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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.

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

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

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

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

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

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

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

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

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.

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.

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

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

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.

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

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.

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.

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.

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

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.

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

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.

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.

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

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

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.

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