Congenital heart defects can affect blood flow to the lungs. In defects with decreased pulmonary blood flow, less blood reaches the lungs for oxygenation, leading to low oxygen levels in systemic circulation. Tetralogy of Fallot is a classic example of such a defect.

Rationale for correct answer:

B. Tetralogy of Fallot (TOF) includes pulmonary stenosis, which limits blood flow to the lungs. This results in low oxygen levels, visible as bluish skin, lips, or nail beds. Children may develop compensatory behaviors, such as squatting, to improve oxygenation during activity.

Rationale for incorrect answers:

A. Ventricular septal defect (VSD) typically causes increased pulmonary blood flow, as blood shunts from the left ventricle to the right ventricle and then to the lungs.

C. Patent ductus arteriosus (PDA) also usually increases pulmonary blood flow, as oxygenated blood from the aorta flows into the pulmonary artery.

D. Atrial septal defect (ASD) allows left-to-right shunting, which also increases pulmonary blood flow over time.

Test-taking strategy:

• Identify the pulmonary blood flow pattern:
  • Decreased pulmonary flow causes bluish skin, cyanosis, hypoxemia, compensatory postures.
  • Increased pulmonary flow causes heart failure symptoms, pulmonary congestion.
• Match the defect with the physiologic effect, not just the name.

Take-home points

• Tetralogy of Fallot is a defect with decreased pulmonary blood flow.
• Look for low oxygen levels and compensatory postures as classic clinical signs.
• Other common defects (VSD, PDA, ASD) generally increase pulmonary blood flow, causing different symptoms.

Tetralogy of Fallot is a congenital heart defect that reduces blood flow to the lungs, leading to low oxygen levels in the systemic circulation. Children often develop compensatory behaviors to improve oxygenation, such as squatting during episodes of exertion, which is a classic sign.

Rationale for correct answer:

B. Squatting increases systemic vascular resistance, reducing right-to-left shunting through the heart. This redirects more blood to the lungs, improving oxygenation. It is a hallmark compensatory mechanism seen in children with TOF, especially during activity or crying.

Rationale for incorrect answers:

A. Continuous machinery-like murmur is characteristic of patent ductus arteriosus (PDA), not TOF.

C. Bounding pulses in all extremities are more typical of aortic regurgitation or patent ductus arteriosus, not TOF.

D. Fixed splitting of the second heart sound is characteristic of atrial septal defect (ASD), not TOF.

Test-taking strategy

• Identify the classic clinical signs of TOF including low oxygen levels, hypoxic episodes, and compensatory behaviors.
• Distinguish TOF from other defects by the presence of squatting during activity and cyanosis.

Take-home points

• Children with TOF may squat to relieve hypoxia and improve oxygen delivery during activity.
• Other murmurs or pulse abnormalities are more typical of different congenital heart defects.
• Recognizing these behaviors helps prompt timely intervention during hypoxic episodes.

Children with tetralogy of Fallot can experience hypercyanotic spells (also called Tet spells), where oxygen levels drop suddenly due to increased right-to-left shunting.

Rationale for correct answer:

C. Morphine reduces infundibular spasm in the right ventricular outflow tract. It slows heart rate, allowing more time for blood to flow to the lungs and decreases the severity and frequency of hypercyanotic episodes.

Rationale for incorrect answers:

A. Furosemide, a diuretic used to manage fluid overload or heart failure. It does not prevent hypercyanotic spells in TOF.

B. Digoxin increases cardiac contractility and may help with heart failure symptoms. It is not specifically used to reduce hypercyanotic episodes.

D. Enalapril is an ACE inhibitor used to reduce afterload and manage heart failure. It does not directly prevent hypercyanotic spells.

Test-taking strategy

• Identify the primary problem in TOF hypercyanotic spells: sudden hypoxemia due to right-to-left shunting.
• Choose medications that reduce heart rate and spasm, not just treat heart failure.

Take-home points

• Morphine is the drug of choice for preventing or treating Tet spells in TOF.
• Other cardiac medications (digoxin, furosemide, enalapril) are used for heart failure management but do not prevent acute cyanotic episodes.
• Recognizing triggers and prophylactic management reduces hypoxic complications while awaiting surgery.

Tetralogy of Fallot is characterized by decreased pulmonary blood flow and right-to-left shunting, leading to chronic hypoxemia. The expected clinical manifestations are those related to low oxygen levels and the child’s compensatory behaviors.

Rationale for correct answer:

C. Cyanosis, irritability, clubbing, and crouching: Cyanosis is the hallmark finding due to right-to-left shunting and decreased pulmonary blood flow. Irritability is common in hypoxic children, especially during Tet spells. Clubbing develops over time from chronic hypoxia. Crouching (squatting) is classic compensatory posture that increases systemic vascular resistance, reducing shunting and improving oxygenation.

Rationale for incorrect answers

A. Cyanosis, hypertension, clubbing, and lethargy: Children with TOF are more likely to experience hypotension, not hypertension. Lethargy is not a classic primary finding unless severe hypoxia is present.

B. Cyanosis, hypotension, crouching, and lethargy: Cyanosis and crouching are consistent with TOF. Lethargy is not a typical expected finding; children are more often irritable due to hypoxia.

D. Cyanosis, confusion, clonus, and crouching: Confusion and clonus suggest neurologic pathology, not typical findings of TOF. These are not standard or expected assessment findings.

Test-taking strategy

• Focus on classic manifestations of TOF:
  • Cyanosis
  • Irritability
  • Clubbing
  • Squatting/crouching
• Eliminate options with neurologic signs or abnormal blood pressure findings not characteristic of TOF.

Take-home points

• Tetralogy of Fallot causes chronic hypoxia, leading to cyanosis and clubbing.
• Irritability is common, especially during hypoxic episodes.
• Crouching or squatting is a hallmark compensatory behavior that improves oxygenation.
• Recognizing classic signs helps nurses identify worsening hypoxia and intervene promptly.

In tetralogy of Fallot, right-to-left shunting allows deoxygenated blood to bypass the lungs, causing chronic hypoxemia. The body compensates by producing more red blood cells to increase oxygen-carrying capacity, a condition known as secondary polycythemia.

Rationale for correct answer:

D. Chronic hypoxemia stimulates erythropoietin production in the kidneys, which in turn increases RBC production. Elevated RBCs help improve oxygen delivery to tissues, partially compensating for the low arterial oxygen saturation. This is a normal physiological response to chronic hypoxia in cyanotic heart defects.

Rationale for incorrect answers:

A. Anemia is characterized by low RBC count, hemoglobin, or hematocrit, not elevated RBCs.

B. Dehydration may increase hemoglobin and hematocrit slightly, but it is not the primary cause in a cyanotic infant. Elevated RBCs in this context are due to chronic hypoxia, not fluid status.

C. Jaundice refers to hyperbilirubinemia, not RBC elevation. Although polycythemia can increase bilirubin breakdown, jaundice is a secondary effect, not the cause of elevated RBCs.

Test-taking strategy:

• Identify the underlying problem in tetralogy of Fallot which is chronic hypoxemia.
• Link laboratory findings (elevated RBCs) with physiologic compensatory mechanisms rather than unrelated conditions.
• Eliminate options that contradict the lab finding (anemia refers to low RBC, jaundice is caused by excess bilirubin, dehydration causes minor hemoconcentration).

Take home points

• Chronic hypoxemia in cyanotic heart defects triggers secondary polycythemia (elevated RBC count).
• This is the body’s compensatory mechanism to improve oxygen delivery to tissues.
• Understanding these lab findings helps guide nursing assessment, monitoring for hyperviscosity, and patient education.

The infant is experiencing a hypercyanotic (Tet) spell, a life-threatening complication of tetralogy of Fallot. Tet spells occur when pulmonary blood flow decreases, causing right-to-left shunting and severe hypoxemia. The priority intervention is to increase systemic vascular resistance and improve pulmonary blood flow.

Rationale for correct answer:

C. Knee-chest positioning increases systemic vascular resistance, which reduces right-to-left shunting, increases blood flow to the lungs, and improves oxygenation and tissue perfusion. This is the first-line intervention during a Tet spell, followed by oxygen, morphine, and fluids as needed.

Rationale for incorrect answers:

A. Oxygen may help, but it is not as immediately effective as knee-chest positioning in increasing pulmonary blood flow. Oxygen alone does not stop the shunt or improve systemic vascular resistance as effectively.

B. Morphine sulfate calms the infant and decreases pulmonary vascular resistance but is secondary to knee-chest positioning. The first priority is mechanical intervention to improve circulation.

D. Placing the infant in Fowler’s position does not increase systemic vascular resistance or improve pulmonary blood flow. It is inappropriate for a Tet spell and may worsen hypoxemia if the infant struggles to breathe.

Test-taking strategy:

• Recognize classic Tet spell signs: sudden cyanosis, tachypnea, diaphoresis, weak pulses.
• Prioritize interventions that increase pulmonary blood flow and systemic vascular resistance first.
• Use the ABCDE approach, focusing on breathing and circulation in cyanotic episodes.

Take home points

• Tet spells are acute, potentially life-threatening events in infants with tetralogy of Fallot.
• Immediate nursing interventions:
  • Place infant in knee-chest position
  • Administer oxygen
  • Give morphine if ordered
  • Provide fluid replacement if needed
• Early recognition and rapid intervention prevent severe hypoxemia and cardiac arrest.

Tetralogy of Fallot (TOF) is characterized by right-to-left shunting caused by a combination of pulmonary stenosis, ventricular septal defect (VSD), overriding aorta, and right ventricular hypertrophy. Children with TOF often develop hypercyanotic episodes ("Tet spells") during crying, feeding, or activity due to increased right-to-left shunting, leading to worsening cyanosis.

Rationale for correct answer:

C. Cyanosis worsens with activities that increase oxygen demand or decrease pulmonary blood flow. Hypercyanotic episodes are classic signs of TOF, often accompanied by irritability or fussiness, tachypnea, and squatting or knee-chest position.

Rationale for incorrect answers:

A. A machinelike murmur is characteristic of a patent ductus arteriosus (PDA), not TOF.

B. Eisenmenger syndrome is a long-term complication of uncorrected left-to-right shunts, leading to pulmonary hypertension and reversal of the shunt. This is not an expected finding in a child with TOF, especially before surgical correction.

D. Higher pressures in the upper extremities than with the lower extremities is typical of coarctation of the aorta, not TOF.

Test-taking strategy:

• Identify various congenital heart defect:
  • TOF causes cyanosis, Tet spells, squatting
  • PDA causes a machinelike murmur
  • Coarctation is characterized by BP differences between upper and lower extremities
  • Eisenmenger is a chronic, late complication of long-standing shunt

Take home points

• Tetralogy of Fallot presents with cyanosis that worsens with activity or crying due to right-to-left shunting.
• Hypercyanotic episodes (Tet spells) are hallmark signs and require prompt recognition and intervention.
• Murmur type, blood pressure differences, and long-term complications help differentiate other congenital heart defects.

Clubbing is a common finding in children with congenital heart defects like tetralogy of Fallot. It develops over time as a compensatory response to prolonged low oxygen levels in the blood (chronic hypoxia). The body adapts to improve tissue oxygenation, resulting in thickening of the distal fingers and toes.

Rationale for correct answer:

B. Chronic hypoxia stimulates vascular endothelial growth and increased blood flow to distal extremities, leading to thickened, bulbous fingertips and toes. Clubbing is directly related to the duration and severity of hypoxia, not an acute event.

Rationale for incorrect answers:

A. Polycythemia, that is increased RBC production, occurs as a compensatory mechanism for chronic hypoxia, but it does not directly cause clubbing. Clubbing is the result of long-term tissue hypoxia, not the high RBC count itself.

C. A murmur is a sound caused by turbulent blood flow, not a cause of physical changes like clubbing. Murmurs indicate structural heart defects, but do not produce hypoxia-induced tissue changes.

D. While chronic hypoxia can affect growth and development, clubbing is not caused by poor growth, but by long-term oxygen deprivation in the extremities.

Test-taking strategy:

• Identify physical manifestations of tetralogy of Fallot:
  • Clubbing, cyanosis, and polycythemia result from chronic hypoxia.
• Distinguish causal vs. associated findings: polycythemia is associated, not the direct cause of clubbing.

Take home points

• Clubbing of fingers and toes is a hallmark sign of chronic hypoxia in cyanotic heart defects.
• Polycythemia, murmurs, or growth delays may be associated findings, but chronic low oxygen levels drive clubbing.
• Early recognition of hypoxia-related changes helps guide long-term monitoring and intervention in children with cyanotic congenital heart disease.

Tetralogy of Fallot is a congenital heart defect characterized by ventricular septal defect (VSD), pulmonary stenosis, overriding aorta, and right ventricular hypertrophy (RVH). The right ventricular hypertrophy causes the heart to appear boot-shaped on chest X-ray, which is a classic diagnostic clue for TOF.

Rationale for correct answer:

A. The prominent right ventricular apex and upturned left upper border of the heart create a boot-shaped appearance. This is a hallmark finding in TOF and correlates with right ventricular hypertrophy caused by pulmonary stenosis.

Rationale for incorrect answers:

B. Oblong appearance of heart on X-ray may be seen in dilated cardiomyopathy or other types of cardiomegaly, not specific for TOF.

C. Increased pulmonary vascular markings are usually associated with left-to-right shunt defects like VSD, PDA, or ASD. In TOF, pulmonary blood flow is often decreased, so markings may be normal or decreased.

D. TOF primarily causes right ventricular hypertrophy due to obstruction to pulmonary blood flow. Left ventricular hypertrophy is not characteristic of TOF.

Test-taking strategy:

• Remember the classic X-ray finding for TOF is a boot-shaped heart.
• Differentiate congenital heart defects:
  • Those that result in decreased pulmonary blood flow cause right-sided hypertrophy.
  • Those with increased pulmonary blood flow, left-sided hypertrophy.

Take home points

• Tetralogy of Fallot features VSD, pulmonary stenosis, overriding aorta, and right ventricular hypertrophy.
• Boot-shaped heart on X-ray is a key diagnostic finding.
• Other defects may show different X-ray patterns, so recognize right-sided vs left-sided hypertrophy and pulmonary vascular markings.

Tricuspid atresia is a congenital heart defect characterized by the absence of a tricuspid valve, which results in no direct communication between the right atrium and right ventricle. This defect leads to obligatory right-to-left shunting through an atrial septal defect (ASD) or patent foramen ovale, and blood flow to the lungs depends on a ventricular septal defect (VSD) or patent ductus arteriosus (PDA).

Rationale for correct answer:

D. “There’s no communication between the right atrium and right ventricle.” This statement accurately describes the primary anatomical defect in tricuspid atresia. Because the right ventricle is underdeveloped (hypoplastic) or absent, blood cannot flow directly from the right atrium to the right ventricle. Pulmonary blood flow is dependent on a VSD or PDA, which explains why children with tricuspid atresia are often cyanotic.

Rationale for incorrect answers:

A. “There’s a narrowing at the aortic outflow tract.” This describes aortic stenosis, not tricuspid atresia.

B. “The pulmonary veins don’t return to the left atrium.” This describes total anomalous pulmonary venous return (TAPVR), a separate congenital defect.

C. “There’s a narrowing at the entrance of the pulmonary artery.” This describes pulmonary stenosis, which can occur in some defects but is not the defining feature of tricuspid atresia.

Test-taking strategy:

• Focus on defining anatomical features of congenital heart defects.
• For tricuspid atresia, the key defect is absence of the tricuspid valve, leading to absent right atrium–right ventricle communication.
• Eliminate options describing other defects affecting valves or pulmonary veins.

Take home points

• In tricuspid atresia there is no direct communication between right atrium and right ventricle.
• Blood flow to the lungs relies on VSD or PDA; cyanosis is present early.
• Understanding the primary anatomical defect helps parents and caregivers recognize symptoms and understand surgical interventions.
• Early detection and monitoring are crucial for oxygenation and growth in affected infants.

Tricuspid atresia is a congenital heart defect caused by the absence of the tricuspid valve, resulting in no communication between the right atrium and right ventricle. This defect leads to right-to-left shunting of blood, causing deoxygenated blood to enter systemic circulation, which manifests as cyanosis.

Rationale for correct answer:

A. Cyanosis is the hallmark sign of tricuspid atresia. Occurs because oxygen-poor blood bypasses the lungs through an atrial septal defect or patent foramen ovale. Severity of cyanosis depends on the degree of pulmonary blood flow and presence of associated defects (VSD, PDA). Often present at birth or in early infancy, and may worsen during stress, crying, or feeding.

Rationale for incorrect answers:

B. A machinelike murmur is characteristic of patent ductus arteriosus (PDA), not tricuspid atresia. Murmurs in tricuspid atresia are usually related to VSD flow or pulmonary stenosis, not a machinelike PDA murmur.

C. Children with tricuspid atresia often increase their respiratory rate to compensate for hypoxia. Tachypnea, not bradypnea, is more likely.

D. Capillary refill is usually normal unless heart failure or shock develops. Delayed refill is not a defining characteristic of tricuspid atresia.

Test-taking strategy:

• Focus on the primary physiologic problem of the defect in tricuspid atresia, that is, impaired blood flow to the lungs resulting in low oxygen levels.
• Choose findings that reflect chronic hypoxemia, not infection, shock, or unrelated murmurs.

Take home points

• Tricuspid atresia causes cyanosis due to right-to-left shunting.
• Early recognition of cyanosis is critical for diagnosis and management, including monitoring oxygenation and planning for surgical intervention.
• Other findings such as murmurs or tachypnea may vary depending on associated defects, but cyanosis is the key consistent sign.

Polycythemia in children with tricuspid atresia is a compensatory response to chronic hypoxemia. When oxygen saturation is chronically low, the body increases erythropoietin production, stimulating the bone marrow to produce more red blood cells.

Rationale for correct answer:

B. There is an increased ability for the oxygen to carry blood: The primary purpose of polycythemia in cyanotic heart disease is to enhance oxygen delivery to tissues. Higher red blood cell mass allows more hemoglobin molecules to transport oxygen, partially offsetting the low arterial oxygen saturation.

Rationale for incorrect answers:

A. The red blood cell count is normal: This is incorrect because polycythemia is defined by an elevated red blood cell count.

C. There is little to no effect on the blood clotting system: Polycythemia can increase blood viscosity, which may predispose the child to thrombosis or stroke, so it does affect the blood clotting system indirectly.

D. The viscosity of the blood is unchanged: Increased RBCs thicken the blood, increasing viscosity, which can lead to complications like headaches, dizziness, stroke, and poor perfusion.

Test-taking strategy:

• Remember that polycythemia is a compensatory mechanism for chronic hypoxia in cyanotic heart defects.
• Consider both benefits such as increased oxygen-carrying capacity and risks such as hyperviscosity and clotting complications.
• Eliminate options that contradict the definition of polycythemia or ignore its physiological effects.

Take home points

• Polycythemia develops in children with chronic cyanosis to increase oxygen transport.
• While beneficial for oxygen delivery, it can increase blood viscosity, leading to complications such as thromboembolism.
• Monitoring and managing hematocrit and hydration are essential in children with cyanotic congenital heart defects.

Tricuspid atresia is a congenital heart defect characterized by absence of communication between the right atrium and right ventricle, leading to underdevelopment of the right ventricle. Definitive diagnosis requires visualization of the heart’s structure, pressure measurements, and assessment of blood oxygen saturation in the chambers.

Rationale for correct answer:

D. Cardiac catheterization provides direct measurement of pressures in the heart chambers. It determines oxygen saturation in systemic and pulmonary circulation. It also visualizes anatomic abnormalities, such as absent tricuspid valve and hypoplastic right ventricle. It guides surgical planning for staged procedures like Fontan operation.

Rationale for incorrect answers:

A. Arterial blood gas (ABG) analysis provides oxygen and CO₂ levels, but does not visualize cardiac anatomy or assess the presence of structural defects.

B. Pulmonary function tests assess lung function, not cardiac structure.

C. ECG detects electrical conduction abnormalities or chamber hypertrophy, but cannot define the precise anatomical defect like tricuspid atresia.

Test-taking strategy:

• Identify cyanotic heart defect symptoms such as cyanosis, tachypnea, murmur.
• Determine which test provides definitive anatomical diagnosis and hemodynamic data → cardiac catheterization.
• Recognize that ABG, ECG, and pulmonary tests are supportive, not diagnostic for structural heart defects.

Take home points

• Tricuspid atresia requires cardiac catheterization for definitive diagnosis and surgical planning.
• Staged surgeries (palliative shunts followed by Glenn the Fontan procedure) are planned based on catheterization data.
• Noninvasive tests (ECG, ABG, echocardiography) may support assessment but cannot confirm anatomy or shunt direction.

Tricuspid atresia is a congenital heart defect in which the right atrium cannot communicate with the right ventricle, making the right ventricle hypoplastic.

Rationale for correct answer:

B. The Fontan procedure is the definitive surgical treatment, designed to divert systemic venous blood directly to the pulmonary arteries, bypassing the underdeveloped right ventricle, and improving oxygenation in children with single-ventricle physiology. It redirects blood from the superior and inferior vena cava directly to the pulmonary arteries, eliminates the need for a functional right ventricle.

Rationale for incorrect answers:

A. Blalock-Taussig operation is a palliative procedure, not definitive. It creates a shunt between the subclavian artery and pulmonary artery to increase pulmonary blood flow temporarily in congenital heart defects like TOF. It is often used in the neonatal period.

C. Jatene procedure is used to correct transposition of the great arteries (TGA), not tricuspid atresia.

D. Patch closure is typically used to repair septal defects (ASD, VSD), not to reroute circulation in single-ventricle defects like tricuspid atresia.

Test-taking strategy:

• Identify the definitive surgical repair for single-ventricle physiology:
  • Fontan is used for tricuspid atresia or hypoplastic right ventricle
  • Blalock-Taussig is palliative for TOF
  • Jatene is used in TGA
• Eliminate procedures that do not address the absent right ventricular pathway.

Take home points

• Tricuspid atresia requires staged surgical repair, with the Fontan procedure as the final corrective surgery.
• The Fontan allows systemic venous blood to flow passively to the lungs, bypassing the nonfunctional right ventricle.
• Early recognition and staged surgery improve survival and quality of life in children with tricuspid atresia.

In tricuspid atresia, blood cannot flow from the right atrium to the right ventricle. Survival in the newborn period depends on the patent ductus arteriosus (PDA) to maintain pulmonary blood flow. Prostaglandin E1 is administered to keep the ductus arteriosus open, ensuring oxygenated and deoxygenated blood can circulate adequately.

Rationale for correct answer:

A. Administering prostaglandin E1 keeps the ductus arteriosus open, which is critical for pulmonary blood flow in ductal-dependent lesions. It provides oxygenation support until surgical intervention can be performed. This is considered a life-saving intervention in neonates with tricuspid atresia.

Rationale for incorrect answers:

B. High-flow oxygen alone does not correct the structural defect or ensure adequate pulmonary blood flow. Excessive oxygen can even reduce pulmonary vascular resistance, decreasing blood flow to the lungs in ductal-dependent lesions.

C. Feeding is important for nutrition but cannot address immediate circulatory needs. Overfeeding may increase metabolic demand and worsen hypoxemia.

D. Administering furosemide for pulmonary edema is incorrect since pulmonary edema is not typically the primary issue in ductal-dependent tricuspid atresia. Furosemide would not improve systemic oxygenation in the immediate neonatal period.

Test-taking strategy

• Ask: Which intervention maintains life in the immediate neonatal period?
• Ductal-dependent defects require maintaining patency of the ductus arteriosus until surgery.
• Prostaglandin E1 is the standard first-line intervention for survival.

Take-home points

• Tricuspid atresia in newborns is ductal-dependent; the PDA must remain open for pulmonary blood flow.
• Prostaglandin E1 is used immediately after birth to maintain ductus arteriosus patency.
• Other interventions (oxygen, nutrition, diuretics) are supportive but not life-saving in the acute phase.

Congenital heart defects (CHDs) are structural problems with the heart or nearby blood vessels that are present at birth. They affect about 1 in 100 babies and can range from mild, like small holes in the heart, to severe such as missing or underdeveloped chambers.

Rationale for the correct answers:

A. A ventricular septal defect (VSD) allows blood to flow from the left ventricle (higher pressure) to the right ventricle (lower pressure). This increases blood flow to the lungs, leading to pulmonary overcirculation and potential heart failure if untreated.

C. A patent ductus arteriosus (PDA) allows blood to flow from the aorta into the pulmonary artery. This results in excess pulmonary circulation and increased workload on the heart.

D. An atrial septal defect (ASD) permits blood flow from the left atrium to the right atrium, increasing right-sided volume and pulmonary blood flow over time. Although symptoms may be subtle early, pulmonary overcirculation is present.

Rationale for incorrect answers:

B. Tetralogy of Fallot (TOF) involves right ventricular outflow obstruction, which limits blood flow to the lungs. This results in reduced pulmonary blood flow, not increased.

E. Coarctation of the aorta is an obstructive defect, characterized by narrowing of the aorta. Pulmonary blood flow is not increased; systemic circulation is affected.

F. In tricuspid atresia, blood flow to the lungs is limited and dependent on shunts. This condition is associated with decreased pulmonary blood flow.

Test-taking strategy:

• Think “extra blood going to the lungs” caused by septal defects and PDA.
• If blood is blocked from reaching the lungs, it is not an increased pulmonary blood flow defect.

Take home points

• Defects with septal openings or persistent fetal connections increase pulmonary blood flow.
• VSD, ASD, and PDA are classic examples.

Obstructive defects and outflow tract abnormalities decrease pulmonary circulation

Children with tetralogy of Fallot (TOF) often experience hypercyanotic (Tet) spells during exertion or crying, when pulmonary blood flow decreases and right-to-left shunting increases, leading to acute hypoxia.

Rationale for correct answer:

D. Squatting increases systemic vascular resistance, which reduces the right-to-left shunt through the ventricular septal defect and forces more blood through the lungs for oxygenation. This position is instinctively adopted by children during hypercyanotic episodes or exercise. It is a classic clinical sign of TOF, often observed in toddlers and young children.

Rationale for incorrect answers:

A. Lying prone does not increase systemic vascular resistance or improve oxygenation. This position does not relieve cyanosis during Tet spells.

B. Semi-Fowler’s position does not significantly affect shunting or systemic vascular resistance.

C. Side-lying has minimal effect on pulmonary blood flow or shunt reduction. It is not a compensatory position for cyanotic spells.

Test-taking strategy:

• Identify positions that improve oxygenation in cyanotic heart defects:
  • Squatting increases systemic vascular resistance resulting in more pulmonary blood flow.
• Eliminate positions that do not affect hemodynamics (prone, side-lying, semi-Fowler’s).

Take home points

• Squatting is a compensatory position for children with TOF to relieve cyanosis during exertion or Tet spells.
• Recognizing this behavior helps nurses:
  • Identify hypercyanotic episodes early.
  • Implement supportive interventions (oxygen, calm environment, knee-chest positioning in infants).
• Other positions such as prone, side-lying, or semi-Fowler’s do not provide hemodynamic benefit in TOF.

Tetralogy of Fallot is a cyanotic congenital heart defect that causes right-to-left shunting of blood. This can lead to hypercyanotic episodes (“tet spells”), particularly during stress, crying, or exertion. Teaching parents to recognize tet spells is a key aspect of disease management and safety.

Rationale for correct answer:

B. “A child with this condition experiences hypercyanotic, or ‘tet,’ spells.” This shows that parents understand the most characteristic symptom of TOF. Tet spells involve sudden cyanosis, tachypnea and irritability, and squatting (in older children) or knee-chest positioning in infants. Recognizing tet spells allows prompt intervention to improve oxygenation, preventing severe hypoxia or cardiac arrest.

Rationale for incorrect answers:

A. “The condition is commonly referred to as ‘blue tets.’” While sometimes informally called “blue tets,” this is not the accurate medical terminology for teaching parents. Parents understanding the clinical signs and management is more important than knowing a nickname.

C. “A child with this condition experiences frequent respiratory infections.” Respiratory infections are not a hallmark of TOF. Cyanosis and tet spells are the key features, not increased infection frequency.

D. “A child with this condition experiences decreased or absent pulses in the lower extremities.” This is a classic finding in coarctation of the aorta, not TOF. Including this would indicate misunderstanding of the defect.

Test-taking strategy:

• Focus on hallmark clinical manifestations of the defect:
  • Cyanosis
  • Tet spells
  • Squatting or knee-chest positioning
• Eliminate answers that describe other cardiac defects or non-specific symptoms.

Take home points

• Tetralogy of Fallot causes right-to-left shunting, leading to cyanosis and hypercyanotic spells.
• Parental understanding of tet spells is crucial for early recognition and intervention.
• Teaching should emphasize how to identify a tet spell and immediate interventions such as knee-chest positioning, oxygen, and calming the child.
• Understanding clinical signs is more important than knowing informal names or unrelated findings.

In tetralogy of Fallot (TOF), there is a right-to-left shunt due to the ventricular septal defect and pulmonary stenosis. Determining the direction and amount of blood shunting is essential for preoperative assessment and surgical planning.

Rationale for correct answer:

D. Cardiac catheterization provides direct hemodynamic data, including oxygen saturations in the right and left heart chambers, pressure gradients across valves and septal defects, and the direction and magnitude of shunting. It is essential for surgical planning, especially if corrective or palliative procedures are considered.

Rationale for incorrect answers:

A. Chest radiography shows cardiac silhouette, pulmonary vasculature, and signs of right ventricular hypertrophy, but cannot quantify shunting or direction of blood flow.

B. Echocardiography provides structural information such as the size of VSD, degree of pulmonary stenosis, and right ventricular hypertrophy. Can estimate shunting, but cannot precisely quantify the amount or exact direction as reliably as catheterization.

C. Electrocardiography (ECG) shows cardiac rhythm, conduction delays, and ventricular hypertrophy. It does not provide information on shunt direction or magnitude.

Test-taking strategy:

• Recognize the difference between structural, functional, and hemodynamic tests:
  • Structural requires echocardiography and chest X-ray.
  • Electrical requires an ECG.
  • Hemodynamic and shunt assessment requires cardiac catheterization.

Take home points

• Cardiac catheterization is the gold standard for assessing the direction and magnitude of intracardiac shunts.
• Noninvasive tests like echocardiography provide important structural and functional information but cannot replace direct measurements.
• Accurate shunt assessment guides surgical planning and risk stratification in tetralogy of Fallot.

Hypoxic spells (also called “Tet spells”) are sudden episodes of severe cyanosis and hypoxia that occur in children with Tetralogy of Fallot (TOF), a congenital heart defect. They are most common in infants and toddlers.

Rationale for correct answers:

A. Prolonged crying increases oxygen demand, intrathoracic pressure, and agitation. This worsens right-to-left shunting and decreases oxygen delivery, commonly triggering hypoxic spells.

B. Straining during bowel movements increases intrathoracic pressure, similar to a Valsalva maneuver. This reduces pulmonary blood flow and can precipitate a hypoxic episode.

D. Dehydration increases blood viscosity, reducing effective circulation and oxygen delivery. This makes hypoxic spells more likely and more severe.

Rationale for incorrect answers:

C. Squatting is a compensatory position, not a trigger. It increases systemic vascular resistance, helping direct more blood to the lungs and relieves hypoxic spells.

E. Calm, resting states reduce oxygen demand. This situation is protective, not a trigger for hypoxic episodes.

Test-taking strategy:

• Identify situations that increase oxygen demand, stress, or intrathoracic pressure.
• Eliminate options that reduce symptoms or improve oxygenation.

Take home points

• Common triggers of hypoxic spells include crying, straining, dehydration, feeding stress, and agitation.
• Squatting or knee–chest positioning is a relief mechanism, not a trigger.
• Preventive care focuses on hydration, minimizing stress, and early intervention.

Tricuspid atresia is a congenital heart defect in which the right atrium cannot communicate with the right ventricle, resulting in limited pulmonary blood flow. Even after staged surgical repairs such as palliative shunt, bidirectional Glenn, and Fontan procedure, children often have residual cyanosis, which may persist for life.

Rationale for correct answer:

A. “My child will have this dusky color for the rest of his life.” This reflects understanding that surgery improves oxygenation but does not fully normalize it. Residual cyanosis is common in children with single-ventricle physiology after the Fontan procedure. Parents who understand this can better monitor for complications and support the child postoperatively.

Rationale for incorrect answers:

B. “These procedures will make my child have a normal heart.” This is incorrect since staged surgeries improve circulation and oxygenation, but the heart remains anatomically abnormal.

C. “Once fixed, my baby will not have to take any more medicine.” Many children require ongoing medications, such as anticoagulants, diuretics, or cardiac medications, even after surgery.

D. “My baby will be just like all of the other children once the surgeries are all done.” Children may have activity limitations, residual cyanosis, and ongoing follow-up, so they may not be identical to peers in terms of exercise tolerance or oxygenation.

Test-taking strategy:

• For congenital cyanotic heart defects requiring staged surgery, realistic understanding of outcomes includes residual cyanosis.
• Eliminate options that suggest complete anatomical correction or return to normal function.

Take home points

• Tricuspid atresia requires staged surgical intervention; surgery improves oxygenation but does not fully normalize anatomy.
• Residual cyanosis is common, and parents should be taught to monitor for signs of hypoxia and complications.
• Realistic expectations help families participate effectively in long-term care and follow-up.

Tetralogy of Fallot is a congenital heart defect caused by right-to-left shunting through a ventricular septal defect (VSD) due to pulmonary stenosis. Administering oxygen can increase the amount of oxygen in the blood that reaches the systemic circulation, but it cannot reverse the anatomical shunt.

Rationale for correct answer:

D. Hypoxia in infants often causes irritability, fussiness, and restlessness. Providing supplemental oxygen can increase arterial oxygen content slightly, which can calm the infant and reduce symptoms of hypoxia-related agitation. Oxygen is supportive but does not correct the underlying structural defect.

Rationale for incorrect answers:

A. Murmurs in TOF are caused by turbulent blood flow through the VSD and stenotic pulmonary valve. Oxygen administration does not alter the structural defect, so the murmur will persist.

B. Cyanosis is due to right-to-left shunting, which is an anatomical problem. Supplemental oxygen may slightly increase oxygen saturation, but cyanosis will not disappear in uncorrected TOF.

C. Clubbing develops over months to years due to chronic hypoxia. It cannot improve acutely with oxygen administration.

Test-taking strategy:

• Determine if the intervention can alter the anatomical defect:
  • Murmurs and cyanosis are caused by structural heart defects and are unlikely to resolve with oxygen.
  • Symptoms caused by hypoxia such as agitation and tachypnea may temporarily improve.

Take home points

• In uncorrected TOF, oxygen temporarily reduces symptoms of hypoxia but does not correct cyanosis or murmurs.
• Agitation and irritability due to hypoxia may improve with oxygen supplementation.
• Definitive treatment for TOF is surgical correction, such as intracardiac repair, to eliminate right-to-left shunting.

The infant is experiencing a hypercyanotic (Tet) spell, a life-threatening complication of TOF caused by sudden right-to-left shunting through the ventricular septal defect due to pulmonary stenosis. The priority is to improve systemic oxygenation and reduce the workload of the heart.

Rationale for correct answer:

B. Placing the infant in knee-chest position increases systemic vascular resistance (SVR) by compressing the lower extremities, which reduces right-to-left shunting, improves pulmonary blood flow, and enhances oxygenation. It helps relieve cyanosis and decrease cardiac workload during a Tet spell. Often combined with calming the infant, administering oxygen, and morphine if ordered.

Rationale for incorrect answers:

A. Placing the infant in Trendelenburg position does not effectively increase SVR and may worsen respiratory effort. It is not recommended for Tet spells.

C. Oxygen may be helpful as an adjunct, but it alone does not correct the shunting or improve SVR. Oxygen is supportive, not definitive.

D. Suctioning is only necessary if the infant has airway obstruction or secretions. It does not relieve the shunt or cardiac workload.

Test-taking strategy:

• Identify hypercyanotic signs: cyanosis, tachypnea, tachycardia, irritability.
• Determine priority intervention that directly improves oxygenation and reduces shunting.
• Remember knee-chest position is the hallmark first-line response for Tet spells.

Take home points

• Tet spells are emergencies in TOF requiring rapid intervention.
• Knee-chest positioning increases systemic vascular resistance and improves pulmonary blood flow.
• Oxygen, sedation (e.g., morphine), and supportive care are secondary interventions.
• Understanding pathophysiology of right-to-left shunt guides correct nursing actions.

Cyanosis is a bluish discoloration of the skin and mucous membranes caused by increased amounts of deoxygenated hemoglobin in the blood. In infants with cyanotic congenital heart defects, a right-to-left shunt or impaired pulmonary blood flow reduces the oxygen content of systemic blood, resulting in visible cyanosis.

Rationale for correct answer:

C. It is related to hemoglobin level and oxygen saturation: Cyanosis occurs when deoxygenated hemoglobin exceeds ~5 g/dL in capillaries. Infants with congenital heart defects often have right-to-left shunting, which decreases arterial oxygen saturation. Rapid onset of cyanosis, irritability, and pallor suggests a hypercyanotic episode or Tet spell, reflecting acute hypoxemia.

Rationale for incorrect answers:

A. It is caused by a left-to-right shunting of blood: Left-to-right shunts (e.g., VSD, ASD) typically cause acyanotic defects, leading to volume overload, not cyanosis.

B. It is associated with liver dysfunction secondary to congestive heart failure: Liver dysfunction may cause jaundice or hepatomegaly, but not acute bluish discoloration.

D. It is due to poor iron levels in the child’s body: Low iron causes anemia, which may contribute to pallor but does not cause cyanosis.

Test-taking strategy:

• Recognize that cyanosis results from increased deoxygenated hemoglobin in systemic circulation.
• Rapid-onset cyanosis in infants with cyanotic defects indicates acute hypoxemia, not chronic anemia or liver dysfunction.
• Differentiate between heart defects that cause cyanotic from those that do not cause cyanosis when explaining skin color changes.

Take home points

• Cyanosis in congenital heart defects is caused by low oxygen saturation in the blood.
• The degree of cyanosis is influenced by hemoglobin concentration and oxygen content.
• Rapid recognition and explanation help reassure parents and guide immediate interventions, such as oxygen therapy, knee-chest positioning, or notifying the provider.

Tetralogy of Fallot is a cyanotic congenital heart defect defined by four classic anatomical features. Clinical manifestations include Cyanosis, “Tet spells”, that is, sudden episodes of deep blue skin, nails, and lips after crying, feeding, or exercise, difficulty breathing, irritability, and fainting during spells.

Rationale for correct answers:

B. VSD (Ventricular septal defect) is hallmark feature of TOF. Blood shunts from right to left, contributing to cyanosis.

C. Right ventricular hypertrophy (RVH) develops secondary to increased pressure from pulmonary stenosis. It is visible on chest X-ray as a boot-shaped heart.

F. Right ventricular outflow obstruction (pulmonary stenosis) causes reduced blood flow to the lungs, leading to cyanosis. Severity of obstruction influences the degree of cyanosis and frequency of Tet spells.

G. Overriding aorta receives blood from both ventricles, contributing to systemic desaturation.

Rationale for incorrect answers:

A. ASD (Atrial septal defect) is not part of the classic TOF defects, although occasionally present as an associated anomaly.

D. Aortic stenosis is a separate congenital defect, not related to TOF.

E. Hypoplastic left heart syndrome is a different cyanotic defect involving underdevelopment of the left ventricle and aorta, unrelated to TOF.

Test-taking strategy:

• Recall “TOF = 4 defects” mnemonic:
  • V – VSD
  • R – Right ventricular hypertrophy
  • O – Overriding aorta
  • P – Pulmonary stenosis (right ventricular outflow obstruction)
• Eliminate options not part of the classic four defects.

Take home points

• TOF is a cyanotic heart defect caused by VSD, RVH, pulmonary stenosis, and overriding aorta.
• Severity of pulmonary stenosis determines cyanosis and frequency of Tet spells.
• Understanding the anatomical defects is critical for nursing assessment, monitoring, and parental teaching.

A Tet spell is an acute episode of severe hypoxia in infants with TOF, often triggered by crying, feeding, or agitation. It is characterized by cyanosis, tachypnea, irritability, and a fetal (knee-chest) position. Immediate nursing intervention aims to increase pulmonary blood flow, reduce right-to-left shunting, and calm the infant.

Rationale for correct answer:

A. Administer oxygen and morphine as ordered: Oxygen increases arterial oxygen saturation but does not fully correct the shunt. It is a supportive measure. Morphine reduces infant agitation and respiratory effort. It also decreases systemic vascular resistance, helping improve pulmonary blood flow. Combined with knee-chest positioning, these interventions are the first-line response to a Tet spell.

Rationale for incorrect answers:

B. Raise the head of the bed and increase the oxygen by 2 L: Raising the head of the bed reduces systemic vascular resistance, which worsens right-to-left shunting. 100% oxygen via face mask should be administered.

C. Call the pediatrician immediately: While notifying the provider is important, initial stabilization is the priority. Waiting could delay lifesaving interventions.

D. Call a code: A code is only indicated if the infant is unresponsive, pulseless, or in cardiopulmonary arrest. Immediate interventions can often resolve Tet spells without resuscitation.

Test-taking strategy:

• Identify Tet spell signs: cyanosis, dyspnea, irritability, fetal (knee-chest) position.
• Recognize priority interventions:
  • Knee-chest positioning to increase SVR
  • Oxygen administration
  • Morphine to calm the infant
• Rescue medications and code activation come after immediate stabilization.

Take home points

• Tet spells are emergencies in TOF requiring rapid nursing action.
• Oxygen, morphine, and knee-chest positioning are the first-line interventions.
• Early intervention prevents hypoxic injury and cardiopulmonary arrest.
• Education of parents to recognize Tet spells and assist with positioning is critical for home management.

Congenital heart defects are structural abnormalities of the heart present at birth. They are primarily classified by how blood flows through the heart and lungs, which affects oxygenation and cardiac workload.

Rationale for correct answers:

C. Defects with increased pulmonary blood flow: Blood is shunted to the lungs, often causing tachypnea, heart failure, or pulmonary congestion. Examples are VSD, ASD, PDA. Left-to-right shunts increase pulmonary circulation without causing initial cyanosis.

D. Defects with decreased pulmonary blood flow: Pulmonary blood flow is restricted, resulting in cyanosis due to right-to-left shunting. Examples are tetralogy of Fallot, tricuspid atresia. Pulmonary obstruction and right-to-left shunts cause cyanosis.

E. Mixed defects: Blood flow involves both systemic and pulmonary circulations in abnormal patterns, as in transposition of the great arteries. Examples include transposition of the great arteries, truncus arteriosus. Oxygenated and deoxygenated blood mix in abnormal patterns, causing variable cyanosis and heart failure.

F. Obstructive defects: Blood flow is impeded by narrowing or blockage of valves or vessels, as in coarctation of the aorta or aortic stenosis. Examples include coarctation of the aorta, aortic stenosis, pulmonary stenosis. Narrowed valves or vessels increase cardiac workload and may cause congestive heart failure.

Rationale for incorrect answers:

A. Cyanotic defect: This is an older, traditional classification. While still used colloquially, they are considered outdated for clinical classification. While this term describes clinical presentations, it is not the official hemodynamic classification used in CHD taxonomy.

B. Acyanotic defect: This is an older, traditional classification. While still used colloquially, it is considered outdated for clinical classification because an "acyanotic" defect (like a large VSD) can eventually cause cyanosis if it leads to Eisenmenger syndrome.

G. Pansystolic murmurs: This describes a heart sound, not a classification of CHD.

Test-taking strategy:

• Focus on hemodynamic changes rather than clinical symptoms or auscultatory findings.
• Identify whether the defect affects pulmonary blood flow, systemic blood flow, or both, and whether there is obstruction.

Take home points

• CHDs are classified by how blood flows:
  • Increased pulmonary blood flow
  • Decreased pulmonary blood flow
  • Mixed defects
  • Obstructive defects
• Terms like cyanotic/acyanotic or murmur type are descriptive but not part of the classification system.
• Understanding these classifications guides nursing assessment, monitoring, and intervention priorities.

Hypoxic spells or “Tet spells” occur when there is a sudden decrease in oxygen saturation, leading to systemic hypoxemia. Chronic or repeated hypoxic episodes can cause physiologic and neurologic complications due to prolonged oxygen deprivation and compensatory mechanisms.

Rationale for correct answers:

A. Polycythemia: Chronic hypoxia stimulates erythropoietin production, increasing red blood cell count. This is a compensatory mechanism to improve oxygen-carrying capacity.

B. Blood clots: Increased blood viscosity from polycythemia can lead to thrombosis, increasing the risk for clots.

C. Cerebrovascular accident (CVA): Hyperviscosity and decreased cerebral oxygenation increase the risk of stroke in infants with cyanotic CHDs.

D. Developmental delays: Repeated hypoxia affects brain development, potentially resulting in cognitive and motor delays.

F. Brain damage: Severe or prolonged hypoxia can cause neuronal injury, leading to permanent neurological deficits.

Rationale for incorrect answers:

E. Viral pericarditis: Pericarditis is inflammatory and caused by infections, not directly by hypoxic spells.

G. Alkalosis: Hypoxic spells often lead to metabolic acidosis due to anaerobic metabolism, not alkalosis.

Test-taking strategy:

• Focus on complications of hypoxia and polycythemia.
• Consider effects on blood, brain, and development.
• Eliminate options that are infection-related or unrelated to oxygenation.

Take home points

• Hypoxic spells in infants with cyanotic CHDs can lead to:
  • Polycythemia causes hyperviscosity resulting in blood clots and CVA.
  • Neurological consequences include brain damage, developmental delays.
• Prompt recognition and management of hypoxic spells are critical to prevent long-term complications.

A Tet spell is an acute episode of cyanosis, hypoxia, and dyspnea in infants with tetralogy of Fallot, often triggered by crying, feeding, or agitation. The goal of nursing intervention is to increase pulmonary blood flow, reduce right-to-left shunting, calm the infant, and manage cardiac workload. Immediate, appropriate interventions prevent hypoxic injury and cardiopulmonary compromise.

Rationale for correct answers:

A. Placing the infant in a knee-chest position increases systemic vascular resistance, reducing right-to-left shunting. It improves pulmonary blood flow and oxygenation. This is a first-line intervention during Tet spells.

C. Morphine reduces agitation and hyperpnea, which decreases oxygen demand. It helps relax infundibular spasm in the right ventricular outflow tract. In preterm infants, IM route is sometimes used if IV access is not immediately available.

D. Using a calm and comforting approach reduces stress and agitation, preventing further hypoxia. It supports effective breathing and oxygenation.

E. Administering oral propranolol (Inderal®), a beta-blocker prevents or reduces infundibular spasm, decreasing the frequency and severity of Tet spells. It can be used as prescribed for ongoing management.

Rationale for incorrect answers:

B. Administering 2 L of oxygen via nasal cannula is incorrect since the infant should receive 100% oxygen via face mask in this condition and not 2L via nasal cannula.

F. Surgery may be planned electively, but acute Tet spell management is medical and nursing stabilization, not immediate surgery.

Test-taking strategy:

• Identify acute signs of a tet spell: cyanosis, dyspnea, irritability, fetal position.
• Prioritize interventions that:
  • Increase pulmonary blood flow (knee-chest)
  • Reduce agitation (morphine, calm approach)
  • Administer medications that reduce infundibular spasm (propranolol)
• Ensure accurate oxygen dosing during a tet spell where 100% oxygen should be administered via face mask.
• Surgery is a secondary consideration in acute management.

Take home points

• Tet spells are life-threatening emergencies in TOF requiring rapid intervention.
• First-line nursing actions:
  • Knee-chest positioning
  • Morphine administration
  • Calm environment
  • Propranolol if prescribed
• Oxygen is supportive, not definitive.
• Early recognition and intervention prevent hypoxic injury and potential cardiac arrest.

Infants with unrepaired congenital heart defects, especially cyanotic or left-to-right shunt defects, are at higher risk for respiratory infections, including RSV, which can cause severe bronchiolitis and pneumonia. Prevention of RSV infection is a key health promotion strategy for these infants.

Rationale for correct answer:

A. Vaccinate against the respiratory syncytial virus (RSV) monthly during the RSV season: Palivizumab (Synagis®) is a monoclonal antibody given monthly during RSV season to high-risk infants, including those with CHD. Prevents severe RSV infection, which can exacerbate heart failure or hypoxia. Evidence-based primary prevention strategy for infants with unrepaired CHD.

Rationale for incorrect answers:

B. Restrict the child’s level of physical activity: Mild activity restriction may be recommended only if fatigue or cyanosis occurs, but normal age-appropriate activity should be encouraged to promote development.

C. Encourage weight loss by restricting caloric intake: Infants with CHD often struggle with growth due to increased caloric needs; restricting intake is contraindicated. Nutrition should focus on adequate calories and growth support.

D. Delay immunizations as the child’s immune system may be too impaired: Most infants with CHD should receive routine immunizations on schedule, as their immune systems are generally functional. Delaying vaccines increases infection risk, which is dangerous for these high-risk infants.

Test-taking strategy:

• Consider preventive strategies for infants with CHD including infection prevention, nutrition, growth, and immunizations.
• Eliminate options that restrict growth or delay standard preventive care.
• RSV prophylaxis is specific to high-risk infants with heart defects.

Take home points

• RSV vaccination (palivizumab) is a priority preventive measure for infants with unrepaired CHD.
• Encourage adequate nutrition and normal activity; avoid unnecessary restrictions.
• Routine immunizations should continue on schedule.
• Early prevention of infections reduces hospitalizations, complications, and hypoxic events.