium-Sized PDA

  • Qp/Qs 1.5 to 2.0 yet small enough to offer some resistance to flow.
  • PA systolic to systemic pressures are < 0.5
  • Unusual for this group to have markedly increased PVR.
  • Due to increased return to the left heart, there is volume overload of the left atrium (LA) and the left ventricle (LV).

Large PDA

  • Defect does not restrict flow.
  • There is pulmonary hypertension at near systemic pressures (PA systolic/systolic pressure is >0.5).
  • Because of the physiologic decrease in the PVR over the first three months of life there is a large left-to-right shunt with Qp/Qs > 2.
  • The large volume overload of the left ventricle may result in LV failure.
  • There is pulmonary hypertension.
  • There may be two courses:
    • A decrease in the relative size of the ductus compared with other cardiovascular structures. This results in a medium-sized defect compared with the course expected for a medium-sized defect.
    • The development of severe pulmonary vascular obstructive disease, can occur at any time from age 3 until early adulthood. The left-to-right shunt converts to a right-to-left shunt with cyanosis and disappearance of the continuous murmur.

Gross Pathology


Shown below is the pictoral image of pathophysiology of patent ductus arteriosus

Pictoral illustration of patent ductus arteriosus

Shown below is the image of pathophysiology of patent ductus arteriosus in the cross-section of the heart

Pathophysiology of PDA

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References

  1. Giuliani et al, Cardiology: Fundamentals and Practice, Second Edition, Mosby Year Book, Boston, 1991, pp. 1653-1663.

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