IGNOU PB Bsc Nsg Entrance-2017
Child Health Nursing (Pediatrics)
Medium

One of the following is a cyanotic congenital heart disease?

Appeared in: IGNOU PB Bsc Nsg Entrance-2017

Explanation

  • Pulmonary stenosis is an obstructive congenital heart defect that narrows the passage from the right ventricle to the pulmonary artery.
  • While mild to moderate forms are acyanotic, severe or 'critical' pulmonary stenosis significantly increases pressure in the right side of the heart.
  • This high pressure can force deoxygenated blood to move from the right atrium to the left atrium (a right-to-left shunt) through an associated opening like a patent foramen ovale (PFO) or atrial septal defect (ASD).
  • The mixing of deoxygenated blood into the systemic circulation results in cyanosis, making it a cyanotic condition in these severe cases.

Why Other Options Were Wrong

  • Option A: Atrial septal defect (ASD) is a classic acyanotic congenital heart disease. It involves a hole in the septum between the atria, causing a left-to-right shunt where oxygenated blood flows from the left atrium to the right atrium.
  • Option B: Ventricular septal defect (VSD) is the most common congenital heart defect and is acyanotic. It features a hole in the septum between the ventricles, leading to a left-to-right shunt of oxygenated blood from the left ventricle to the right ventricle.
  • Option D: Patent ductus arteriosus (PDA) is an acyanotic defect. It is the failure of the ductus arteriosus (a fetal blood vessel) to close after birth, resulting in a left-to-right shunt where oxygenated blood from the aorta mixes with blood in the pulmonary artery.

Related Visual

Visual explanation — Related Visual
Clinical Relevance
  • Nursing practice connection: Knowing Classification of congenital heart diseases as cyanotic or acyanotic helps nurses interpret findings accurately and avoid errors in routine assessment, medication administration, and patient teaching.
  • Nurses must be skilled in the early recognition of cyanosis in newborns, as it can signal a critical cardiac emergency requiring immediate prostaglandin infusion and surgical consultation.
  • A key nursing assessment is differentiating between central cyanosis (blue tongue and mucous membranes), which indicates true hypoxemia, and peripheral cyanosis (acrocyanosis), which can be normal in newborns.
  • Monitoring oxygen saturation via pulse oximetry is a critical nursing intervention for any infant suspected of having congenital heart disease.
How to Approach the Question
  • First, identify the core concept being tested: the classification of congenital heart disease into cyanotic and acyanotic types.
  • Recall the fundamental difference: Acyanotic defects typically involve a left-to-right shunt (oxygenated blood recirculates to the lungs), while cyanotic defects involve a right-to-left shunt (deoxygenated blood enters systemic circulation).
  • Systematically evaluate each option. Recall that Atrial Septal Defect (ASD), Ventricular Septal Defect (VSD), and Patent Ductus Arteriosus (PDA) are the most common examples of acyanotic defects.
  • Consider Pulmonary Stenosis. It is an obstructive lesion, not a shunt. However, think about the hemodynamic consequences. Severe obstruction increases right-sided pressure.
  • Deduce that this high pressure can force a right-to-left shunt if an interatrial communication (like a PFO or ASD) exists, thus causing cyanosis.
  • Conclude that among the given choices, Pulmonary Stenosis is the only one that can present as a cyanotic condition at birth.
Concept Tested & Keywords
  • Concept Tested: Classification of congenital heart diseases as cyanotic or acyanotic.
  • Stem keywords: cyanotic, congenital heart disease
  • Lead-in keywords: One of the following is
  • Negative lead-in flag: false

Question ID

QRUjgKlkFLZXAZoHRBZmBO

Reference Book

E6 Pathology-Textbook of PATHOLOGYHarsh Mohan Part 2 (215-514) p. 1

E6 Pathology- ROBBINS & COTRAN PATHOLOGIC BASIS OF DISEASE 10TH Ed p. 541-543

E6 Midwifery Obstetrics and Gynecology Nursing Sandeep Kaur p. 25-33

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