A 1-month-old boy is brought to the emergency department due to poor feeding. Over the past 2 weeks, the patient has been breathing harder and faster during feeds with associated diaphoresis and pallor. He has not had fever and has never turned blue, stopped breathing, or lost consciousness. The patient has no sick contacts. Medical history is unremarkable, and he takes no daily medications. Temperature is 36.7 C (98 F), blood pressure is 90/46 mm Hg, pulse is 124/min, and respirations are 62/min. Oxygen saturation is 95% on room air. There is no stridor. Mild retractions are present. Physical examination reveals a 4/6 holosystolic murmur at the left lower sternal border associated with a palpable thrill. The lungs have rales at both bases. The liver is palpable 3 cm below the right costal margin. Which of the following is the most likely cause of this patient's clinical presentation?

Question

A 1-month-old boy is brought to the emergency department due to poor feeding.  Over the past 2 weeks, the patient has been breathing harder and faster during feeds with associated diaphoresis and pallor.  He has not had fever and has never turned blue, stopped breathing, or lost consciousness.  The patient has no sick contacts.  Medical history is unremarkable, and he takes no daily medications.  Temperature is 36.7 C (98 F), blood pressure is 90/46 mm Hg, pulse is 124/min, and respirations are 62/min.  Oxygen saturation is 95% on room air.  There is no stridor.  Mild retractions are present.  Physical examination reveals a 4/6 holosystolic murmur at the left lower sternal border associated with a palpable thrill.  The lungs have rales at both bases.  The liver is palpable 3 cm below the right costal margin.  Which of the following is the most likely cause of this patient's clinical presentation?

Quizplus · Accepted Answer

11ec25c8_d63e_a855_bc81_89a30fa08d72_MD0003_00 This infant exhibits signs of heart failure and a holosystolic murmur at the left lower sternal border, characteristic findings of a ventricular septal defect (VSD). In utero, this abnormal communication between the right and left ventricles has no hemodynamic consequence due to nearly equivalent right- and left-sided cardiac pressures (ie, high pulmonary vascular resistance [PVR]). At birth, the lungs replace the placenta as the site for oxygenation, and PVR and right-sided pressures drop, creating a left-to-right shunt of oxygenated blood through the VSD. ventricular septal defect (VSD) With a large VSD, the right ventricle becomes volume overloaded with flow from both the right atrium and left ventricle. In turn, pulmonary blood flow and left-sided blood return increase. To maintain systemic blood flow, left ventricular (LV) output increases but cannot keep up with the increased blood return, resulting in high-output cardiac failure. Symptoms from both the high-output LV failure and pulmonary overcirculation include increased work of breathing (eg, tachypnea, retractions), tachycardia, diaphoresis, and pallor, particularly during times of exertion (eg, feeding in infants). Bilateral rales from increased extravascular transudate in the lungs and a palpable thrill due to turbulent intracardiac flow may be present. Signs of right-sided heart failure (eg, hepatomegaly) are also common. (Choice A) Heart failure from VSD is due to the inability of the left ventricle to keep up with left-sided volume overload despite normal or increased output. LV contractility remains normal. (Choice B) Impaired LV diastolic relaxation can occur with the concentric LV hypertrophy that occurs with chronic LV pressure overload (eg, systemic hypertension). By contrast, VSD involves LV volume (rather than pressure) overload with compensatory eccentric hypertrophy and an increase in diastolic filling capacity. eccentric hypertrophy (Choice C) LV afterload is decreased, not increased, with VSD because the connection to the right ventricle provides a relatively low resistance pathway for LV outflow. (Choice E) An untreated VSD can cause pulmonary vascular disease due to the prolonged increase in pulmonary blood flow. Rising PVR eventually leads to a reversal of the intracardiac shunt to right-to-left flow (Eisenmenger syndrome), causing cyanosis, which is not seen here. Eisenmenger syndrome Educational objective: Ventricular septal defects (VSDs) cause left-to-right shunting that leads to volume overload of the right ventricle, increased pulmonary circulation, and volume overload of the left side of the heart. In infants, VSDs may present with tachypnea, tachycardia, and poor feeding due to high-output heart failure and pulmonary overcirculation. References: Ventricular septal defect. (http://www.ncbi.nlm.nih.gov/pubmed/29261884)

A 1-Month-Old Boy Is Brought to the Emergency Department Due