18.1 Heart Murmurs, Hypertension & Syncope

Cardiology is clinical category #11 on the CPNP-PC outline. Items sit in Assessment (Domain II) and Management (Domain III). You are not the pediatric cardiologist. You are the clinician who decides whether a murmur is Still’s or a VSD, whether a blood pressure is a percentile problem or a coarctation, and whether a faint is vasovagal or a sudden-death story. Acute Kawasaki criteria live in infectious diseases (13.1). This section owns the later coronary problem and the everyday cardiac exam.

Quick Answer: Innocent murmurs are systolic, grade 1–2, musical, without a thrill, symptoms, or a fixed split S2. Refer/echo for diastolic, holosystolic, grade ≥3, thrill, symptoms, or fixed S2 splitting. Check femoral pulses for coarctation. Shock as the duct closes is an emergency. AAP: annual BP ≥3 years by age/sex/height tables; confirm elevated readings; work up stage 2 or a young child. Vasovagal syncope has a prodrome; exertional, no prodrome, or family sudden death needs ECG and referral. Chest pain in primary care is usually musculoskeletal. Kawasaki coronary disease is later cardiology follow-up.

Innocent versus pathologic murmurs

Most childhood murmurs are innocent flow sounds. The exam still expects you to know which features are never innocent.

Diastolic murmurs are pathologic in children (aortic or pulmonary regurgitation, mitral stenosis). Holosystolic murmurs are VSD, mitral regurgitation, or tricuspid regurgitation until imaging says otherwise. A grade ≥3 murmur, a thrill, heart-failure symptoms, or a fixed split S2 are not watch-and-wait well-child findings. Those children get pediatric cardiology and echocardiography, not a six-month recheck of a “flow murmur.”

A newborn or infant with a concerning murmur, abnormal pulses, failed pulse-oximetry screen, or poor feeding does not wait for the 2-month visit. An older, thriving school-age child with a classic Still’s murmur and a normal exam can be followed in primary care.

Named innocent murmurs: Still’s, venous hum, PPS of the newborn

Still’s murmur is the most common innocent murmur of childhood, typically ages 3–7. It is a low-pitched, musical or vibratory midsystolic sound at the left lower sternal border or toward the apex, grade 1–2, louder when supine, softer sitting or standing. There is no thrill and no diastolic component. Do not call a harsh holosystolic LLSB murmur Still’s.

Venous hum is a continuous innocent sound in preschoolers, usually infraclavicular (often right). It is louder sitting, softer or gone supine, and it disappears with gentle jugular compression or turning the head. Continuous murmurs are otherwise PDA until you prove a venous hum with those maneuvers. Do not refer every continuous sound if it vanishes with neck compression; do not dismiss a continuous murmur that is unchanged lying down.

Peripheral pulmonary stenosis (PPS) of the newborn is a soft systolic ejection murmur from relative branch-pulmonary-artery hypoplasia. It radiates to both axillae and the back. It is common in the first weeks and typically resolves by about 3–6 months. Persistence, increasing grade, poor growth, or unequal pulses is not PPS — that is a different lesion.

Other innocent sounds (pulmonary flow in thin adolescents, a Still’s-like vibratory sound) still must pass the systolic, grade 1–2, asymptomatic, normal S2, normal pulses test.

When to refer and when to echo

Primary-care echocardiography or same-day cardiology is indicated for pathologic timing or grade, symptoms of heart failure or cyanosis, abnormal S2, abnormal pulses, a failed newborn critical-CHD screen, a concerning family history of cardiomyopathy or sudden death, and any murmur you cannot name as a classic innocent pattern with confidence. Do not order a “routine echo in 3 months” for a holosystolic grade 3 murmur in an infant who is tiring with feeds.

Femoral pulses, coarctation, and shock when the duct closes

Palpate femoral pulses on every infant exam and whenever you evaluate a murmur or hypertension. Diminished, absent, or delayed femorals compared with brachial pulses is coarctation of the aorta until proven otherwise. Check four-extremity blood pressures: higher in the arms than the legs supports coarctation. Leg BP that is not higher than arm BP in a child is a clue, not a trivia fact.

Critical congenital heart disease with ductal-dependent systemic flow (critical coarctation, interrupted aortic arch, hypoplastic left heart, critical aortic stenosis) can look well in the nursery while the ductus arteriosus is open, then present at 1–3 weeks of life with poor feeding, gray color, tachypnea, metabolic acidosis, and shock as the duct closes. That infant is an emergency: EMS/ED, prostaglandin in a setting that can give it, not an office observation hour and not a Friday outpatient echo. Newborn pulse-oximetry screening misses some lesions; a “passed screen” does not exclude critical CHD in a collapsing neonate.

AAP hypertension: measure, confirm, work up the right child

The 2017 AAP clinical practice guideline is the exam language.

• Measure blood pressure annually beginning at age 3 at well visits. Measure every visit if the child has obesity, renal disease, diabetes, a history of aortic-arch obstruction or coarctation, or is on a drug that raises BP.
• Use AAP tables by age, sex, and height percentile through age 12. From age 13, adult cut-points apply (elevated 120/80 to <130/80, stage 1 130/80–139/89, stage 2 ≥140/90).
• Technique: correct cuff (bladder ~40% of mid-arm circumference, length covering 80–100% of the arm), right arm, seated, feet on the floor, after a few minutes of rest. An elevated oscillometric reading is confirmed by auscultation.

Confirm elevated readings before you label a child hypertensive. White-coat effect is real; so is a cuff that is too small. Once confirmed, work up stage 2 hypertension and hypertension in a young child (especially under 6 years), who is more likely to have a secondary cause: renal parenchymal disease, coarctation, endocrine disease, or a drug. Do not call a 4-year-old’s stage 2 reading “essential hypertension” and send the family home with a low-salt pamphlet only. History (umbilical lines, UTI, sleep-disordered breathing, family kidney disease), exam (femorals, four-limb BP, fundi, thyroid, abdominal bruit), UA, chemistries, and, when indicated, renal ultrasound and echocardiography for left-ventricular hypertrophy belong in that workup — often with pediatric nephrology or cardiology rather than a solo primary-care titration of adult antihypertensives.

Lifestyle (DASH-style eating, activity, sleep, weight, sodium) is first-line for elevated BP and much of stage 1 disease. It is not a substitute for evaluating coarctation or kidney disease.

Syncope, Kawasaki coronaries later, and chest pain

Vasovagal (neurocardiogenic) syncope is the common faint: a prodrome of nausea, diaphoresis, pallor, and visual gray-out, often after standing, heat, pain, or a needle. Recovery is prompt. After a normal exam, a 12-lead ECG is reasonable, and primary-care counseling (hydration, salt in selected patients, sit/lie at the prodrome) is appropriate when the story is classic.

Cardiac syncope is the miss: exertional collapse, no prodrome, syncope while swimming or mid-exercise, chest pain or palpitations, a known heart lesion, an abnormal exam, or a family history of sudden death, cardiomyopathy, or unexplained drowning. Those children get an ECG and cardiology referral, not a “drink more water” plan as the only action. Do not return an athlete with exertional syncope to practice pending that workup.

Kawasaki coronary disease later. Acute complete and incomplete Kawasaki disease is referred the same day for hospital IVIG and aspirin (13.1). Primary-care cardiology follow-up is the later problem: coronary aneurysms can persist or appear after discharge; stenosis and thrombosis are long-term risks. Document that the child has cardiology follow-up and echo timing per AHA Kawasaki guidance. Do not clear unrestricted collision sport until coronary status is known. A school-age child with remote Kawasaki and no records is a records-and-cardiology problem, not a PPE signature.

Chest pain in primary care is usually musculoskeletal: costochondritis with reproducible wall tenderness, precordial-catch (brief, sharp, positional), strain after coughing or sport. Cardiac chest pain is uncommon. Exertional pain, syncope, radiation, known CHD, or an abnormal exam/ECG leaves the musculoskeletal bin.

Exam traps

• Calling a diastolic or holosystolic grade 3 murmur innocent.
• Missing coarctation because you never felt femorals.
• Sending a gray 10-day-old home as gastroesophageal reflux while the duct is closing.
• Labeling a single high school BP as hypertension without confirmation, or ignoring stage 2 and young-child hypertension.
• Treating exertional syncope as vasovagal because the ECG “can wait until sports end.”
• Clearing a post-Kawasaki athlete without knowing coronary anatomy.
• Working up every chest-wall twinge as ischemia.

Name the innocent murmur, feel the femorals, treat ductal shock as an emergency, confirm the BP, ECG the worrisome faint, and remember that Kawasaki’s coronary story continues after the fever.