Neonatal CCRN Exam

The cardiovascular items reward physiology thinking more than memorization. If you can explain where the blood is going, what the ductus arteriosus is doing for the patient, and what happens to flow when pulmonary vascular resistance rises or falls, you can reason through almost any scenario, even with a defect you have rarely seen at the bedside.

This chapter reviews fetal circulation, the changes that occur at birth, and the conditions that arise when transition is incomplete: patent ductus arteriosus, patent foramen ovale and persistent pulmonary hypertension of the newborn.

The fetus is oxygenated by the placenta, not the lungs. Oxygenated blood travels from the placenta through the single umbilical vein. About half of it bypasses the liver through the ductus venosus and enters the inferior vena cava, then the right atrium. Because of the streaming pattern in the right atrium, much of this better-oxygenated blood is directed across the foramen ovale into the left atrium, left ventricle and ascending aorta, so the heart and brain receive the most oxygen-rich blood.

Deoxygenated blood from the superior vena cava flows mainly into the right ventricle and pulmonary artery. Fetal pulmonary vascular resistance (PVR) is very high because the lungs are fluid-filled and the fetal environment is relatively hypoxic, so only a small fraction of right ventricular output perfuses the lungs. Most crosses the ductus arteriosus into the descending aorta and returns to the placenta through the two umbilical arteries. The placenta is a low-resistance circuit, so systemic vascular resistance (SVR) is low in the fetus.

Fetal Shunts and Their Fate After Birth

Three events drive transition. First, lung aeration and the rise in alveolar oxygen dilate the pulmonary arterioles, so PVR falls sharply and pulmonary blood flow increases many-fold. Second, clamping the cord removes the low-resistance placenta, so SVR rises. Third, increased pulmonary venous return raises left atrial pressure above right atrial pressure, pushing the foramen ovale flap closed.

The ductus arteriosus constricts in response to the higher arterial oxygen tension and the drop in circulating prostaglandin E2 (formerly made and cleared by the placenta and lungs). In healthy term newborns functional closure usually occurs within the first 24 to 72 hours; anatomic closure takes weeks. Preterm infants have a ductus that is less sensitive to oxygen and more sensitive to prostaglandins, so it often stays open.

Anything that keeps PVR high (hypoxia, acidosis, hypothermia, hypercapnia, sepsis, lung disease, meconium aspiration) can keep the fetal pathways open with right-to-left shunting. That is the core physiology of persistent pulmonary hypertension of the newborn (PPHN), covered in detail in Section 2.

Memory Aid: Oxygen opens the lungs and closes the duct. Low oxygen and acidosis do the opposite: they squeeze the pulmonary arteries and keep the fetal shunts open.

A patent ductus arteriosus (PDA) is common in preterm infants, especially under 28 weeks. After PVR falls, flow across the ductus reverses to left-to-right (aorta to pulmonary artery). The lungs are over-circulated and the systemic circulation loses part of its output during diastole, which is called diastolic steal.

Signs of a hemodynamically significant PDA include:

Bounding peripheral pulses and easily palpable palmar or dorsalis pedis pulses

Widened pulse pressure (low diastolic pressure), often more than about 25 mm Hg or more than half the systolic value in a preterm infant

Systolic or continuous machine-like murmur at the left upper sternal border (may be silent when the shunt is very large)

Hyperactive precordium

Increasing ventilator or oxygen requirement, failure to wean, apnea, pulmonary edema or pulmonary hemorrhage

Hypotension that responds poorly to fluids, metabolic acidosis, oliguria, feeding intolerance from reduced mesenteric flow

Chest radiograph with cardiomegaly and increased pulmonary vascular markings

Diagnosis is by echocardiogram, which shows ductal size, direction of flow, left atrial enlargement (left atrium to aortic root ratio) and reversal of diastolic flow in the descending aorta.

Management depends on gestational age, symptoms and unit philosophy. Many units now use conservative management for a period because many ducts close on their own. Options include:

Supportive care: careful fluid management (avoid excess fluid; modest restriction per order), adequate PEEP to reduce pulmonary edema, hematocrit maintained per protocol, and avoidance of routine furosemide in the first days (it stimulates renal prostaglandin and may keep the ductus open).

Pharmacologic closure with a cyclooxygenase inhibitor (indomethacin or ibuprofen) or acetaminophen.

Procedural closure: surgical ligation through a left thoracotomy or transcatheter device closure, which is now done even in small preterm infants at many centers.

Medications for PDA Closure

Common contraindications to NSAID therapy include active bleeding (including significant intraventricular hemorrhage that is evolving), platelet count under about 50,000 per microliter, suspected or confirmed necrotizing enterocolitis or intestinal perforation, significant renal impairment (oliguria under 1 mL/kg/h or rising creatinine), and, most important, a ductal-dependent congenital heart lesion. An echocardiogram should exclude ductal dependence before closure.

Typical ibuprofen lysine regimen is 10 mg/kg for the first dose followed by 5 mg/kg at 24 and 48 hours, per order and unit protocol. Feeds are often held or limited to trophic volumes during treatment per protocol.

Worked calculation: A 0.9 kg infant has received 12 mL of urine output in the last 12 hours. Urine output = 12 mL divided by 0.9 kg divided by 12 h = 1.11 mL/kg/h. That is just above the 1 mL/kg/h threshold, so the nurse reports the trend before the next NSAID dose and checks the creatinine order.

Common Trap: Giving indomethacin to an infant who has not had an echocardiogram. If the infant has an undiagnosed ductal-dependent lesion, closing the duct can cause shock or profound cyanosis. The safest answer confirms anatomy first.

Postoperative care after surgical ligation includes monitoring for post-ligation cardiac syndrome (hypotension and rising oxygen need about 6 to 12 hours after ligation as the left ventricle suddenly faces higher afterload), vocal cord paralysis from left recurrent laryngeal nerve injury (stridor, hoarse or weak cry, feeding difficulty), chylothorax, pneumothorax and phrenic nerve injury.

A patent foramen ovale (PFO) is a normal finding in many newborns. Shunting is usually small and left-to-right. It becomes important when right atrial pressure rises, as in PPHN or right-sided obstructive lesions, because blood then shunts right-to-left and causes cyanosis. In d-transposition of the great arteries, an adequate atrial opening is lifesaving because it allows mixing.

PPHN produces right-to-left shunting across the ductus and foramen ovale. The hallmark cardiovascular finding is a preductal (right hand) saturation higher than the postductal (foot) saturation by more than about 3 to 5 percentage points when the ductus is the main shunt. Cardiac evaluation by echocardiogram is essential to rule out structural heart disease, especially obstructed total anomalous pulmonary venous return, which can mimic PPHN. Ventilator and medication management is taught in Section 2.

Exam Tip: When a question shows a preductal saturation of 96% and a postductal saturation of 84%, think right-to-left ductal shunting, as in PPHN or a left-sided obstructive lesion with the duct supplying the descending aorta. A reversed difference (postductal higher than preductal) suggests d-transposition with pulmonary hypertension or with an aortic arch obstruction.

Clinical Scenario: A 26-week infant on day 5 has a ventilator FiO2 that rose from 0.25 to 0.40 over 12 hours. The nurse finds bounding brachial pulses, BP 48/22 mm Hg (mean 31), and a new systolic murmur. The nurse reports the findings as a suspected hemodynamically significant PDA, anticipates an echocardiogram, reviews the platelet count, creatinine and urine output before any NSAID order, and checks that fluid intake matches the ordered total. The widened pulse pressure (26 mm Hg) and rising oxygen need point to pulmonary over-circulation.

PVR falls and SVR rises at birth; oxygen and lower prostaglandin levels constrict the ductus.

A significant PDA causes bounding pulses, widened pulse pressure, a murmur, rising ventilator needs and diastolic steal.

Before NSAID closure, exclude ductal-dependent heart disease and check platelets, renal function, bleeding and NEC.

Ibuprofen displaces bilirubin; indomethacin reduces renal and mesenteric flow; acetaminophen requires liver monitoring.

A preductal saturation well above the postductal saturation means right-to-left ductal shunting.