Pediatric Cardiology
Core concepts
Separate cyanotic from acyanotic congenital heart disease and understand the physiology of each. Know the classic lesions: ventricular septal defect (harsh pansystolic murmur), atrial septal defect (fixed split S2), patent ductus arteriosus (continuous machinery murmur), tetralogy of Fallot (cyanosis, squatting, boot-shaped heart, diminished pulmonary flow), transposition of the great arteries (cyanosis with inadequate mixing, duct-dependent), and coarctation (differential blood pressures, weak femoral pulses). Understand duct-dependent lesions and the role of prostaglandin E1. Recognize heart failure in infants (tachypnea, poor feeding, failure to thrive, hepatomegaly) and the difference between respiratory and cardiac causes of distress. Know Kawasaki disease criteria and the risk of coronary aneurysms, and the basics of rheumatic fever (Jones criteria). Understand innocent murmurs (soft, systolic, positional, no symptoms) versus pathologic murmurs (diastolic, loud, continuous, associated symptoms).
Traps
- A normal oxygen saturation does not exclude serious congenital heart disease.
- Confusing a benign flow murmur with a pathologic one - diastolic or continuous murmurs are always abnormal.
- Missing coarctation because upper-limb saturations and pressures are normal.
- Forgetting that prostaglandin E1 can cause apnea and that duct-dependent lesions deteriorate when the duct closes.
- Overlooking Kawasaki in a child with prolonged fever and no other clear source.
Worked example / rule of thumb
A neonate with cyanosis and a normal or mildly decreased saturation that does not improve with oxygen, plus a single second heart sound, suggests transposition - start prostaglandin E1 and obtain urgent echocardiography. Rule of thumb: cyanosis unresponsive to oxygen = cardiac until proven otherwise; a diastolic or continuous murmur is always pathologic.