AACN CCRN (Neonatal)Free Critical-Care Registered Nurse (Neonatal) practice test

Correct answer: D. Adenosine

This presentation — a regular, narrow-complex tachycardia arising abruptly — points to supraventricular tachycardia (SVT), the tachydysrhythmia most often seen pathologically in newborns; a reentry circuit through the AV node or an accessory pathway usually drives it. Once vagal maneuvers fail in a stable infant, adenosine becomes the pharmacologic agent of choice: by briefly interrupting AV nodal conduction, it breaks the reentry loop and lets sinus rhythm resume. Its half-life is so short that a rapid IV push immediately followed by a saline flush is required for it to reach the heart. Refractory or more complicated tachyarrhythmias are where amiodarone, a broad-spectrum antiarrhythmic, has a role — but not as the initial agent for converting stable SVT. Rather than terminating the tachycardia, epinephrine would drive the heart rate and contractility even higher; its place is in cardiac arrest or severe bradycardia, not SVT. Symptomatic bradycardia from vagal stimulation or AV block is what atropine treats, by boosting sinus firing and AV conduction — a mechanism that does nothing to break a reentrant SVT circuit.

Correct answer: B. Under the right clavicle at the midclavicular line within the rib cage frame

CSTS relies on cardiorespiratory monitoring to catch apnea, bradycardia, and desaturation, so lead placement has to be accurate. The right arm (RA) lead is the white electrode, and it sits under the right clavicle at the midclavicular line, inside the rib cage frame. Because semi-upright positioning puts head flexion and reduced tone at risk of narrowing the airway, reliable heart-rate detection from correct lead placement matters most in exactly this population — late-preterm and preterm infants prone to cardiorespiratory instability in the car seat. Placement under the left clavicle at the midclavicular line belongs to the left arm (LA) lead instead; swapping RA and LA leads distorts waveform interpretation and invites monitoring errors. The left leg (LL) lead, not the white electrode, is what goes on the left lower abdomen within the rib cage frame. Placing an electrode on the lower abdomen doesn't correspond to the right arm position at all and would give inaccurate heart-rate readings.

Correct answer: A. Closely monitor for any increase in intensity or quality

Up to 10% of neonates have a heart murmur, and this is often a normal finding rather than a sign of disease. As the ductus arteriosus closes — typically within the first 48 hours after birth — nearly every newborn going through normal cardiac transition will briefly have a murmur from that closure. Because murmurs in this period don't reliably signal heart disease, but do need attention, the nurse should track the intensity, quality, location, and radiation of the sound closely, since these features guide diagnosis; conversely, a murmur's absence doesn't rule out significant cardiac disease either. Since this finding fits the expected transitional process, there's no need to notify the physician at this stage — that call is reserved for a murmur that worsens, persists, or comes with new symptoms. Other signs and symptoms would typically accompany a true congenital heart defect. And ordering diagnostic tests independently falls outside the nurse's scope; physician approval is required first.

Correct answer: A. Left-to-right shunting

Among congenital heart defects, VSD is the single most common — occurring in 2 of every 1,000 live births and making up 37% of all congenital heart disease. Because pulmonary vascular resistance runs lower than systemic vascular resistance, a large VSD lets blood shunt left to right in significant volume: well-oxygenated blood coming back from the lungs crosses the defect and is redirected to the lungs again. The lungs end up overcirculated, and CHF, pulmonary edema, respiratory distress, and failure to thrive follow. On auscultation, this produces a pansystolic murmur over the left sternal border.

Correct answer: C. Tricuspid atresia

With the tricuspid valve entirely absent, tricuspid atresia blocks blood from moving out of the right atrium into the right ventricle. Instead, systemic venous blood has to cross an atrial septal defect to reach the left heart — mixing oxygenated and deoxygenated blood along the way. Since every drop of systemic output is now mixed blood, cyanosis is a constant feature, though how severe it looks shifts with pulmonary blood flow; this obligatory mixing is what makes tricuspid atresia inherently cyanotic. Cyanosis isn't a built-in feature of pulmonary stenosis — it would only show up if right-to-left shunting develops, which isn't universal. Left-to-right shunting and pulmonary overcirculation are the typical neonatal presentation of atrioventricular septal defects; cyanosis only shows up consistently when other defects or severe pulmonary hypertension are also present. As an obstructive lesion affecting systemic outflow, coarctation of the aorta doesn't produce cyanosis on its own unless it's paired with a separate cyanotic defect.

Correct answer: D. Horizontal to V5 at the left midaxillary line

Precordial leads on a standard 12-lead ECG capture the heart's electrical activity as seen in the horizontal plane. V6 sits level with V5, out at the left midaxillary line. Getting this placement right matters for correctly reading ventricular depolarization and catching hypertrophy, ischemia, or conduction problems — and because neonates are so small, anatomic landmarks can be tricky to find, which makes knowing them well even more important. A misplaced V6 can shift QRS amplitude and axis readings enough to cause a diagnostic error. That description of 'horizontal to V5 at the left anterior axillary line' is actually where V5 goes, not V6 — mixing these two up is a frequent mistake that puts the lateral leads in the wrong spot. Adult V4 sits at the left midclavicular line, fifth ICS — a landmark that doesn't apply to V6; in neonates, V4 instead goes at the left midclavicular line, fourth ICS. Depending on which side, the left sternal border at the fourth ICS marks either V1 or V2 — neither of which tells you anything about lateral ventricular activity.

Correct answer: D. To maintain ductal patency and support systemic blood flow

Because HLHS leaves the left ventricle, mitral valve, aortic valve, and ascending aorta underdeveloped, the left ventricle simply can't drive systemic circulation on its own. These infants instead depend on a right-to-left shunt across a patent ductus arteriosus (PDA), which lets blood ejected from the right ventricle reach the body. A continuous PGE1 infusion keeps that ductus from closing — closure would otherwise occur within the first days of life. Should the ductus close in HLHS, systemic perfusion collapses abruptly, triggering profound acidosis, shock, and death; since the ductus can constrict quickly once prostaglandin levels drop, the infusion has to run continuously. Balancing pulmonary against systemic blood flow sometimes calls for raising pulmonary vascular resistance as a supportive measure, but that's not why prostaglandin therapy is given — PGE1 itself doesn't raise pulmonary vascular resistance. When the atrial septum is restrictive or intact, the left atrium may need decompressing, often via balloon atrial septostomy; that intervention matters in select cases, but it doesn't substitute for keeping the ductus open to preserve systemic circulation. Neither correcting metabolic acidosis nor boosting myocardial contractility directly is something PGE1 does — acid–base status improves only as a downstream effect once ductal flow restores systemic perfusion.

Correct answer: B. 3 to 5 g/dL

Once deoxygenated hemoglobin in the arterial circulation reaches roughly 3 to 5 g/dL, cyanosis becomes visible to the eye. Because this threshold depends on total hemoglobin as much as oxygen saturation, presentations can be deceptive: an infant with polycythemia might look cyanotic even at a relatively higher saturation, simply because more total hemoglobin is available to desaturate, while an anemic infant could be severely hypoxemic yet show no visible cyanosis for lack of enough hemoglobin to produce the discoloration. This is exactly why cyanosis is an imperfect gauge of oxygenation. A deoxygenated hemoglobin level of only 1 to 2 g/dL generally isn't enough to make cyanosis visible. Deoxygenated hemoglobin levels of 8 to 10 g/dL or 15 g/dL would reflect far more profound desaturation than what's needed for cyanosis to first appear.

Correct answer: B. Polycythemia

Right-to-left shunting is the hallmark of cyanotic congenital heart defects, letting deoxygenated blood skip the lungs and enter systemic circulation — the tissues end up chronically hypoxemic as a result. The kidneys respond by ramping up erythropoietin, which drives excessive red blood cell production. That polycythemia thickens the blood, and with it comes a risk of poor tissue perfusion, thrombosis, stroke, and sluggish microcirculatory flow. Rather than helping, this compensatory response can actually worsen overall oxygen delivery in neonates with cyanotic heart disease, which is why polycythemia stands out as a major, ongoing risk demanding close monitoring and management. Rather than a complication, a heart murmur is simply a physical exam finding; although common in congenital heart disease, it doesn't itself raise morbidity or reflect the downstream effects of chronic hypoxemia. As the leading cause of cyanotic congenital heart disease, tetralogy of Fallot is a diagnosis, not a consequence of cyanosis — this question is asking about physiologic fallout, not disease classification. Renal perfusion can eventually suffer from prolonged hypoxemia, but renal injury isn't among the earliest or most frequent risks for neonates with cyanotic congenital heart defects; hematologic complications tied to increased viscosity show up sooner and more often.

Correct answer: D. Fluid restriction

TOF carries a risk of hypercyanotic ('tet') spells, which can arise when the right ventricular outflow tract obstruction transiently worsens, cutting pulmonary blood flow to minimal or nothing. These true spells are uncommon, but because even one can turn life-threatening, a single significant episode should prompt earlier surgery. Knee-chest positioning is the first step in managing a spell medically, with oxygen, morphine, and fluid boluses added as needed; quickly calming the infant matters too. A beta-blocker such as propranolol, or a systemic vasopressor, are additional options that may be tried.